The diagram illustrates modifications in hemoglobin (Hb) and IgAk monoclonal spike (left Y axis), platelets (PLT) and symptoms (right Y axis) by treatment in our patient. Symptom Scale: 0-100-point scale, based on patient's reported symptoms. Higher scores indicate more severe symptoms. RCD: Rituximab-Cyclophosphamide-Dexamethasone; CHOP: Cyclophosphamide-Doxorubicin-Vincristine-Prednisone. Red arrow: initiation of ibrutinib.


Magnetic resonance image demonstrates a 3.0x2.5 cm size solid mass with mildly enhancement on left kidney lower pole with a central necrotic portion.


Left kidney coronal opening specimen shows a well-circumscribed encapsulated mass measuring 2.7x2.8 cm size, involving the lower pole. The mass revealed areas of myxoid change necrosis, and cystic change.


Microscopic findings. (A) The low power appearance demonstrating a capsule of dense collagenous fibrous tissue and myxoid zone and inflammation with cellular zone consisting of spindle cells arranged in fascicles.


Microscopic findings. (B) The area of myofibroblastic proliferation showing densely cellular fascicles.


Microscopic findings. The tumor cells were potive for smooth muscle actin.


Microscopic findings. And vimentin.


Imaging Results: Normal Chest X-Ray.


Chest CT without evidence of intrathoracic lymphadenopathy or pulmonary parenchymal lesions.


Morphology of leukemia at diagnosis (case report #1: BCP-ALL). A; Blood smear showing small to medium size blast cell, with fine and pearly chromatin, evocative of lymphoid blast.


Morphology of leukemia at diagnosis (case report #1: BCP-ALL). B; Bone marrow aspirate picture in optic microscopy (May-Grunwald-Giemsa) showing extensive marrow necrosis. Cells cannot be identified.


Morphology of leukemia at diagnosis (case report #1: BCP-ALL). C; Bone marrow trephine biopsy showing a fibrotic marrow with a low cellularity but a massive blastic infiltration.


Morphology of leukemia at diagnosis (case report #2: AML). A; Blood smear showing an aspect of myeloid blasts with monocytic differentiation.


Morphology of leukemia at diagnosis (case report #2: AML). B; Bone marrow aspirate picture in optic microscopy (May-Grunwald-Giemsa) showing extensive marrow necrosis. Cells cannot be recognized, showing indistinct outlines and pycnotic nuclei.


Morphology of leukemia at diagnosis (case report #2: AML). C; Bone marrow trephine biopsy showing a hypercellular marrow with extensive necrosis. Majority of cells are necrotic but however suggestive of blastic cells.


Positron emission tomography-computed tomography scan of the patient revealing multiple enlarged lymph nodes in the root of the left side of neck, mediastinum, bilateral hilus of the lungs, right cardiophrenic angle, hepatic portal area, peripancreatic area, diaphragm angle, posterior peritoneum, inter-mesangial area and anterior sacral area, and along the iliac blood vessels, bilateral iliac fossa, pelvic wall and bilateral lingual areas. The scans reveal multiple nodules in the bilateral lungs, an enlarged liver with nodular appearance of the parenchyma, an enlarged spleen with multiple low-density shadows in the parenchyma, and multiple regions of elevated fluorodeoxyglucose metabolism in the bones, such as the sternum, multiple vertebrae, and the bilateral ilia, pubis and ischia. A diagnosis of lymphoma was therefore considered.


Four times CT-guide needle biopsy. (A) Jan 2016, CT-guided needle biopsy in the enlarged lesion in his right lung.


Four times CT-guide needle biopsy. (B) Oct 2016, CT-guided needle biopsy in lesion A after resistant to IO.


Four times CT-guide needle biopsy. (C) Oct 2016, CT-guided needle biopsy in lesion B after resistant to IO.


Four times CT-guide needle biopsy. (D) Apr 2017, CT-guided needle biopsy in the enlarged lesion of right lung after apatinib.


Fluctuation of serum NSE and pro-GRP. (A) The fluctuation of serum NSE (12.26 ng/mL at baseline, 38.48 ng/mL, at the time of resistant to AZD9291,45.35 ng/mL at time of resistant to EC after 4 cycles, 17.71 ng/mL at time of response to IO after 2 cycles, 52.9 ng/mL at time of resistant to IO after 4 cycles, 18.17 ng/mL at time of response to abraxane after 4 cycles, 25.09 ng/mL at time of resistant to abraxane after 4 cycles,18.93 ng/mL at time of treatment of apatinib after 6 weeks).


Fluctuation of serum NSE and pro-GRP. (B) The fluctuation of serum pro-GRP (22.35 pg/mL at time of response to IO after 2 cycle, 27.94 pg/mL at time of resistant to IO after 4 cycles, 21.05 pg/mL at time of response to abraxane after 4 cycles, 17.79 pg/mL at time of resistant to abraxane after 4 cycles, 18.94 pg/mL at time of treatment of apatinib after 6 weeks).


The change of chest CT after different regimens. (A) PR after 2 cycles of EC (right lower lobe, from 6.71 to 3.1 cm).


The change of chest CT after different regimens. (B) PD after 4 cycles of EC (right lower lobe, from 2.9 to 3.9 cm).


The change of chest CT after different regimens. (C) PR after 2 cycles of IO (left upper lobe, from 2.72 to 1.65 cm).


The change of chest CT after different regimens. (D) PD after 4 cycles of IO (left upper lobe, from 1.9 to 3.1cm).


The change of chest CT after different regimens. (E) PR after 2 cycles of Abraxane (right lower lobe, from 5.41 to 0.4 cm).


The change of chest CT after different regimens. (F) PD after 4 cycles of Abraxane (right upper lobe,from 2.8 to 4.0 cm).


The change of chest CT after different regimens. (G) Shrunken lesion of left lung after Apatinib (left lower lobe,from 3.47 to 2.34 cm).


The change of chest CT after different regimens. (H) Enlarged lesion at right lung after Apatinib (right upper lobe,from 3.74 to 5.73 cm).


Serum protein electrophoresis revealing monoclonal gamma/lambda gammopathy (IgG1) of unknown significance with lambda light chains, confirmed by an immunofixation study.


Ultrasonography of the cyst four years previously.


Ultrasonography of the cyst prior to surgery.


Computerized tomographic appearance of the cyst prior to surgery. Punctate calcification consistent with extramedullary hematopoiesis is circled.


Fibrous cyst wall demonstrating the tumor focus (hematoxylin and eosin; magnification, x2).


In spite of the clear cell type, in which the cytoplasm appears empty (not stained) due to glycogen content, the cell cytoplasm in this tumor contains mitochondria, which are stained by H&E (grey) (magnification, x20).


Bone trabeculae and cyst wall (H&E, x4). The inset shows the following bone marrow cells: 1, erythroblasts; 2, myeloid series; and 3, megakaryocytes (H&E; magnification, x20). H&E, hematoxylin and eosin.


A; Hematoxylin and eosin staining (HE), high power. Florid endocapillary hypercellularity with prominent monocytes and granulocytes within capillary loops with minimal mesangial matrix expansion and variable capillary wall thickening, morphologically consistent with cryoglobulinemic glomerulone-phritis.


B; HE, high power. Florid intimal arteritis involving the interlobular caliber artery.


C; HE, high power. Arteriole with inflammatory cell infiltration and eosinophilic material within the vessel wall consistent with cryoprecipitate.


D; HE, medium power. Monomorphic small lymphoid cells infiltrating the perinephric fat can be seen.


A; The lymphoid infiltrate showed strong diffuse CD20 staining.


B; CD3 staining highlighted only scattered reactive T lymphocytes.


(a) Gadolinium-enhanced magnetic resonance imaging (MRI) revealed an enhanced mass in the cerebellar vermis.


(b) Brain CT image revealed massive SAH in the posterior fossa after rebleeding.


Preoperative left vertebral angiogram note the tumor stain. The tumor is fed by the vermian branch of the left posterior inferior cerebellar artery. A flow-related aneurysm (arrow) is seen in the arterial phase.


(a) Intraoperative findings. Note the ruptured aneurysm (arrow) on the feeder near the vascular-rich tumor (asterisk).


(b) Microphotograph of the aneurysm showing disruption of the internal elastic lamina and rupture of the adventitia (Elastica van Giesson staining, original magnification x10).


Serial panoramic radiograph monitoring the resolution of the lesion:. Orthopantomogram radiograph at the initial presentation.


4 months after the first triamcinolone injection.


8 months after the first triamcinolone injection.


18 months from the initial injection.


PET scan which shows metabolic activity only in the right breast.


MRI scan of spine shows soft tissue mass posterior to T9 causing moderate cord compression.


Trend of hemolytic parameters with plasma exchanges and eculizumab.


Multiple splenic nodules.


Endothelial cells are CD31- and CD8-positive. . Notes: (A) CD31, arrow indicates positive endothelial cells.


Endothelial cells are CD31- and CD8-positive. (B) CD8, arrows indicate positive endothelial cells. . Abbreviation: CD, cluster of differentiation.


Vascular channels are CD34+. . Notes:. Capillary proliferation in microscopy.


Vascular channels are CD34+. CD34; arrows indicate positive endothelial cells. . Abbreviation: CD, cluster of differentiation.


Vascular channels are HHV8-negative. . Abbreviation: HHV8, human herpesvirus 8.


Bivalirudin dosing and relevant ACT in the present patient with HIT. (A) The dosage of bivalirudin and the ACT monitoring during bivalirudin treatment. Red squares indicate ACT values while the blue dos indicate bivalirudin doses.


Bivalirudin dosing and relevant ACT in the present patient with HIT. (B) The linear relationship between bivalirudin dosage and ACT value undergoing ECMO with CRRT.


Bivalirudin dosing and relevant ACT in the present patient with HIT. (C) The linear relationship between bivalirudin dosage and ACT value undergoing ECMO without CRRT. HIT, heparin-induced thrombocytopenia; ECMO, extracorporeal membrane oxygenation; CRRT, continuous renal replacement therapies; ACT, activated clotting times. Y (dependent variable): ACT(s), x (independent variable): dosage of bivalirudin (mg/kg/hour).


Platelet counts in the present patient with HIT are displayed during ECMO support with heparin therapy and bivalirudin anticoagulation, respectively. The red squares indicate platelet counts (*109/L). HIT, heparin-induced thrombocytopenia; ECMO, extracorporeal membrane oxygenation.


Pathological findings. EMA (x200).


Pathological findings. S-100 (x100).


Pathological findings. INI-1 (x100).


Pathological findings. Ki-67 (x200).


Pathological findings. Vim (x40).


Pathological findings. CK (x100).


(Giemsa, 200x) depicts a hypercellular bone marrow, featuring expansion of the eosinophilic lineage, comprising maturing to fully mature eosinophils.


While tryptase stain [; 200x] delineates the presence of scattered aggregates of epitheliod to spindled mast cells, featuring at least partial CD25-positivity (inset, 400x).


Bone marrow biopsy at 3 months from Imatinib initiation [, Giemsa, 200x] shows a reduction of cellularity, eosinophilic compartment.


Mast cells [; tryptase, 200x], which appear scattered.


Restitutio ad integrum of the hematopoiesis is steadily apparent in subsequent biopsies [, Giemsa, 200x],. With only scattered tryptase+ cells [ insets.


Electrocardiogram revealed sinus rhythm, low voltages in limb leads, QS waves indicative of pseudoinfarction in precordial and inferior leads, first-degree atrioventricular block, and prolonged QTc.


A four-chamber apical view echocardiogram showing biatrial dilatation, valve thickening, thick ventricular walls (left ventricular wall is 15 mm and interventricular septum is 19 mm), and interventricular septum with speckled appearance, which suggests amyloid infiltrate. . Abbreviations: RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium.


Rectum biopsy: amyloid deposits are confirmed by a positive Congo red stain (arrow), which gives the characteristic salmon pink color (200x).


Extraoral facial asymmetry on left side of face.


Orthopantomograph revealed multilocular radiolucency on left side extending from 35 to condylar process.


Computed tomography scan revealing buccal and lingual cortical expansion with cortical perforation at 37 region.


Macroscopic specimen.


Specimen with impacted tooth.


Computed tomography images of the chest of a patient with multiple lung metastases from renal leiomyosarcoma. . Notes:. Before sunitinib malate treatment.


Computed tomography images of the chest of a patient with multiple lung metastases from renal leiomyosarcoma. 4 weeks after sunitinib malate treatment (37.5 mg/d).


Computed tomography images of the chest of a patient with multiple lung metastases from renal leiomyosarcoma. 1 month after withdrawal of sunitinib malate due to severe adverse effects.


Computed tomography images of the chest of a patient with multiple lung metastases from renal leiomyosarcoma. After resuming use of sunitinib malate at the dose of 25 mg/d.


Computed tomography images of the chest of a patient with multiple lung metastases from renal leiomyosarcoma. 26 months after sunitinib malate treatment. Arrows indicate sites of lesions.


Adverse effects of sunitinib malate included hand-foot syndrome (grade 3). . Notes:. Hand.


Adverse effects of sunitinib malate included hand-foot syndrome (grade 3). Foot.


(A) Fluid attenuation inversion recovery (FLAIR) image showed hyperintensity in the cortical region of right frontal and parietal lobes without white matter involvement (Case 1).


(B) Diffusion weighted imaging (DWI) showed no obvious signal change in the cortex (Case 1).


(C) MRI scan showed the abnormality disappeared at the follow-up scan (Case 1).


(D) Hyperintensity in the cortical regions of left parietal lobes in MRI FLAIR images 7 years before this episode (Case 1).


(E) DWI showed no obvious signal change in the cortex (Case 1).


(F) MRI scan showed the abnormal lesions disappeared at the follow-up scan (Case 1).


(G) Hyperintensity in the cortical regions of left frontal and parietal lobes in MRI FLAIR images (Case 2).


(H) DWI showed mild hyperintensity in the involved cortical regions (Case 2).


(I) Gadolinium enhanced T1-weighted image showed meningeal linear enhancements in the sulci of left brain lobes (Case 2).


(J) T2-weighted image showed hyperintensity in the spinal cord from thorax 2 to 9 segments. (Case 2).


Computed tomography of abdomen showing bilateral large adnexal masses with bilateral hydronephrosis due to compression of ureters.


Sagittal T1 flair showing an expansive tumor that affects the right parietal bone in a 42-years old patient with primary non Hodgkin's lymphoma of the cranial vault.


Diffuse large B cell lumphoma positive for CD20 (immunohistochemistry CD20 orginal magification x400).


MRI findings. . (
1-A) - Axial MRI FLAIR image from the affected female child done at 4.5 years of age shows hyperintensities in the periventricular (primarily periatrial) white matter (arrows).


MRI findings. (
1-B) Axial FLAIR and sagittal T1 MRI images from the affected male child at 2.5 years of age. This shows bilateral periventricular (periatrial) and subcortical white matter hyperintensities consistent with dysmyelination (arrows). Brain architecture (corpus callosum, cerebellum, and cortical gyration) was normal.


CT scan spine sagittal view: showing D5 to D7 laminectomy defects with D6 collapse.


MRI dorsal spine sagittal view: the heterogeneous tumor mass spread around the vertebra with collapse of the D6 vertebra.


MRI dorsal spine axial view: the widespread tumor mass causing significant engulfing of spinal cord.


PET scan axial view: lytic lesion seen involving D5, D6, and D7 vertebral body with intraspinal and right paravertebral soft-tissue component.


Biopsy section: sheets and clusters of plasma cells consisting of immature forms having focal nuclear pleomorphism.


Papulonodular lesions over the face with crusting.


Conjunctival nodule with congestion in the right eye.


Bone marrow aspirate smears showing a reactive marrow with few extracellular and intracellular histoplasma within macrophages (Leishman stain, x100).


Histopathological section of the conjunctival specimen showing numerous macrophage aggregates with Period Acid Schiff (PAS)-positive histoplasma (PAS stain, x100).


Photomicrograph showing granular cells with indistinct cell borders interspersed with muscle fibers (H&E stain, x100).


Photomicrograph showing strong positivity of granules for the S-100 protein (IHC stain, x100).


Photomicrograph showing strong positivity of granules for inhibin (IHC stain, x100).


Photomicrograph showing granular cells staining positive for CD68 (IHC stain, x100).


PET-CT before treatment. . PET-CT was performed after the biopsy of the nasal tumor. Accumulation of FDG was noted in the mesenteric nodes, mediastinal nodes, pleura and pelvic mass.


Intraoral photograph showing smooth lobulated swelling, 2 x 5 cm in diameter extending from maxillary first premolar to first molar on right side and posteriorly to the maxillary tuberosity area.


Panoramic CBCT demonstrating the lesion causing loss of bony structures with internal calcifications and resorption of root in relation to 14.


Axial CBCT section at level of maxillary alveolus demonstrate buccal and palatal cortical plates destruction with areas of calcification and soft tissue extent of the lesion.


3-D CBCT volumetric reconstruction demonstrates complete perforation of buccal and lingual cortical plates with flecks of calcification.


alpha-SMA-positive staining in vicinity of blood vessels in odontogenic islands.


Histologic findings showed proliferation of histiocytes and eosinophil infiltration. Immunohistochemical stains were positive for S100 and CD1a, and negative for CD68.


A: On MRI an ovoid mass lesion seen in the right parieto-occipital region measuring 10 x 7 x 4 cm with peritumoral edema.


B: The tumor showed intermediate-low signal intensity in the T1-Weighted Image (T1WI). The mass was attached to tentorium and was seen extending into the right transverse sinus.


A: Photomicrograph depicting a spindle cell tumor with a "PAtternless-pattern with hypercellular and hypocellular areas. (H& E-40 X).


B: Tumor cells are spindle shaped and collagen fibres are seen to separate them. Hypercellular areas showed interlacing fascicles of spindle-shaped cells with moderate amount of eosinophilic cytoplasm and oval to elongated nuclei exhibiting variable pleomorphism. (H&E-200X).


C: Reticulin fibres are seen to separate the tumor cells (RETICULIN-200X).


D: On IHC, CD 99 Is strongly positive in tumor cells. (100x).


E: Stat 6 strongly positive in tumor cells (100X).


Clinical course of the patient (schematic). BDG, (1,3)-b-D-glucan; PCT, procalcitonin; CRP, c-reactive protein; CT, computed tomography; MRI, magnetic resonance imaging; MRA, magnetic resonance angiography; VRC, voriconazole; IPI, Imipenem; VAN, Vancomycin; TEC, teicoplanin; AmBL, liposome-associated amphotericin B; mNGS, metagenomics next-generation sequencing; PB, peripheral blood; CSF, cerebral spinal fluid; BAL, bronchoalveolar lavage fluid.


Daily course of the patient's treatment. Horizontal thick blue lines show the medications administered; VRC, voriconazole; AmBL, Liposome-associated amphotericin B; TZP, piperacillin-tazobactanm; IPI, Imipenem; PCT, procalcitonin; CRP, C-reactive protein.


Colonoscopy showed diffuse mucosal edema, ulcer formation and bleeding from the sigmoid colon.


To the ascending colon.


Abdominal computed tomography showed that the whole colon wall was markedly thickened, with huge ascites (c).


The resected specimen showed hemorrhagic necrosis of the transverse colon.


Postoperative clinical course.


Patient 1. Platelet counts and platelet transfusions during intensive care hospitalization. Combined therapy including romiplostim as emergency management for severe immune thrombocytopenia complicated by intracranial hemorrhage (ICH). Intracranial pressure monitoring (ICPM); Romiplostim dose: 1 mug/kg subcutaneously; intravenous immunoglobulin (IVIg) dose: 1 g/kg; and high-dose methyl prednisolone (HDMP): 15 mg/kg/day.


Patient 2. Platelet counts and platelet transfusions during intensive care hospitalization. Combined therapy including romiplostim as emergency management for severe ITP complicated by intracranial hemorrhage (ICH). ICPM = intracranial pressure monitoring (intraparenchymal probe). MP = methylprednisolone. Romiplostim dose: 10 mug/kg subcutaneously; intravenous immunoglobulin (IVIg) dose: 1 g/kg.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. Compression fractures and kyphoscoliosis of the spine in CT.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. , MRI scan showing fragility fracture of the lateral condyle of the right tibia.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. , X-ray of the fragility fracture of left femoral neck.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. And X-ray of pelvis showing arthroplasty of the left hip and osteosynthesis performed after fragility fractures in right femoral shaft and lateral condyle after surgery.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. CT scan of the tumor in the mandible , hematoxylin.


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. Eosin staining. (18.4 x).


Radiological images of the fragility fractures diagnosed before the diagnosis of TIO. Vimentin staining (positive) (15.9 x). Of the tumor.


Timeline showing serum phosphate and FGF23 (C-terminus) concentrations at diagnosis and postoperatively. Time of surgery is marked with the black triangle and X-axis presents the time in months relative to surgery. Reference ranges are 0.76-1.41 mmol/l, and 26-110 kRU/l are marked to the y-axes with a bar, respectively.


Cellular morphology of bone marrow aspirate smear and chromosome karyotypes. (A, B) Bone marrow smear showing a proliferation of blasts (Giemsa-Wright stain). (A, B) The blasts exhibited medium sizes, round, round-like or irregularly shape, the cytoplasm were less with trailing and burr-like changes (100 x oil immersion).


Cellular morphology of bone marrow aspirate smear and chromosome karyotypes. (C) The cytochemiscal staining was negative for POX (peroxidase).


Cellular morphology of bone marrow aspirate smear and chromosome karyotypes. (D) Chromosome analysis demonstrated + 4 (arrow) in 4 of 10 metaphases examined.


Immunophenotypic analysis of the blasts cells exhibited ETP-ALL. Through the flow cytometry analysis, blast cells were gated and showed in blue (P3). Normal mature lymphocytes were showed in green for comparison (P2). The immunophenotype of blasts were CD7, CD117, CD34, CD33, CD38, CD3 (dim), cytoplasmic CD3, and negative for TDT, CD123, CD36, HLA-DR, CD64, CD11b, CD13, CD16, CD14, CD15, CD64, CD11c, CD4, CD5, CD8, CD10, CD19, lambda, kappa, CD20, CD22, MPO, CD1a, CD99, CD2. The phenotype was consistent with early T-cell precursor acute lymphoblastic leukemia (ETP-ALL).


Relevant genetic aberrations detected by NGS in patient's sample. A) Mutations in ASXL1, CBL, SRSF2 and TET2 genes, presented as screenshots from IGV. *Provided is an ID of an ASXL1 mutation which arises from insA instead of G but results in a similar frameshift. VAF - variant allele frequency.


Relevant genetic aberrations detected by NGS in patient's sample. B) Focal deletion on chr12 detected in sequencing coverage analysis, resulting in monoallelic loss of locus containing ETV6 and CDKN1B.


Relevant genetic aberrations detected by NGS in patient's sample. C) Allele frequencies of common variants detected on chromosome 11 in patient sample. Each point of the chart represents VAF of a single variant. VAF shift on 11q arm suggests a loss-of-heterozygosity event.


Avulsive wound over the lower lip.


Processing of platelet-rich fibrin.


Platelet-rich fibrin membrane.


Two weeks follow up.


Six weeks follow up.


Clinical course of Case 1. After treatment with lenalidomide, the renal impairment and proteinuria caused by LCDD was improved. BCD: bortezomib (2 mg, once weekly), cyclophosphamide (200 mg, once weekly), and dexamethasone (20 mg, once weekly); Rd: lenalidomide (25 mg daily, on Days 1 through 21 of each 28-day cycle) and dexamethasone (20 mg once weekly).


Clinical course of Case 2. After treatment with lenalidomide, the renal impairment and proteinuria caused by LCDD was aggravting. BCD: bortezomib (2 mg, once weekly), cyclophosphamide (200 mg, once weekly), and dexamethasone (20 mg, once weekly); Rd: lenalidomide (25 mg daily, on Days 1 through 21 of each 28-day cycle) and dexamethasone (20 mg once weekly).


Pictures of chest radiographs during ECMO therapy. . Note:. Two hours post ECMO.


Pictures of chest radiographs during ECMO therapy. 6 days post ECMO. . Abbreviation: ECMO, extracorporeal membrane oxygenation.


ECMO circuit with an inline hemofilter system. . Abbreviation: ECMO, extracorporeal membrane oxygenation.


Computed tomography scan showing entrance of the thorn through left C3-C4 foramen.


The 5-cm thorn.


FLAIR.


DWI. Sequences of cranial MRI showed diffuse thickening of the skull and increasing signal intensity.


Lumbar MRI prompted lumbar vertebra multiple bone changes.


Skull X-ray prompted that the skull and maxillofacial bone (A,B) were found to have diffuse worm-like low-density bone destruction and there was no obvious hardening at the edge.


(C) Pelvis X-ray showed small and low-density bone destruction zone in the pelvis and proximal femur.


The changes of beta2-MG, IL-6, VEGF, LDH. The series of beta2-MG, IL-6 are drawn on the primary axis, and the series of VEGF, LDH are drawn on the secondary axis.


PET/CT finding. (A-C) Before chemotherapy. (The largest lymph nodes was in the lower abdominal mesenteric region 68mm x 42mm, SUVmax =8.2). (A) Widespread lymph node enlargement and hypermetabolism, splenomegaly, kidney hypermetabolism (blue arrows) and diffuse bone marrow hypermetabolism.


PET/CT finding. (A-C) Before chemotherapy. (The largest lymph nodes was in the lower abdominal mesenteric region 68mm x 42mm, SUVmax =8.2). Its inferior border approached the upper margin of pelvis (SUVmax= 2.9);. Spinal hypermetabolism (blue arrow), (SUVmax =9.0).


PET/CT finding. (A-C) Before chemotherapy. (The largest lymph nodes was in the lower abdominal mesenteric region 68mm x 42mm, SUVmax =8.2). Iliac hypermetabolism (blue arrows).


PET/CT finding. (D-F) After three courses of chemotherapy (The spleen reduced obviously, whose metabolism was normal (SUVmax=2.6)). No abnormal lymph nodes were found.


PET/CT finding. (D-F) After three courses of chemotherapy (The spleen reduced obviously, whose metabolism was normal (SUVmax=2.6)). The volume of spleen was smaller than before, and the metabolism of bone marrow, kidney metabolism were normal (red arrows);. Normal spine metabolism, (SUVmax =3.3) (red arrow).


PET/CT finding. (D-F) After three courses of chemotherapy (The spleen reduced obviously, whose metabolism was normal (SUVmax=2.6)). Normal ilium metabolism (red arrows).


Fluorescence interphase in situ hybridization on lymph node biopsy. (A) IGH-BCL2 dual-colour dual-fusion probe displays two fused green and red signals, one isolated green and one isolated red signal in most of tumour nuclei with t(14;18) (q21;q32)/IGH-BCL2. Arrow indicates positive nuclei.


Fluorescence interphase in situ hybridization on lymph node biopsy. BCL2 dual-colour break-apart (BAP) probe shows one co-localised green, and ,red signal, one isolated green, and ,one isolated red signal in most of tumour nuclei.


Fluorescence interphase in situ hybridization on lymph node biopsy. BCL6 dual-colour break-apart (BAP) probe shows two co-localised green, and ,red signal.


The immunostaining of bone marrow after one course of chemotherapy. (b-FGF,x200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (CD19,x200), negative.


The immunostaining of bone marrow after one course of chemotherapy. (CD117x200), negative.


The immunostaining of bone marrow after one course of chemotherapy. (IL-1beta,x200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (IL-2,x200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (IL-6,x200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (IL-10,x200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (PDGFx200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (TGF-betax200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (TNF-alphax200), positive.


The immunostaining of bone marrow after one course of chemotherapy. (VEGFx100), positive.


The immunostaining of bone marrow after one course of chemotherapy. Reticular fiber staining x200, MF-1.


The immunostaining of bone marrow after two courses of chemotherapy. (b-FGF,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (CD19,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (CD117,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (IL-1beta,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (IL-2,x100), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (IL-6,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (IL-10,x200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (PDGFx200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (TGF-betax200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (TNF-alphax200), negative.


The immunostaining of bone marrow after two courses of chemotherapy. (VEGFx100), positive.


The immunostaining of bone marrow after two courses of chemotherapy. Reticular fiber staining 100x, MF 0-1.


Sequencing the genomic PCR products, heterozygous missense mutation (R81P)(G changing to C) was identified.


(a) Generalized gingival enlargement involving maxillary and mandibular arch.


(b) Boggy, reddish-blue gingiva on the buccal, labial, palatal and lingual aspect of marginal and attached maxillary gingiva.


(c) Enlarged gingiva covering the crown surface with a mild ecchymosis in the floor of the mouth.


Peripheral blood smear showing numerous monoblasts and promonocytes and scarcity of platelets.


52-year-old female with Von Hippel-Lindau syndrome. . Transaxial contrast enhanced CT (A) of abdomen show large (9.6 x 7.4 x 5.4 cm) mass lesion in region of body and tail of pancreas with intense post contrast enhancement (arrow). Multiple cysts of varying sizes are noted in rest of pancreas (asterix). Also, note tortuous blood vessels in peripancreatic and perisplenic location.


52-year-old female with Von Hippel-Lindau syndrome. Transaxial PET . Focal 68Ga-DOTANOC uptake (SUVmax = 13.2) was also seen in segment III of liver (B, C, broken arrow) suggesting liver metastasis from pancreatic NET. This was confirmed at fine needle aspiration cytology.


52-year-old female with Von Hippel-Lindau syndrome. PET-CT. Images show intense heterogeneous uptake of 68Ga-labelled [1, 4, 7, 10-tetraazacyclododecane-1, 4, 7, 10-tetraacetic acid]-1-Nal3-Octreotide (68Ga-DOTANOC) (SUVmax = 18.6) in pancreatic mass (arrow), thus confirming it to be NET. Focal 68Ga-DOTANOC uptake (SUVmax = 13.2) was also seen in segment III of liver (B, C, broken arrow) suggesting liver metastasis from pancreatic NET. This was confirmed at fine needle aspiration cytology.


52-year-old female with Von Hippel-Lindau syndrome. Transaxial contrast enhanced CT (D) of abdomen also shows another mass (7.8 x 5.8 x 5.1 cm) arising from interpolar region of left kidney and showing intense post contrast enhancement (arrow). Multiple feeding vessels are seen to arise from left renal artery and supply mass. These findings were suggestive of RCC. Also noted are bilateral multiple renal cortical cysts (asterix).


52-year-old female with Von Hippel-Lindau syndrome. PET.


52-year-old female with Von Hippel-Lindau syndrome. PET-CT. Images reveal mild 68Ga-DOTANOC uptake (SUVmax = 3.1) in renal mass (arrow).


52-year-old female with Von Hippel-Lindau syndrome. Transaxial PET.


52-year-old female with Von Hippel-Lindau syndrome. PET-CT. Images of brain show focal area of 68Ga-DOTANOC uptake (SUVmax = 9.9) in hypodense lesion (2 x 2 cm) in left cerebellum (arrow).


52-year-old female with Von Hippel-Lindau syndrome. Transaxial T2 weighted gadolinium enhanced MRI (I) of brain reveals nodular lesion in lateral half of left cerebellar hemisphere with intense post contrast enhancement (arrow), suggesting hemangioblastoma.


52-year-old female with Von Hippel-Lindau syndrome. PET-CT. Images also revealed focal 68Ga-DOTANOC uptake (SUVmax = 8.3) in lateral part of left globe, corresponding to heterogeneous nodular lesion (arrow).


52-year-old female with Von Hippel-Lindau syndrome. Transaxial T2 weighted gadolinium enhanced MRI (L) showed eccentric nodule in lateral part of left globe with intense post contrast enhancement, suggesting retinal hemangioblastoma (arrow).


Computerized tomography of Case 2 showing calcification of aorta.


Calcification of coronary artery.


Beaded appearance of aorta on CT angiogram with calcification of both common iliac arteries.


Right adrenal pheochromocytoma and paraganglioma at left renal hilum.


Histology and immunohistochemistry. Hematoxylin-eosin stained image from a representative area of the tumor shows a small to medium sized primitive cellular population. A desmoplastic micronodular architecture is revealed by reticulin staining. The tumor cells are positive with synaptophysin and weakly with GFAP. INI-1 expression is preserved. The proliferative index (MIB-1) reaches 70%.


Copy number profile. Array data showed a low density copy number profile which indicates an almost flat genome without relevant chromosomal aberration.


Immunohistochemical analysis performed on paraffin sections. Neoplastic cells show positive staining for the T-cell antigen, CD3 (magnification, x400).


Bone marrow aspirate: Blast cells are seen along with many plasma cells (acute myelomonocytic leukemia) (Giemsa stain, 100x).


Serum and urine protein electrophoresis: Polyclonal rise in gamma globulins and nonselective proteinuria, respectively.


Myeloperoxidase stain: Myeloid blasts are positive (100x).


Alpha naphtyl butyrate esterase stain: Monocytic lineage is positive (monoblasts, promonocytes and monocytes) (100x).


Timeline of disease progression and treatment. Black bordered months indicate diagnosis or definitive progression on surveillance MRI. The graph shows CAR T-EGFRvIII levels in the peripheral blood as measured by qPCR.


(a) Cellular smear showing loose clusters of cells with preponderance of histiocytes with few of them showing kidney shaped nucleus (arrow), alongwith neutrophils (N), lymphocytes (L) in the background. (Pap, x400); (b) Cells showing pseudoinclusion (arrow) (Pap, x400); (c) Binucleated histiocyte (arrow) (Giemsa, x400).


(a) Biopsy showing variable histiocytes with mononucleate, binucleate and multinucleate cells amidst lymphocytes and polymorphs (H and E, x400); (b) Immunostaining with S100 showed diffuse positivity in the atypical histicytes (IHC, x100).


Panoramic radiograph showing a diffuse radiolucent lesion in lower left molar region.


Computed tomagraphy showing a wide osteolytic area in the left part of the mandible.


Computed tomography showing a wide osteolytic area in the left part of the mandible.


Photomicrograph of immunohistochemical stain shows sheets of large mononuclear cells positive for CD20.


Axial view displaying left renal vein thrombosis.


Coronal view displaying thrombosis in the renal vein with further extension into the inferior vena cava (top arrowhead). Also displayed is the ovarian vein clot (bottom arrowhead).


Normal glomerulus without proliferative changes (Periodic acid-Schiff, original magnification x 400).


Glomerulus with granular capillary loop staining for IgG (direct immunofluorescence; original magnification x 400).


Glomerular basement membranes with subepithelial electron dense deposits (original magnification x 12,000).


Histopathological examination in hematoxylin-eosin. A: BM at the initial diagnosis of PMF, showing hypercellularity with some fat cells left (circle), clusters of mature granulocytes (closed arrow), singular and groups of atypical megakaryocytes (open arrow).


Histopathological examination in hematoxylin-eosin. B: BM at follow up, showing maximal cellularity without any fat cells left, no organized hematopoiesis with only singular mature granulocytes, a few atypical megakaryocytes, and clusters of immature cells and blast cells (asterisk). (Pictures: Friedemann Leh, Department of Pathology, Haukeland University Hospital).


Abdominal CT scan demonstrating a 15 mm hypervascular lesion in segment VII of the liver in arterial phase.


Venous phase.


Histologic analysis. (A) The well-demarcated and unencapsulated tumor is seen in the liver.


Histologic analysis. (B) The tumor is composed of fascicles featuring cells with bland, elongated cigar shaped nuclei and eosinophilic cytoplasm.


Histologic analysis. (C) Higher magnification depicting bland tumor cells with cigar shaped nuclei and indistinct eosinophilic cytoplasm. Note the absence of mitotic activity.


Histologic analysis. (D) Palisading of the nuclei was present at many tumor foci.


(A) Computed Tomography scan showing a 3 cm heterogeneous right adrenal mass of undetermined significance.


(B) Strong Meta-iodobenzylguanidine (MIBG) uptake of the 2 x 2 x 3 cm right adrenal mass with no evidence of distant metastasis.


(a) ECG shows sinus tachycardia with lowering and inverted T wave on leads II, III, and avF.


(b) Echo shows a dilated, poorly functioning left ventricle (EF 35.


(c) Echo shows a severe TR.


(a) V-A ECMO via neck cannulation with a 15-Fr cannula in the right atrium and a 12-Fr cannula in the right common carotid aorta.


(b) Chest X-ray post-ECMO.


Bone marrow biopsy showing hemophagocytosis. Arrows depict red blood cells engulfed by macrophages in the bone marrow.


Representative image from the removed cervical lymph node showing erythrophagocytosis (arrows).


(a) Hematoxylin and eosin stain (100x original magnification) demonstrates amyloid deposition (asterisk) with tumoral cell infiltration (arrowheads).


(b) Hematoxylin and eosin stain (400x original magnification) of the tumoral infiltration area reveals typical clock face pattern nuclei (arrowheads) in plasma cells diagnostic of plasmacytoma.


Lung volumes and DLco in patient 1.


CTA chest showing an embolus in a branch of the left pulmonary artery (arrow).


Effect of immune modulation on biomarkers, organ dysfunction, and cytokine levels during HSV-associated secondary HLH. The time course of clinical laboratory values of serum C-reactive protein (CRP), creatinine (Cr), and INR levels.


Effect of immune modulation on biomarkers, organ dysfunction, and cytokine levels during HSV-associated secondary HLH. , ferritin levels.


Effect of immune modulation on biomarkers, organ dysfunction, and cytokine levels during HSV-associated secondary HLH. , as well as the timing of the administration of the immune suppressive agents is shown.


Effect of immune modulation on biomarkers, organ dysfunction, and cytokine levels during HSV-associated secondary HLH. While IL-6 and TRAIL levels fell precipitously after admission, CXCL9 and IL-18 levels fell more gradually (D) (*Actual INR resulted as >15.7).


Histopathology of a Sweet's syndrome lesion. Closer views (A) of Sweet's syndrome lesions located on the upper arms are shown.


Histopathology of a Sweet's syndrome lesion. The biopsy specimen (B) shows a confluent neutrophilic infiltrate in the reticular dermis and edema in the papillary dermis (hematoxylin and eosin staining).


Bone marrow aspiration at diagnosis (A,B). Hypocellular bone marrow with 14% blasts and dysplasia in all cell lineages (May-Giemsa).


Endoscopic examination reveals a 4 cm sized irregularly margined mass with intact mucosa (margin) and shallow ulcer (central) in descending colon.


Trans-axial view.


Coronal view. Show a 4.0 cm sized homogeneous enhancing intra-luminal mass (arrow) in descending colon.


Tumor is composed of cytologically bland spinle cells arranged in hyaline stroma with scattered inflammatory cells. Inflammatory cells are composed of lymphocytes, histiocytes and plasma cells. H&E, x40.


Tumor is composed of cytologically bland spinle cells arranged in hyaline stroma with scattered inflammatory cells. . H&E, x400).


Tumor cells stain strongly for vimentin and variably with myoid markers including smooth muscle actin, muscle-specific actin and desmin. Vimentin, x200.


Actin, x200).


68-year-old male referred to our hospital due to multifocal hepatic lesions, subsequently diagnosed as diffuse hepatic hemangiomatosis. A) Ultrasound examination demonstrates multiple ill-defined yperechoic nodules dispersed throughout the hepatic parenchyma, mostly sub-centimeter and with right hemi-liver predominance. Some nodules are larger and better defined (arrows).


68-year-old male referred to our hospital due to multifocal hepatic lesions, subsequently diagnosed as diffuse hepatic hemangiomatosis. B) Color Doppler shows no evident vascularity in the lesion.


Graphic representation of the patient's serum Tg values and TgAb titer between 2004 and 2018.


Bilateral exophthalmos (left > right), periorbital oedema, conjunctival hyperaemia.


Detail of left eye.


The exophthalmos, periorbital oedema, conjunctival hyperaemia disappeared after first cycle of therapy.


Detail of left eye after first cycle of therapy.


(a) Orthopantomograph showing multilocular radiolucency in the mandibular body-ramus area on the left side.


(b) Cone beam computed tomography image showing buccal expansion due to the lesion.


(a) Photomicrograph demonstrating follicles of ameloblastoma in mature fibrous stroma (H&E, x10).


(b) Foreign body and associated granulomas (H&E, x10).


(c) Multinucleated giant cells phagocytosing hyaline ring-like foreign particles (H&E, x40).


(d) The foreign body demonstrating periodic acid-Schiff positivity (periodic acid-Schiff, x10).


(a) Foreign body showing peripheral smaller rectangular cells (demonstrated by arrowhead) and arrow pointing larger more angular cells in the center enclosing amorphous eosinophilic material (H&E, x40).


(b) Processed pulse showing structure similar to the foreign body (H&E, x40).


Finally, plate fixation and cementation were performed (left).


After the cryoablation, contrast-enhanced CT showed the frozen region (middle).


On CT, the density of right metastatic femur was different from that of opposite side (right).


In the histopathological findings of curettage tissue, tumor cells were not observed.


Trends in. Hemoglobin.


Platelet count in case 1.


Trends in platelet count and serum creatinine in case 2, both during initial disease presentation.


During relapse.


Microscopic: sections show dense spindle cell proliferation with storiform growth pattern associated with patchy infiltration of lymphoplasma cells.


Positive reaction of tumor cells with SMA.


Brain magnetic resonance imaging.


Surgical steps:. Macular hole, submacular hemorrhage, and ,arterial macroaneurysm are present.


ILM peeling.


RtPA injection using vitrectomy probe via the macular hole, and ,extension of the submacular hemorrhage area after injection of rtPA.


Fluid-air exchange at the end of the surgery.


The patient had three ulcers on the mucosa of the upper palate and uvula. The surface of the ulcers is covered with a layer of white plaque (arrow).


The protruding masses can be seen around the anus. In addition, a rash can be seen around the anus and inguinal region.


The patient carries one heterozygous mutation, c.301 c > T, P. (Arg 101 Trp), in exon 3 of the IL-10RA gene, which is a missense mutation (a, arrow). Her father also carries one heterozygous mutation, c.301 c > T, P.


The patient carries one heterozygous mutation, c.301 c > T, P. (Arg 101 Trp), in exon 3 of the IL-10RA gene (b, arrow).


The patient carries one heterozygous mutation, c.301 c > T, P. Her mother has no abnormalities in this coding region of the IL-10RA gene (3-c).


Preoperative view.


Orthopantomograph view.


Histopathological slide of gingival biopsy showing an encircled dystrophic gingival calcification.


Computed tomography showing agenesis of the left kidney and slight calcification in the right kidney (encircled).


Postoperative healing and crown preparation.


Full-mouth crown rehabilitation after 1 month.


The 2,8 dihydroxyadenine stones removed from our patient on ureterolithotomy.


Gd-EOB-DTPA enhanced MRI of this patient. (A) T1-weighted MRI showing that the liver nodules (red arrows) were highly intense.


Gd-EOB-DTPA enhanced MRI of this patient. (B) T2-weighted MRI, showing that the liver nodules were iso-intense.


Gd-EOB-DTPA enhanced MRI of this patient. (C) Gd-EOB-DTPA-enhanced MRI, showing the showed were highly intense during the hepatobiliary phase.


Gd-EOB-DTPA enhanced MRI of this patient. (D) Plain-CT examination 1 year before liver biopsy, showing small, high-density nodules.


Gd-EOB-DTPA enhanced MRI of this patient. (E) FDG-PET CT examination at liver biopsy. No abnormal FDG uptake was detected.


Gd-EOB-DTPA enhanced MRI of this patient. Dynamic CT examination during the. Arterial.


Gd-EOB-DTPA enhanced MRI of this patient. Portal phase.


Gd-EOB-DTPA enhanced MRI of this patient. Equivalent phases. No enhancement was detected.


Histological findings. Hematoxylin-eosin (HE) staining. X4.


Histological findings. . X200).


Histological findings. (C) Melan-A staining (X400).


Histological findings. (D) MIB-1 staining (X400).


Histological findings. CD4 staining. X100.


Histological findings. . X400); T indicates tumor area, N indicates non-tumor area.


Histological findings. CD8 staining. X100.


Histological findings. . X400).


Histological findings. (I) Number of infiltrating cells. Y-axis represents the number of infiltrating cells. The average number of cells in three high power fields is shown. Black bar means the number of cells in tumor area, whereas white bar means that of non-tumor area. Asterisk indicates statistical significance (p<0.05).


Clinical course of present case with images. Red arrow and arrow head indicate the metastatic tumors detectable with imaging studies.


(A) Immunohistochemical staining (IHC) of programmed cell death ligand 1 (PD-L1) from biopsy specimens after treatment with osimertinib as the eighth-line treatment showed PD-L1 tumor proportion score (TPS). 90.


(B) IHC of PD-L1 from surgical specimens before chemotherapy and epidermal growth factor receptor tyrosine kinase inhibitors showed PD-L1 TPS 1%-24.


Pembrolizumab followed by gemcitabine therapy showed antitumor effects. . Notes: Chest computed tomography scan images obtained before administration of pembrolizumab.


Pembrolizumab followed by gemcitabine therapy showed antitumor effects. And at 2 months after three cycles of pembrolizumab showing stable disease.


Pembrolizumab followed by gemcitabine therapy showed antitumor effects. And after 2 months of administration of gemcitabine showing a partial response Arrowheads indicate pulmonary metastatic lesions.


Cerebral MRI presenting the temporal evolution within 3 days (from left to right) and EEG excerpt. First row: axial T2-weighted FLAIR images showing increasing bilateral confluent widespread hyperintensities of the supratentorial white matter predominantly on the left. Second row: axial T2-weighted FLAIR images revealing new hyperintensities of the left cerebellar peduncle. Third row: axial SWI demonstrating subtle and small susceptibility artifacts in the splenium of the corpus callosum. Fourth row: axial pre- and post-contrast T1-weighted MPRAGE showing enhancement of the left parieto-occipital region. FLAIR, Fluid-Attenuated Inversion Recovery; SWI, Susceptibility Weighted Imaging; MPRAGE, Magnetization-Prepared Rapid Acquisition with Gradient Echo.


(A,B) Histologic workup of the biopsy of the left frontal lobe and the cerebral autopsy. (A) Histology of the biopsy of the left frontal lobe showing perivascular infiltrates (arrow) of neutrophils, eosinophils, and macrophages (Hemalaun Eosin [HE] stain).


(A,B) Histologic workup of the biopsy of the left frontal lobe and the cerebral autopsy. (B) Histology of the cerebral autopsy revealing diffuse generalized inflammation and acute hemorrhages (arrow) (Hemalaun Eosin [HE] stain).


Serial serum platelet count post-vaccination and chronological evolution of symptoms after steroid treatment and high-dose immunoglobulin.


Skin biopsy showing lymphocytic infiltrate with histiocytes and giant cells [H and E, x100.


Skin biopsy showing multinucleated giant cells (arrow) with an amorphous eosinophilic cytoplasm [H and E, x400.


MRI of thoracic spine showing T8 fracture.


Patient 1: Sprouting erosive growth over the scrotum.


Patient 3: Computerized tomography (CT) of the abdomen and pelvis. Contrast-enhanced axial CT image through the lower pelvis. Heterogeneously enhancing soft tissue mass destroying the sacrum. It displaces the urinary bladder anteriorly and also extends into the right side. Another large lymphnode mass is also noted adjacent to the iliac vessels.


Immune dysregulation and exposure to associated immunomodulatory therapies from the cases presented. (A) Timeline of C-reactive protein (CRP) and ferritin values from case 1 showing progressive immune dysregulation. This patient was exposed to methylprednisolone, anakinra, intravenous immunoglobulin (IVIG), and plasma exchange, as shown along the top of the panel.


Immune dysregulation and exposure to associated immunomodulatory therapies from the cases presented. (B) Timeline of CRP and ferritin values from case 2 showing two distinct periods of immune dysregulation. This patient was exposed to methylprednisolone, tocilizumab, anakinra, etanercept, infliximab, and plasma exchange, as shown along the top of the panel.


Extended family pedigree of our patient with Chronic Granulomatous Disease illustrating the extensive family history of the disease. Square- Male, Darkened square- Affected male, Circle- Female, Dotted Circle- Carrier, Strikethrough- Deceased.


Dihydrorhodamine test results for. The shipping control.


Our patient with CGD showing fluorescence after incubation of serum sample with dihydrorhodamine and phorbol myristate acetate (PMA). Note the lack of fluorescence shift in B indicating lack of oxidative phosphorylation.


(A) Computed tomography (CT) scan at diagnosis demonstrating acute intracerebral hemorrhage (ICH) in the right frontal lobe.


(B) CT scan demonstrating ICH re-occurrence at day 3 after the first craniotomy.


(C) CT scan demonstrating rebleeding after the second craniotomy.


(D-F) Magnetic resonance images showing multiple intracranial lesions (arrow) 1 month after the first craniotomy.


Timeline with relevant data from the episode of the case.


Delayed postcontrast head CT obtained with CT angiography showing suggestion of a filling defect (arrows) in the region of the left sphenoparietal sinus.


T1 with contrast.


T2 flair.


Medical image.


FSPGR BRAVO.


DWI. MRI sequences demonstrating findings of FLAIR hyperintensity, diffusion restriction, susceptibility blooming, and mild enhancement in the region of the left frontal-temporal operculum and insula indicative of venous infarct.


Noncontrast head CT obtained with CT angiography demonstrating tubular hyperdensity indicated by arrows (a-c) adjacent to areas of hypoattenuation in the left frontal operculum, temporal operculum, and insula.


Swelling of the right lower eyelid due to the tumor in the anterior inferior orbit.


Histopathological analysis of an orbital hemangiopericytoma. . Notes: (A) Low-power view showing the lobular pattern of highly cellular areas separated by fibrous tissue (hematoxylin and eosin [H&E], 40x).


Histopathological analysis of an orbital hemangiopericytoma. (B) Large, dilated vascular channels within the neoplastic cells (H&E, 100x).


Histopathological analysis of an orbital hemangiopericytoma. (C) A high-power view of the cellular areas (H&E, 400x).


Histopathological analysis of an orbital hemangiopericytoma. (D) The fibrotic areas separating the lobules were mostly acellular (H&E, 400x).


Histopathological analysis of an orbital hemangiopericytoma. (E) Factor VIII-positive immunostaining (100x).


Histopathological analysis of an orbital hemangiopericytoma. (F) Ki-67 immunostaining (200x).


MRI where we observed a serpentigenous path of the arteriovenous malformation at the parieto-occipital region. (a) Axial T2-weighted sequence.


MRI where we observed a serpentigenous path of the arteriovenous malformation at the parieto-occipital region. (b) Axial T2-FLAIR sequence.


MRI where we observed a serpentigenous path of the arteriovenous malformation at the parieto-occipital region. (c) Axial 3D TOF.


MRI where we observed a serpentigenous path of the arteriovenous malformation at the parieto-occipital region. (d) Sagittal 3D TOF.


Scanning findings for bones. (A) Disseminated hypermetabolic lesion (maxSUV=9.0, L2 body) at the whole spine by PET. A hypermetabolic lesion suggesting a primary malignant lesion was not detected in the lung, intraabdominal and pelvic organs.


Scanning findings for bones. (B) No increased bone uptake of hypermetabolic lesions on bone scan, with little osteoblastic effect.


Histopathological findings of bone marrow biopsy. (A) Non-cohesive proliferation of large pleomorphic neoplastic cells with large round-to-oval nuclei with vesicular chromatin and abundant foamy cytoplasm (H&E stain, x400).


Histopathological findings of bone marrow biopsy. Immunostaining with antibodies to. CD99.


Histopathological findings of bone marrow biopsy. CD68.


Histopathological findings of bone marrow biopsy. CD56.


Histopathological findings of bone marrow biopsy. HMB45 (each, x100).


Histopathological findings of bone marrow biopsy. S100 (x200).


Axial computed tomography scan. Showing a well-demarcated mass in the tip of the left temporal fossa extending into the orbital apex, and accompanying bony erosions in the medial sphenoid ridge. Sequences, and intensely enhanced on contrast examinations.


Magnetic resonance images The tumor appears isointense on both T1- The left optic nerve is considerably compressed by the tumour at the orbital apex (b, arrow).


Magnetic resonance images. And T2-weighted.


Magnetic resonance images. Sequences, and intensely enhanced on contrast examinations.


Intraoperative photos showing drilling of the medial sphenoid ridge overhanging the tumour ,exposure of a dura-based.


Medical image.


Microscopic appearance of the tumor comprised by spindle-shaped cells, lacking findings of atypia or necrosis (a). Immunohistochemical stains showing positive staining for bcl2 (b), CD34 (c), CD99 (d), and STAT6 (e), with the MIB-1 index of 10% (f). A: Hematoxylin and eosin stain, x200; b: bcl2; c: CD34; d: CD99; e: STAT6; f: MIB-1, x100.


Computed tomography (CT) findings. A; Local recurrence of thymoma at the first relapse.


Computed tomography (CT) findings. B; A pleural dissemination of thymoma at the second relapse.


Computed tomography (CT) findings. C; Complete remission following cyclosporine therapy.


Flow cytometry of mantle cell lymphoma in the peripheral blood (2015) shows CD19/CD5 coexpression (depicted in dark blue).


Lambda light-chain restriction.


Flow cytometry of T-cell large granular lymphocytic leukemia in bone marrow (2018) shows CD3+/TCR gammadelta+ (depicted in green).


CD5-/TCR gammadelta.


CD7+/TCR gammadelta+. Expression.


(a and b) Multiple erythematous papules over the face.


(c) Multiple erythematous papules and edematous urticarial plaques over the back.


(d) Purpuric lesion over the thenar aspect of right palm.


(a) Moderately dense perivascular and interstitial infiltrate of lymphocytes, eosinophils, and neutrophils with spongiosis in the superficial and mid-dermis. (Hand E staining, x10).


(b) Interstitial infiltrate of many mature eosinophils intermixed with neutrophilswith areas of leukocytoclasia without vasculitis (Hand E staining, x40).


(a and b) Resolution of facial lesions after treatment.


(c) Significant decrease in the number and size of lesions after treatment.


(d) Clearance of palmar lesion after treatment.


Non-enhanced coronal view CT of head and orbit, showing ill-defined soft tissue mass measuring about 2.7 cm, height 0.2 cm* transverse 1.3 cm located in the superomedial aspect of left orbit, extra-conal involving underlying bone erosion and periosteal reaction with opacification of left ethmoid and both maxillary sinuses.


Non-enhanced sagittal view CT of head and orbit, showing ill-defined soft tissue mass of superomedial aspect of left orbit causing inferolateral displacement of left eye globe.


Non-enhanced axial view CT of head and orbit, showing ill-defined soft tissue mass at the medial aspect of left orbit causing lateral displacement of left globe.


T2 weighted image, coronal view of head and orbit, showing extra-conal isointense soft tissue mass of superomedial aspect of left orbit causing inferolateral displacement of left globe and medial orbital wall erosion with periosteal reaction, and opacification of left ethmoid and both maxillary sinuses. Surrounding fat planes are preserved.


T2 weighted image, sagittal view of head and orbit, showing slightly homogenously enhanced lesion seen at superomedial aspect of left globe.


T2 weighted image, axial view of head and orbit, showing homogenous isointense lesion, seen at superomedial aspect of left globe causing mild lateral proptosis of left eye globe.


In bronchoalveolar lavage, a large number of hemosiderin-laden macrophages are histologically confirmed, which indicate an alveolar hemorrhage (Berlin blue stain).


Clinical course in this case. PE = plasma exchange; mPSL = methylprednisolone; SBP = systolic blood pressure; DBP = diastolic blood pressure; NPPV = noninvasive positive pressure ventilation; Cr = creatinine; Plt = platelet count.


Specimen radiographic appearance of the jaw eliciting the multilocular radiolucency with root resorption postero-anteriorly.


Radiographic appearance of the jaw eliciting the multilocular radiolucency with root resorption.


The microscopic appearance exhibiting fibrous connective tissue exhibiting numerous odontogenic epithelial islands with peripheral tall columnar cells showing reversal of polarity. The center of the island shows stellate reticulum like cells which is replaced by granular cells (inset) (under x10 magnification).


The microscopic appearance shows central stellate cells replaced by large eosinophilic rounded or polyhedral granular cells (under x10 magnification).


The microscopic appearance of granular cell (under x40 magnification).


Coronal CT image showing bilateral perinephric collections with otherwise normal kidneys.


Axial CT scan showing fluid attenuation perinephric collections.


FNAC shows numerous lymphoid cells without atypia.


Histological findings. A; Thick fibrous septa intersecting the tumor cells into lobules. Hematoxylin-eosin stain, x40.


Histological findings. B; Tumor cells have a round nucleus with remarkable nucleolus. Hematoxylin-eosin stain, x400.


Histological findings. Immunohistochemical studies showed the tumor was CD5 partially positive.


Histological findings. And Ki-67 positive.


Case one, 2008: Fluid attenuated inversion recovery (FLAIR) MRI sequences showing multifocal hyperintensity in the subcortical U-fibres of the right basifrontal, right temporal, and left parieto-occipital regions (see arrows). The corresponding T1 post contrast images (lower row), demonstrate an absence of enhancement.


Case one, 2011: FLAIR MRI sequences from 2011 again show hyperintensity in the right basifrontal (see arrows) and left parieto-occipital regions, now with enhancement on corresponding post contrast T1 images (lower row) in the right basifrontal region only.


Case one, 2013: FLAIR hyperintensity has increased in the left parieto-occipital region (see arrows, top images), with new gyriform enhancement (see arrows, bottom images) on corresponding pre-contrast FLAIR sequences. The right basifrontal contrast enhancement has shown a complete resolution.


Case two, 2006: FLAIR MRI sequences demonstrating multiple poorly defined bright foci in the central and periventricular white matter, with subcortical U-fibre involvement (see arrows) in the frontoparietal region.


Case two, 2012: FLAIR MRI sequences showing new lesions in the posterior fossa (see arrow) and an increase in the number of lesions in the high frontoparietal white matter bilaterally (see arrows). There was also increased cerebral atrophy. There was no mass effect, perilesional oedema, or enhancement after contrast administration (not shown).


CT of the chest (in lung window) showing multiple thick-walled cavities in both upper lobes with diffuse tree-in-bud nodularities. . Abbreviation: CT, computed tomography.


Brain MRI.


The residual mass on the right side of the post-operative cavity, which was ~26 mm*35 mm*30 mm (arrow) in volume, and the mass disappeared 1 month after infusion.


No relapse occurred in subsequent follow-up (C).


The levels of fourth-generation CART19 and CART70 cells in peripheral blood at the indicated time points after CAR T-cell infusion. Both 4SCAR19 and 4SCAR70 reached their peaks in the peripheral blood on day 7, with the former accounting for 2.28% of circulating mononuclear cells and the latter accounting for 0.46%.


MRI of the brain shows a residual lesion in the left nucleocapsular region (red arrow).


Total cystectomy tissue sample. Hematoxylin and eosin staining.


Total cystectomy tissue sample. And immunohistochemical staining with the anti-hCG antibody Positive staining of the tumor cells was detected (indicated by arrowhead).


Preoperative brain MRI The white arrow (a; axial Flair sequence) points to the tumor invading the cerebellar parenchyma bilaterally. The lesion appears slightly hyperintense. The 4th ventricle is invaded (white arrowhead), causing a hydrocephalus (dilatation of the lateral ventricles in b).


Preoperative brain MRI.


Preoperative brain MRI The tumor expands clearly in the vermis as shown on a sagittal image (c). Early postoperative axial FLAIR slice shows postoperative sequelae at the level of dentate nuclei bilaterally (white arrows in d).


Medical image.


The hydrocephalus is resolved (e). The 4th ventricle is moderately dilated, including in the rostral direction. The superior medullary velum is visible (white arrow in f). The superior cerebellar peduncles are involved (white arrows in g), with a slight extension towards the corpora quadrigemina at the level of inferior colliculi (white arrows in h). Crus cerebri are spared bilaterally (white arrows in i). R: right side.


Multiple yellowish-brown coalescing papular lesions located in the patient's left cheek.


Yellowish-brown, slightly elevated papular lesions located in the left cheek after treatment.


Response evaluation during the clinical course including changes in imaging and quantitative data. IuPD (immunity unconfirmed progressive disease); icPD (immunity confirmed progressive disease). (A) Trends in the levels of tumor monitoring indicators, including AFP (left Y-axis) and tumor diameters (right Y-axis) corresponding to the treatment timeline. X-axis showing the date of the disease course. The frequency of imaging evaluations is less than that of AFP.


Response evaluation during the clinical course including changes in imaging and quantitative data. IuPD (immunity unconfirmed progressive disease); icPD (immunity confirmed progressive disease). (B) Representative images of the CT scan revealed the increasing and decreasing process of both primary and metastatic lesions in the liver and lung after PD-1 antibody (tislelizumab) and sorafenib treatment. Red arrows indicate tumor lesions.


The whole clinical timeline of the patient, with major treatment and disease status. DFS, disease-free survival; PFS, progression-free survival.


Histopathology and immunohistochemistry (IHC) of the lymph node of this patient. Microscopic observation (10x) of H&E staining showed a dense diffuse lymphoid cells infiltration (A).


Histopathology and immunohistochemistry (IHC) of the lymph node of this patient. Immunohistochemical staining of CD20 and Bcl-2 expression (20x) showed that tumor cells were positive for CD20 and Bcl-2, respectively (B, D).


Histopathology and immunohistochemistry (IHC) of the lymph node of this patient. The Ki-67 proliferative index (20x) was low (C).


Treatment history of our case and schematic diagram of tumor evolution. (A) Clinical treatment history and gene tests results of the patient. Numbers indicate time (in months) from the diagnosis of lung adenocarcinoma (LADC). Scale bar in histopathologic picture indicates 100 mum.


Treatment history of our case and schematic diagram of tumor evolution. (B) Presumed clonal evolution of our case which refers to Lee et al. 's study. The horizontal axis suggests the clinical history, and the vertical axis represents tumor volume.


Postoperative Magnetic Resonance Images (a) Axial T1-weighted MRI demonstrating normal postoperative changes.


(b) Sagittal T1-weighted postcontrast MRI demonstrating normal postoperative changes.


Preoperative photograph of case 1 showing expansile swelling over the left anterior maxilla.


Orthopantomograph showing a well-defined unilocular radiolucent lesion affecting left maxilla with multiple displaced teeth.


Intraoperative photograph showing the tumor involving the left maxilla exposed via modified Weber-Ferguson incision.


Resected tumor after sub-total maxillectomy.


Postoperative photograph after 6 months.


Preoperative photograph of Case 2 showing swelling over left mid and lower face.


Case 2: Intraoral view showing the swelling involving left mandibular alveolus, obliterating the vestibule with buccal cortical expansion.


Orthopantomograph showing multiple ill-defined radiolucencies over the angle and ramus region of left side of mandible with displaced adjacent teeth.


Operated site after the resection of tumour (hemimandibulectomy) done followed by placement of 2.4 mm titanium reconstruction plate.


Resected hemi-mandible with 2 cm margin.


Case 2: Recurrence with marked swelling over left side lower face extending to the neck after 8 months of surgery.


Skin manifestation after bagatelle injury on day 11 after admission.


Intraoperative appearance after initial radical debridement on day 11 after admission.


Areactive necrosis of subcutaneous fat and fascia without detection of bacteria (H&E, 200x).


Diagram of the course of disease.


Bone marrow biopsies. (A) Eosinophilia and micro-megakaryocyte proliferation.


Bone marrow biopsies. Evident signs of fibrosis, original magnification 5x; (B) Micro-megakaryocytes characterized by hypo-lobated nuclei, original magnification 20x.


Pre-operative view.


Pre-operative X-ray.


11 prepared.


Implant with cover screw.


Post-operative radiograph.


One month after implant placement.


Fenestration defect around an implant.


PRF gel.


Bone graft mixed with PRF.


Bone graft and PRF mixture placed over defect.


PRF and GTR membrane placed over defect.


Flap sutured.


Final restoration.


Histological sections of excised lymph node showing increased volume. Histiocyte containing numerous lymphocytes (emperipolesis) (hematoxylin and eosin at 400x magnification);. Immunohistochemical staining for protein S100 expression (400x magnification).


MRI brain images at 3 months follow-up. T2 axial image shows decrease in the number of T2-isointense lesions.


Perilesional edema (arrow).


DWI does not show any restriction. Post-contrast images show fewer enhancing nodular lesions in the subependymal regions and deep gray nuclei (arrows).


(a) T2 sagittal MRI cervical spine showing complete destruction C4 with partial destruction of C3 and C5 body with anterior epidural collection with compression of cervical spinal cord between C3 and C5.


(b) T1 gadolinium contrast-enhanced sagittal MRI cervical spine showing contrast-enhanced epidural lesion anterior to C3-C5.


(c) Axial contrast-enhanced cervical MRI at C4 showing canal compromise.


(d) Postoperative NCCT cervical spine shows adequate decompression between C3 and C5 with expandable titanium cage in situ.


Negative anaplastic lymphoma kinase-1 staining in the atypical cells (Immunoperoxidase, x400).


T1-Turbo inversion recovery magnitude (TIRM) coronal MRI.


T1-Turbo spin-echo (TSE) coronal MRI.


Clinical and histopathological appearances. (a and b) HE staining results from thickened rectum showing adenocarcinoma.


Clinical and histopathological appearances. (c) Bone marrow cytology results showing increased plasmocyte.


Clinical and histopathological appearances. (d-g) Pathological and immunohistochemical results of bone marrow showing CD138 (+), CD38 (+), CD56 (partial +), Kappa (+), myelodysplastic activity and increased plasmocyte.


Clinical and histopathological appearances. (h) Excised rectal cancer.


ECG of patient during treatment. Normal ECG before atrial fibrillation, and ,RR interval prolongation.


ECG of patient during treatment. The first holt result showing atrial fibrillation occurring during thalidomide treatment.


ECG of patient during treatment. The first holt result showing serious RR interval prolongation (RR interval = 5.2 s) during thalidomide treatment.


ECG of patient during treatment. Atrial fibrillation did not disappear after withdrawal.


(a) T2-weighted sagittal magnetic resonance image of the thoracolumbar spine showing the isointense extradural lesion (arrow) causing thecal sac and spinal cord compression and signal intensity changes within the cord.


(b) The T2-weighted axial image showing thecal and spinal cord compression (curved arrow) by the extradural lesion (straight arrow).


(a) Myeloid cells (arrow) admixed with erythroid cells and megakaryocytes (H and E, x40). (b) Increased reticulin (arrow) on bone marrow biopsy (Retic x40).


At presentation, BCVA of a 52-year-old male patient with multiple myeloma was 20/50 in the right eye and 20/800 in the left eye. . Notes: (A and B) Color fundus image showed scattered flame-shaped hemorrhages, Roth spots, and serous macular detachment in both eyes.


At presentation, BCVA of a 52-year-old male patient with multiple myeloma was 20/50 in the right eye and 20/800 in the left eye. (C and D) FFA revealed scattered microaneurysms and hypofluorescent areas, but no macula leakage.


At presentation, BCVA of a 52-year-old male patient with multiple myeloma was 20/50 in the right eye and 20/800 in the left eye. (E and F) OCT revealed bilateral serous macular detachment, prominent middle limiting membrane (yellow arrow), and cysts in the outer plexiform layer of the left eye (white arrow). . Abbreviations: BCVA, best-corrected visual acuity; FFA, fundus fluorescein angiography; OCT, optical coherence tomography.


One month after presentation, BCVA was 20/32 in the right eye and 20/100 in the left eye. . Notes: (A and B) Color fundus image showed retinal hemorrhages, Roth spots, and yellow macular deposits.


One month after presentation, BCVA was 20/32 in the right eye and 20/100 in the left eye. (C and D) Fluorescein angiography showed a reduction in microaneurysms.


One month after presentation, BCVA was 20/32 in the right eye and 20/100 in the left eye. (E and F) SD-OCT showed a decrease in serous macular detachment in both eyes, and subretinal hyperreflective deposits.


One month after presentation, BCVA was 20/32 in the right eye and 20/100 in the left eye. (G and H) Fundus autofluorescence showed hyperautofluorescent macular deposits. . Abbreviations: BCVA, best-corrected visual acuity; SD-OCT, spectral-domain optical coherence tomography.


Two months after presentation, BCVA was 20/20 in the right eye and 20/32 in the left eye. . Notes: (A and B) Color fundus image showed complete resolution of retinal hemorrhages and Roth spots and decrease in yellow macular deposits.


Two months after presentation, BCVA was 20/20 in the right eye and 20/32 in the left eye. (C and D) FA showed complete resolution of microaneurysms.


Two months after presentation, BCVA was 20/20 in the right eye and 20/32 in the left eye. (E and F) SD-OCT showed subretinal hyperreflective deposits and left serous macular detachment. . Abbreviations: BCVA, best-corrected visual acuity; FA, fundus autofluorescence; SD-OCT, spectral-domain optical coherence tomography.


Four months after presentation, BCVA was 20/20 in both eyes. . Notes: (A and B) Fundus examination revealed retinal hemorrhages had completely resolved.


Four months after presentation, BCVA was 20/20 in both eyes. (C and D) FA revealed microaneurysms had completely resolved.


Four months after presentation, BCVA was 20/20 in both eyes. (E and F) Fundus autofluorescence showed reduction in hyperautofluorescent macular deposits.


Four months after presentation, BCVA was 20/20 in both eyes. (G and H) SD-OCT revealed complete resolution of serous macular detachment. . Abbreviations: BCVA, best-corrected visual acuity; FA, fundus autofluorescence; SD-OCT, spectral-domain optical coherence tomography.


(a) Showing a T2-weighted sagittal view with a heterogeneously iso-hypointense mass lesion located in the sphenoid sinus.


Shows heterogonous enhancement of lesion after gadolinium administration.


Lesion is isointense on plain T1-weighted images.


(d) Microphotographs showing a cellular spindle cell tumor with interlacing fascicles; inset (1) showing the increased MIB-1 labeling and inset (2) showing positive staining for smooth muscle actin. Vimentin positive but negative for S100, desmin, creatine kinase, and CD99 suggestive of leiomyosarcoma.


(a) Shows a T2-weighted sagittal magnetic resonance imaging with a hyperintense mass lesion in the sphenoid sinus with enlargement of sphenoid sinus.


The lesion is hyperintense on plain T1-weighted images.


Not enhancing on postgadolinium injection axial.


Coronal imagesab.


Preoperative X-ray whole spine anteroposterior and lateral view showing osteolytic lesions in D8 and L3 vertebral bodies with erosion and collapse of D8 vertebra.


Preoperative MRI sagittal and axial T1- and T2-weighted images showing collapsed D8 vertebral body with surrounding free fluid extending posteriorly from D7 to D9 vertebra and causing significant compression of spinal cord with a lesion in L3 vertebral body causing dural sac indentation.


Histopathological examination report showing inflammatory granulation tissue.


(a) PET-CT scan showed metabolically active osteolytic lesion predominantly in D8 vertebra and in multiple regions such as D7, D9, D11 vertebral bodies, left 7th rib, sternum, and right iliac bone along with bilateral pleural effusions, mediastinal, and left supraclavicular lymphadenopathy and soft-tissue lesions in the left orbit and left temporal region of brain.


Timeline of Events for Case 1. HCT, hematopoietic cell transplant; ICU, intensive care unit; ECMO, extracorporeal membrane oxygenation; CD, cluster of differentiation; G-CSF, granulocyte-colony stimulating factor.


Serial chest radiographs for Case 1 demonstrating the progression and subsequent improvement of diffuse bilateral interstitial and alveolar opacities. Initial decline prompting transfer to the ICU.


Serial chest radiographs for Case 1 demonstrating the progression and subsequent improvement of diffuse bilateral interstitial and alveolar opacities. Mild respiratory improvement.


Serial chest radiographs for Case 1 demonstrating the progression and subsequent improvement of diffuse bilateral interstitial and alveolar opacities. Worsening ARDS leading to transfer for ECMO evaluation.


Serial chest radiographs for Case 1 demonstrating the progression and subsequent improvement of diffuse bilateral interstitial and alveolar opacities. Pre-decannulation.


Timeline of Events for Case 2. HCT, hematopoietic cell transplant; ICU, intensive care unit; ETT, endotracheal tube; BAL, bronchoalveolar lavage; ECMO, extracorporeal membrane oxygenation; CRRT, continuous renal replacement therapy; TA-TMA, transplant-associated thrombotic microangiopathy.


Serial chest radiographs for Case 2 demonstrating the progression and subsequent improvement of diffuse bilateral interstitial and alveolar opacities. Following intubation.


Prior to transfer for ECMO evaluation.


Following ECMO cannulation.


Prior to ECMO decannulation.


Post-transfer back to referring center.


The patient's lymphoma chemotherapy timeline. Abbreviations: Ara-C, cytarabine; CDI, Clostridiumdifficile infection; CTX, cyclophosphamide; DXM, dexamethasone; IFO, ifosfamide; MTX, methotrexate; NHL, Non-Hodgkin's lymphoma; R, rituximab; VCR, vincristine; VP 16, etoposide. V-AA-RBB-RCC was the chemotherapy regimen combination used to treat the patient. V regimen: prednisone + CTX; AA regimen: DXM + IFO + VCR + Ara-C + MTX +VP 16; RBB regimen: R + DXM + CTX + VCR + MTX + Adriamycin; RCC regimen: R + DXM + vindesine + Ara-C +VP 16.


Jelly-like stool from the patient before treatment.


Stool from the patient 3 days after the initiation of treatment.


Normal stool from the patient after 10 days of treatment.


Computed tomography scan of the chest and abdomen showing multiple consolidations in both lung fields:. Pleural effusion, and ,atelectasis bilaterally.


Massive ascites.


(a) Orthopantomography showing mixed radiolucentradiopaque lesion from distal of 33 to distal of 36, intact inferior border and periosteal reaction along the lower border of mandible (Sun-burst appearance).


(b) Radiograph showing periosteal reaction along the lower border of mandible (Sun-burst appearance).


(c) Axial computed tomography showing soft tissue density mass surrounding left mandible with erosion of underlying bone.


(d) Reduction in size of lesion involving left mandibular body after chemotherapy and radiotherapy.


Photomicrographs of immunohistochemical markers that were positive: (a) Terminal deoxynucleotidyl transferase (IHC stain, x100), (b) CD99 (IHC stain, x200), (c) PAX5 (IHC stain, x400), (d) CD10 (IHC stain, x100), (e) CD20 (IHC stain, x100), (f) Diagnostic flow-chart of pre-B-cell lymphoblastic lymphoma.


Chest computed tomographic images showing a pulmonary mass in the left upper lobe with pleural effusion at the patient's first visit (a).


This tumor grew rapidly to occupy the entire left upper lobe 1 month after the patient's first visit (b).


Postoperative 18F-fluorodeoxyglucose positron emission tomographic images showing abnormal and diffuse accumulation of 18F-fluorodeoxyglucose in the left pleural cavity.


Which disappeared after five cycles of chemotherapy.


Histopathological findings showing an admixture of spindle-shaped and circular cells, arranged in a storiform pattern (hematoxylin and eosin, x100) (a).


Immunohistochemical staining revealed cells positive for vimentin (x100) (b).


18F-FDG-PET images at relapse Multiple indications of abnormal 18F-FDG uptake (a) disappeared after RIC-HSCT.


507 days after RIC-HSCT.


Fundus photograph showing active juxtamacular retinitis before treatment.


Inactive lesion after treatment with intravitreal clindamycin.


Spectral-domain optical coherence tomography showing hyperreflective spots in the vitreous, macular edema with intra-, and ,sub-retinal fluid before treatment, hyperreflectivity of the neurosensory retina can be noted in the temporal aspect precluding the individualization of the different layers.


Normal retinal thickness and foveal contour after treatment.


Fundus photograph showing active juxtamacular toxoplasmic retinochoroiditis before treatment.


Sharpening of lesion borders after treatment with intravitreal clindamycin.


Spectral-domain optical coherence tomography showing elevation of the neurosensory retina, and ,retinal pigment epithelium with the presence of intra-, and ,sub-retinal fluid before treatment, hyperreflectivity of the neurosensory retina can be noted in the inferior nasal aspect precluding the individualization of the different layers.


Normal foveal contour with evidence of retinal pigment epithelial and outer retinal atrophy after treatment.


Fundus photograph showing active juxtamacular focal retinitis before treatment.


Spectral-domain optical coherence tomography showing increased retinal thickness, subretinal fluid.


Vitreous hyperreflectivity before treatment. Normal retinal thickness and foveal contour after treatment.


Fundus photograph showing active juxtapapillary retinitis before treatment.


Quiescent lesion after treatment with intravitreal clindamycin.


Clinical photograph of the erythematous swelling of the left eyelid.


Enhanced extraconal and intraconal infiltrations in the left orbit, and an inferolateral view of the silicone ball sphere in the eyelid.


The tumors were composed of cells with hyperchromatic eccentric nuclei (suggesting signet ring cells), prominent eosinophilic cytoplasm, and intracytoplasmic vacuolations (H&E, x400).


A positron emission tomography image revealed the multiple intense hypermetabolic foci on the left orbit and the skull as well as along the spine.


Abdominopelvic CT scan with contrast is primarily nonrevealing for a malignant process. . Nonspecific gastric fold thickening in the fundus is observed (
arrow). An incidental finding in the liver was noted by a small focal hypoattenuation in the middle segment of the left lobe of the liver adjacent to the fissure for ligamentum teres (
arrowhead). This nodule was confirmed as PET-negative on later PET/CT studies.


Pathology demonstrates an invasive poorly differentiated adenocarcinoma.


Pre-chemotherapy staging PET scan shows a locally advanced gastric cancer. . PET from skull to mid-thigh reveals extensive, diffuse hypermetabolism throughout the gastric wall compatible with a PET-avid infiltrating gastric neoplasm. Imaging revealed involvement of at least one hepatogastric lymph node. Thus, the patient was determined to have stage III disease (T3N1). Scattered areas of contrast uptake within the bowel are likely physiologic and limit evaluation for lesions. Contrast uptake within the brain and genitourinary system are physiologic.


Case report timeline. . Presented according to CARE guidelines.


Pseudotumor orbitae and lymphocytic dakryadenitis as rare extrahepatic manifestations of hepatitis C. A; Presentation of our patient with bilateral ptosis on the left side more than on the right.


Pseudotumor orbitae and lymphocytic dakryadenitis as rare extrahepatic manifestations of hepatitis C. B; MRI of the brain and orbit (T1-weighted contrast-enhanced image) demonstrating left-sided pseudotumor orbitae.


Pseudotumor orbitae and lymphocytic dakryadenitis as rare extrahepatic manifestations of hepatitis C. C; Lacrimal gland with a prominent lymphocytic infiltration. Giemsa. X200.


Pseudotumor orbitae and lymphocytic dakryadenitis as rare extrahepatic manifestations of hepatitis C. D; Abundant CD20-positive B cells. CD20. X100.


Contrast axial.


Coronal T2. Magnetic resonance images at initial presentation showing solid enhancing cerebellopontine angle mass with adjacent nonenhancing cerebellar cyst.


T2-weighted. Axial magnetic resonance images at recent presentation.


Coronal. Magnetic resonance imaging showing solid densely enhancing tumor in left cerebellopontine angle.


Preoperative digital subtraction angiography showing feeders from left posterior inferior cerebellar artery.


Feeders from ascending pharyngeal branch of external carotid artery.


"En-bloc" excision of the tumor.


(a) Photomicrograph showing tumor with blood vessels containing glue material (blue arrow) and fibrin thrombi (white arrow) (H and E, x20). (b) Tumor showing stromal edema, hyalinization, and micro cystic changes (H and E, x100).


Postoperative axial.


Coronal. Contrast magnetic resonance imaging showing complete tumor excision.


Preoperative view of discoloured maxillary lateral incisor.


Preoperative radiograph showing radiolucency along distal aspect of maxillary lateral incisor to the apex.


Separation of platelet rich plasma from the collected autologous blood.


Platelet rich fibrin after activation with calcium chloride.


Curettage of the defect after reflection of soft tissue flap using intracrevicular incision.


Placement of graft into defect.


Placement of PRF.


Follow-up radiographs. At 6 months, postoperative view showing bone fill.


At 12 months.


X-ray of the forearm showing a soft tissue tumor with areas of calcification (arrows).


Magnetic Resonance Imaging (MRI) showing a soft tissue mass in the subcutis. The lesion is isointense to muscle in T1-weighted sequence.


Magnetic Resonance Imaging (MRI) showing a soft tissue mass in the subcutis. , hyperintense on T2-weighted sequence.


Magnetic Resonance Imaging (MRI) showing a soft tissue mass in the subcutis.shows contrast medium enhancement on T1-weighted sequence.


Low power view showing the two abruptly separated components of the tumor. Well-differentiated leiomyosarcoma is shown in the lower and high-grade osteosarcoma in the upper right (40x).


Well-differentiated leiomyosarcoma consisting of spindle cells arranged in intersecting fascicles (200x).


High-grade osteosarcoma consisting of highly atypical cells with osteoid matrix production (a; 200x).


In other areas neoplastic cells produced cartilage matrix (b; 100x).


Is positive for alpha smooth muscle actin. 40x, inset 400x).


The leiomyosarcoma component (on the right in a and . Desmin. 100x), whereas the osteosarcoma component (on the left in a, and . . Is negative.


SATB2 was positive in the nuclei of neoplastic cells in the osteosarcoma component. 400x).


Negative in the leiomyosarcoma. 400x).


(a) Conjunctival flap done for nonhealing fungal corneal ulcer (right eye).


(b) Healthy limbus and leukomatous corneal opacity (right eye).


Maximum intensity projection image of FDG PET/CT in an 11-month old boy done after injection of 37MBq of F18-FDG intravenously, showing FDG avid foci in neck, mediastinum, upper abdomen and spleen.


Axial PET.


Low dose CT.


Fused PET/CT images showing enlarged hypermetabolic mediastinal lymph nodes (eg, right paratracheal, maximum standardized uptake value 3.9). Similar enlarged FDG avid lymph nodes were seen involving multiple lymph node groups including right intraparotid, cervical, lung hilum, splenic hilum, mesenteric, and inguinal nodal stations.


Sonogram of the abdomen showing splenomegaly , diffusely heterogeneous spleen.


With hypoechoic subcentimeter splenic nodules , which could be secondary to fungal infection or multiple abscesses.


CT of abdomen and pelvis with intravenous contrast revealing right-sided PA with multiloculation and contiguous spread, as shown by the arrows in the coronal.


Sagittal. Sections.


Plain CT after AVS. Immediately after AVS, pooling of contrast medium in the entire right adrenal gland was observed (arrow).


Results of AVS. Blood sampling site numbers are in parentheses. Plasma aldosterone concentration (pg/mL)/plasma renin activity (ng/mL/h) = aldosterone-renin ratio.


Pedigree of the three-generation (I-III) patient's family. Squares denote males while circles denotes females. Shadow symbols indicate affected individuals, while open symbols represent unaffected individuals. Diagonal lines are used to show that a person is died. Information regarding HLA genotypes associated with EM is also included in the pedigree. II-2 without a history of EM shows the same haplotypes (HLA-DQB1*03:01) as the patient with EMM (III-2).


Histologic findings of biopsied specimens from the anterior aspect of the antrum in the first patient. (A) On microscopic findings at a low magnification, the nodular mucosa is expanded by a marked lymphoplasma cell infiltration with the presence of a prominent germinal center (H&E stain, x100).


Histologic findings of biopsied specimens from the anterior aspect of the antrum in the first patient. (B) On microscopic findings at a higher magnification, diffuse lymphoplasma cell infiltration is noted in the lamina propria, and a few lymphocytes are infiltrating the epithelium. Low grade gastric MALT lymphoma is suspected, but no definite lymphoepithelial lesion is found (H&E stain, x400).


Left pheochromocytoma (arrows); dog. Neoplastic vascular invasion (asterisk) in caudal vena cava (CVC) and abdominal phrenic vein (APV). Left kidney (LK). Right kidney (RK).


Right pheochromocytoma (asterisk), sagittal section; dog. Thinning (between arrows) of adrenal cortex (AC). Adrenal medulla (AM).


Parathyroid adenoma (asterisk); dog. Caudal parathyroid gland (Pc) and left thyroid lobe (LTL).


Parathyroid chief cell adenoma; dog. Section showing cubic cells arranged in tortuous trabeculae and packets supported by a delicate fibrovascular stroma (HE).


Right pheochromocytoma; dog. Section showing large polyhedral cells forming irregular packets, delimited by a delicate fibrovascular stroma. HE. Smaller box: section of adrenal cortex not invaded by pheochromocytoma, with traces of zona glomerulosa (Zg) and atrophy of zona fasciculata (Zf) and zona reticularis (Zr). Capsule (C) (HE).


Left pheochromocytoma; dog. Section showing more than 90% of cells with positive staining to anti-synaptophysin antibody in histochemical procedures (Avidin-biotin complex). Smaller box: Strongly positive cytoplasmatic staining of neoplastic cells (Avidin-biotin complex).


Radiation exposure assessment during radioiodine treatment of the thyroid: Radiation exposure assessment data provided by the National Hospital.


Tumor specimen showing the pinkish white color, soft, friable nature of the tumor.


Immunohistochemistry with S-100 positivity.


CD68 immunopositivity.


Lysozyme immunopositivity.


Clinical image shows noduloulcerative growth with keratin plugging seen on left vermilion of the lower lip.


Histopathological image shows hyperkeratotic epithelium with parakeratin plugging overlying connective tissue stroma with epithelial proliferations superficially in the stroma (H&E, x40).


Histopathological image shows epithelial tissue entrapment with cystic degeneration in the center and keratinization (H&E, x100). Inset (H&E, x400).


Histopathological image shows periodic acid-Schiff-stained section showing negative staining for glycogen granules (H&E, x100). Inset (PAS, x400).


(a and b) Hemangiopericytoma and solitary fibrous tumor (HPC/SFT) in a 10-day-old girl. Left: Magnetic resonance imaging (MRI) axial postcontrast T1-weighted image of HPC/SFT, Right: MRI coronal of HPC/SFT. Postcontrast T1-weighted image.


Postoperative computed tomography scan with obstructive hydrocephalus after subtotal resection.


(a and b) Postoperative magnetic resonance imaging postcontrast T1-weighted image axial (left) and coronal (right) after completion of chemotherapy.


MRI performed at the beginning of the first hospital admission showing bilateral hemispheric infarction. In DWI.


A time of flight imaging. Revealing bilateral ICA-stenosis including the right C3-C5 segments and the left C3-C4 segments (see arrows, classification according to Bouthillier 1996).


Duplex sonography.


PW-Doppler image.


MRI time of flight imaging. Of the left sided extra-intracranial bypass.


CT-scan showing a bilateral heterogeneous mass of about 6 cm in diameter in both adrenal glands.


CT-scan at the end of chemotherapy treatment showing complete response.


An axial, non-contrast enhanced view of the brain shows severe diffuse cerebral and cerebellar edema. . Notes: The normal definition between gray and white matter tissue is poor because of the edema. The quadrigeminal and ambient basal cisterns (white arrows) are no longer seen due to upward transtentorial herniation. The fourth ventricle (black circle) is not seen as edematous cerebellum displaces the CSF. The cystic (asterisk) and calcified suprasellar mass is seen.


Non involuting hemangioma with ulcerated areas.


Wilms' tumor composed of tubuloglandular and mesenchymal component. A) (40x, H&E stain).


Wilms' tumor composed of tubuloglandular and mesenchymal component. B) (200x, H&E stain).


Wilms' tumor composed of tubuloglandular and mesenchymal component. C) rosette- like structure (400x, H&E stain).


Wilms' tumor composed of tubuloglandular and mesenchymal component. D) mesenchymal stroma (400x, H&E stain).


SNP microarray analysis of bone marrow sample of patient at diagnosis. SNP array analysis of chromosomes 9.


SNP microarray analysis of bone marrow sample of patient at diagnosis. And 22 Gain of 9q34 from genomic position (hg19) 133,624,374-139,394,573 (5.8 Mb) including ABL1, and gain of 22q11 from 16,114,244-23,648,478 (7.5 Mb) including BCR are indicated by the right shift of log R as well as change of B allele frequencies. Loss of heterozygosity at 22q12 (5 Mb) in 100% of the cells is observed, which most likely represents a constitutional change also seen in a few regions on other chromosomes in this patient.


Liver with lymphocytic infiltrate (H&E, 440x).


CD20 immunostaining, Liver (440x) demonstrating malignant lymphoid infiltrate which stains positive for CD20.


Images of hepatic transjugular biopsy: in the middle, the red arrows showed the expansion of hepatic sinusoid spaces, on the right the figure showed a centrilobular vein.


Diagnostic interventions with liver function profile from clinical onset of VOD until resolution, and treatment of VOD in case 1.


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. The nodules are Periodic acid-Schiff (PAS).


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. And silver positive.


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. Numerous periodic acid-Schiff-negative fuchsinophilic casts are present within the tubular lumens, some of which have a cracked appearance and associated inflammation (c).


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. The cortical tubulointerstitial tissue has moderate interstitial edema (d). Immunofluorescence - Frozen sections of tissue submitted show no glomeruli.


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. On a scale of 0-3+, tubular casts stain with kappa light chain (3+, focal) Tubular basement membranes stain with kappa light chain (2.


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. And lambda light chain (1+, focal). And are negative for lambda light chain.


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. Electron microscopy - The two glomeruli evaluated show punctate granular subendothelial electron-dense deposits that have a linear distribution throughout the glomerular basement membranes (g).


Histopathology seen on renal biopsy. . Light microscopy - The non-sclerotic glomeruli show nodular glomerulosclerosis. The tubular basement membranes show similar powdery granular electron-dense deposits (h).


Computed tomography (plain) of the brain at presentation showing the hemorrhagic lesion in the third ventricle obstructing the foramen of Monro, and ,causing hydrocephalus.


Magnetic resonance imaging demonstrating [ T1-weighted axial.


T2-weighted sagittal.


Susceptibility-weighted Imaging (SWI) axial.


Contrast-enhanced T1-weighted axial.


Contrast-enhanced T2-weighted sagittal images] a pituitary macroadenoma with suprasellar extension with evidence of apoplectic change.


Magnetic resonance imaging [ contrast-enhanced T1-weighted coronal.


Contrast-enhanced T2-weighted sagittal images] at 6-month follow-up exhibiting near total resection of the pituitary adenoma.


A; Tumor cells were positive for AFP, which was mainly expressed in the cytoplasm of tumor cells (x70).


B; Tumor cells were positive for CEA, which was mainly expressed in the apical surfaces of tumor cells (x70).


C; CDX2 was expressed strongly in the tumor cell nuclei (x70).


D; CD10 was positive in the luminal surfaces in some tumor cells (x140).


Imaging examination results. (A) The yellow arrows indicate the enlarged right cervical lymph nodes, which were suspicious for metastasis.


Imaging examination results. (B) CT showed an oval mass with low attenuation in the right lobe of the thyroid and a round nodule with discontinuous peripheral annular calcification. (The yellow arrow indicates the tumor; the green arrow indicates the tumor focally broke into the nodule below and caused the interruption of the annular calcification; the red arrow indicates airway deviation caused by tumor compression).


Imaging examination results. (C) The yellow arrow indicates the left lobe of the thyroid gland; the red arrow indicates airway deviation caused by tumor compression; the green arrow indicates a nodule with interruption of the annular calcification. . Abbreviation: CT, computed tomography.


(A) No postoperative recurrence of the left adrenal lesion was observed, and the right adrenal lesion was unchanged and showed 123I-MIBG accumulation.


(B) 123I-MIBG accumulation showed no change compared to that recorded 7 years ago.


Pedigree chart of the patient's family members (arrow indicates the index patient).


The chest X-ray showed a large dense shadow with an unclear boundary in the left lung field, and the heart was obviously compressed and shifted to the right.


Hematoxylin-eosin staining (a), 40 times magnification: microscopically, there were obviously degenerate fusiform and ovoid tumor cells with loose reticular arrangement, hyperchromatic nuclei, inconsistent cell sizes, and can see the fat composition between the cells.


Immunohistochemical staining showed tumor cells positive for AFP.


Medical image.


Vimentin.


(a) PET/CT examination of the patient with mediastinal MGCT after chemotherapy; whole-body MIP (maximum density projection) images showed large patches of slightly increased radioactivity uptake in the left lung field (black arrow), SUVmax 5.2.


(b) Axial PET/CT fusion images showed varying levels of uptake of radioactive tracers in the lesions, but no uptake in the cystic necrosis area (white arrow).


(c) Coronal PET/CT fusion image.


Serum protein electrophoresis showing the presence of a monoclonal peak migrating in the gamma globulin area amounted at 6.9 g/L.