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+A 9-year-old girl with Alagille syndrome was referred to our hospital. She had been diagnosed with biliary atresia at the age of 1 month and treated with surgical bile duct reconstruction, vitamins D and K, and ursodeoxycholic acid. However, her liver dysfunction and hyperbilirubinemia worsened. When she was running during physical education, she suddenly felt an acute pain in her right knee. She could not walk and was taken to the emergency department of another hospital. She was found to have a sustained pathological fracture of the right femoral shaft and was treated with skeletal traction. However, repositioning the fractured bone was difficult. Because of her low weight (19 kg), application of skeletal traction with a heavy weight was difficult. On examination, she was malnourished with stunted growth (height: 126 cm, < 3rd centile; weight: 19 kg, < 3rd centile). She had most of the features of Alagille syndrome, including a characteristic face, mild peripheral pulmonary artery stenosis, butterfly vertebrae, posterior embryotoxon, and hyperbilirubinemia. Blood tests revealed anemia (hemoglobin, 8.3 mg/dL) and liver dysfunction with high serum aspartate transaminase (186 U), alanine aminotransferase (253 U), gamma-glutamyl-transpeptidase (1445 IU/L), serum total cholesterol (23.5 mmol/L), and serum alkaline phosphatase (3546 U) levels, as well as hyperbilirubinemia (218.9 μmol/L). Radiographs showed a left femoral shaft fracture (Orthopaedic Trauma Association classification: 32–A3.2) . Elastic nailing was considered; however, because of her narrow intramedullary canal, this was judged to not be a viable fixation method. Furthermore, we wanted to prevent increased bleeding caused by use of a locking plate because of the anemia. The left femur was osteoporotic, with beaking and cortical thickening . Therefore, there appeared to be a risk of pathological fracture of the left femur. We decided to use a closed indirect reduction technique with an Ilizarov ring fixator and to decrease bleeding. One day after admission to our institute, Ilizarov ring fixator surgery was performed with the patient under general anesthesia in the supine position without a thigh tourniquet. For the Ilizarov technique, a closed indirect reduction technique was performed under image guidance, by first using ligamentotaxis to compress the fracture ends . Repositioning was simple and complete. There was no need to open the fracture site, fixation was stable, and the growth plate was preserved. The tota1 operative time was 69 minutes. The hemog1obin concentration decreased from 8.3 mg/dL preoperative1y to 8.1 mg/dL the next day. This patient was not transfused. Immediately after surgery, treatment with a low-intensity pulsed ultrasound stimulation (LIPUS) device (SAFHS 2000, Exogen, Inc., Piscataway, NJ) was started for 20 min/day in September 2000. This device had a frequency of 1.5 MHz, a signal burst width of 200 microseconds, a signal repetition frequency of 1 kHz, and an intensity of 30 mW/cm2. There was no need for additional external immobilization. Physical therapy involving walking with weight-bearing on the operated leg was started immediately after surgery. The patient could walk without any support 1 week later. The hospital stay was 14 days. The patient was well after being discharged from hospital and enjoying school life with the frame. Use of LIPUS was continued, and the patient was allowed to walk without crutches. Radiographs showed healing of the fracture at 53 days postoperatively . In such cases, before actually removing the frame, the patient may be allowed full weight-bearing, in which all the uprights connecting the proximal and distal segments of the bone are disconnected, and the patient is asked to use the limb in a functional manner with weight-bearing for the lower limb for 3 weeks. This was performed in our case. Seventy-four days postoperatively, the frame was removed, and the patient had anatomically and functionally recovered. Two years postoperatively, there was no leg-length discrepancy and no angular malalignment of the lower extremities as determined clinically and radiographically. Furthermore, 2 years postoperatively, the range of motion of the hip, knee, and ankle of the patient’s operative leg matched the range of motion in the nonoperative leg .

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+A 41-year-old primigravid woman, at 18 weeks gestation, with acute liver failure was referred to our transplant center for a trans-jugular liver biopsy and assessment for a potential liver transplant. Past medical history was unremarkable. The patient exhibited a ten-day history of persistent fever, headache, and acute hepatitis. Despite outpatient treatment with amoxicillin, cefixime, and acetaminophen, up to 1 gr three times per day for seven days, her symptoms did not improve. At admission (day zero), she was febrile (T 38.7 °C), alert, oriented, and hemodynamically stable. Physical examination revealed severe asthenia, pallor, sub-icteric sclera, and abdominal pain. Laboratory findings showed anemia (hemoglobin 8.3 g/dL), lymphopenia (1.4 × 103/μL), elevated transaminases (AST 7864 units/L, ALT 3012 units/L), hypoalbuminemia (1.5 g/dL), INR 1.4, increase in total bilirubin (1.6 mg/dL), and creatinine was 0.57 mg/dl. Inflammatory markers were elevated, with C-reactive protein (CRP) at 136 mg/L, (normal value 0–5 mg/L) procalcitonin (PCT) at 10.3 ng/mL, and ferritin at 36,185 ng/mL. Minimal peri-hepatic ascites was observed on abdominal ultrasound. Empiric antibiotic treatment with meropenem was initiated. The pathologist, at first evaluation of urgent liver biopsy, observed cytolytic liver damage with extensive centrilobular necrosis (acinar zone 3), suggestive of drug-induced damage. On day one after admission, the peripheral blood smear showed activated reactive and apoptotic lymphocytes. Serological tests for hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), cytomegalovirus (CMV), toxoplasmosis, and hepatitis E virus (HEV) were negative for acute infection. The plasma viral load of HSV-1 and 2, CMV, adenovirus, and varicella-zoster virus (VZV) was negative. Fecal samples tested negative for adenovirus, and molecular testing for respiratory viruses was also negative.
+Despite a negative HSV-1 and -2 viral load, serological analysis demonstrated positive HSV-1/2 IgM and borderline IgG antibodies. Consequently, a histological review of the liver biopsy was requested, revealing numerous cells with viral nuclear inclusions and a highly suggestive morphology for herpes virus cytopathic effects. Immuno-histochemical staining and real-time polymerase chain reaction (PCR) for HSV-2 were positive in the hepatic tissue , confirming the diagnosis. This was a primary HSV infection rather than a reactivation, as confirmed by the fourfold rise in IgG title observed four weeks after the first serological evaluation.
+Acyclovir treatment was initiated, leading to a progressive reduction in transaminases and inflammatory markers . However, on the fourth day, the patient’s clinical condition deteriorated, concomitantly with the development of anasarca attributed to severe hypoalbuminemia (1.8 g/dL) and an elevation in total bilirubin level (5.25 mg/dL). On the following day, the HSV-2 viral load became detectable, quantified at 28.750.000 copies/mL. The observed increase in inflammatory markers and high serum ferritin, despite optimized HSV-2 treatment, raised concerns of unregulated hyper-inflammation suggestive of a cytokine storm. Probability of hemophagocytic lymphohistiocytosis (HLH) using H score was 25–40% on day 4 and 80–88% on day 5 [, ]. By considering that steroids are usually not recommended in acute HSV infections and that cyclosporin may be unsafe during pregnancy .
+We decided to administer human polyvalent immunoglobulin at a dose of 400 mg/kg/day for five days . The patient started to recover with a reduction in H score (with probability of HLH 25–40% on day 7, 8, 10, and 16–25% on day 12), inflammatory markers and in HSV-2 viral load to 1.361.205 copies/mL within one week. The patient became afebrile while HSV-1/2 DNA on the vaginal swab remained detectable. Thus, we recommended a cesarean delivery.
+After a total hospital stay of 20 days, including 19 days of acyclovir treatment, the patient was discharged with normalized inflammatory markers and recovery of liver function. On the follow-up visit, a month after discharge, she was asymptomatic with a viral load of HSV-2 of 120 copies/mL and a detectable HSV-1/2 vaginal swab. Obstetric examination revealed no discernible abnormalities in the fetus. The patient underwent a cesarean delivery at 33+s3 weeks of pregnancy. The newborn was a healthy girl with a birth weight of 1800 gr. HSV-1/2 DNA in plasma and cerebrospinal fluid of the newborn was undetectable. Both mother and baby are alive and well at the 6-month follow-up.
+Using Luminex technology and the R software tool (version 4.1.2), we retrospectively analyzed plasma cytokine levels (stored at − 80 °C until their use) at five designated time points (day: 0–3–4–18–62) and correlated them with the clinical data after a z-score transformation. The heatmap generated in Fig. E revealed three discernible temporal biomarker clusters. The first cluster, represented by the acute phase (day 0 and day 3 after admission) in the absence of viremia, revealed an impaired specific antiviral immune response and, conversely, the production of cytokines and chemokines, including monokine induced by interferon-gamma (MIG), interferon-gamma (IFNγ), hepatocyte growth factor (HGF), monocyte chemoattractant protein-1 (MCP-1), interferon-gamma induced protein-10 (IP-10), C–C motif chemokine ligand 11 (CCL-11), and interleukin-8 (IL-8), IL-6, IL-1RA, IL-2R, and IL-10, all involved in inflammation. This profile was accompanied by increased hepatic (AST, ALT, bilirubin, gamma-GT, alkaline phosphatase, INR) and inflammatory (CRP, PCT, LDH, ferritin) biomarkers. In the second cluster, the viremic phase (day 4–18), we observed a reduction in the aforementioned inflammatory profile and an increase in total bilirubin, WBC, and neutrophils. Finally, in the third cluster (day 62, follow-up), we observed a complete recovery of hepatic markers and an increase in different cytokines involved in antiviral immunity, suggesting the onset of T cell responses involved in viral clearance and recovery from the infection. In Fig. F, we show the pairwise Pearson correlation analysis, which associates cytokine expression levels and laboratory values across the five-time points.

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+A 25 year old Sinhalese Sri Lankan female presented with a 1 day history of bilateral lower limb weakness, and numbness with urinary incontinence. She had no back pain and no history of constitutional symptoms such as fever, loss of appetite, or recent subjective weight loss.
+On examination she had atonic lower limbs, with absent muscle power, and absent bilateral lower limb reflexes below knee level, with sensory impairment up to T6 level. She had no spinal deformities or tenderness, and no papilloedema. Upper limb examination was unremarkable except for a hard non tender bony mass on the left scapular region. She had a blood pressure of 140/80 mmHg, pulse rate of 78 beats per minute and had no respiratory compromise.
+She was investigated with a suspicion of metastatic disease and X-ray of the left shoulder showed a soft tissue and bony mass on the dorsal aspect of the left scapula with multiple lytic lesions suggestive of a primary bone neoplasm , but chest radiograph, ultrasound scan of the neck, and Computed tomography (CT) of abdomen were normal. Magnetic resonance imaging (MRI) of the spine showed an intradural extramedullary mass with an extra spinal component at C7-T2 level causing severe cord compression , hence intravenous dexamethasone regimen was started.
+Ultrasound guided core needle biopsy from the left scapular mass showed malignant small round blue cell tumour suggestive of Ewing sarcoma. Blood investigations showed Heamoglobin of 9.2 g/dl, white blood cell count of 12 × 103/μl, Erythrocyte sedimentation rate (ESR)of 150 mm/h, C-reactive protein level of 96 mg/l, normal liver enzyme levels and liver functions tests, and serum alkaline phosphate level of 173 μ/l. Her blood picture showed increased rouleaux formation with anaemia of chronic disease.
+She had no improvement of symptoms following treatment with dexamethasone. Before implementing on oncological management, 3 days after onset of symptoms, she developed sudden onset progressive ascending neurological impairment with upper limb and bulbar involvement, and unfortunately resulted with respiratory failure and death.

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+A 10-year-old white girl presented to our emergency room in January 2015 with a 1-month history of headache and morning vomiting. On examination, she appeared slightly pale, with body temperature of 36.5 °C, heart rate of 90 beats per minute, blood pressure of 106/62 mmHg, respiratory rate of 18 breaths per minute, and oxygen saturation of 100% in ambient air. Her neurological status was normal. Laboratory test results are shown in Table . A chest X-ray was within limits. An urgent non-enhanced brain computed tomography (CT) scan showed a focal lesion in the left frontal subcortical region with prominent surrounding edema and mass effect . She was therefore admitted to our hospital. Magnetic resonance imaging (MRI) demonstrated ring enhancement on post-contrast T1-weighted (T1W) sequences; fluid-attenuated inversion recovery (FLAIR) sequences confirmed extensive vasogenic edema . She lived with her parents and siblings in Southern Italy. Before the onset of the current illness, at 5 years of age she had undergone surgical excision of a pleomorphic adenoma of the parotid gland. No evidence of a pre-existing congenital airway malformation was referred. She was not sexually active, and she did not smoke cigarettes, drink alcohol, or use illicit drugs. Her father, a heavy tobacco smoker, was a merchant. Her mother, a housewife, reported three miscarriages. Her maternal grandfather had died from colon cancer at 40 years. Her paternal aunt was affected by , and a second-degree cousin presented ovarian immature teratoma. After multidisciplinary discussion, neuronavigation and left frontal craniotomy with tumor resection with direct cortical and subcortical stimulation was done under general anesthesia. She received preoperative steroid medication which was tapered post-surgery. MRI scanning within 72 hours after surgery documented total resection .
+Microscopy on tissue sections showed malignant neoplasms with extensive necrosis, composed of atypical columnar and cuboidal cells, which had vesicular nucleolated nuclei and eosinophilic cytoplasm. Tumor cells covered papillary structures with fibrovascular cores or formed small glands and micropapillae lacking stroma. The surrounding brain parenchyma showed evidence of reactive gliosis and lymphohistiocytic infiltrate . On immunohistochemical examination, neoplastic cells were positive for cytokeratin 7, thyroid transcription factor 1 (TTF-1) , cytokeratin AE1/AE3, and epithelial membrane antigen (EMA), whereas all other markers tested were negative: cytokeratin 20, carcinoembryonic antigen (CEA), thyroglobulin, vimentin, cluster of differentiation (CD) 10, WT1, calretinin, inhibin, CD117, CD30, S100 protein, melan-A, actin, chromogranin, synaptophysin, and glial fibrillary acidic protein (GFAP). INI1 expression was retained. Thus, a diagnosis of metastatic lung adenocarcinoma was proposed. A chest CT scan showed a parenchymal nodular lesion in the lower lateral basal segment of the right lobe, measuring 32 mm × 18 mm × 17 mm, thought to be the primary lung cancer with mediastinal nodal metastasis. Tumor spread was confirmed by positron emission tomography (PET)/CT showing a primary lung tumor and with high fluorodeoxyglucose (FDG) uptake: maximum standardized uptake value (SUVmax) of 8.5 and 8, respectively .
+At fluorescence in situ hybridization (FISH) analysis, no rearrangements of anaplastic lymphoma kinase (ALK), c-ros oncogene 1, receptor tyrosine kinase (ROS1), and rearranged during transfection (RET) genes were found. ROS1 gene was found deleted in 57% of neoplastic cells. Next generation sequencing (NGS) analysis was applied to genomic deoxyribonucleic acid (DNA) extracted from formalin-fixed paraffin-embedded tissue. Both the “Cancer Hotspot Panel” (50 genes) and the “Comprehensive Cancer Panel” (444 genes) through the Personal Genome Machine with Ion Torrent™ technology (Life Technologies, Applied Biosystems) were applied. NGS analyses with Comprehensive Cancer Panel highlighted the presence of multiple non-targetable mutations in fms-related tyrosine kinase 4 (FLT4), ubiquitin-protein ligase E3 component N-recognin 5 (UBR5), ataxia telangiectasia mutated (ATM), and TATA-box binding protein associated factor 1 (TAF1). Epidermal growth factor receptor (EGFR) mutation status was negative.
+One month after admission our patient started chemotherapy treatment for NSCLC with cisplatin and vinorelbine for six cycles over a 5-month period. Two months later, an MRI 3 months after diagnosis revealed cerebral recurrence; therefore, she underwent a second surgical resection, followed by radiosurgery (CyberKnife). A brain MRI and PET/CT scan after completion of her last dose of chemotherapy showed absence of cerebral metastasis and partial regression of the lesion of the lower lobe of her right lung (RLL); thus, between 7 and 8 months after admission she received adjuvant thoracic radiation therapy. Unfortunately, 1 month later surveillance imaging revealed lung tumor progression and multiple brain metastases. She subsequently started whole brain radiotherapy (WBRT) and three cycles of docetaxel. One year after admission a rapid lung tumor progression was documented. One month later she developed headache and vomiting due to increased cerebral edema and growth of brain metastases. Therefore, she started corticotherapy and third-line pemetrexed treatment (five cycles), but 5 months later a PET/CT scan revealed further worsening of intracranial lesions and skeletal metastases. She underwent radiosurgery by CyberKnife technique on brain metastases and the following month she received nivolumab at 3 mg/kg intravenously every 2 weeks compassionately. Due to worsening of clinical conditions, a month later PET/CT was performed, revealing disseminated (skeletal, pulmonary, cerebral, lymphonodal) disease. She continued nivolumab, receiving a total of five cycles without adverse events. Given the ongoing clinical and imaging deterioration, palliative treatment was initiated and she died of respiratory failure 23 months after diagnosis of metastatic lung adenocarcinoma . Autopsy was declined by parents.

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+A 74-year-old man was intubated in emergency for acute ischemic stroke, and then referred to Anesthesiology and Intensive Care Unit of our hospital. The patient’s medical history included cardiac disease and COPD. PDT was then performed, and patient returned to spontaneous breathing 15 days later. Despite systemic administration of broad-spectrum antibiotics (Vancomycin, Cefepime, and Azithromycin), he developed APF following necrotizing pneumonia that complicated with pneumothorax, empyema and subcutaneous emphysema . A 32 French tube was placed at the 5th intercostal space anterior axillar line with drainage of 1.500 l of brownish, putrid, and foul-swelling fluid. A negative suction (− 20 mmHg) was applied to chest drainage and daily chest X-ray showed the expansion of upper and middle lobe, but a loculated pneumothorax within lower lobe was seen on chest CT scan performed 15 days . A second 28 French chest tube was then placed using ultrasound as guide at the 8th intercostal space posterior axillar line with drainage of 500 mL of purulent material. The microbiological cultures of pleural fluid showed the presence of Pseudomonas aeruginosa; thus, ofloxacin (400 mg every 12 h) and ceftazidime (2 g every 8 h) were intravenously administered, in addition to clindamycin to provide empiric coverage against anaerobes and gram-positive cocci bacteria. The pleural space was also irrigated with 0.1% povidone-iodine solution (Betadine; 40 mL/h) until the eradication of pleural infection was obtained. However, the formation of dense adhesions trapped the lower lobe, and prevented its expansion ; yet, the persistence of large bubbles in the drainage suspected the presence of APF. Methylene blue (1 ampoule diluted in 1-l saline solution) was injected via chest drainage into the pleural cavity, and was bronchoscopically identified within RB9 segment . The resolution of air leaks obtained by occluding the RB9 segment with an inflated-balloon catheter confirmed it to be the culprit segment. Thus, a Zephyr 5.5 EBV (Zephyr, PulmonX Corporation-Redwood City, CA, USA) was placed within RB9 segment with temporary resolution of air leaks that recurred 4 days later due to valve dislocation. The valve was removed and the RB9 segment closed by intrabronchial injection of 10 mL of FG (Tisseel: Baxter Healthcare Corp, Deerfield, IL, USA) . The procedure was repeated twice at 1-week interval, but in both cases the fibrin clot dislocated.
+Finally, fiber bronchoscopy, introduced through the chest drainage, explored the pleural cavity and showed a small APF that was marked by methylene blue following intrabronchial injection of the blue solution within RB9 segment . The APF was filled by 20 mL of FG using a dedicated double-lumen catheter introduced through the working channel of fiber bronchoscopy . Furthermore, the RB9 segment was occluded by intrabronchial injection of 10 mL of FG. The chest drainage was then clamped, and a bronchial blocker was left with the balloon inflated within intermedius bronchus to prevent the intrapleural, and intrabronchial dislocation of fibrin clot, respectively. Two days later, the bronchial blocker was deflated, and the chest drainage opened. No recurrence of air-leaks occurred; drainage of non-purulent fluid was < 100 mL/24 h; chest CT scan showed no evidence of worsening pneumothorax, and of progressive subcutaneous emphysema; thus, chest tube was removed . Patient was then transferred to a rehabilitation center. He died 11 months later for cardiac failure. The entire procedure was summarized in Additional file 1: Video S1.

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+A 48-year-old Chinese woman with no smoking history presented to the Union Hospital of Tongji Medical College of Huazhong University of Science and Technology in October 2020 for chest tightness and chest pain. The 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) revealed a soft tissue density shadow in the right lower lobe with a size of 3.4*2.4 cm; enlarged bilateral supraclavicular and mediastinal lymph nodes, thickened bilateral pleura and increased pericardial effusion were metabolism increased; the metabolism in thoracic vertebrae T4, lumbar vertebrae L1, L5, and right ilium were also increased . Baseline lung enhanced CT images are shown in . Brain MRI showed no abnormalities . In October 2020, the patient underwent ultrasound-guided pericardiocentesis of pericardial effusion. Upon pathological examination of the pericardial effusion, cancer cells were detected, which was consistent with lung adenocarcinoma . Immunohistochemistry yielded the following: PCK (+), TTF-1(+), i+), CK5/6 (–), EGFR (–), C-met (–), Ros-1 (–), ALK (+). Next-generation genetic sequencing (whole-exome sequencing by company of gloriousmed) suggested the ALK EML4 (, ) - ALK (, ) fusion. Variant allele frequency (VAF) was 3.81%. Another driver mutation was CUX1 (mutation region: chr7: 101821924, 11 exon c.1004delA, p. Asn335fsTer20, VAF 1:00%), and others were somatic mutations of no clinical value, such as INPP4A, MED12, CDC73, CIC, SACS, NOTCH3, ARID2, RPS2, IRS2, INHA. Therefore, the patient was initially diagnosed with lung adenocarcinoma stage cT2N3M1c IVB with EML4-ALK gene fusion (AJCC 8th Edition). She started treatment with crizotinib (p.o. 250 mg bid) in October 2020 for financial reasons. In January 2021, the patient’s lung CT showed that the lesion in the lower lobe of the right lung was 2.2*1.7 cm, and the pericardial effusion was significantly reduced (. According to the criteria of resist1.1, the therapeutic effect was evaluated as partial response (PR). The patient started to have headache and dizziness in September 2021, and brain MRI showed that the pituitary gland was full in shape on September 7, 2021, approximately 1.4*1.4*1.3 cm in size, and the lung lesion was stable . Then, a lumbar puncture was performed, and no significant abnormalities were seen in the cerebrospinal fluid panel, cerebrospinal fluid biochemistry or cerebrospinal fluid cytology. ACTH (0 am): 5.83 pg/ml, ACTH (8 am): 10.20 pg/ml, ACTH (4 pm): 7.03 pg/ml (normal value: 7-64 pg/ml); cortisol (0 am):7.0μg/L, cortisol (8 am):3.0μg/L, cortisol (4 pm): 1.0μg/L (normal values: 37.0-194 μg/L); prolactin: 113.35 ng/ml (normal values: 1.2-29.9 ng/ml). No abnormalities were seen in sex hormones, thyroid hormone, growth hormone, or insulin-like growth factor. Afterward, our team conducted a multidisciplinary consultation with neurology, neurosurgery, and endocrinology and recommended a follow-up MRI after 1 month of supplemental hormone therapy. However, one month later, the patient’s symptoms of headache and dizziness worsened, and the brain MRI re-examination showed that the pituitary gland was enlarged with a size of approximately 1.8*1.4*1.6 cm. On November 15, 2021 , the patient underwent sphenoid sinus exploration and nasal endoscopic saddle area tumor excision in our neurosurgery department. During the operation, the neurosurgery team found an occupying lesion in the sellar area with high dural tension, approximately 2*1.5 cm in size, pink in color, and tightly adherent to the surrounding tissues. The postoperative pathology showed that it was consistent with metastatic adenocarcinoma with neuroendocrine marker expression in some areas of pulmonary origin. Immunohistochemistry yielded the following: PCK (+), TTF-1 (+), Napsin A (+), ACTH (–), GH (–), PRL (–), FSH (–), LH (–), TSH (–), Ki67 (Li: 5%) . The next-generation sequencing (whole-exome sequencing by company of gloriousmed) conducted on the pituitary metastasis suggested EML4 -ALK fusion with VAF of 2.63%. Interestingly, the ALK gene then revealed a missense mutation (mutation region: chr2: 29445213, 22 exon p. Ile1171Ser, VAF: 29.2%). Four non-clinically relevant somatic gene variants (missense mutations) were also detected, namely INPP4A, MAGI2, AMER1, MED12.The patient’s postoperative headache and dizziness were significantly relieved compared to before. The patient’s hormone levels were reviewed on November 29, 2021, and most of the abnormal hormone levels returned to normal. On December 01, 2021, the pituitary gland MRI was reviewed and showed that the pituitary tumor was significantly smaller than before. Based on the patient’s gene sequencing results, we recommended that the patient replace crizotinib with ceritinib. On February 7, 2022, the patient’s lung CT showed that the lesion in the lower lobe of the right lung had shrunk further with a size of 1.8*1.4 cm, and the brain MRI re-examination showed no abnormalities . The patient was reexamined every two months by brain MRI and lung CT. The latest reexamination was on August 7, 2022, and no progression was observed .

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+A 71-year-old woman was diagnosed with diabetes mellitus at 56 years of age. She had a history of hyperthyroidism due to Basedow disease when she was 52 years of age. After three years of anti-thyroid therapy, her hyperthyroidism went into remission. She received oral drugs after being diagnosed with diabetes mellitus at 56 years of age.
+Seven months later, blood examination revealed an elevated level of anti-glutamic acid decarboxylase antibody (869 U/ml). She then received insulin injection therapy for type 1 diabetes mellitus. Her glycated hemoglobin (HbA1c) level was approximately 8%, and she had no history of ketosis or ketoacidosis.
+She was treated with insulin glulisine (13 units/day, pre-breakfast 4 units, pre-lunch 4 units, pre-dinner 5 units), insulin degludec (pre-dinner 3 units), and a SGLT-2 inhibitor, ipragliflozin (25 mg/day). Her fasting blood glucose levels in the morning before COVID-19 vaccination ranged from 93 to 169 mg/dl. Her HbA1c levels at approximately three months and one month before admission were 8.3% and 8.1%, respectively. She received the Pfizer-BioNTech COVID-19 (BNT162b2) vaccine (Pfizer, Inc; Philadelphia, Pennsylvania) three days prior to admission. Immediately after COVID-19 vaccination, she developed nausea and fatigue, and her water and dietary intake decreased. From the next day, the patient showed impaired consciousness, which made it impossible for her to inject insulin or take SGLT-2 inhibitor. Her symptoms worsened, and she was taken to the emergency room of Tokyo Medical University Hachioji Medical Center, Hachioji, Tokyo, Japan.
+On arrival, she had tachycardia and tachypnea, and her Glasgow Coma Scale was 12 (E3V4M5). A laboratory evaluation showed severe acidosis, ketonuria, ketonemia . Chest X-ray, electrocardiography, abdominal computed tomography, and urinary sediments showed no abnormalities. Thus, an infectious disease was unlikely. The patient was diagnosed with ketoacidosis. Immediately after admission, continuous intravenous insulin, Ringer’s solution, and glucose infusion were initiated in the intensive care unit.
+With the above combined treatment, her ketoacidosis gradually improved . On admission, the plasma glucose, HbA1c, and glycated albumin levels were 944 mg/dL, 8.0%, and 27.7%, respectively. She tested positive for anti-glutamic acid decarboxylase antibody, but was negative for insulinoma associated antigen-2 antibody and insulin autoantibody . Serum C-peptide and urinary C-peptide were undetectable. After her ketoacidosis improved, intensive insulin therapy without SGLT-2 inhibitor was resumed. Serum C-peptide was also below the limit of detection in a glucagon load test . When the patient was discharged, she was treated with insulin glulisine (17 units/day, pre-breakfast 7 units, pre-lunch 6 units, pre-dinner 4 units) and insulin degludec (pre-dinner 4 units).
+The patient was a 52-year-old woman who received insulin infusion therapy with multiple daily injections after being diagnosed with type 1 diabetes mellitus at 47 years of age. At the time of the diagnosis, she was admitted to another facility due to diabetic ketosis. She noticed thirst and >10 kg body weight loss in comparison to 6 months before her admission. A blood examination showed an elevated HbA1c level (15.5%), an elevated anti-glutamic acid decarboxylase antibody level (1230 U/ml), and an elevated islet antigen 2 antibody level (or*insulinoma-associated protein-2 antibody) (>41 U/mL). The urinary c-peptide level (45 µg/day) indicated that her insulin secretory capacity remained. She was diagnosed with latent autoimmune diabetes in adults and insulin treatment was continued.
+She was treated by a family doctor with insulin aspart (25 units/day, pre-breakfast 11 units, pre-lunch 8 units, pre-dinner 6 units) and insulin degludec (before sleeping 12 units). However, the transition of her HbA1c level was poor (10-11%). Her fasting blood glucose levels in the morning before COVID-19 vaccination ranged from 106 to 262 mg/dl. She received her second vaccination the day before admission. For both vaccinations, she received the Pfizer-BioNTech COVID-19 (BNT162b2) vaccine (Pfizer, Inc; Philadelphia, Pennsylvania). She had a drinking habit and consumed approximately 20 g of alcohol on the night before vaccination.
+Immediately after the second COVID-19 vaccination, she had symptoms of nausea, palpitation and respiratory distress. Her symptoms worsened, she could not inject insulin or eat from noon on that day. The following day she was taken to the emergency room of Tokyo Medical University Hachioji Medical Center, Hachioji, Tokyo, Japan.
+On arrival, she had tachycardia and tachypnea, but her consciousness was clear (E4V5M6). A laboratory evaluation showed severe acidosis, ketonuria, and ketonemia . The patient was diagnosed with diabetic ketoacidosis. Immediately after admission, continuous intravenous insulin, Ringer's solution, and glucose infusion were initiated in the intensive care unit. With these combined treatments, her ketoacidosis gradually improved . On admission, her plasma glucose and HbA1c values were 494 mg/dL and 11.6%, respectively . Serum C-peptide and the urinary C-peptide were slightly detected. Her thyroid hormone levels were normal. After her ketoacidosis improved, intensive insulin therapy was resumed.
+When the patient was discharged, she was treated with insulin glulisine (27 units/day, pre-breakfast 11 units, pre-lunch 8 units, pre-dinner 8 units) and insulin degludec (before sleeping 13 units).

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+A 21-year-old Caucasian woman presented to an outside facility with altered mental status after being found lethargic by family. On arrival to the emergency department, plasma glucose was 20 mg/dl. The patient was hospitalized and started on dextrose infusion, including 10% dextrose in water but remained hypoglycemic with capillary glucose ranging between 50 and 60 mg/dl. She was transferred to our facility on suspicion of an insulinoma as the patient was unable to recall her prior diagnosis.
+Medical records from our hospital revealed treatment for hypoglycemia as a neonate. The patient reported repeated episodes of seizures, syncope, dizziness, headaches, palpitations, and sweating around age 12; however, symptoms were never formally investigated as she did not seek expert care. These symptoms were also reported to have been present since birth but had been intermittent and of varying severity. She remained seizure-free and without syncopal episodes until 17 when she experienced another syncopal episode. At that time, she underwent extensive inpatient hypoglycemia evaluation with the following results: blood glucose of 47 mg/dl after 2 h of fasting, proinsulin levels varying from 10.4 to 84.1 pmol/l (normal range 0–10 pmol/l), C-peptide level 3.1 ng/ml (normal range 1.1–4.4 ng/ml), negative insulin antibodies and sulfonylurea screen. Magnetic resonance imaging of the abdomen showed no insulinoma, but genetic studies revealed Val452 Leu activating mutation of the GCK gene. She was successfully treated with diazoxide and discharged home on oral diazoxide 250 mg daily, which she discontinued due to side effects of hirsutism and fluid retention.
+On current admission, the patient was treated with dextrose boluses initially. Her blood glucose level remained low in spite of a continuous infusion of 5% dextrose necessitating transfer to an intensive care unit. Both fasting and postprandial blood glucose levels were low. As review of her medication list did not show any implicating drugs, no additional work-up was pursued. She was then placed on octreotide 200 µg subcutaneously twice daily and diazoxide suspension 100 mg three times a day on consultation with the pediatric endocrinologist. Neuroglycopenic symptoms of hypoglycemia improved. The patient's hypoglycemia improved with capillary glucose of 55–110 mg/dl by the time of discharge. Importance of compliance with the treatment and follow-up with an endocrinologist was emphasized.

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+A 19-month-old girl with no known immunocompromise presented with persistent unilateral neck lumps two weeks after lacerating her chin on a wooden shelving unit. While the laceration and swelling had healed uneventfully without specific therapy, neck swelling and overlying erythema developed following her injury, further increasing over the following four weeks. An ultrasound revealed several mild to moderately enlarged left submandibular and upper cervical lymph nodes—changes in keeping with inflammation.
+Examination revealed two prominent lymph nodes on the left side of her neck but was otherwise unremarkable. An 18 mm lymph node was located in the submandibular area, and another node (22 mm) towards the tail of her parotid . Both were fluctuant with erythema of the overlying and surrounding skin. There were no fistulae present. Incision and drainage with curettage was performed under general anaesthesia. Copious purulent discharge was drained and sent along with tissue for histological review and culture. A full blood count performed was within normal limits and C-reactive protein was not elevated. A ten-day course of Clarithromycin 150 mg twice daily was taken post-operatively. The wound healed without complication and no further therapy was required.

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+A 43-year-old female presented to the Department of Neurology of the Second Affiliated Hospital of Zhejiang University in March 2021. She was diagnosed with WD 12 years ago. Physical examination showed the patient had reduced facial expression and impaired articulation. The patient's left hand mildly trembled when she was asked to raise it flatly. She was also found to have increased extremity muscular tension, upper extremity tendon reflex +++++, and was unable to walk straight. Laboratory tests showed a low ceruloplasmin level (23 mg/L, reference 200–600 mg/L), and no abnormal serum copper concentration was found. Skull MRI showed hepatolenticular degeneration. Abdominal ultrasound revealed liver cirrhosis and splenomegaly. The patient was hospitalized and given sodium dimercaptopropane sulfonate for copper removal, zinc gluconate to inhibit copper metabolism, and supportive treatment such as amantadine and vitamin C supplements. During hospitalization, the patient complained of progressive bilateral vision decrease over 10 years, for which she was referred to our Eye Center. She volunteered that the night blindness began in early childhood, and her parents were close relatives. Her parents and sister were healthy, denying a similar medical history. The patient's best corrected visual acuity (BCVA) at presentation was 0.8 (logarithm of the minimum angle of resolution, logMAR) in both eyes, and intraocular pressure (Non-contact tonometer, Topcon CT-80, Topcon Corporation, Tokyo, Japan) was 10.0 mmHg in the right eye (OD) and 13.5 mmHg in the left eye (OS), respectively. Slit lamp biomicroscopy (SL-D8Z; Topcon Corporation, Tokyo, Japan) revealed bilateral corneal K-F ring and sunflower-like cataract . Fundus photography (TRC-NW8; Topcon Corporation, Tokyo, Japan) showed thinner retinal blood vessels and retinal osteocyte-like pigmentation in bilateral eyes . Cystoid macular edema (CME) and outer retina atrophy was observed in both eyes via optical coherence tomography (OCT) . Visual field examination (Octopus 900, Haag-Streit, USA) revealed binocular tunnel vision . The patient was subsequently diagnosed with WD combined with binocular RP and complicated cataract.
+After informed consent form the patient, phacoemulsification and posterior chamber intraocular lens implantation was performed in the right and left eye, respectively. Postoperatively, topical Tobradex (Tobramycin and Dexamethasone, Alcon) and Pranoprofen (Senju Pharmaceutical Co.Ltd, Japan) eyedrops were prescribed four times a day for anti-inflammatory treatment. Drug therapy for CME was not started before the surgery, and there was no significant change in the central retinal thickness (CRT) of both eyes during the 8-months follow-up. Unfortunately, there was limited improvement in her visual acuity. The BCVA remains 0.8 logMAR for both eyes at her last visit .
+Whole exome sequencing (WES, by Beijing Giantmed medical diagnostics Lab) was performed on the patient and her parents . The results showed an ATP7B gene c.G2333T: p.R778L homozygous mutation, CNGA1 gene c.C453A: p.Y151X homozygous mutation, RP2 gene c.T248C: p.l83T heterozygous mutation, and SNRNP200 gene c.C1898T: p.A633V heterozygous mutation in the patient . Both parents were heterozygous carriers of ATP7B and CNGA1 genes. The mother was of the RP2 heterozygous genotype, and the father was of the SNRNP200 heterozygous genotype, which were both found in the patient. However, the parents did not show any WD or RP-related manifestations.

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+A 27-year-old male involved in a motor vehicle accident was brought to Emergency Department room with respiratory distress. He was intubated upon arrival due to low Glasgow Coma Scale (GCS) with extensive maxillofacial injuries. Thoracic examination showed reduced air entry at right chest wall region with palpable crepitus on his right neck region due to subcutaneous emphysema from the neck to the anterior chest wall. The heart sound was barely audible. A curvilinear transducer on the right second intercostal ribs shows the absence of sliding signs, suggestive of right pneumothorax. A FAST scan was performed, but, on subxiphoid view of the heart, only the right ventricle is seen during diastole. Part of the cardiac image was obscured by A-lines . This raised a suspicion of pneumopericardium given the subxiphoid window was showing partly A-lines and the other half of anatomy partially obscured. We proceeded with focused cardiac ultrasound, and only A-lines were visible on parasternal long axis (PLAX), parasternal short axis (PSAX), and apical four chamber (A4C) views.
+The patient underwent head and chest CT scan that confirmed the diagnosis of Le Fort II facial bone injury, right pneumothorax, and right pulmonary contusion with pneumopericardium . The pneumopericardium was treated conservatively, but other injuries were treated accordingly.

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+A 39-year-old Caucasian man presented in 2009 with an 8-week history of fevers, night sweats, nausea, abdominal pain and distension and 5 kg weight loss. He reported no respiratory or other gastrointestinal symptoms and did not have any unwell contacts or history of overseas travel. He cared for an aviary of Gouldian finches (Erythrura gouldiae), which included cleaning and removing dead birds. There is no personal or family history of recurrent or opportunistic infections.
+Three years earlier, he was diagnosed with acetylcholine receptor (AChR) antibody-positive myasthenia gravis (MG) after presenting with ptosis, dysarthria and dysphagia. A type B2 thymoma was confirmed on surgical resection and treatment with prednisolone and pyridostigmine was commenced.
+In 2008, he suffered a myasthenic crisis with severe bulbar and respiratory muscle involvement necessitating a feeding tube (Myasthenia Gravis Foundation of America (MGFA) grade 4b). This improved with treatment (3-weekly plasma exchange, cyclosporine 150 mg two times per day, azathioprine 50 mg daily and prednisolone 25 mg alternate days) and he remained clinically stable until this presentation. At presentation, he had mild residual bulbar features, including dysarthria, dysphagia and fatigable chewing.
+On examination, he was afebrile, and had splenomegaly, periumbilical and epigastric tenderness. There was no palpable lymphadenopathy.
+Full blood examination showed haemoglobin of 111 g/L (130–170 g/L) and lymphocytes of 1.0×109/L (1.2–2.7 x 109 /L). C reactive protein was 63 mg/L.
+Lymphocyte subsets, including CD4 T-cell counts, were all within normal limits except for reduced CD19 pan B-cell count at 0.03×109/L (0.05–0.41×109/L). Immunoglobulin levels were not reduced, and HIV screen was negative. Bacterial and mycobacterial blood cultures were unrevealing.
+CT scan demonstrated splenomegaly (15 cm) and periaortic and mesenteric lymphadenopathy with no evidence of thymoma recurrence or residual thymic tissue. Gastroscopy showed a macroscopically abnormal duodenum with a fine, nodular appearance. Gastric and duodenal biopsies revealed broad, shortened villi and marked diffuse to confluent infiltrates of histiocytes in the lamina propria. Innumerable acid-fast bacilli were seen on Ziehl-Neelsen stain . Mycobacterium genavense was identified on molecular sequencing, leading to a diagnosis of disseminated M. genavense infection in an immunocompromised patient. Empirical therapy with rifampicin, ethambutol, moxifloxacin and clarithromycin was started. Cyclosporine and azathioprine were discontinued and the frequency of plasma exchange was increased with sequential intravenous immunoglobulin.
+Despite treatment, interval abdominal CT scan revealed progressive splenomegaly (17.8 cm) and intra-abdominal lymphadenopathy, raising concerns of refractory infection or lymphoma, as well as potential splenic rupture. Further biopsies of the mesenteric lymph nodes, stomach and duodenum demonstrated countless mycobacteria, consistent with ongoing infection. Drug sensitivities were unavailable as M. genavense could not be cultured.
+Following a multidisciplinary discussion, subcutaneous interferon-gamma (IFN-γ) was trialled, resulting in substantial fever. Dose was reduced to induce only low-grade fevers and chills (25 μg three times a week). Over the next 12 months, the patient’s symptoms resolved. Repeat CT scan demonstrated a reduction in the degree of splenomegaly and intra-abdominal lymphadenopathy. Antimicrobials were slowly weaned off over 6 years and he remains well 11 years later, with controlled myasthenia.
+Given the rare opportunistic infection, stored and newly collected blood samples were investigated for cytokine antibodies producing immunodeficiency. Due to ease of use and wide availability, the tuberculosis IFN-γ release assay was used to screen for reduced IFN-γ production. After incubation, a multiplex assay was used to measure cytokine production within the supernatant. The patient’s sample showed a markedly reduced IFN-γ response to mitogen stimulation compared with healthy controls . Moreover, the analysis also revealed a reduced concentration of interleukin-12 (IL-12).
+Research-based inhibition studies showed that adding the patient’s sample to IL-12p40 resulted in inhibition of analyte recovery at sample concentrations above 1:16 , suggesting the presence of an IL-12p40 inhibitor. This inhibitory effect was similar to that seen with ustekinumab, a human monoclonal antibody specifically directed against the p40 subunit shared by IL-12 and IL-23. Interestingly, plasma exchange did not substantially reduce inhibition , suggesting that the patient had a very high inhibitor concentration.

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+A 75-year-old woman was referred to our hospital with a gastroesophageal lesion. Upper gastrointestinal endoscopy revealed a raised lesion with ulceration on the posterior wall of the greater curvature of the cardia. The endoscopy also indicated tenderness in the lower esophagus and tumor invasion was suspected . Immunostaining of the tumor biopsy showed positive staining for Melan-A, human melanoma black-45 (HMB45), and S-100 protein (+), indicating malignant melanoma of the esophagogastric junction. Contrast-enhanced computed tomography (CT) of the abdomen showed a mildly stained lesion protruding into the cardiac part of stomach and enlarged perigastric lymph nodes (the right paracardial lymph node and lesser curvature lymph node were lumped together) . No obvious distant metastasis was observed. Serum analysis indicated that squamous cell carcinoma antigen, carcinoembryonic antigen, and carbohydrate antigen 19–9 were within normal limits. A positron emission tomography (PET)– CT scan showed a high degree of fluorodeoxyglucose accumulation (maximum standardized uptake value: early = 13.2, delayed = 19.2) in the upper stomach and enlarged lymph nodes. Based on these findings, we performed proximal gastrectomy, lower esophagus resection, and double-tract reconstruction. We also performed resection of the enlarged lymph node in the lesser curvature of stomach and no obvious distant metastasis in the abdominal cavity was found. Histological examination of the resected tissue indicated an elastic, soft tumor that was located in the esophagogastric junction (6 × 5 cm, Fig. a). Analysis of the tumor cell morphology demonstrated large, round tumor cells with nuclear atypia and high mitotic activity . Immunostaining was positive for Melan-A, HMB45, S-100 protein and SRY-box transcription factor 10 , and the patient was diagnosed with malignant melanoma of the esophagogastric junction with regional lymph node metastases. Postoperative recovery was good, and the patient was discharged on 22 days post-operation. Three months after the surgery, a follow-up CT showed subpleural masses in the lower lobe of the left lung, with bilateral pleural effusion . As previous analyses of the primary tumor had revealed BRAF-wild-type, the patient was prescribed with nivolumab, human immunoglobulin G4 monoclonal antibody, and inhibitor of programmed death-1 (PD-1) in accordance with melanoma treatment guidelines. Following three courses of nivolumab treatment, the patient presented with grade 3 renal dysfunction (Common Terminology Criteria for Adverse Events version 5.0) . The patient was prescribed steroid therapy for the immune-related adverse events that developed in response to the nivolumab treatment. Despite improved renal function, chemotherapy was discontinued at the patient's request. Five months after the presentation of renal dysfunction, a CT scan demonstrated an unstained nodule in the pancreas with dilation of the caudal pancreatic duct , although the size of the pleural metastasis was unchanged. Intensity-modulated radiotherapy (IMRT) was initiated for pancreatic metastasis treatment at 66 Gy. Six months after IMRT treatment, a CT scan revealed pancreatic nodule and pleural metastasis was shrunk. Eight months after the IMRT (13 months after nivolumab treatment completion), the pleural mass and pleural effusion had disappeared . PET–CT showed no obvious abnormal accumulation . We hypothesized that the abscopal effect was caused by the radiation therapy, and further enhanced by the nivolumab treatment, which had finished 5 months earlier; the timeline of these events is shown in Fig. . Twelve months after the onset of the abscopal effect, no additional lesions were observed and the patient had discontinued all treatment.

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+A 68-year-old man was examined in the outpatient department of our hospital by transoesophageal echocardiogram (TOE) because the attending cardiologist suspected mitral valve endocarditis. The patient’s medical history revealed permanent AF, drug-, and hepatitis E-induced liver cirrhosis (CHILD Score B) being on vitamin-K-antagonist (VKA), a biological aortic valve replacement in 2011 and long-standing hypertension. Due to a history of cirrhosis-associated major gastric bleeding complications in February 2014, while being on VKA and rheumatoid arthritis with long-term glucocorticoid therapy, an LAA closure procedure was planned 3 months later in our hospital. At that time, the patient had a CHA2DS2-VASc score of 2 points (age 65–74 years +1 and hypertension +1) and a HAS-BLED score of 5 points (age, hypertension, abnormal liver function, labile International Normalized Ratio (INR), and prior major bleeding; each +1). Despite antihypertensive combination therapy, including a diuretic, the patient’s blood pressure remained increased. Therefore, in combination with the glucocorticoid therapy, the bleeding risk (estimated risk 9–12%) was substantially higher than the risk for ischaemic stroke (estimated at 2.2%). At the time, guidelines did not recommend direct oral anticoagulants as an alternative to VKA use as there was insufficient data. As a result, a percutaneous LAA closure was performed in May 2014 and a 33-mm WATCHMAN device was implanted in the LAA of a chicken wing type and a left atrial (LA) size of 22 cm2. The WATCHMAN device size was chosen based on a maximum LAA ostium size of 30 mm, for which a 33-mm WATCHMAN device is recommended. The manufacturer’s standard guidelines and recommendations were followed and the procedure was performed without any adverse events. Post-interventional TOE assessment showed an appropriate closure of the LAA. The patient was discharged with dual antiplatelet therapy (DAPT) comprising aspirin 100 mg/day and clopidogrel 75 mg/day for 3 months, to which he was compliant.
+In July 2015, the patient was diagnosed with an ischaemic stroke due to the occlusion of the right internal carotid artery and carotid endarterectomy performed. A TOE performed at the time showed no intracardiac thrombus. Systemic lysis was performed, which resulted in intracranial bleeding. As a result, the CHA2DS2-VASc score increased to 4 points (age 65–74 years +1, hypertension +1, and stroke +2; estimated risk 4%) and the HAS-BLED score increased to 6 points [age, hypertension, abnormal liver function, labile INR, prior major bleeding, and (NEW) stroke; each +1 point; estimated risk higher than 9.1%], respectively. After conservative treatment, the patient was discharged to outpatient care with only slight neurological deficits (insecure gait) and his daily life was not impaired. The patient again received DAPT for 3 months, but no oral anticoagulation.
+In April 2016, the patient was invited by the outpatient cardiologist for a routine transthoracic echocardiographic assessment, which included the evaluation of the prosthetic aortic valve function. Examination revealed a mobile mass towards the mitral valve, which was suspected to be potentially endocarditis-related. The size of the left atrium was only slightly larger than in 2014 (25 cm2). A TOE, which was performed shortly after hospital admission, confirmed this mobile mass (∼40 mm × 15 mm in size) arising from a cleft of the LAA and located between the pulmonary vein ridge and the LAA device itself . The structure periodically prolapsed through the mitral valve leaflets and was of dense texture with only minor mobility. Anticoagulation with partial thrombopplastin time (PTT)-controlled heparin (PTT 50–80 s) was initiated. The patient remained completely asymptomatic, without showing any clinical evidence of peripheral embolism or neurological event. Fever and elevation of serological inflammation markers were also absent. Because of the high bleeding risk with a HAS-BLED score of 5 points, surgery was chosen as the therapy of choice instead of long-term anticoagulation.
+The patient was transferred to the cardiac surgery unit of a tertiary hospital and the device together with the thrombus was removed. Surgery was performed by a standard procedure with moderate hypothermia, utilizing a cardiopulmonary bypass manoeuvre, and by surgical closure of the LAA thereafter. In situ analysis showed that the closure did not cover the LAA completely and the device was only partially coated by the endothelium. A gap was identified between the device and the LAA from where the thrombus developed.
+On Day 21 post-extirpation of the thrombus, the patient was discharged in good clinical condition on DAPT for the following 3 months. A TOE 6 weeks later showed no further thrombus formation and a completely closed LAA. In follow-ups at 6 and 12 months after surgery, transthoracic echocardiography was performed in an outpatient setting and did not reveal any clinically relevant findings. At this point, the patient was in a stable clinical condition. Further follow-up is planned on a yearly basis.

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+A 24-year-old Chinese pregnant woman presented to the emergency department with complaints of anemia for 3 mo, gingival bleeding for 1 mo, and hematuria for 2 wk.
+She was 24 wk pregnant and presented to the emergency department complaining of anemia for 3 mo, gingival bleeding for 1 mo, and hematuria for 2 wk.
+Before pregnancy, she had a history of chronic seizures for 22 years that occurred about every 2-3 mo. The patient was on a long-term regimen of levetiracetam tablets (1000 mg per day) but stopped taking antiepileptic drug 1 d before admission.
+The patient had no family medical history of lipid disorders.
+Although she had a normal physique (height: 1.58 m, weight: 61 kg; body mass index: 24.4 kg/m2) with no impaired intelligence, she was anxious with a characteristic round “doll-like” face.
+The biochemistry of this patient was found to be abnormal as indicated by various biochemical tests : hemoglobin: 67 g/L, extremely elevated triglyceride: 5483.5 mg/dL (normal value < 150 mg/dL), cholesterol: 836.6 mg/dL (normal value < 200 mg/dL), elevated lactic acid: 13.3 mmol/L (normal value 0.5-1.7 mmol/L), slightly elevated uric acid: 412 μmol/L (normal value 89-360 μmol/L), albumin: 33.6 g/L, qualitative urine protein: 0.3 (1+) g/L, urinary erythrocyte++++/haptoglobin, and elevated thyroid-stimulating hormone: 8.080 mU/L (the recommended value for pregnant women is less than 2.5 mmol/L). The patient’s enzymes such as amylase and lipase were in the normal range.
+Ultrasound examination showed abnormal enlargement of the liver where the maximum oblique diameter of the right lobe was found to be about 17.2 cm. Two stones smaller than 0.5 cm were found in the left kidney. The patient had been undergoing regular prenatal check-ups after pregnancy and the nuchal translucency thickness, as well as Down’s syndrome screening, were normal. Obstetric ultrasound examination at 24 wk of gestation revealed a live single fetus in the uterus with a thickened and sail-shaped placenta, which needed to be closely monitored during the pregnancy.
+After eating, the patient’s blood glucose returned to normal levels (6-9 mmol/L) after two episodes of intermittent fasting hypoglycemia (minimum 2.66 mmol/L). We highly suspected that she was suffering from GSDI. To confirm this diagnosis, we treated the patient with cornstarch diet therapy and performed genetic testing using samples of her blood and fingernails. The genetic test results showed that there was a gene c.648G>T mutation on chromosome 17q21, indicating that the patient had glucose-6-phosphatase (G6Pase) deficiency.

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+A 50-year-old woman presented in the outpatient department with severe abdominal pain, especially in the left iliac region, for the past six months. The pain was dull aching in nature and continuous and used to be relieved with oral analgesics. The patient also complained of shortness of breath, which worsened in the supine position and was eased in the sitting posture. She also stated that she had lost her appetite and lost a large amount of weight. There was no history of vaginal bleeding. There was no previous medical or surgical history.
+On physical examination, the patient looked cachexic with mild degree of pallor with stable vital parameters. Abdomen examination showed a mass of 20 weeks of gestation size with irregular surface, heterogeneous consistency, tender, margins well defined but the lower pole was usually not reached, with restricted mobility. Ascites was present and positive shifting dullness was noted. A vaginal examination showed nodules on the right posterior fornix, tenderness was present. Left fornix was free.
+The patient was advised for contrast-enhanced computed tomography (CECT) of the abdomen and pelvis, which revealed a large cystic lesion with peripheral enhancing solid areas in the pelvis in midline, probably arising from the left ovary, a possibility of malignant ovarian lesion . Another heterogeneously enhancing lesion was seen in the right adnexa. The right ovary was not seen separately from the lesion. There was a large ill-defined heterogeneously enhancing central mesenteric lesion with omental extension showing dense calcification, most likely metastatic deposit. Loculated ascites and left-sided moderate pleural effusion with few peripheral lung parenchymal nodules in the right middle and bilateral lower lobes were suggestive of stage 4A of the International Federation of Gynecology and Obstetrics system 2014.
+CA-125 (cancer antigen 125) value was more than 1000 units/ml. NACT was given to the patient with paclitaxel 175 mg/m2 and carboplatin 675 mg/m2 (area under the curve (AUC)=5-6, calculated by Calvert’s formula). After two cycles of NACT with intervals of three weeks, CA-125 was 452 units/ml. The patient then underwent further four cycles of NACT. CA-125 was repeated, which showed normal values, and CECT was done, which revealed a complex cystic lesion in the pelvis and the infra-umbilical region at midline and para midline locations . A lesion of 2-3 cm thickness and peripherally enhancing solid mass of 8.6 x 5.8 cm in size was displacing the adjacent bowel loop. There was para midline location-significant regression in size of the mass. There was significant regression in ascites.
+USG revealed a solid cystic lesion in the left adnexa measuring 5 x 4.2 x 3.6 cm; the solid component showed vascularity. Left ovary not seen separately. Findings were consistent with left ovarian complex cyst-neoplastic etiology. Omental thickening was seen in midline in the epigastric region.
+The patient was taken for exploratory laparotomy. A vertical incision of 10 cm was made and the abdomen was opened in layers so as to expose the maximum area. In order to assess the extent of the primary tumor and metastatic disease, the peritoneal cavity and retroperitoneum were thoroughly inspected and palpated. All abdominal viscera were palpated and checked, and adhesions between sigmoid and left corn structures were lysed. Ureters were identified and placed away. Dissection of mass, uterus, cervix, bilateral fallopian tube, and ovaries was done by retroperitoneal approach and sent for frozen section according to which it was labeled as bilateral papillary cystadenocarcinoma. Then retroperitoneal resection was done. Bilateral pelvic lymph nodes were removed and an omentectomy was done. No para-aortic lymph nodes were identified. The bowel was inspected for injury. Drain was inserted and hemostasis was achieved. Rectus was closed with prolene 1-0. All laparotomy sponges and instruments were removed from the abdomen and counted. The abdomen was closed in layers with Vicryl 1. Skin closure was done in layers with Ethilon 2-0 mattress sutures. The patient withstood the procedure satisfactorily and was shifted to the postoperative ward. Specimens were sent for histopathology, which confirmed bilateral serous cystadenocarcinoma. The specimen is shown in Figure .
+The patient was discharged on postoperative day 12 after suture removal and advised to follow up every month for the first three months and then every three months for the next one year. On her last follow-up, the patient was better clinically and had no signs of recurrence.

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+A prepubertal, Caucasian 11 years-old girl was admitted to the Pediatric Department of Chieti for evaluation of severe hypertension (200/114 mmHg) in the context of severe obesity [Weight: 86.9 kg, Height: 144 cm, BMI: 41.9 kg/m2 (SDS-BMI: 3.25)]. She had a family history of obesity (both parents and the 17 years-old brother) and both parents were affected by T2D. The girl had a normal weight at birth, developed obesity since the age of 5 years-old. Clinical examination revealed marked acanthosis nigricans and striae rubrae. Essential Hypertension was diagnosed and therapy with amlodipine and bisoprololo was successfully started. The girl presented normal glucose metabolism (fasting glycaemia: 79 mg/dL, HbA1c: 5.4%) with insulin resistance (fasting insulin: 51 mU/mL, HOMA-IR index: 9.9), normal lipid profile (total Cholesterol: 197 mg/dL, HDL: 23 mg/dL, LDL Cholesterol: 137 g/dL, Triglycerides: 185 g/L) and hepatic steatosis with mildly increased transaminases levels (AST: 62 U/L, ALT: 122 U/L). Lifestyle change was recommended including a detailed dietary scheme and physical activity program. Thereafter, during the ambulatory follow-up hypertension was well controlled but the patient was lost after 2 months.
+After six months she was admitted to the emergency department [Weight: 78.5 kg, Height: 146 cm, BMI: 36.8 kg/m2 (SDS-BMI: 2.97)] for lethargy. She had an history of chest pain associated with increasing dyspnoea and progressive drowsiness over the last two days before presentation. Weight lost and intense polyuria over the 4 weeks was reported.
+On admission, Glasgow Coma Scale (GCS) was 13/15, heart rate 120 beats/min, respiratory rate 40 acts/min, blood pressure 140/70 mmHg and pulse oximetry 100% on room air. At clinical evaluation she appeared severely dehydrated. Neurological examination confirmed profound drowsiness although awakeable, with eye opening response to speech and mild confused verbal response. She denied headache and no neurological alterations were reported.
+Kidney function (creatinine: 0.70 mg/dL) and potassium levels were normal. In contrast, on blood gas evaluation severe hyperglycaemia (647 mg/dL), increased sodium levels (corrected Na: 152 mmol/L) associated with high serum osmolality (326 mmol/Kg) were detected. In addition, severe acidosis with low bicarbonates and high ketonemia levels (pH: 7.11, BE: -23.9, HCO3-: 9.2 mmol/L, ketonemia >8 mmol/L) were demonstrated establishing a diagnosis of combined HHS and DKA. Clinical history together with well-known insulin resistance state and long lasting polyuria oriented towards metabolic derangement due to unknown T2D. In this respect therapy was started with the aim to control primarily the hyperosmolar state .
+In fact, rehydration with isotonic saline (0.9% NaCl) infusion was initially started and after four hours continued with 0.45% NaCl together with continuous low-dose insulin administration . Infusion treatment was stopped after 60 hours when normal serum osmolality and pH levels were achieved, although blood ketones were still present. Therefore, subcutaneous basal-bolus insulin administration was started. Over the infusion period general condition progressively ameliorated and no neurological or other complications were developed.
+The suspicion of T2D complicated by combined HHS and DKA, was confirmed by detection of high percentage of HbA1c (11.6%), high levels of C-peptide (3.24 ng/mL) and the undetectable titre of antibodies against pancreatic islets’ antigens (ICA, GAD, IA2) while ZnT8 antibodies were not been performed. She stopped basal-bolus insulin administration after 17 days and continued with degludec therapy once a day and metformin therapy twice daily obtaining normal glucose metabolism after two months (HbA1c: 5.2%). Lifestyle changes were endorsed but after some months the girl was lost for follow-up.
+After 2 years, she presented again to the emergency department with a similar episode characterized by increased dyspnoea, nausea, lack of appetite, sporadic vomiting and a poor glycaemic control over the last seven days [Weight: 95.5 kg, Height: 155 cm, BMI: 39.8 kg/m2 (SDS-BMI: 3.41), Pubertal stage: P5B5]. Parents reported poor compliance over the last months.
+On admission neurological examination was normal (GCS 15/15). She did not complain headache, neither other neurological symptoms. She was severely dehydrated.
+Blood tests performed showed again normal potassium values, while kidney function was borderline (creatinine: 1.26 mg/dL, BUN: 16 mg/dL). Blood gas demonstrated hyperglycaemia (402 mg/dL), increased sodium concentrations (corrected Na: 152 mmol/L), associated with mild increased serum osmolality (316.4 mmol/Kg). Moreover, acidosis and ketonemia (pH: 7.23, BE: -18.8, HCO3-: 26.4 mmol/L and ketonemia: 5.6 mmol/L) were documented.
+Initial combined HHS/DKA was supposed and isotonic saline (0.9% NaCl) infusion was started first and subsequently substituted by 0.45% NaCl for rehydration . After two hours, continuous low dose insulin administration was started and associated thereafter with glucose 5% after 11 hours. Moreover, when osmolality was acceptable but metabolic acidosis with high blood ketone levels persisted after 20 hours, glucose infusion at 10% was started and maintained up to 60 hours post admission with insulin infusion (0.042 U/kg/h). Normal serum osmolality, pH levels and resolution of ketonemia were achieved. General condition ameliorated progressively and no neurological symptoms appeared.
+Poorly controlled T2D (HbA1c: 11.6%) in the presence of detectable levels of C-peptide (1.64 ng/mL, normal range 0.69-2,45 ng/mL) was found and undetectable titre of antibodies against pancreatic islets’ antigens (ICA, GAD, IA2) were confirmed. Degludec therapy once a day and metformin therapy twice daily was confirmed obtaining good metabolic control.

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+In May 2005, a 43-year-old man was admitted to the hospital with mitral regurgitation. In 1981, he had been in a car crash and developed a destructive nosocomial Staphylococcus aureus endocarditis of the mitral valve. A bioprosthesis was inserted which failed in 1988 and was replaced. In May 2005, regurgitation through the valve was once again detected and the patient was hospitalized for a further valve replacement. The patient was afebrile and had a systolic murmur over the mitral area. He had no leukocytosis (leukocyte count was 3.63 × 109/l with 50.2% neutrophils). The low neutrophil count corrected itself spontaneously. The erythrocyte sedimentation rate (16/43 mm) and C-reactive protein (<5 mg/l) was normal and hepatic enzymes were elevated (ALT: 69 IU/L; normal ≤ 40 IU/L). Three routine blood cultures were negative (Bactec, Becton Dickinson, Sparus, Maryland) and no rheumatoid factor was detected. Transthoracic echocardiography revealed mitral insufficiency but there were no vegetations and IE was not considered as a possible diagnosis. However, no transesophageal echocardiography was performed. Histology of the prosthetic valve removed at surgery using reported methods [,], revealed an IE with a vegetation containing micro-organisms that stained with Warthin-Starry and Giemsa . Standard cultures of cardiac valve tissue remained sterile, but with cell-cultures (human endothelial cell) a strain of B. henselae was isolated in 3 weeks . Also, DNA of B. henselae was demonstrated to be present in the valve by PCR and sequencing with primers for the eubacterial 16S rRNA gene and Bartonella ITS region Genotyping of the B. henselae strain was carried out using the multi-spacer typing (MST) method as previously described . Sequences obtained from the nine studied spacers classified the strain within MST genotype five, previously described to contain cat isolates from various countries including France, Germany and USA . Serum tested retrospectively was found to contain antibodies to B. henselae and B. quintana at an IgG titer of 1:200 , which is not suggestive of IE. However, western blotting was positive for antibodies to B. henselae and B. quintana and showed a reactivity pattern typical for endocarditis . Immunoblotting with a serum sample adsorbed with B. henselae confirmed the diagnosis of B. henselae IE.
+The diagnosis of IE was made retrospectively based on the combination of histology of the cardiac valve lesions, culture of Bartonella from the valve, presence of a predisposing heart condition, and serological evidence of Bartonella infection. Without the histology of the valve the patient would not have had a positive score using the Duke criteria; he would only have had 2 minor criteria. After surgery, the patient recovered rapidly with routine post-surgical amoxicillin administration for 4 days, followed by gentamycin for 15 days and doxycycline for 1 month .
+Retrospectively, it was found that six months before the patient had had suspected lymphoma of an inguinal lymph node. Histology of the node, however, showed a necrotizing lymphadenitis suggested of CSD. Numerous microabscesses containing fragmented neutrophils were observed in homogenous necrotic areas. These necrotic regions were surrounded by a ring of macrophages and epithelioid histiocytes to form stellate inflammatory granulomas . No bacteria were detected by immunohistochemical examination or Warthin-Starry staining. Unfortunately, the lymph node sample was not available for PCR analysis to confirm the diagnosis of CSD.
+The patient did not own a cat but reported a single contact with a stray cat that scratched him one month before the enlargement of the inguinal lymph node. We report the development of IE after a likely episode of CSD in a patient with a mechanical mitral cardiac valve. In previous studies , B. henselae was described in patients who have regular contact with cats and with pre-existing valvulopathies [,], but to the best of our knowledge the progression of CSD to IE has not previously been reported.

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+A 43-year-old Caucasian man on anti-retroviral therapy (lopinavir/ritonavi and emtricitabine/tenofovir) for HIV/AIDS presented in September 2008 with a three-month history of low grade fevers, night sweats, generalized fatigue, lethargy, unintentional weight loss, and bilateral lower extremity swelling. He had a CD4 count of 196 cells/mm3, and a viral load of <50 copies/mL. He had been diagnosed with HIV-infection in 1990; his CD4 nadir was 4 (0.6%) in February 2004 with high viremia, 175,671 copies/mL. After initiation of potent anti-retroviral therapy the HIV viral load has been undetectable since October 2004.
+A physical exam of our patient revealed diffuse lymphadenopathy in his cervical, axillary and inguinal areas, splenomegaly, and pitting edema in both lower extremities. Computed tomography of his chest, abdomen and pelvis demonstrated widespread mediastinal, hilar, axillary, retro-peritoneal and pelvic lymphadenopathy, as well as the splenomegaly. A laboratory workup revealed a hemoglobin level of 8.5 mg/dL, a white blood cell count (WBC) of 4,600 cells/μL, an albumin level of 2.5 mg/dL, and a Westergren sedimentation rate of 90 mm/hr. A lower extremity Doppler was negative for deep venous thrombosis.
+Histological examination of lymph node biopsy material revealed marked plasma cell infiltration, and follicles that were variable in appearance, from marked follicular hyperplasia to involution and dendritic cell hyperplasia . Immunohistochemical studies demonstrated HHV-8 positive , and plasmablastic foci associated with an intense polytypic plasma cell infiltrate. These findings were consistent with the diagnosis of MCD--plasma cell variant. Our patient was discharged from the hospital and was scheduled to start treatment for MCD.
+Three weeks later our patient presented with lower abdominal pain, urinary retention, and lower extremity weakness. Neurological examination revealed bilaterally reduced motor power (4/5) in all major muscle groups in his lower extremities, along with a positive Babinski sign on the right. Deep tendon reflexes were normal bilaterally. An ultrasound of his pelvis demonstrated bladder distention. A Foley catheter was inserted and 2 liters of urine was evacuated, with complete relief of pain.
+A Gadolinium magnetic resonance imaging (MRI) of his spine was done to rule out spinal cord compression; it revealed abnormal spinal cord signal intensity involving several cervical and thoracic segments, associated with expansion of the cord and mild enhancement of the areas of abnormal T2 signal . MRI of the brain revealed a few patchy areas of abnormal T2 signal in the peri-ventricular and pontine white matter.
+A lumbar puncture was performed: cerebrospinal fluid (CSF) contained an elevated WBC of 50 cells/mm3, with 90% lymphocytes, and a high protein level of 243 mg/dL; cytological analysis identified mature reactive lymphocytes with no evidence of lymphoma on flow cytometry. Polymerase chain reaction (PCR) was positive for EBV DNA in the CSF, but negative for HHV-8, cytomegalovirus (CMV), herpes simplex virus (HSV) and Varicella-Zoster virus (VZV). Treatment with high-dose dexamethasone was initiated. Our patient was then transferred to the National Institute of Health (NIH) and started on a treatment protocol of high-dose zidovudine (AZT) and valganciclovir for MCD (ClinicalTrials.gov identifier: NCT00099073). Subsequent laboratory follow-up revealed marked improvement over the first seven days of treatment, including a marked decrease in WBC and protein in his CSF. A follow-up MRI demonstrated resolution of all spinal cord lesions. He is now doing well, his last CD4 was 322 (15%), viral load < 50 copies/mL in August 2010.

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+A 21-year-old man was diagnosed with B-ALL 5 years ago (August 2015) and received chemotherapy consisting of one cycle of VCDLP (CTX, vindesine, daunorubicin, prednisone, PEG-aspargase) for induction ), and one cycle of MTX plus PEG-aspargase for consolidate . After these two cycles of therapy, minimal residue disease (MRD) was still positive. Therefore, he underwent a second-line therapy with MA (MTX and Arac) , and reached MRD-negative complete remission (CR). In March 2016, he received allo-HSCT (allogenic hematopoietic stem cell transplantation) from an HLA-matched unrelated donor, and all went well with no occurrence of CMV reactivation. Four months later, a disease relapse was suspected, and the patient was admitted to our hospital for further treatment, where he underwent bone marrow (BM) examination. Flow cytometry revealed 18.5% abnormal B lymphoblasts, and immunohistochemistry showed significant hyperplasia of abnormal lymphoblasts with CD34+ TdT+ CD79a+ CD10+ CD19+ CD22+ CD3- BCL2+ MPO- and Ki-67 Li 90%. Gene examination revealed a missense mutation in the NOTCH2 gene and a splice variant of the IKZF1 gene. No evidence of central nervous system (CNS) invasion or any other extramedullary diseases were identified. Serological tests were negative for HBV antigens/antibodies except for HBsAb, but they were not performed for CMV antibodies. No CMV DNA or HBV DNA was detected in the blood. The chest CT scan and hematobiochemical results were consistently normal. He was allergic to ofloxacin and had no history of exposure to HBV, HIV, tuberculosis, or any other infectious diseases. No other clinical history, familiar or psycho-social history of importance.
+Given the relapse after HSCT, we treated the patient with the sequential infusion of anti-CD19 and anti-CD22 CAR-T cells (ChiCTR-OPN-16008526). It took two weeks to manufacture the patient’s own anti-CD19 and anti-CD22 CAR-T cells from collected peripheral blood mononuclear cells (PBMCs). The transfection rates of CD19 CAR and CD22 CAR were 35.6% and 40.9%, respectively . The patient was treated with 3-day conditioning chemotherapy consisting of fludarabine 25 mg/m2 and cyclophosphamide 20 mg/kg per day, and was sequentially transfused with CD19 CAR-T cells and CD22 CAR-T cells at doses of 1.5x106 cells/kg and 1x106 cells/kg, respectively. As shown in , CAR-T cells expanded well in vivo with CD19 and CD22 CAR copy numbers of 1,034,286 and 52,857.14 per µg genomic DNA, respectively, on day 6. Meanwhile, after the infusion of CAR-T cells, the patient developed grade 3 CRS manifested as high fever (max temperature of 41°C), hypotension (lowest at 88/42 mmHg, responsive to fluids therapy), hypoxia (requiring high-flow nasal cannula oxygen), coagulopathy (requiring fresh frozen plasma), pulmonary edema characterized by extensive rales among both lower lobes of the lung, and grade 3 immune effector cell-associated neurotoxicity syndrome (ICANS) with two-side blurred vision. Eye examinations found patchy bleeding around the infratemporal branch of the central retinal vein and scattered exudation in the other parts of the right retina (suspected to be associated with coagulopathy and severe thrombocytopenia), and mild retinal edema (no hemorrhage was observed) in the left eye. Laboratory testing revealed markedly increased levels of IL-6 and ferritin after CAR-T cell infusion, as shown in , with peak values of 1,260 pg/mL and 30,014 µg/L on day 6 and day 8, respectively. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), N-terminal B-type natriuretic peptide (NT-proBNP), and hypersensitive troponin were also abnormally elevated. After one session of plasma exchanges [to selectively eliminate inflammatory cytokines ], two 40-mg doses of methylprednisolone, and other supportive treatments, the inflammatory cytokine storm was gradually controlled, with both the levels of IL-6 and ferritin falling to baseline levels 2 weeks after the infusion as well as the levels of AST, ALT, NT-proBNP, and hypersensitive troponin. The blurred vision disappeared spontaneously two days later. In addition, the patient experienced severe myelosuppression but recovered two weeks later, as depicted in . The patient received prophylactic anti-infective treatment (excluding antiviral therapy) after CAR-T cell infusion, and no severe infection was observed during treatment. BM aspiration was performed on day 14, indicative of complete remission by flow cytometry.
+On December 3, three months after CAR-T cell treatment, the patient was hospitalized with a 10-day history of low fever (37-38 °C) and cough, and a 3-day history of palpitations, chest tightness and dyspnea. The primary disease was well controlled, and B cells were still absent . The findings on chest X-ray suggested pulmonary infection and interstitial infiltration . CMV DNA, rather than bacterial DNA or fungal DNA, was detected in the peripheral blood by next-generation sequencing (NGS) sequencing. Given the patient’s previous medical history, clinical manifestations, and laboratory and radiographic evidence, he was diagnosed with suspectable CMV pneumonia (fiberoptic bronchoscopy was contraindicated as the patient was oxygen dependent, and therefore, no pneumonia tissue was available to confirm CMV infection). On December 4, the patient received antiviral (ganciclovir 5mg/kg q12h) therapy, as well as preventive anti-bacteria (tigecycline 50mg q12h, and sequential use of cefoperazone/sulbactam 3g q8h, meropenem 0.5g q6h and imipenem/cilastatin 1g q8h) and anti-fungi (sequential use of voriconazole 0.2g q12h and caspofungin 50mg qd) therapy (all intravenously). However, the symptoms worsened rather than alleviated, with the occurrence of diarrhea (yellow watery stool) and an SpO2 of 90% despite using oxygen mask on December 7. Therefore, we introduced intravenous gamma globulin 20 g/day, methylprednisolone 40 mg/day and bilevel positive airway pressure (BiPAP) ventilation on December 8, after which his pulmonary symptoms gradually improved. Ganciclovir was changed to penciclovir (5mg/kg q12h, intravenous drip) due to the side effects of limb numbness, chills and pain at the infusion site. During treatment with these two antiviral drugs, the patient’s WBC count and platelet count decreased progressively . We stopped penciclovir on December 18 when the clinical symptoms had improved. Meanwhile, CMV DNA was negative in the blood, and a chest X-ray showed reduced inflammatory filtration. However, the side effects of myelosuppression aggravated, and three days after treatment discontinuation with penciclovir, the patient again reported chest tightness and shortness of breath. We reintroduced penciclovir on December 21, but the patient’s symptoms gradually worsened. He died on December 25 from respiratory failure. The key events in this case are summarized in .

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+A 9-year-old female patient arrived at the emergency room because of a 36-h history of intermittent right lower abdominal pain, anorexia, vomit, and quantified high-grade fever. She had no pathological personal or family history of interest. On examination, the right iliac fossa was tender to palpation and no frank peritoneal signs were observed. Initial laboratory evaluation showed leukocytosis, neutrophilia, and an elevated C-reactive protein. Ultrasonography of the abdomen was inconclusive. A heterogeneous lesion of 40 × 37 mm within the colon, no appendix and some swollen mesenteric nodes of at least 10 mm were reported. A complementary abdominal CT scan revealed findings suggestive of ileocolic intussusception with an invagination area of approximately 6.6 × 4.9 cm. After surgical consult, the patient underwent an exploratory laparoscopy that required laparotomy conversion. A well-defined, 5 cm mass at ileo cecal valve and multiple hard pericecal lymph nodes were observed. Preserved permeability between the ileum and colon, complete integrity of the cecum wall and lack of vermiform appendix were also reported. The possibility of an auto-digested appendix and a cecal tumor were discussed. At this time, surgeons decided to resect retrocecal and pericecal lymph nodes and send these samples to pathology before any further intervention. The patient was admitted to the inpatient floor where antibiotic therapy based on ampicillin sulbactam, and metronidazole was initiated. The oncologist department was consulted and complementary laboratory exams including liver and renal function tests, uric acid, electrolytes, lactic dehydrogenase, and quantiferon-TB tests were ordered. Only lactic dehydrogenase was altered. A chest x-ray ruled out mediastinal masses. No alarming findings were reported. However, the patient presented gastric distension, abdominal pain and fever by the second hospitalization day. The content inside the suprapubic JP drain changed from a serohematic aspect to a dense cloudy fluid. A culture and cytochemical analysis of peritoneal fluid was performed without significant results. CBC showed mild leukocytosis and neutrophilia. Reactive C-protein remained elevated. Two blood cultures and an urinalysis were negative. Due to the uncertainty of the etiology of her clinical picture, infectology decided to change antibiotic therapy to piperacillin/tazobactam and amikacin. An abdominal x-ray showed air fluid levels in the small bowel and a colonic distention projected at mesogastrium. Gastroenterology suggested initiating bowel rest and placing a central line for parenteral nutrition.
+After five more days, elevated inflammatory markers, abdominal distension and pain, and the unusual JP drain aspect persisted. A new ultrasound confirmed that the mass and surrounding area had the same aspect as days before. The histopathological description of paracecal-retrocecal lymph nodes and the sample of mesenteric omentum obtained during the first intervention failed to detect neoplastic cells. Macroscopically, three encapsulated lymph nodes from 0.8 to 2 cm were received. Their physiological architecture was preserved; secondary lymphoid follicles with hyperplastic germinal centers containing macrophages with cellular debris were reported. The interfollicular population was polymorphic and contained frequent large cells with prominent immunoblast-like nucleoli. Other areas showed sinusoidal histiocytosis with eosinophils and neutrophils. There was fibrosis with a predominantly neutrophilic mixed inflammatory infiltrate that spread to neighboring adipose tissue in the periphery of the nodes. The immunohistochemical study confirmed the presence of follicular dendritic cells and B lymphocytes in the germinal centers (CD23 + + +/+ + + and CD20 + + +/+ + + respectively), T lymphocytes in the mantle zone (CD3 + + +/+ ++), macrophages in germinal centers and sinusoidal area (CD68 +/+ ++). Frequent CD30 + + +/+ + + immunoblasts and actin + + +/+ + + myofibroblasts within areas of fibrosis were also observed. EBV study using EBER in situ hybridization was negative. Ziehl Neelsen and PAS did not show any pathogen. The 22 × 0.6 cm omentum sample showed fibrous thickening of the septa and the presence of a mainly lymphocytic infiltrate. Fibrino-leukocytic material was also seen in the serosa. Pathologists concluded the possibility of an unspecified acute versus chronic epiploitis, lymphadenitis and serositis. Nevertheless, due to her unfavorable clinical evolution and the elevated inflammatory markers, a second surgical intervention was decided. The patient underwent an omentectomy and resection of approximately 40 cm of terminal ileum, cecum and ascending colon. Pericolonic lymph nodes were resected as well. A sample of a collection observed near the cecum was taken for culture and cytochemical studies before aspiration and drainage. After surgery, the patient remained hemodynamically stable, without abdominal pain or distention. A nasogastric tube was placed and parenteral nutrition continued. The peritoneal fluid analysis was negative. Improvement in inflammatory markers lead to amikacin discontinuation. And by the fifth postoperative day, JP drain, and nasogastric tube were removed. Later, a regular diet was successfully initiated, and the patient was finally discharged.
+The histopathological final report described an 8 cm ileal segment, and a 14 cm ascending colon including the cecum with a diameter that ranged from 1 to 3 cm. The external surface was covered by a pinkish-gray serosa with fibrinopurulent material over the ileocecal area. A completely subserous dilated appendix was identified within the cecum wall. It contained a white-yellowish purulent material at the tip . A well-defined nodular lesion of approximately 1.5 cm was also identified . The mucosa of the cecum was pink while ileal mucosa had a granular appearance. Nine nodules, which measured between 0.3 and 3 cm, were isolated from the surrounding area. The 12 × 4.5 cm omentum sample had no palpable nodes. A second omentum sample showed multiple whitish irregular fragments of bland tissue that measured between 0.8 and 1.5 cm. Microscopically, the histological findings of the fourteen isolated lymph nodes were compatible with follicular hyperplasia. The subserosal cecal appendix showed transmural necrosis and perforation causing leakage of purulent material and an acute inflammatory reaction of the surrounding adipose tissue which extended up to the cecal and ileal serosa. All layers of the appendix were independent and unrelated to the cecum wall . The distal portion of the appendix showed the proliferation of cellular nests that were composed of round uniform nuclei with a “salt and pepper” appearance . No mitotic activity was evidenced. It seemed to infiltrate the muscular layer of the appendix and reach a diameter of 1.5 cm. No lymphovascular or perineural invasion was observed. Disease free margins were reported. Ileum dissection showed Peyer’s patches hyperplasia with wide germinal centers. Tumoral cells’ immunochemical studies showed a Ki67 proliferative index of 2%, a positive (+ + +/+ + +) cytoplasmic granular pan-cytokeratin, a positive (+ + +/+ + +) cytoplasmic chromogranin and a negative synaptophysin reaction . Pathologists concluded the presence of an incidental well differentiated neuroendocrine tumor grade I pT1 pN0 at the tip of the appendix in the middle of a clinical picture caused by an acute necrotizing appendicitis of a complete subserosal appendix. Due to the stage, no further intervention was required. She fully recovered in subsequent controls. Nevertheless, correct management of short bowel syndrome will become a key feature for the preservation of her future quality of life.

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+Here, we report the case of a 63-year-old Japanese man with no medical or psychiatric history, except for type-2 diabetes mellitus and essential hypertension. He had no previous history of psychotropic drug use, including antidepressants and antipsychotics. Additionally, he had no developmental abnormalities or neurodevelopmental disorders. He held a steady job from college graduation until retirement age, and his wife described his premorbid personality as dependable, sociable, and patient. He had no family history of psychiatric disorders, migraine, or epilepsy.
+One year before his first admission to an inpatient psychiatric unit, he started experiencing mild depressive moods and fatigue that did not disrupt his day-to-day functioning. Two months before the first hospital admission, he began complaining about typical AIWS symptoms, including micropsia, altered perception of his body image, and a disturbed sense of the passage of distance and time. All sorts of objects in his environment, such as buildings and cars, looked extremely small to him. He gave up driving because cars looked so small that he lost his sense of speed and distance in relation to the cars around him. Nearby objects also looked very small, with the single exception of pill strips that he had difficulty opening. Moreover, even though he knew it was not possible, he felt as if he could ‘step over’ long distances in a flash, such as the 50 km from his suburban town to the center of Tokyo. Additionally, he felt that days passed extremely quickly, as if in a single moment. He also sometimes felt his body was slightly enlarged or shrunken compared with normal. These AIWS symptoms persisted all day long during the depressive episodes.
+In addition to the typical AIWS symptoms described above, he also complained of disturbances in high-order cognition. For instance, he said, “I cannot sense how important the news is. For example, when I see news about a serial murder on television, I can understand intellectually how sad it is, but I cannot realize it emotionally”. Similarly, he said, “I cannot appreciate the value of money. Even if there were a ¥10,000 bill in front of me, I wouldn’t care about it because I can’t realize how much value it would have”. Although his bowel movements and urination were normal, he complained of a decreased urge to defecate and urinate.
+The depressed mood, loss of interest and pleasure, psychomotor retardation, fatigue, and reduced concentration gradually worsened. He was referred to a neurologist. Organic causes were ruled out as follows: his blood-sugar level and blood pressure were well controlled with insulin injections and oral medications; he was a non-drinker, had no history of head trauma, and took no medications associated with adverse reactions that could mimic depression, such as beta-blockers and cimetidine. Neurological examinations and laboratory tests including endocrine evaluations and an HIV test, electroencephalography, and brain magnetic resonance imaging (MRI) detected no abnormalities. He was then referred to a psychiatrist. After confirming that he was not experiencing a manic episode, was not using illicit drugs, and had not experienced any recent stressful life events, he was diagnosed as having a severe depressive episode with AIWS. His condition worsened to the degree that he could not continue working despite taking paroxetine, and he was hospitalized for the first time.
+At this first admission, he was bed-ridden all day because of severe depressive symptoms. Administration of amitriptyline (75 mg/day) and perphenazine (6 mg/day) induced gradual improvement of depressive and AIWS symptoms. He was discharged on day 47 after he had remitted almost completely from the depressive episode, with the exception of easily becoming fatigued and waking at night. At that time, he was also completely remitted from AIWS. His day-to-day functioning returned to normal, and his work and life continued as they had before the episode began.
+Three years after discharge, he relapsed into another major depressive episode, again simultaneously presenting with AIWS. The symptoms worsened despite the use of amitriptyline (50 mg/day) and aripiprazole (6 mg/day) in the outpatient clinic. The Visual Perception Test for Agnosia detected nothing abnormal. His thoughts became stunted and he became very inactive, lying in bed all day. He continuously refused inpatient treatment because he delusionally believed he was too poor. Upon the strong recommendation from his family, 8 months after this recurrence, he was admitted to the hospital with recurrent severe depressive symptoms and AIWS at the age of 67 years.
+At this second admission, he was alert and oriented, but had prolonged speech latency and spoke in a slow and quiet manner without making eye contact. His face was unshaven and he did not smile. Dementia was ruled out as a plausible cause of his symptoms for the following reasons: 1) his Mini-Mental State Examination (MMSE) score was 28/30 during this depressive episode, 2) he made a complete recovery from the observed reduction in concentration and processing speed after treatment of the first episode, 3) he exhibited no other signs of recognizable cognitive decline such as impaired executive function, learning, memory, language, or social recognition, and 4) he did not exhibit any typical symptoms of common dementia subtypes, such as amnesia, fluctuating cognition, visual hallucinations, extrapyramidal symptoms, or behavioral symptoms. Evidence of depressive symptoms and AIWS was comparable between the first and second episodes. He scored 30/63 on the Beck Depression Inventory-II (BDI-II), indicating severe depression. An ophthalmologist confirmed no eye/visual abnormalities with the exception of bilateral cataracts. Pre-therapy FDG-PET was performed as described below. After 2 weeks of maprotiline (75 mg/day) had no effect, twice-weekly ECT, duloxetine (60 mg/day) and mirtazapine (45 mg/day) were administered. He remitted completely from AIWS and almost completely from the depressive episode after 12 ECT sessions, except for a mild reduction in concentration. He scored 12/63 on the BDI-II, which also indicated significant recovery from depression. He was discharged after 75 days, just after post-therapeutic FDG-PET was performed.
+We obtained the pre- and post-treatment FDG-PET images of the brain during the second admission. The patient was kept at rest in supine posture with a blinder in a quiet and dim room from 10 min before each PET examination until the end of the scan. Scans were recorded with a PET scanner (Advance NXi; GE Medical Systems, Milwaukee, WI, USA) 45 min after the injection of 296 MBq FDG.
+Upon visual inspection, the pre-treatment FDG-PET images depicted moderate hypometabolism in the frontal cortex and relative hypermetabolism in the occipital and parietal cortices . These abnormalities improved slightly after treatment .
+Statistical analysis was performed in the following steps: (1) morphological co-registration between pre-and post-treatment FDG-PET; (2) normalization of voxel values to the global mean voxel counts using proportional scaling; (3) subtraction of pre-treatment from post-treatment images to obtain pre-post difference images; (4) mean and standard deviations of voxel values were calculated for the difference images; and (5) identification of area with statistically significant difference, using a cutoff value of z > 2 and extent threshold k > 200. These methods are part of the standard process for subtracting ictal single photon emission computed tomography (SPECT) coregistered to MRI (SISCOM), which is generally used for comparing ictal and interictal SPECT images in epileptic patients . The statistical analysis showed that metabolism decreased after treatment in the posterior half of the cerebral cortex, including the posterior part of the bilateral temporal cortex, the occipital cortex, the inferior part of parietal cortex, precuneus, and posterior cingulate cortex . No area showed statistically significant increases in metabolism after treatment.

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+A 48-year-old Japanese woman had a sudden onset of severe headaches early in the morning during work and was transported to a local hospital. She was alert-oriented and had no neurologic deficits. She had a medical history of atopic dermatitis and metal allergy that had discouraged her from wearing any jewels.
+A head computed tomography (CT) scan demonstrated a subarachnoid hemorrhage (SAH) around the basal cistern with predominant SAH in the left sylvian cistern. A three-dimensional-CT angiography revealed a left internal carotid artery (ICA)-posterior communicating artery (Pcom) aneurysm. Although an emergent aneurysm clipping surgery was scheduled, the patient preferred a coil embolization rather than an open surgery so that she was referred to us for a coil embolization.
+On the next day after the onset, a coil embolization was performed using a simple technique under the general anesthesia. The left ICA angiogram confirmed an irregular-shaped aneurysm measuring 7.7 mm in the maximum diameter at the left ICA-Pcom junction. Besides the ICAPcom aneurysm, aneurysms at the bilateral middle cerebral artery (MCA) bifurcations and at the top of the right ICA were also revealed. Given the distribution of SAH as well as the size and the shape of the aneurysm, the left ICA-Pcom aneurysm was believed to be the cause of the SAH.
+A guiding sheath (Flexor shuttle 7F × 90 cm ST 0.100”/2.54 mm) was advanced to the pre-petrous portion of the left ICA. A microcatheter (Excelsior SL-10 pre-shaped 90°) was placed in the aneurysm using a manual-shaped intermediate catheter (TACTICS 120 cm STR). Seven coils were used for the complete obliteration of the aneurysm (Raymond-Roy occlusion classification class I) and are listed in . The patient recovered well without any neurologic deficits. The head CT scan right after the embolization showed no abnormal findings, as shown in
+Despite no neurologic deficits after the surgery and no abnormal findings on a MRI 7 days after the coil embolization, an MRI study performed 24 days after the embolization demonstrated a round lesion beside the posterior horn of the left lateral ventricle, as shown in . The lesion showed homogeneously moderately high intensity on the T2-weighted image (T2WI) and the fluid-attenuated inversion recovery (FLAIR) sequence, mildly high intensity on the apparent diffusion coefficient (ADC) map but isointensity on diffusion-weighted imaging (DWI). An MRI taken 44 days after the surgery showed multiple patchy lesions at separate locations of the left frontal and parietal lobes. The lesions demonstrated high intensity on FLAIR as the previous one. An MRI obtained 70 days after the surgery still demonstrated an even larger high intense lesion on T2WI, FLAIR, and ADC map and an isointensity on DWI in the left frontal lobe, though the previous lesion had disappeared. An MRI taken 146 days after the surgery showed complete disappearance of the abnormal high intense lesions finally.
+Meanwhile, the ratio of eosinophils (EOS) among the leukocytes was 3.0% (0.0–7.0%) before the surgery, and it elevated up to 9.7% 16 days after the coil embolization and got back to 2.6% 147 days after the surgery, as shown in .
+Despite the MRI findings, the patient showed no neurologic deficits and complained of only mild headaches throughout the course. No specific treatments were performed, and the headaches gradually subsided and finally resolved completely.
+The patient subsequently underwent a metal skin patch test that showed positive against only zinc though the patch test covered neither titanium, tungsten, nor molybdenum, as shown in .

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+A 3-week-old girl, with a family history of maternal unilateral retinoblastoma, presented for evaluation of leukocoria right eye (OD). On examination, visual acuity was fix and follow in both eyes (OU) and intraocular pressures were normal OU. External examination documented obvious leukocoria OD. Fundus evaluation OD revealed a white macular tumor measuring 16.0 mm in largest basal dimension and 6.1 mm in thickness, and with overlying mild vitreous seeding and surrounding extensive serous retinal detachment. Fundus evaluation of the left eye (OS) detected a solitary mass measuring 2.0 mm in basal dimension and 1.0 mm in thickness, located within 2.0 mm from the foveola. A diagnosis of bilateral familial retinoblastoma, group D OD and group B OS, was rendered and treatment with intravenous chemoreduction (CRD) using vincristine, etoposide, and carboplatin was initiated. Following therapy with individual tumor consolidation, all retinoblastomas were regressed.
+At 6-months follow-up, the right eye remained under control, but the left eye revealed a subtle recurrence of the juxtafoveal tumor and HH-OCT (iVue Optovue, Fremont, CA) revealed an intact macula with adjacent tumor recurrence , measuring 2750 µm in diameter and 792 µm in thickness. The recurrence was 615 µm from the foveola. Treatment with intraarterial chemotherapy (IAC) using Melphalan 5 mg was performed and complete tumor control was achieved with 1 cycle , leaving a concave scar of 2750 µm in diameter and 120 µm in thickness, located 663 µm from the foveola. In addition, there was underlying choroidal thinning and preservation of the foveal microanatomy documented by HH-OCT OS . The findings remained stable on last follow-up at 2 years following IAC.

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+A 45-year-old man was referred to our center due to Wolff-Parkinson-White (WPW) syndrome for radiofrequency ablation. General physical examination was normal. Electrocardiography (ECG) showed pre-excitation in favor of left posterior accessory pathway (AP). Echocardiography was also normal.
+Guided by fluoroscopy, right atrium (RA), right ventricle, and coronary sinus catheters were introduced into the corresponding heart chambers. Basic electrophysiology study confirmed that AP was located in the posterior part of mitral valve ring; so we decided for TSP. This was the first time we used HeartSpan Steerable (Merit Medical Systems, South Jordan, UT, United States) sheath and the needle for TSP; in the previous TSP procedures, we used the AgilisTM sheath (Abbott, Saint Paul, MN, United States). Withdrawal of trans-septal sheath from superior vena cava into RA after 2 jumps usually places the introducer system in the fossa ovalis; but in this patient, this maneuver did not work despite several attempts. Finally, we could place the sheath into lower part of the interatrial septum, just above coronary sinus catheter in left anterior oblique projection. Jerky puncture with the needle was done and small amount of contrast injection showed that the needle has traversed the interatrial septum. So, we advanced the steerable sheath over the needle to the left side, and then the needle was withdrawn. However, to our surprise, contrast injection into the side branch of the sheath showed that it was in the left ventricle (LV) rather than the left atrium (-A). We advanced the 0.032” guidewire through the sheath to LV, and retracted the sheath to RA. Continuous arterial blood pressure monitoring did not show hemodynamic compromise, nor did echocardiography show pericardial effusion; so we decided to perform radiofrequency ablation of AP via the retrograde trans-aortic approach that was successful (-B).
+We transferred the patient to coronary care unit (CCU) for better hemodynamic monitoring. On the next day, transthoracic and trans-esophageal echocardiography showed LV outflow tract to RA jet (-C and -D respectively). The patient was discharged uneventfully. Follow-up echocardiography showed that the tract was present for up to 18 months without any evidence of cardiac enlargement . Since the patient was asymptomatic, endovascular or surgical closure was not attempted.

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+An 82-y-old woman, gravida 2 para 2, suffering from right vulvar swelling and pus drainage for 1 week was transferred to our hospital. She presented with a remarkable swelling of her vulva as well as her right leg. Computed tomography scan and magnetic resonance imaging showed a 75 mm irregular mass in her right vulva; additionally, her pelvic and inguinal lymph nodes were markedly swollen. However, we did not detect any instance of distant metastases, and neither did the patient have a family history. Incidentally, the patient had been diagnosed with endometrial cancer stage IA, and she had undergone a total abdominal hysterectomy and bilateral salpingo-oophorectomy 3 y ago. Histological diagnosis of the hysterectomy specimen had confirmed endometrioid carcinoma (grade1, pT1a cN0 cM0) (shown in Fig. a). However, lymphovascular space invasion was observed over the uterine wall (shown in Fig. b). No adjuvant therapy had been administered post-surgery. The current vulvar biopsy revealed small atypical cells with necrosis, a high nucleo-cytoplasmic ratio, and a proliferating solid mass (shown in Fig. c, d). The patient’s tumor marker levels were as follows: cancer antigen 125 – 20.2 U/mL (normal value: ≤ 35.0 U/mL), cancer antigen 19–9 < 2.0 U/mL (normal value: ≤ 37.0 U/mL), squamous cell carcinoma antigen – 1.0 ng/mL (normal value: ≤ 1.5 ng/mL), neuron-specific enolase > 370 mg/mL (normal value: ≤ 16.3 mg/mL), and pro-gastrin releasing peptide – 53.4 pg/mL (normal value: ≤ 80.00 pg/mL). The vulvar SCNEC was thought to be a primary or secondary SCNEC. The tumors grew daily. However, owing to the patient’s age and poor prognosis, only palliative care was provided for the pain management. Unfortunately, the patient died of the disease within 1 month.
+Immunohistochemical staining of the vulvar mass revealed that most of the vulvar tumor cells were positive for AE1/AE3, CAM5.2, neuron-specific enolase, CD56, and chromogranin A (shown in Fig. a). On the contrary, the tumor cells tested negative for MCPyV (shown in Fig. b), CK20, synaptophysin, c-kit, estrogen receptor, progesterone receptor, p16, and adrenocorticotropic hormone. Retrospectively, immunohistochemical and virological analyses had been performed for the initial endometrial endometrioid carcinoma. Immunohistochemical staining had revealed that the tumor cells were positive for CD56 and chromogranin A (shown in Fig. c). Notably, endometrial cancer cells infiltrated into lymphatic vessels are also positive for chromogranin A. Additionally, the tumor cells were negative for MCPyV and CK20. Furthermore, the HPV DNA typing analysis (types 6, 11, 16, 18, 30, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 66) of the formalin-fixed, paraffin-embedded specimens of the vulvar tumor was negative (PapiPlex™, GeneticLab Co., Hokkaido, Japan) (shown in Fig. ). Therefore, the vulvar tumor was suggested to be a recurrence of the endometrial cancer rather than a primary vulvar HGNEC (shown in Table ).

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1440_en.txt

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+A 42-year-old man with no previous medical history presented with mild dyspnea on exertion and abdominal distension that lasted for a week. Computed tomography (CT) revealed a huge homogeneous mass completely obstructing the right ventricle and extending into the pulmonary trunk . CT findings showed little evidence of blood clots and moderate amounts of pericardial effusion . The patient was admitted via the emergency room for further evaluation and scheduled for echocardiography the next day. However, he suddenly collapsed the next day while on his way to an echocardiography. Cardiopulmonary resuscitation (CPR) was performed immediately by medical staffs, but heart rhythm did not recover. Accordingly, an extracorporeal membrane oxygenation (ECMO) device was inserted percutaneously via the left femoral artery and right femoral vein and ECMO support was urgently initiated. Subsequently, a pericardial window was created at bedside, and about 350 cc of dark blood colored effusion was drained. Soon afterward, blood pressure stabilized but consciousness was not confirmed. But his light reflexes remained intact. Based on consideration of right ventricular outflow tract (RVOT) obstruction in the initial CT scan, we decided to remove the mass from the right ventricle immediately. Surgery was performed using a median-sternotomy approach. Initially, an arterial cannula was placed in the distal aspect of the ascending aorta, and the superior and inferior venae cavae were cannulated to establish cardiopulmonary bypass (CPB). After aortic cross-clamping, the pulmonary trunk and RVOT were incised. By intra-operative gross visualization, the tumor was located in the RVOT and protruded from endocardium of the right ventricle out of epicardium of the right ventricle and also extended toward and was attached to the right leaflet of the pulmonary valve . The tumor was fragile and considered highly likely to be malignant and impossible to completely control, and thus, we planned chemotherapy after surgery. The main mass was resected to relieve the RVOT obstruction, and after the operation, the ECMO was removed from the operation room. However, the patient failed to regain consciousness and electroencephalography (EEG) and subsequent magnetic resonance imaging (MRI) indicated severe hypoxic brain damage. We assume CPR was unsuccessful because the mass completely blocked the RVOT. Pathology revealed the mass was an undifferentiated spindle cell sarcoma .

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1452_en.txt

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+A 4-year-old girl visited her local hospital due to abdominal pain and vomiting for one day. Then, she was admitted to our department for a giant retroperitoneal lesion, which was considered an NB.
+The girl’s abdominal computed tomography (CT) scan showed a giant retroperitoneal lesion, which was considered an NB. For further diagnosis and treatment, she visited our department. Her symptoms such as abdominal pain and vomiting had disappeared spontaneously without treatment after admission.
+Previously, she did not have a specific past medical history.
+The girl did not have any significant family history. Both her father and mother were healthy.
+On physical examination, a mass was found on palpation of abdomen, mainly in the left upper and left lower quadrants, extending to the right lower quadrant, of about 10 cm × 7 cm in size. It was firm mass without tenderness, and had an unclear boundary and limited mobility.
+Tumor markers revealed a neuron-specific enolase level of 42.45 ng/mL. All other blood test findings, including other tumor markers, coagulation, liver and renal function tests, were within normal values.
+Ultrasonography showed a giant hypoechoic mass in the left retroperitoneal space, and the mass had a patchy strong echogenicity and no obvious cystic area. The lesion size was 12.4 cm × 10.5 cm × 6.3 cm with irregular morphology, and the mass crossed the midline. A tumor blood supply vessel with a diameter of 0.3 cm branched from the abdominal aorta . Contrast-enhanced CT showed that the huge lesion appeared well defined and was 123 mm × 85 mm in maximum cross-section, while the inferior mesenteric artery was fully encased 360°. Mixed density and patchy calcification were seen within the mass, the solid component was significantly enhanced, and adjacent structures were pushed out. The radiologists considered it to be a tumor (NB?) .
+To clarify the diagnosis and decide the next treatment, ultrasound-guided abdominal mass aspiration biopsy was performed. Pathology revealed a retroperitoneal neoplastic lesion, and some cells were spindle-shaped and considered Schwann stroma. As a whole, the tumor was differentiated, while some of the cells were suspected to have undergone ganglion cell differentiation. Some areas appeared to be immature, but no definite NB nesting mass was observed. Immunohistochemical results showed calretinin (+-), Syn (+-), NF (+-), and SOX10 (+-). Therefore, the pathologists first considered it to be a GN .

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1479_en.txt

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+A 47-year-old Caucasian man with a past medical history significant for noninsulin-dependent diabetes mellitus, hepatitis C, past alcohol abuse and cirrhosis was admitted to our medical intensive care unit with an upper gastrointestinal bleed. On presentation, his blood pressure was 104/70mmHg, heart rate 137 beats per minute, temperature 37.2°C and respiratory rate 24 breaths per minute. On examination, he was pale and icteric, and had a mildly distended abdomen with no discernable organomegaly. Cardio-respiratory examination was normal. He was confused and agitated with no focal neurological signs. His white blood count was elevated at 23.7 × 109//L with 24% bands, with a hemoglobin of 78g/L and platelets of 83 × 109/L. Albumin was 19g/dl (normal 32 to 49g/L), total bilirubin 83.3μmol/L (normal 3.4 to 20.4μmol/L), aspartate aminotransferase (AST) 32 IU/L (normal 7 to 42 IU/L), alanine aminotransferase (ALT) 35 IU/L (normal 1 to 45 IU/L), alkaline phosphatase (ALP) 32 IU/L (normal 25 to 120 IU/L), international normalized ratio (INR) of 1.84, arterial ammonia 151μmol/L (normal 11 to 35μmol/L) and lactate of 6.1mmol/L (normal 0.6 to 1.7mmol/L). His blood urea nitrogen (BUN) and creatinine were 9mmol/L and 124μmol/L, respectively.
+The patient was electively intubated for airway protection and to facilitate endoscopy. He was resuscitated with crystalloids, 5% albumin, packed cells and fresh frozen plasma and treated with vancomycin and piperacillin/tazobactam for presumed sepsis. Ultrasound and Doppler of his upper quadrants was consistent with cirrhosis with normal blood flow and splenomegaly. An upper endoscopy revealed grade 4 esophageal varices with no active bleed. Over the next few days, the patient became progressively unresponsive (off sedation) with his ammonia level rising above 200μmol/L despite aggressive treatment with lactulose and rifaximin. Neurologic assessment revealed posturing to painful stimuli with a poorly reactive pupillary reflex. Computed tomography of the head revealed diffuse white matter edema prominent in the posterior temporal, parietal and occipital lobes. Brain MRI confirmed diffuse white matter edema with temporal and occipital lobe predominance consistent with the diagnostic pattern for PRES . His course was complicated by the development of tonic-clonic seizures which were controlled with intravenous levetiracetam. His pupils became fixed and non-responsive. Transcranial Dopplers (TCD) of the middle and posterior cerebral arteries demonstrated a marked reduction in cerebral blood velocity consistent with severely increased intracerebral pressure (ICP). As an extraordinary salvage method to control the patient's severe ICP, we lowered his core body temperature to 32°C with the addition of propofol and mannitol, titrated to keep serum osmolarity < 310mmol/L. Induced hypothermia was maintained for 48 hours during which time he regained normal pupillary reflexes with marked improvement in TCD velocities. During the passive rewarming phase, the patient developed massive hematemesis. He required massive transfusion and Minnesota tube placement as attempted banding via endoscopy was unsuccessful. The patient underwent an emergency transjugular intrahepatic portocaval shunt (TIPS) placement followed by repeat induced hypothermia (32 to 34°C). Due to the anticipated increase in the serum ammonia level following the massive gastrointestinal hemorrhage, we initiated high-flow continuous venovenous hemodiafiltration (CVVHD) to facilitate ammonia removal. The CVVHD was associated with a fall in the ammonia level . At this time, the patient was again passively rewarmed and the propofol discontinued. His neurological status improved slowly over the following week becoming more alert and responsive and allowing extubation. A repeat MRI of the brain showed interval improvement in extensive white matter signal abnormality most consistent with resolving PRES. He was discharged home with no neurological sequela apart from amnesia for the entire hospital stay. The patient has returned to work part-time and is currently listed for liver transplantation.

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+A 67 year-old male presented to his local hospital with six weeks of extreme lethargy. He complained of non-radiating chest and epigastric pain with associated breathlessness and anorexia. On further questioning he admitted to 25 kg weight loss over the previous six months. He reported a past history of empyema occurring decades previously.
+Examination revealed normal heart sounds, an irregular tachycardia with a pulse of 100 beats/min, raised jugular venous pulse, widespread peripheral edema, vesicular air entry to lungs, no abdominal signs, and no lymphadenopathy.
+Vital signs revealed a pyrexia of 39 °C, relative hypotension of 110/67 mmHg, pulse oximetry 95 % on air, a tachypnea of 26 breaths/min and normal urine output.
+Laboratory investigations showed hemoglobin 57 g/L (125–160 g/L), MCV 71 fL (80–100 fL), white cell count 33.6 × 109/L (4-11 × 109/L), CRP 218 mg/L (<5 mg/L), sodium 127 mmol/L (135–145 mmol/L), potassium 5.9 mmol/L (3.5–5.5 mmol/L), creatinine 111 mmol/L (60–110 mmol/L), albumin 17 g/L (35–55 g/L), bilirubin 9 mg/L (0–17 mg/L), ALT 182 U/L (7–56 U/L), ALP 203 (44–107 U/L). Blood film demonstrated neutrophilia with left shift consistent with severe bacterial infection, and evidence of anemia including microcytosis, polychromasia, target cells and pencil red blood cells.
+Initial treatment included transfusion of 4 units of packed red blood cells, treatment of heart failure with diuresis and of sepsis with intravenous broad-spectrum antibiotics (tazobactam/piperacillin).
+Serial electrocardiograms showed sinus tachycardia with paroxysmal atrial fibrillation and widespread ST elevation of about 2 mm in leads II, III, aVF, V3-V6 , which later normalized. Serial troponin I ultra over a 24 h period after presentation were 695, 538, 491 ng/L (<20 ng/L) respectively. It was thought this represented cardiac stress secondary to persistent tachycardia and profound anemia. Thoracic radiogram showed a small left-sided pleural effusion .
+Echocardiography was obtained and showed mild left ventricular dilatation with severe dysfunction and an ejection fraction of 25 %. There was also a 0.9 cm apical, 1.4 cm anterior and 1.3 cm posterior simple pericardial effusion without hemodynamic compromise or tamponade. For this reason, pericardiocentesis was not performed.
+Computed tomogram of chest abdomen and pelvis demonstrated right lower lobe pulmonary artery embolus with infarction of lung parenchyma, pneumopericardium and pericardial effusion , fixed large hiatus hernia with a mass , enlarged 18 mm celiac node and unremarkable appearances elsewhere. Subsequent gastroscopy confirmed a large hiatus hernia with a bleeding ulcerated gastroesophageal junction tumor . Serosal breaching by this mass led to fistulation into the adjacent pericardium. Histological diagnosis was subsequently confirmed as poorly differentiated adenocarcinoma.
+After an initial improvement with antibacterial therapy and hemodynamic stabilization, drainage of his contaminated pericardial cavity was considered, but the patient rapidly deteriorated with uncontrolled sepsis and multi-organ failure. Management of a complex case such as this requires multidisciplinary team discussion. It was felt that aggressive management of a cachectic man with a poor cancer prognosis and a multiple serious clinical conditions arising from this was not in his best interest as he was unlikely to survive intervention or surgery. These discussions included the patient and his family, and led to a palliative management approach.

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+Our patient was a 48-year-old woman with a history of two previous cervical surgeries, the first one in 1987 and the second in 2003, with placement of titanium plates and screws at C4-C5 and C5-C6. She was seen at the clinic in 2005 with a 2-month history of fatigue, chills, headache, nausea, and asymmetric arthralgia. She also had episodes of malar rash after sun exposure and cutaneous fluctuating rash in the trunk. Physical examination revealed arthritis of the left shoulder and left ankle, livedo reticularis, and erythematous cutaneous rash in the thorax. No infection foci were detected. Laboratory studies revealed thrombocytosis 485,000 cells/mm3 (normal range 130,000–400,000 cells/mm3), elevated C-reactive protein (CRP) 75 mg/dl (normal range 0.1–1.0 mg/dl), and erythrocyte sedimentation rate (ESR) 40 mm/h (normal range 0–20 mm/h). Autoantibodies were negative, and complement levels were within normal range.
+From 2005 to 2007, she had no treatment, and her symptoms had a fluctuating course. In 2007, fatigue, rash, and arthralgia appeared again, and she developed edema in her hands and feet. Rheumatology started prednisone and methotrexate without improvement. Six months later, dysphagia, halitosis, and “sputum” production of purulent aspect were added to the patient’s symptoms. She consulted an ear, nose, and throat specialist, who did not find any abnormality.
+She continued with elevated CRP, ESR, and thrombocytosis. Labeled leukocyte single-photon emission computed tomography (SPECT) suggested spondylitis in the cervical spine (C4-C6) and revealed an inflammatory process in the nasopharynx, an increase in the prevertebral space of > 2 cm, and free air in this area . An esophagogram with hydrosoluble contrast revealed a posterior pharyngoesophageal diverticulum with a fistula to C6 . The patient’s x-rays of the lateral column after the cervical spine anterior fixation in 2003 showed preserved prevertebral space, and intersomatic C4-C5 box and plate were 5 mm anterior to the vertebral bodies, pressing the esophagus .
+The patient was taken to surgery; screws and plates were removed from C4 to C6; surgical debridement was performed; and the fistula and diverticulum were removed with cricopharyngeal myotomy and esophageal repair. Esophagography with water-soluble contrast showed no leak after surgery, but the lumen of the esophagus at C4–C6 was increased in diameter with diminished compliance. Removed plates, screws, and tissue were cultured and grew Streptococcus milleri. The patient was treated with oral amoxicillin 1 g every 8 h and probenecid for 4 months, until a gammagram was negative. Her fatigue, arthralgia, rash, and livedo reticularis as well as dysphagia disappeared. Her acute-phase reactants normalized.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1497_en.txt

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+A 49-year-old man was hospitalized due to pleuropneumonia. Transthoracic echocardiography in parasternal and modified apical view showed a markedly dilated coronary sinus . There was no evidence of valvular heart disease and diameters of cardiac chambers were within normal limits. Systolic and diastolic function of the left ventricle and estimated pulmonary systolic pressure were in normal range. All pulmonary veins drained into the left atrium. In order to reveal the cause of coronary sinus dilation an agitated saline injection was given into the left antecubital vein. The contrast entered first into the coronary sinus and subsequently appeared in the right atrium. Similarly, when the saline injection was given into the right antecubital vein, the contrast agent appeared first in the dilated coronary sinus and thereafter entered into the right atrium . Transesophageal echocardiography showed absence of right SVC, presence of left SVC at lateral border of left atrium and no evidence of any other structural abnormalities of the heart and great thoracic vessels . An upper venous digital subtraction cavography confirmed the absence of the right SVC and the presence of persistent left SVC . Surface electrocardiogram and laboratory exams were within normal limits. Abdominal sonography verified normal position and structure of visceral organs.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_149_en.txt

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+We report the case of a 46-year-old female non-smoker without medical history of interest, who had been working in a cosmetics packaging company for 20 years. She had undergone daily exposure to several substances including a red azo dye known as Sudan red.
+Over the past 15 years, the patient had experienced dyspnea, dry cough, occasional wheezing, facial edema, rhinitis and conjunctivitis. These symptoms had worsened in the last 3 years; she had frequently required emergency-room assistance for acute episodes of bronchospasm and had been admitted to hospital on four times. The patient’s symptoms responded to inhaled long acting beta-2 agonist and inhaled corticosteroids, and were clearly work-related since they improved on weekends, during vacations, and after she finally left her job.
+Physical examination and chest radiograph were normal. Blood tests showed eosinophilia (500 cells/mm3) and increased total serum IgE (846 KU/L). Lung function study revealed an obstructive ventilatory pattern with a forced vital capacity (FVC) of 3.14 L (91%), a forced expiratory volume in one second (FEV1) of 2.12 L (76%) and FEV1/FVC of 67%. Methacholine challenge test was positive, with a PC20 of 0.85 mg/mL and a fractional exhaled nitric oxide test (FENO) of 47.2 ppb.
+With a suspected diagnosis of OA, the patient underwent a specific inhalation challenge (SIC) with the azoic dye, in accordance with the recommendations in the European Respiratory Society guidelines . The patient was exposed to a mixture of 2 g of “Sudan Red” and 100 g of lactose powder, tipped from one tray to another 30 cm away from her face for 10 min; she continued treatment with inhaled long acting beta-2 agonist and inhaled corticosteroids due to the persistence of bronchospasm. During the procedure, she suffered dyspnea and cough, and experienced a dual positive response with a fall in FEV1 of 22% in the first 20 min and another of 33% approximately 10 h after the exposure. No significant changes in FEV1 were observed in response to a control challenge of lactose powder alone conducted on a separate day .
+Induced sputum samples were obtained previously and in the 24 h following the procedure, with a rise in the percentage of eosinophils from 10 to 65%. Methacholine and FENO tests did not present significant variations from the results obtained prior to the SIC. The diagnosis of OA due to Sudan Red was established, and the patient was advised to avoid the causal agent.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1521_en.txt

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+A 56-year old woman presented with chronic back pain. No history of trauma and no other associated symptoms. Patient’s personal and family medical histories did not show positive signs and symptoms of any splenic pathology. Physical examination likewise did not show any palpable splenic mass or splenomegaly. Laboratory workup was within the normal limits. She underwent thoracolumbar MRI to investigate her chronic back pain which incidentally showed 5 cm splenic mass which appeared hyperintense on T1-weighted images .
+She was admitted in our institution and was subsequently prepared for laparoscopic splenectomy. Preoperative cardiopulmonary screening did not reveal any significant comorbidities. She had previous immunization as per established protocols for elective splenectomy. On surgery under general anesthesia, she was positioned in right lateral semi-decubitus position. A 10 mm Hasson trocar was inserted through the left periumbilical area followed by CO2 insufflation. Three more trocars (10 mm, two 5 mm trocars) were inserted at the left subcostal area. Abdominal inspection was done. Splenic artery and vein were identified and doubly ligated and clipped. Afterwards, splenocolic, lienorenal and phrenicosplenic ligaments were dissected and proceeded with ligation of the short gastric vessels. The spleen was then extracted. Grossly, the spleen was enlarged to 6 × 4 × 10 cm (A and 2B) and weighed 380 g with well-defined 3.8 × 3.2 × 4.2 cm mass predominantly cysts measuring less than 5 mm in diameters and containing serous and mucinous fluid. No solid or complex areas were identified. The rest of the splenic parenchyma is normal. Perioperative course was uneventful and the chronic back pain resolved. Final histopathological result was splenic lymphangioma.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1549_en.txt

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+On July 24, 2022, a 4-year-old pregnant Simmental beef cow (approximately 600 kg, 268 days gestation) stopped eating and had not drunk water for 8 days. The cow was not producing any feces despite being given 1 kg of sodium sulfate and 8 l of vegetable oil twice.
+Primary symptoms
+The affected cow had an increased abdominal circumference , was dehydrated (as evident by the recession of the eyes in the orbits and skin tent duration >2 seconds), and transabdominal palpation revealed a large accumulation of fluid in the rumen. The cow had a body temperature of 39.4°C, respiration rate of 42 breaths/minute, and heart rate of 74 beats/minute. The left 1–3 ribs had high-pitched “pinging” based on auscult ation and percussion. The right abomasum area was enlarged , which was hard and clearly defined on palpation. On rectal examination, the intestine was found to be empty, the intestinal wall was dry, and a small amount of black sticky feces was attached to the rectum . The fetus was confirmed to be alive by the rectal touch of the uterus.
+Laboratory examination
+Blood routine examination showed an elevated white blood cell count of 18.4 × 109/l (reference range: 4.9–12.0 × 109/l) and neutrophil count of 9.6 × 109/l (reference range: 1.8–6.3 × 109/l). There were also marked increases in the number of red blood cells (10.8 × 1012/l; reference range: 5.1–7.6 × 1012/l), hemoglobin content (154 g/l; reference range: 85–122 g/l), and hematocrit (0.75 l/l; reference range: 0.22–0.33 l/l).
+Biochemical results showed reduced potassium ions (3.2 mmol/l; reference range: 3.9–5.8 mmol/l), chloride ions (88 mmol/l; reference range: 95–110 mmol/l), and calcium ions (2.0 mmol/l; reference range: 2.43–3.10 mmol/l), with elevated creatinine (384.46 μmol/l; reference range: 88–175 μmol/l), urea nitrogen (28.2 mmol/l; reference range: 2.0–9.6 mmol/l), total bilirubin (19.23 μmol/l; reference range: 0.17–8.55 μmol/l), and γ-glutamyltransferase (29.7 U/l; reference range: 6.1–17.4 U/l).
+X-ray examination revealed a metallic foreign body in the reticulum . The rumen fluid pH was approximately 8.5. Based on the above results, the cow was diagnosed with TR and AI. Based on previous reports , the diagnosis of TR can be confirmed by foreign body tests and X-ray examination. However, the differential diagnoses include forestomach atony (FA), rumen obstruction (RO), omasal obstruction (OO), left displaced abomasum (LDA), abomasal torsion (AT), and intestinal obstruction (IO) .
+Treatment plan
+Both TR and AI were treated surgically. To save the fetus, a cesarean section was performed on the cow before the two operations were carried out. Medication was administered 3 hours before surgery to correct the dehydration, electrolyte disturbances (hypokalemia, hypocalcemia, and hypochloremia), and acid-base disturbances (metabolic alkalosis). describes the specific treatment plan in the present case.
+Antibiotics and anti-inflammatory agents were administered in the following preoperative injections: (i) 500 ml Ringer’s solution, 5 mg vitamin C, and 50 ml of 10% potassium chloride; (ii) 100 ml of 10% glucose and 500 ml of 10% calcium gluconate; and (iii) 500 ml of 5% glucose and 5 g ampicillin, each as a one-time intravenous injection; and (iv) 0.3 g meloxicam as a one-time intramuscular injection.
+Before surgery, the accumulated fluid in the rumen was extracted by inserting a gastric tube via the oral cavity, further relieving the abdominal pressure. After local-infiltration anesthesia with a 0.5% procaine solution, an incision was made in the middle of the paralumbar fossa in the lef t flank to open the abdominal cavity. Intraperitoneal exploration rev ealed that the wall of the reticulum had adhered to the diaphragm, although no inflammatory purulent exudate from the abdomen. The omasum was found to be approximately 0.5 times larger than normal and located in a more ventral position than normal. The volume of the abomasum was approximately 5–7 times normal and was very firm on palpation. The bowel was empty and the fetu s was active. The cesarean section was then performed. Part of the uterus was pulled out at the incision, the uterus was cut open, and the fetus was removed. The uterus was then sutured. Subsequently, the rumen was cut open and the wire attached to the wall of the reticulum was removed. The rumen was then sutured.
+The abomasum was cut open to eva cuate its contents. Xylazine hydrochloride (60 mg) w as injected intramuscularly to sedate the cow while lying down on the left side. After administering local-infilt ration anesthesia using a 0.5% procaine solution around the right lower abdominal wall in the abomasum region, the surgical incision was sele cted at the location where the AI was the hardest and made contact with the body surface. The feed material was removed a nd the abomasum was sutured. It is worth noting that we apply a slightly different approach for suturing the rumen, abomasum, and uterus from the traditional method. In particular, continuous spiral sutures were made on the mucosa of the uterus, and on the mucosa and submucosa of the rumen and abomasum with thinner polyglycolic acid (PGA) sutures (USP: 2–0), followed by continuous spiral sutures throughout the layer with thicker PGA sutures (USP: 0). Finally, cushing sutures were made with the same thicker PGA suture.
+Postoperative treatment was provided for 5 days, including (i) 2 l Ringer’s solution, 5 g vitamin C, and 50 ml 10% potassium chloride; (ii) 1 l 10% glucose and 300 ml 10% calcium gluconate; (iii) 500 ml 10% concentrated sodium chloride; (iv) 500 ml 5% glucose and 5 g ampicillin; (v) 500 ml normal saline and 600 mg ranitidine, each as a single intravenous injection once per day; (vi) 20 mg neostigmine methylsulfate as a single subcutaneous injection twice a day; (vii) 20 ml compound vitamin B as a single intramuscular injection twice a day; and (viii) 100 IU of oxytocin as a single intramuscular injection once a day.
+On the seco nd day after the surgery, the cow began to ruminate, had an appetite, was in good spirits, and passed a large amount of black mucous feces. The cow fed on 3 kg hay and 2 kg concentrate. On the third and fourth days after surgery, feed intake increased, with 7 kg hay and approximately 5 kg concentrate consumed. On the fifth day, the fetal coat was completely excreted, but the feed intake decreased, the number of ruminations was reduced, the rumen peristalsis was weakened, and only a small amount of feces was excreted. On the sixth day after surgery, the cow began to drink a substantial amount of water, the abdominal circumference increased, rumination stopped, only a small amount of hay was eaten, and no excrement was observed. With rumen effusion, the high-pitched “pinging” could be heard by auscultation of the left side of ribs 1–3 with percussion, and palpation of the genuine stomach area was slightly hard. Therefore, we suspected that the abomasum had become obstructed again.
+Routine blood examination showed an elevated white blood cell count of 14.5 × 109 and neutrophil count of 7.2 × 109/l, whereas no obvious abnormalities were found in biochemical parameters. On the eighth and ninth days after the operation, Zeng Ye Cheng Qi Tang (a traditional Chinese medicine powder consisting of 300 g rhubarb, 600 g mirabilite, 60 g Magnolia officinalis, 80 g Fructus aurantii immaturus, 120 g Scrophularia ningpoensis, 120 g Ophiopogon japonicus, 120 g Rehmannia glutinosa, 150 g areca nut, 60 g Aucklandia, and 200 g Raphanus seed) was administered, which is often used to treat ruminal impaction and IO, along with 1 l of vegetable oil. The abomasum area was massaged at the same time as the administration of the formulation (1 hour each time, three times/day). Furthermore, a subcutaneous injection of 10 mg neostigmine was administered four times/day. The cow was fed hay only (2 kg a day) and concentrate feed was stopped. As of the 11th day, the ruminant returned to normal, feed intake gradually increased, the rumen and abomasum peristaltic sound was enhanced as detected by auscultation, and normal defecation was observed. The amount of hay fed daily was gradually increased (but not more than 10 kg). After continued observation for 5 days, all indices of the diseased cow returned to normal . After 120 days, the cow made a full recovery and became pregnant again. The calf born by cesarean section is in good health .
+The animal study was reviewed and approved by the College of Animal Science and Technology, Chongqing Three Gorges Vocational College. Written informed consent was obtained from the owners for the participation of their animals in this study.

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+An 81-year-old Lithuanian woman was tested for faecal occult blood during preventive colorectal cancer screening. Test results were positive and she underwent a colonoscopy. The colonoscopy revealed a tumour in her caecum. Abdominal and thoracic computed tomography (CT) scanning revealed no metastasis. She then underwent elective surgery. During the operation, a 6×5cm tumour was found in her caecum. Her MD was found 40cm from the hepatoduodenal ligament . A right hemicolectomy was performed to excise the MD from her jejunal loop. After the operation, she underwent chemotherapy. There were no complications related to the surgery. Histological results showed a poorly differentiated G3 adenocarcinoma of the caecum. In her small intestine a muscular layer of excised MD and mesenteric adipose tissue was found, which was pancreatic tissue morphologically. Microscopic analysis revealed pancreatic tissue without islets of Langerhans in the small intestine and mesenteric adipose tissue. Moreover, in the HP tissue, dilatation of the pancreatic ducts was observed.

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+A 53-year-old Caucasian man with FD presented to our cardiology department for regular follow-up. He reported symptomatic ventricular extrasystoles with palpitations for over ten years while he has been in good physical shape. Moreover, he complained of pain and cramps in the lower limbs. In the past, he had two operations (retractile testicles, operation of his knee), but denied further comorbidities. The family history for FD was negative. The physical examination revealed an arrhythmic pulse and a mild atrial hypertension. The ECG showed a shortened PendQ interval, i. e. PQ interval minus P-wave, of 40 ms and negative T-waves . The echocardiographic examination presented LVH about 15 mm and a mildly reduced global longitudinal strain (, Video 1). The left ventricular ejection fraction was in a normal range and no valvular damage was observed. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) was mildly elevated (160 ng/L, normal range <121 ng/L).
+FD was suspected in 2018 after performing a CMR. The CMR presented LVH [left ventricular mass (LVM) 146 g] and short T1 relaxation time, which is indicative of sphingolipid storage in an early FD. Moreover, it showed prolonged T1 time with an intramural hyperenhancement in the inferolateral wall in late enhancement sequences as a sign for fibrosis (, Video 2). Biochemical testing revealed a reduced GLA activity [<2.8 µmol/L/h (limit of quantification), normal range ≥15.3 µmol/L/h] and an increased concentration of lyso-globotriaosylceramide (lyso-Gb3, 20.0 ng/mL, normal range ≤1.8 ng/mL). The diagnosis was confirmed by a hemizygous pathogenetic mutation in exon 6 of the GLA gene [c.902G>A, p.(Arg301Gln)]. Afterwards, the patient was admitted to the Department of Nephrology to evaluate organ involvement in a multidisciplinary approach. Arterial hypertension was treated with an angiotensin receptor blocker. Kidney biopsy was performed due to unclear aetiology of proteinuria in the presence of arterial hypertension. It showed ‘zebra bodies’ and vacuoles in podocytes as a renal involvement of FD. Neurological examination detected bilateral carpal tunnel syndrome and cerebrovascular magnetic resonance showed microbleeds and white matter lesions. According to the detected mutation, an ERT with Agalsidase Beta was started in 2018. The patient presented regularly for follow-up examinations in our Fabry Centrum (CeRKiD). In 2019, CMR detected increased T1 relaxation time (1079 ms in 2019 vs. 1060 ms in 2018) and reduced LVM (−14 g) and, in 2020, lyso-Gb3 concentration decreased to a level of 9 ng/mL.
+In retrospective analysis, ECG characteristics of FD have already been present in 2008 and progressed over time . In particular, the first ECG (2008) showed a sinus rhythm with a PendQ interval of 40 ms, a PQ interval of 160 ms, a QT interval of 360 ms, and negative T-waves in II, III, aVF, V5, and V6. ST elevations were present in V1-V4 with a maximum of 0.2 mV in V2 and V3. Seven years later, the ECG showed additional negative T-waves in I and V4. The duration of the PQ interval remained stable over time while PendQ decreased. The ECG findings correlated well with echocardiographic measurements. While the diameter of the interventricular septum was constant with 15-16mm, the posterior wall exhibited an increasing thickness from 11 mm (2008) to 14 mm (2018, before ERT) and up to 15 mm (2020, two years after ERT was started). In addition, in 2020, lateral and posterior longitudinal left ventricular function was reduced.

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+A 43-year-old man, who had undergone hemodialysis therapy for chronic renal failure owing to diabetic nephropathy for 6 years and whose blood pressure had been under control (<140/80 mmHg), developed mild elevation of blood pressure (150/100 mmHg) for 2 weeks. He has not been treated with immunosuppressant agents. He suddenly showed weakness in both of his legs, and he realized that he had postural instability and that he could not walk. Subsequently, his consciousness level deteriorated. On admission, his blood pressure was 156/96 mmHg. Neurological examination showed a Glasgow Coma Scale of 14(E3V5M6). His facial expression was flat and his voice was barely audible. He had paraparesis in both lower limbs. Brain MRI demonstrated hyperintense lesions in the bilateral basal ganglia, bilateral frontal cortices, and left cerebellum on FLAIR images, and those lesions were hyperintensity on DWI and ADC maps . No arterial stenosis on MR angiography was found . He was treated with anti-hypertensive agents and continued hemodialysis therapy, and his blood pressure were controlled to 130/70 mmHg within 2 weeks. On the 7th day after admission, disturbance of consciousness and paraparesis improved, and he could walk by himself. However, we noticed that he showed parkinsonian signs including FOG, bradykinesia, and postural instability. His FOG fulfilled the criteria of “brief, episodic absence or marked reduction of forward progression of the feet despite the intention to walk” based on the 2010 workshop of clinicians and scientists interested in FOG . The score from part III of the Unified Parkinson’s Disease Rating Scale (UPDRS) was 28 points. He did not show cerebellar ataxia. Concurrently, MRI showed hyperintense basal ganglionic lesions on FLAIR images, DWI, and ADC maps persisted, although lesions on bilateral frontal cortices were diminished . His FOG and postural instability gradually improved, and UPDRS part III scores were 22 and 5 points at 2 and 4 weeks after admission, respectively. Follow-up MRI at 4 weeks after admission showed significant alleviation of the bilateral basal ganglionic lesions on FLAIR . Thus, he was diagnosed as PRES based on the acute transient neurological symptoms and MRI findings. He was treated with 150 mg of amantadine, and a combination of 300 mg of levodopa and 30 mg of carbidopa at 15th and 22st day after admission for 7 days, respectively, but he did not show dramatic improvement of FOG. Thereafter, those anti-parkinsonian drugs were discontinued.

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+A healthy, nonimmunocompromised 43-year-old female with bilateral lower extremity radiculopathy had a fluoroscopically guided percutaneous ozone treatment for degenerative lumbar disc disease . Three months later, she presented with severe back pain (VAS 9/10), bilateral lower extremity radiculopathy (leg VAS-7/10), and a partial right-sided foot drop. The C-reactive protein (CRP 27 mg/dl) and erythrocyte sedimentation rate (ESR 58 mm/h) rates were both elevated, the leukocyte count was at 7.03 thous/ul with 2100 lymphocytes; and she was also anemic (hemoglobin 11.7g/dl).
+The repeat MR of the lumbar spine demonstrated L4–L5 spondylodiscitis with paradiscal erosion consistent with a tubercular type of infection [ and ]. The patient underwent a L4–L5 transforaminal lumbar interbody fusion , with soft-tissue debridement; the purulent/ infected epidural tissues were sent for bacterial, fungal, and tubercular cultures. The rapid AFB cultures showed MA.
+The patient was discharged on intravenous cefoperazone- sulbactam 1.5 g twice daily. She, however, returned after 6 weeks with a fluid collection in the wound, and the CRP and ESR studies remained elevated. The wound was debrided and then she was discharged on intravenous amikacin 500 mg (intravenously) twice daily for 6 weeks, supplemented with oral clarithromycin 500 mg twice daily. Subsequently, she was continued on oral clarithromycin for another 6 weeks following resolution of the primary infection.

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+A 23-year-old male patient came to the emergency department at Universitas Airlangga Hospital presenting fever, anosmia, headache, and nausea 5 days before. He was diagnosed with COVID-19, confirmed by the RT-PCR amplification of SARS-CoV-2 virus nucleic acid on a nasopharyngeal swab. The patient had abnormal laboratory findings, such as lymphopenia, neutrophilia, thrombocytopenia, and high CRP, with a normal chest X-ray . The patient was treated with Favipiravir at 1600 mg per 12 h on day 1, then 600 mg per 12 h on day 2-day 5, intravenous drip of paracetamol 1000 mg every 8 h, oral vitamin C 500 mg per 8 h, and oral vitamin D 1000 IU per day according to Indonesian national COVID-19 treatment guidelines. After 10 days of treatment, the patient was still PCR positive despite no complaints. He was then discharged to continue self-quarantine at home.
+He returned to the hospital two weeks later with general weakness and fever. The fever did not resolve during his self-quarantine, was raised intermittently every 2 days, and was marked by a chilling-fever-sweating cycle. The fever temperature measured was around 39.7°–40 °C. The fever improved when the patient took paracetamol, but the fever returned 6 h later. The fever was accompanied by malaise and muscle pain. The next day the patient was fever-free and able to carry out his daily activities. The physical examination revealed a body temperature of 38 °C, a blood pressure of 112/72 mmHg, a heart rate of 93 bpm, a respiratory rate of 20 breaths/minute, and oxygen saturation of 98% under ambient air. The patient weighs 65 kg with a height of 170 cm (BMI 22.5 kg/m2). Other physical examinations were normal.
+The laboratory results reflected a white blood cell count of 8750/µL with 76.3% neutrophils, 13.5% lymphocytes, and 0.6% eosinophils. Haemoglobin level and platelet counts were 12.2 g/dL and 231,000/µL, respectively. CRP and D-dimer levels were 41.51 mg/L and 9.52 mg/L, respectively. Serum electrolytes and renal function tests were normal, with urea and creatinine serum 6 mg/dL and 0.4 mg/dL, respectively. The liver enzymes test was normal, with ALT being 14 IU/L and AST being 25 IU/L. Electrocardiography showed normal sinus rhythm and axis. The chest X-ray was unremarkable . The RT-PCR amplification of the SARS-CoV-2 virus nucleic acid test from the nasopharyngeal swab was still positive.
+From the previous history, he said that he traveled to Timika District, Papua, for office work for the last 2 years. In May 2021, the patient was infected with P vivax, with initial symptoms including fever, dizziness, nausea, and muscle pain. The patient was treated until declared fully cured. A laboratory test for malaria was performed. The rapid malaria test was positive for PAN antigen, and microscopic diagnosis on blood smear revealed Plasmodium vivax on ring form, trophozoite, and gametocyte stage . Based on anamnesis, physical examination, and laboratory results, the patient was diagnosed with confirmed COVID-19 with hypercoagulopathy and malaria vivax relapse . According to Indonesian National Guidelines for Antimalarial Treatment , he was treated with dihydroartemisinin-piperaquine (DHP) 4 tablets per day for 3 days and primaquine 2 tablets per day for 14 days. The G6PD status was not tested. The patient was given an intravenous drip of paracetamol 1000 mg every 8 h and a subcutaneous injection of heparin 5000 IU every 12 h during treatment. After six days of treatment, the patient had no complaints, and the results of laboratory tests had improved. The patient was discharged from the hospital, continued self-isolation at home, and followed up with the internal medicine outpatient clinic two weeks later. Furthermore, the patient was called later and reported feeling healthy with no complaints.

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+A 75-year old Caucasian man with a long-standing history of tophaceous gout and several recurrent episodes of arthritis during the past five years presented with a large, painful, ulcerated tophus located on the first metatarsophalangeal joint of his left foot to our emergency department. He had intentionally interrupted treatment with allopurinol four months previously; however, he did not report any recent deviations from his standard diet, any alcohol abuse or diuretic treatment. Five days before presenting to the emergency department, a tophus on the first toe of his left foot had become painful, red and swollen. He tried a course of non-steroidal anti-inflammatory drugs (NSAIDs) without improvement. Ten hours before seeking medical assistance, the tophus burst releasing a viscous, chalk-like material.
+On physical examination he had a mild fever of 37.8°C. A greyish, voluminous and ulcerated nodule containing chalky material was located on the first metatarsophalangeal joint of his left foot . Further examination revealed multiple other tophi overlying the first and second metacarpophalangeal joints of his left hand and the interphalangeal joints of his right hand , wrists, elbows , ankles, interphalangeal and metatarsophalangeal joints of the feet and heels . Two smaller ulcerated tophi were also seen on the fingertip of the left thumb and over the first interphalangeal joint of the right foot. Many joints were also deformed. The first metatarsophalangeal joint of his left foot was totally nonfunctional.
+Laboratory workup revealed leukocytosis (14.524/mm3), elevated C-reactive protein (7.21 mg/dl) and elevated serum uric acid (14 mg/dl). Radiographs of the foot showed soft tissue swelling and total destruction of the first metatarsophalangeal joint . Moderate periarticular alterations were also observed in the other joints of the foot. Cultures from the ulcerated tophus were negative. Antibiotic treatment with ciprofloxacin (800 mg/day) and intravenous administration of NSAIDs (lornoxicam 16 mg/day) was initiated.
+Due to the extraordinary size of the ulcer and the complete destruction of the underlying joint, amputation of the left foot was considered. However, before resorting to this solution, a surgical debridement with lavage of the joint was performed. Debridement was also performed on the minor ulcers. Five days after admission treatment with allopurinol (300 mg/day) was initiated. The patient improved clinically and was discharged two days later. For the next 33 days foam silver-containing wound dressing (CELLOSORB® Ag) and heterologous lyophilized collagen (BIOPAD®, equine collagen) were used on the largest of the three ulcers, on an outpatient basis, while efforts were made to keep serum uric acid levels within normal limits. All three ulcers healed completely within eight, 10 and 40 days after initial presentation, respectively . Six months after treatment, he remains symptom free, although he still refuses to comply with the prescribed uric acid lowering regimen and rejects any further surgical intervention.

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+A 52-year-old female developed mandibular sensory paresthesia and pain after 3 mo of lurasidone administration, without orofacial dyskinesia, hands tremor, limbs rigidity, bradykinesia, axial dystonia, retrocollis, torticollis, or blepharospasm.
+A 52-year-old female had been diagnosed with schizophrenia since April 2001, and was treated with various antipsychotics, including risperidone 1 mg/d, amisulpride 200 mg/d, quetiapine 200 mg/d, ziprasidone 40 mg/d, and clozapine 125 mg/d, with a duration of a few months, respectively. The most long duration of main regimen was olanzapine 10-25 mg daily (June 2013-March 2021), which was fully effective, but was discontinued due to the adverse side effect of weight gain. Consequently, the main regimen was shifted to lurasidone, initiate dose 40 mg/d then up titration to 120 mg/d since March 2021. However, she developed mandibular sensory paresthesia and pain after 3 mo of lurasidone administration, without orofacial dyskinesia, hands tremor, limbs rigidity, bradykinesia, axial dystonia, retrocollis, torticollis, or blepharospasm.
+A 52-year-old female with no history of medical disease, movement disorders or sensory paresthesia had been diagnosed with schizophrenia since April 2001.
+The patient had no developmental delay, and had elementary school education level with poor academic performance. She had introverted personality as premorbid personality and poor interpersonal relationship. She could keep her occupational function as a cleaner since young adult until now. She got married at her 20’s and divorced at her 32’ while she was diagnosed of schizophrenia. The patient denied psychiatric family history.
+We also consulted a dentist to rule out oral infection or other lesions. Both the aforementioned laboratory tests and dental consultation showed negative findings. Due to the defining features, TSS was suspected. Severity was evaluated on the basis of an Extrapyramidal Symptom Rating Scale (ESRS) score of 18 points before we changed antipsychotics to quetiapine monotherapy.
+A series of laboratory tests including complete blood count, liver function, renal function, diabetes mellitus lipid profile, copper, ceruloplasmin, thyroid function, rheumatoid factor, antinuclear antibody, immunoglobulin (Ig)A, IgG, anti-2 glycoprotein 1Ab, anticardiolipin Ab IgG, anticardiolipin Ab IgM. Anti-ENA, a venereal disease research laboratory test, HBs antigen, hepatitis C virus antibody, cryoglobulin identification, a homocysteine test and brain computed tomography (CT), were performed to rule out a secondary organic etiology. We also consulted a dentist to rule out oral infection or other lesion. The aforementioned laboratory tests and dental consultation both showed negative findings.
+The brain CT image and report are demonstrated in Figure . Technique of examination: Axial brain CT with 5 mm section from vertex to skull base without contrast enhancement; normal ventricular size; normal appearance of cerebral fissures, cisterns & sulci; no evidence of intracranial hemorrhage; no midline deviation; no abnormal parenchymal attenuation change; no definite bony fracture; well pneumatization of bilateral mastoid cells; unremarkable of paranasal sinus; symmetrical and smooth contours of nasopharynx; and left frontal scalp swelling. There is no evidence of intracranial hemorrhage.

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+The patient was a 66-year-old Chinese man with a past medical history significant for AF, not on anticoagulation per the patient’s preference, and coronary artery disease (CAD) status post-percutaneous coronary intervention to left anterior descending artery about 1 year ago, currently on aspirin, clopidogrel, and rosuvastatin. He initially presented with 2 days of chest tightness, and acute coronary syndrome was ruled out. He then suddenly developed intermittent and sharp left-sided abdominal pain. Systemic review was negative for fever, chills, nausea, vomiting, diarrhea, or hematuria. He lives in a rural town working as a farmer, and is a current smoker with about 30 pack year smoking history. He denies any alcohol abuse or illicit drug use, and has no known drug allergies. Family history is non-contributory. Current home medications include aspirin (100 mg), clopidogrel (75 mg), rosuvastatin (10 mg), furosemide (20 mg), spironolactone (20 mg), and isosorbide mononitrate (10 mg). No known drug allergies were documented.
+On admission, his vitals were normal, with blood pressure of 100/70 mmHg, heart rate of 68 beats/minute, and oral temperature of 36.3 °C. On examination, his heart rate was irregularly irregular without heart murmurs, jugular venous pressure (JVP) was normal, with no pitting edema in lower extremities. Lungs were clear on auscultation. His abdominal examination was notable for mild tenderness to palpation over the left quadrant without rebound or guarding. Bowel sounds were normal. The rest of the examination was unremarkable.
+Routine laboratory tests showed normal complete blood count, liver function tests, amylase, lipase, and thyroid function tests. Creatinine was normal at 56 μmol/L (normal range, 40–130 μmol/L) with mildly elevated blood urea nitrogen (7.29 mmol/L [normal range, 2.3–7.1 mmol/L]). Urinalysis was negative for proteinuria, infection, and hematuria. Fecal occult blood test was negative. Both lactate dehydrogenase (LDH) and alpha-hydroxybutyrate dehydrogenase (α-HBDH) were elevated (283 U/l [normal range, 135–225 U/l] and 239 U/l [normal range, 76–195 U/l], respectively). Bedside abdominal and renal vascular Doppler ultrasound were normal. Due to persistent abdominal pain of unclear etiology, a contrast-enhanced CT scan was then performed, revealing renal infarction of the left kidney . Coronary (data not shown) and aortic angiograms were negative for coronary stenosis and aortic dissection. Given the CT findings and unresolved abdominal pain, a renal angiogram was performed and showed distal occlusion of both superior and inferior segments of the left renal artery . Next, attention was paid to the left renal artery. Two guide wires were introduced into the left renal superior and inferior segments , and the Pt wire was then passed through the distal end of the occluded superior artery. A 5 × 4 mm thrombus was aspirated by a suction catheter and locally inflated using a Maverick 1.5 × 15 mm balloon, and 0.1 mg nitroglycerin and 1 mg diltiazem were injected through the microcatheter . Blood flow restoration to both superior and inferior segments of the renal artery and vessel potencies were confirmed by angiography after the aforementioned interventions , which is more clearly observed in the amplification of the images for renal angiograms after the surgery compared with before the surgery . Abdominal symptoms resolved 6 hours after the operation. LDH (230 U/L) and α-HBDH (216 U/L) decreased and eventually normalized by postoperative day 5. He was continued on all home medications and started on warfarin post-procedure with an international normalized ratio (INR) goal of 2–3. The patient was discharged on triple therapy with aspirin (100 mg), clopidogrel (75 mg), and warfarin (3.125 mg) for 1 month, followed by clopidogrel and warfarin for a further 6 months. At 6 months follow-up, the patient was symptom-free and renal function remained normal (creatinine 74 μmol/L [normal range, 57–111 μmol/L]). Repeat angiography was not performed at follow-up to avoid additional radiation exposure given low suspicion for persistent or recurrent renal infarction.

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+A 13-year-old male presented with complaints of painless swelling which was insidious in onset and gradually progressive over the right distal forearm for 3 years. He had multiple bony swelling all over the body which was asymptomatic.
+On examination of the right wrist, there was an ulnar deviation of the wrist, which was passively correctable. The distal radioulnar joint (DRUJ) was unstable. There was a palpable, non-tender, osseous prominence in the distal aspect of the ulna . He had pain on the wrist range of motion and was unable to lift heavy objects. The skin over the affected site was normal with no distal neurovascular deficit. The examination of the ipsilateral elbow and other joints was normal.
+Anteroposterior and lateral radiographs of the right forearm show distal ulnar exostosis approximately 5*2 cm in size which was Type I according to Masada classification ( and ). At the wrist, a negative ulnar variance of 15 mm was observed. There was substantial radial bowing compared to the contralateral side and the length of the ulna was 3 cm shorter.
+The patient was planned for excision of distal ulna osteochondroma through the Volar approach of the ulna . The osteotomy was done at proximal one-third of the ulna and was stabilized with LRS (two-pin above and two-pin below) and gradual ulnar lengthening was done . Deformity of the radius was not corrected as it will itself get remodeled with time ( and ). Postoperatively, the full range of motion of wrist and elbow is present . DRUJ is stable at subsequent follow-up, no additional procedure was done for DRUJ. We are still following up on the patient until skeletal maturity.

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+An Asian male, aged 63 years, presented with sudden severe bilateral leg edema. His past medical history included hypertension that was made stable by medication for over 10 years. Abdominal CT showed various lymph node swellings, including in the left subclavian, para-aortic, and intrapelvic regions . Biopsy of the para-aortic lymph node was performed; histopathological findings revealed a poorly differentiated adenocarcinoma . Immunohistochemical staining was positive for AE1/3 , PSA , and negative staining for TTF1 , synaptophysin , and chromogranin A . The patient was referred to our department since such results indicated the primary tumor occurred in the prostate. The serum PSA level of the patient was 20.3 ng/mL. Various serum tumor markers were within normal range, including NSE. MRI of the prostate showed an indistinct hypo-intensity in the left peripheral zone on T2-weighted images with a focal area of diffusion restriction (apparent diffusion co-efficient 0.63 × 10−3 mm2/s; Fig. ), diagnosed as prostate cancer of PI-RADS-v.2 category 4. MRI-fusion ultrasound-guided prostate biopsy showed PCa with a Gleason score of 4 + 3 . The final diagnosis was prostate cancer of stage IV (T2N1M1a) with aggravation in the short term. After informed consent, the patient agreed to be treated with a combination of surgical castration and abiraterone acetate. As a result, his serum PSA quickly decreased to 1.34 ng/mL and adverse events did not occur; all lymph node swellings gradually reduced on CT by 4 months after the initiation of treatment.
+However, 10 months after the initiation of treatment, serum NSE was elevated to 27.4 ng/mL (normal range: 0–10 ng/mL), without elevation of serum PSA. Furthermore, CT revealed multiple liver nodules and bone metastasis in the fourth lumbar vertebra. Pathological findings of the specimen obtained by biopsy of liver tumor, on HE staining, nests of round to polygonal cells with scant cytoplasm and infiltrated necrosis were observed as shown in Figure . The cells were immunohistochemically positive for PSMA , CD56 , synaptophysin , and negative for chromogranin A . Consequently, the patient was diagnosed with t-SNPC, and combination chemotherapy of etoposide and cisplatin was administered. The serum NSE levels quickly decreased to a nadir level of 7.9 ng/mL and metastatic sites uniformly reduced at 3 months after the initiation of chemotherapy; however, those increased after seven cycles of treatment. After informed consent, second-line amrubicin treatment was administered but the reduction in tumor growth was insufficient. FoundationOne® CDx (Foundation Medicine Inc, Cambridge, MA, USA) was used for cancer-related gene profiling of a formalin-fixed paraffin-embedded liver tumor specimen that identified a BRCA2 mutation at H1223fs*9. Considering this result, a PARP inhibitor was promising drug, however, progression of the tumor was very rapid, and finally, the patient died because of cancer-related disseminated intravascular coagulation 10 months after the initiation of first-line chemotherapy.

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+A 29-year-old man was taken to our hospital by ambulance, suffering from severe headache. He had no past medical history and did not take any medication. Head computed tomography (CT) revealed an extensive subarachnoid hemorrhage (SAH) filling basal cisterns, especially the thick hemorrhage in the interhemispheric fissure . CT angiography showed an Acom with fenestration, but no evidence of aneurysm . Three-dimensional-digital subtraction angiography (3D-DSA) demonstrated the fenestration of Acom with a small saccular aneurysm (2 mm) [Figure –]. The aneurysm arose from the inferior limb of the fenestrated segment, and it projected posteriorly [Figure –]. In addition, an accessory ACA arose from the upper limb of the fenestrated segment [Figure and ]. This patient underwent a clipping surgery via an interhemispheric approach. At the operation, we had difficulty in getting a good surgical view for an aneurysm existing behind the Acom, because we could not mobilize the Acom complex enough. Additionally, the surgical dissection behind the Acom complex was interfered by an accessory ACA . The intraoperative premature rupture occurred, and a fenestrated clip was applied to be able to preserve an accessory ACA . Immediately after the clip application, the bleeding from the ruptured aneurysm stopped. The remnant of aneurysm was not identified in the visible range, and then we finished off the operation. Postoperatively, we performed the management of brain swelling and cerebral vasospasm. Unfortunately, the re-rupture from an Acom aneurysm occurred on Day 13 [Figure –]. 3D-DSA demonstrated the recurrence of an aneurysm next to the clip . Cerebral vasospasm became progressively worse under the influence of re-rupture, and the patient died on the same day.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_184_en.txt

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+A 43-year-old male patient presented to the emergency department with a 20-day history of fever, predominantly at nights and headaches. His previous medical history is unremarkable; he only referred to a 20-year history of smoking and denied use of intravenous or recreational drugs, any prior sexually transmitted diseases, or blood transfusions. At presentation, the patient had a blood pressure of 109/75 mmHg, heart rate 87 bpm, respiration rate 24 breaths/minute, temperature 38.5°C, and oxygen saturation of 70% at atmospheric pressure. Physical examination revealed pale skin and mucosa; tongue and soft palate had lesions consistent with oral candidiasis and congestive pharynx. Pulmonary fields revealed decreased sounds without crackles or wheezing and painful hepatomegaly and extremities with hyperchromic nodular lesions on both ankles, suggestive of Kaposi sarcoma. Due to these findings, initial blood tests included HIV serology that came out positive; CBC: Hb 11.1 g/dL, hematocrit 33.8%, WBC 7,100/mm3, lymphocytes 3%, and neutrophils 95%; IgE 788.2 UI/ml; VSG 77 mm/hr; TGO 91 UI/L; TGP 66 UI/L; and DHL 2250 UI/L. Chest X-ray revealed disseminated infiltrates in both lungs. Medical management was initiated with omeprazole, metamizole, and oxygen with nasal prongs 3 L/min. On day 2 of hospitalization, the bronchoscopy fluid examination resulted positive for C. albicans and negative for other pathogenic bacteria and fungi. However, we decided to start dexamethasone 6 mg IV, trimethoprim/sulfamethoxazole 160/800 mg, nebulization with ipratropium, and budesonide due to high suspicion of P. jirovecii infection. On day 3 of hospitalization, HIV infection was confirmed with a viral load of 531,000 copies/ml and CD4+ T-cell count of 11 cells/mm3. Other studies were performed including a PPD (negative test 0 mm) and anticytomegalovirus serology (IgG positive). On day 4 of hospitalization, the infectious disease division started ART with ritonavir/lopinavir, tenofovir, and emtricitabine. During the subsequent days, the patient showed clinical improvement. However, on day 13, his clinical condition declined with progressive dyspnea, severe dysphagia, and abdominal pain. Auscultation showed basal rales in both lungs; a new chest X-ray demonstrated no changes compared with the previous one. New blood tests included CBC: Hb 14.5 g/dl, hematocrit 44%, VCM 90 fL, platelets 284,000 × 103, WBC 18,400/mm3, neutrophils 89%, and lymphocytes 5%. Serum electrolytes, glucose, BUN, and creatinine had no alterations. He developed dysphagia and episodes of oxygen desaturation partially corrected with nasal prongs. On day 19 of hospitalization, due to continuous episodes of low oxygen saturation, a chest CT-scan was ordered , showing generalized lung involvement and mediastinal adenopathy (Video 1 in Supplementary Material ).
+Supplementary Video 1 showed digitalized CT-scan of the thorax in coronal sectioning.
+Later that day, an endoscopy showed chronic reflux esophagitis (Grade D of the Los Angeles Classification System), with ulceration . On day 23 of hospitalization, dyspnea worsened; oxygen supply was administered with continuous positive airway pressure (CPAP). A pulmonary biopsy was performed on day 24, which reported CMV pneumonia ; the patient was transferred to the intensive care unit (ICU) due to persistent hypoxemia and was started on methylprednisolone 500 mg IV (maintained for 2 days) and ganciclovir 500 mg IV, and ART was changed to efavirenz, emtricitabine, and tenofovir, to decrease pill intake (1 pill/day). Intravenous sedation was initiated and oxygen supply was maintained with CPAP. The patient had 2 episodes of heart failure that required management with furosemide and nitroglycerin. He developed fever and respiratory distress with episodes of delirium treated with antipsychotics; we suspected the development of IRIS due to a paradoxical worsening of his condition despite being treated with ART and ganciclovir. Therefore, we started methylprednisolone and thalidomide 100 mg/day for immunosuppression and immunomodulation, respectively. After 17 days in the ICU, the oxygen requirements began to drop and the mental status improved. He remained hemodynamically stable with clinical and radiological improvemt. A new viral load reported 12,800 copies/ml. A new CBC reported hemoglobin 8 g/dL, hematocrit 26.4%, MCV 29 pg., platelets 366,000, WBC 7,400 mm3, neutrophils 86%, and lymphocytes 6%. Patient was discharged from the hospital after 45 days of treatment .

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1908_en.txt

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+A multigravid 31-year-old white woman and her 35-year-old white husband were admitted for pre-pregnancy consulting for their fourth pregnancy. In their first pregnancy, no fetal movement was detected by sonography at the 18th gestational week. Subsequently, three-dimensional ultrasound imaging showed a fetus with cystic kidneys and fusion of the lower limbs, so the pregnancy was terminated by induced abortion. The woman later gave birth to a normal baby at gravida 2, but at 32 weeks of her gravida 3, vaginal delivery following intrauterine fetal death (IUFD) occurred. The physical examination of the stillborn baby showed typical Potter facies and normal upper part of the body with fused lower limbs and two feet. The two feet were fused, and the femur and tibiae with four toes were discriminable. The external genitalia and anal opening were absent, as shown in Fig. . Although the exact type of anomaly cannot be identified in the absence of radiographic findings, it may be classified as type II or III based on the Stocker and Heifetz classification, since the fusion somewhat affects superficial tissue. There was no report of diabetes mellitus (DM) or other anomalies in the mother’s medical history or familial medical history. Moreover, their marriage was non-consanguineous, and the mother had not had exposure to any intrinsic or extrinsic factors (such as teratogenic drug intake) associated with sirenomelia during her pregnancy. Further investigation could not be conducted because the parents refused autopsy.
+Eventually, the follow-up to her fourth pregnancy indicated that she gave birth to a normal baby.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1926_en.txt

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+A 71-year-old man presented with a lengthy history of benign prostatic hypertrophy.
+He was asymptomatic without any hematuria, pain, or other urinary symptoms. The ECOG performance status was 1.
+He had a lengthy history of benign prostatic hypertrophy.
+Height: 6 feet (1.83 m); Weight: 225 lbs (102 kg); Body mass index: 30.5 kg/m2.
+A computed tomography (CT) scan of the abdomen and pelvis showed a 1.8 cm left retroperitoneal lymph node which was concerning for malignancy . There was no evidence of renal pathology. A positron emission tomography/CT revealed intense fluorine-18-deoxyglucose activity in the left retroperitoneal soft tissue nodule adjacent to the medial limb of the left adrenal gland . The standard uptake volume was 12.4.
+A core biopsy was performed under CT guidance of the left para-aortic lymph node. The immunohistochemical stains were strong and diffusely positive for PAX8 and cytokeratin (CK) AE1 and AE3 and negative for prostate-specific antigen (PSA), prostate specific acid phosphatase, Inhibin, and melanocyte antigen related to T-cells-1. Although the primary tumor site was unknown, the morphological and immunohistochemical features were most consistent with CCRCC.
+Restaging studies by bone scan 6 wk later were negative for skeletal metastasis. An abdominal and pelvic CT scan with and without Gadolinium contrast demonstrated a significant increase in size of the hypoenhancing retroperitoneal lymph node (4.3 cm × 4.4 cm compared to 1.8 cm × 2.8 cm 8 mo earlier). A primary lesion in the renal collecting system or ureters was not observed, although the prostate was markedly enlarged and there was diffuse bladder wall thickening.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1965_en.txt

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+A 68-year-old man was scheduled for elective coronary artery bypass graft surgery. He had a past history of hypertension, bronchial asthma, cerebral infarction, and myelodysplastic syndrome and has been on hemodialysis because of autosomal dominant polycystic kidney disease. He was alert and preoperative laboratory data were unremarkable except white blood cell count 2.24 × 103/μL, red blood cell count 3.83 × 103/μL, platelet count 9.1× 104/μL, creatinine 4.15 mg/dL, and B-type natriuretic peptide 161.9 pg/mL. Echocardiography demonstrated left ventricular ejection fraction 34%, mild aortic regurgitation, mild aortic stenosis, and mild mitral regurgitation. An IABP catheter (TRANS-RAY®, 7.5 Fr, 34 mL, Getinge AB, Lindholmspiren, Göteborg, Sweden) was inserted via the right femoral artery and connected to the console (Cardiosave® IABP Hybrid, Getinge AB), and circulatory support was started before surgery.
+In the operating room, a radial arterial catheter was inserted and an electrode for monitoring PSI was placed on the forehead in addition to routine monitors. General anesthesia was induced with midazolam 3 mg and remifentanil 0.3 μg/kg/min and was maintained using sevoflurane in an air–oxygen mix after tracheal intubation. PSI value prior to CPB was between 30 and 50. Propofol was continuously infused with a target concentration of 3 μg/mL using an infusion pump (TERUMO TE-371, Diprifuser™, TERUMO, Tokyo, Japan), and heart rate was approximately 60 bpm during CPB. IABP was continuously operated using electrocardiogram-triggered mode (1:1) in order to provide pulsatile flow.
+PSI value was increased from 30 to 50 immediately after starting CPB and remarkably decreased after stopping IABP before partial clamping of the ascending aorta for anastomosis with the saphenous vein . PSI was increased to approximately 70 abruptly after resuming IABP, which did not respond to an increase of infusion rate of propofol and remifentanil and to a bolus administration of fentanyl 100 μg or midazolam 10 mg. PSI values varied between 6 and 88 in accordance with the stopping and restarting of IABP. It decreased to 14 after stopping IABP for hemostasis around the anastomosis and again rapidly increased to 80 corresponding to restart of IABP before weaning from CPB . EEG remained almost electrically silent, mean arterial blood pressure was around 40 mmHg, and rectal temperature was 35.3 °C during CPB with a flow rate of 2.5 L/min. Based on the EEG findings, we were certain that the patient was adequately anesthetized. After weaning the patient from CPB, the PSI value and EEG pattern spontaneously showed sedative status. Postoperatively, there was no evidence of intraoperative awareness, anesthetic drug delivery, or instrument trouble.