Input: Late fulminant posterior reversible encephalopathy syndrome after liver transplant. OBJECTIVES: Posterior leukoencephalopathy due to calcineurin - inhibitor - related neurotoxicity is a rare but severe complication that results from treatment with immunosuppressive agents (primarily those administered after a liver or kidney transplant). The pathophysiologic mechanisms of that disorder remain unknown. CASE: We report the case of a 46 - year - old woman who received a liver transplant in our center as treatment for alcoholic cirrhosis and in whom either a fulminant course of posterior leukoencephalopathy or posterior reversible encephalopathy syndrome developed 110 days after transplant. After an initially uneventful course after the transplant, the patient rapidly fell into deep coma. RESULTS: Cerebral MRI scan showed typical signs of enhancement in the pontine and posterior regions. Switching the immunosuppressive regimen from tacrolimus to cyclosporine did not improve the clinical situation. The termination of treatment with any calcineurin inhibitor resulted in a complete resolution of that complication. CONCLUSIONS: Posterior reversible encephalopathy syndrome after liver transplant is rare. We recommend a complete cessation of any calcineurin inhibitor rather than a dose reduction.

posterior reversible encephalopathy syndrome

Posterior leukoencephalopathy

neurotoxicity

alcoholic cirrhosis

posterior leukoencephalopathy

posterior reversible encephalopathy syndrome

Posterior reversible encephalopathy syndrome

tacrolimus

cyclosporine

tacrolimus

posterior reversible encephalopathy syndrome

tacrolimus

Posterior leukoencephalopathy

tacrolimus

posterior leukoencephalopathy

tacrolimus

posterior reversible encephalopathy syndrome

tacrolimus

Posterior reversible encephalopathy syndrome


Input: Prolonged hypothermia as a bridge to recovery for cerebral edema and intracranial hypertension associated with fulminant hepatic failure. BACKGROUND: To review evidence - based treatment options in patients with cerebral edema complicating fulminant hepatic failure (FHF) and discuss the potential applications of hypothermia. METHOD: Case - based observations from a medical intensive care unit (MICU) in a tertiary care facility in a 27 - year - old female with FHF from acetaminophen and resultant cerebral edema. RESULTS: Our patient was admitted to the MICU after being found unresponsive with presumed toxicity from acetaminophen which was ingested over a 2 - day period. The patient had depressed of mental status lasting at least 24 h prior to admission. Initial evaluation confirmed FHF from acetaminophen and cerebral edema. The patient was treated with hyperosmolar therapy, hyperventilation, sedation, and chemical paralysis. Her intracranial pressure remained elevated despite maximal medical therapy. We then initiated therapeutic hypothermia which was continued for 5 days. At re - warming, patient had resolution of her cerebral edema and intracranial hypertension. At discharge, she had complete recovery of neurological and hepatic functions. CONCLUSION: In patients with FHF and cerebral edema from acetaminophen overdose, prolonged therapeutic hypothermia could potentially be used as a life saving therapy and a bridge to hepatic and neurological recovery. A clinical trial of hypothermia in patients with this condition is warranted.

hypothermia

cerebral edema

intracranial hypertension

fulminant hepatic failure

cerebral edema

fulminant hepatic failure

FHF

hypothermia

FHF

cerebral edema

toxicity

FHF

cerebral edema

hyperventilation

paralysis

hypothermia

cerebral edema

intracranial hypertension

FHF

cerebral edema

overdose

hypothermia

hypothermia

acetaminophen

acetaminophen

acetaminophen

acetaminophen

acetaminophen

fulminant hepatic failure

acetaminophen

fulminant hepatic failure

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

fulminant hepatic failure

acetaminophen

fulminant hepatic failure

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

fulminant hepatic failure

acetaminophen

fulminant hepatic failure

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

fulminant hepatic failure

acetaminophen

fulminant hepatic failure

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

FHF

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

intracranial hypertension

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema

acetaminophen

cerebral edema


Input: Binasal visual field defects are not specific to vigabatrin. This study investigated the visual defects associated with the antiepileptic drug vigabatrin (VGB). Two hundred four people with epilepsy were grouped on the basis of antiepileptic drug therapy (current, previous, or no exposure to VGB). Groups were matched with respect to age, gender, and seizure frequency. All patients underwent objective assessment of electrophysiological function (wide - field multifocal electroretinography) and conventional visual field testing (static perimetry). Bilateral visual field constriction was observed in 59% of patients currently taking VGB, 43% of patients who previously took VGB, and 24% of patients with no exposure to VGB. Assessment of retinal function revealed abnormal responses in 48% of current VGB users and 22% of prior VGB users, but in none of the patients without previous exposure to VGB. Bilateral visual field abnormalities are common in the treated epilepsy population, irrespective of drug history. Assessment by conventional static perimetry may neither be sufficiently sensitive nor specific to reliably identify retinal toxicity associated with VGB.

Binasal visual field defects

visual defects

epilepsy

seizure

Bilateral visual field abnormalities

epilepsy

retinal toxicity

vigabatrin

vigabatrin

VGB

VGB

VGB

VGB

VGB

VGB

VGB

VGB

VGB

vigabatrin

Binasal visual field defects

vigabatrin

visual defects

vigabatrin

Bilateral visual field abnormalities

vigabatrin

Binasal visual field defects

vigabatrin

visual defects

vigabatrin

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

VGB

Binasal visual field defects

VGB

visual defects

VGB

Bilateral visual field abnormalities

vigabatrin

retinal toxicity

vigabatrin

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity

VGB

retinal toxicity


Input: Smoking of crack cocaine as a risk factor for HIV infection among people who use injection drugs. BACKGROUND: Little is known about the possible role that smoking crack cocaine has on the incidence of HIV infection. Given the increasing use of crack cocaine, we sought to examine whether use of this illicit drug has become a risk factor for HIV infection. METHODS: We included data from people participating in the Vancouver Injection Drug Users Study who reported injecting illicit drugs at least once in the month before enrolment, lived in the greater Vancouver area, were HIV - negative at enrolment and completed at least 1 follow - up study visit. To determine whether the risk of HIV seroconversion among daily smokers of crack cocaine changed over time, we used Cox proportional hazards regression and divided the study into 3 periods: May 1, 1996 - Nov. 30, 1999 (period 1), Dec. 1, 1999 - Nov. 30, 2002 (period 2), and Dec. 1, 2002 - Dec. 30, 2005 (period 3). RESULTS: Overall, 1048 eligible injection drug users were included in our study. Of these, 137 acquired HIV infection during follow - up. The mean proportion of participants who reported daily smoking of crack cocaine increased from 11. 6% in period 1 to 39. 7% in period 3. After adjusting for potential confounders, we found that the risk of HIV seroconversion among participants who were daily smokers of crack cocaine increased over time (period 1: hazard ratio [HR] 1. 03, 95% confidence interval [CI] 0. 57 - 1. 85; period 2: HR 1. 68, 95% CI 1. 01 - 2. 80; and period 3: HR 2. 74, 95% CI 1. 06 - 7. 11). INTERPRETATION: Smoking of crack cocaine was found to be an independent risk factor for HIV seroconversion among people who were injection drug users. This finding points to the urgent need for evidence - based public health initiatives targeted at people who smoke crack cocaine.

crack cocaine

crack cocaine

crack cocaine

crack cocaine

crack cocaine

crack cocaine

crack cocaine

crack cocaine

HIV infection

HIV infection

HIV infection

HIV seroconversion

HIV infection

HIV seroconversion

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion

crack cocaine

HIV seroconversion


Input: Fluoxetine improves the memory deficits caused by the chemotherapy agent 5 - fluorouracil. Cancer patients who have been treated with systemic adjuvant chemotherapy have described experiencing deteriorations in cognition. A widely used chemotherapeutic agent, 5 - fluorouracil (5 - FU), readily crosses the blood - brain barrier and so could have a direct effect on brain function. In particular this anti mitotic drug could reduce cell proliferation in the neurogenic regions of the adult brain. In contrast reports indicate that hippocampal dependent neurogenesis and cognition are enhanced by the SSRI antidepressant Fluoxetine. In this investigation the behavioural effects of chronic (two week) treatment with 5 - FU and (three weeks) with Fluoxetine either separately or in combination with 5 - FU were tested on adult Lister hooded rats. Behavioural effects were tested using a context dependent conditioned emotional response test (CER) which showed that animals treated with 5 - FU had a significant reduction in freezing time compared to controls. A separate group of animals was tested using a hippocampal dependent spatial working memory test, the object location recognition test (OLR). Animals treated only with 5 - FU showed significant deficits in their ability to carry out the OLR task but co administration of Fluoxetine improved their performance. 5 - FU chemotherapy caused a significant reduction in the number of proliferating cells in the sub granular zone of the dentate gyrus compared to controls. This reduction was eliminated when Fluoxetine was co administered with 5 - FU. Fluoxetine on its own had no effect on proliferating cell number or behaviour. These findings suggest that 5 - FU can negatively affect both cell proliferation and hippocampal dependent working memory and that these deficits can be reversed by the simultaneous administration of the antidepressant Fluoxetine.

Fluoxetine

5 - fluorouracil

5 - fluorouracil

5 - FU

SSRI

Fluoxetine

5 - FU

Fluoxetine

5 - FU

5 - FU

5 - FU

Fluoxetine

5 - FU

Fluoxetine

5 - FU

Fluoxetine

5 - FU

Fluoxetine

memory deficits

Cancer

5 - fluorouracil

memory deficits

5 - fluorouracil

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits

5 - FU

memory deficits


Input: Liver - specific ablation of integrin - linked kinase in mice results in enhanced and prolonged cell proliferation and hepatomegaly after phenobarbital administration. We have recently demonstrated that disruption of extracellular matrix (ECM) / integrin signaling via elimination of integrin - linked kinase (ILK) in hepatocytes interferes with signals leading to termination of liver regeneration. This study investigates the role of ILK in liver enlargement induced by phenobarbital (PB). Wild - type (WT) and ILK: liver - / - mice were given PB (0. 1% in drinking water) for 10 days. Livers were harvested on 2, 5, and 10 days during PB administration. In the hepatocyte - specific ILK / liver - / - mice, the liver: body weight ratio was more than double as compared to 0 h at day 2 (2. 5 times), while at days 5 and 10, it was enlarged three times. In the WT mice, the increase was as expected from previous literature (1. 8 times) and seems to have leveled off after day 2. There were slightly increased proliferating cell nuclear antigen - positive cells in the ILK / liver - / - animals at day 2 as compared to WT after PB administration. In the WT animals, the proliferative response had come back to normal by days 5 and 10. Hepatocytes of the ILK / liver - / - mice continued to proliferate up until day 10. ILK / liver - / - mice also showed increased expression of key genes involved in hepatocyte proliferation at different time points during PB administration. In summary, ECM proteins communicate with the signaling machinery of dividing cells via ILK to regulate hepatocyte proliferation and termination of the proliferative response. Lack of ILK in the hepatocytes imparts prolonged proliferative response not only to stimuli related to liver regeneration but also to xenobiotic chemical mitogens, such as PB.

hepatomegaly

phenobarbital

phenobarbital

PB

PB

PB

PB

PB

PB

phenobarbital

hepatomegaly

phenobarbital

hepatomegaly

PB

hepatomegaly

PB

hepatomegaly

PB

hepatomegaly

PB

hepatomegaly

PB

hepatomegaly

PB

hepatomegaly


Input: Decreased Expression of Na / K - ATPase, NHE3, NBC1, AQP1 and OAT in Gentamicin - induced Nephropathy. The present study was aimed to determine whether there is an altered regulation of tubular transporters in gentamicin - induced nephropathy. Sprague - Dawley male rats (200 ~ 250 g) were subcutaneously injected with gentamicin (100 mg / kg per day) for 7 days, and the expression of tubular transporters was determined by immunoblotting and immunohistochemistry. The mRNA and protein expression of OAT was also determined. Gentamicin - treated rats exhibited significantly decreased creatinine clearance along with increased plasma creatinine levels. Accordingly, the fractional excretion of sodium increased. Urine volume was increased, while urine osmolality and free water reabsorption were decreased. Immunoblotting and immunohistochemistry revealed decreased expression of Na (+) / K (+) - ATPase, NHE3, NBC1, and AQP1 in the kidney of gentamicin - treated rats. The expression of OAT1 and OAT3 was also decreased. Gentamicin - induced nephropathy may at least in part be causally related with a decreased expression of Na (+) / K (+) - ATPase, NHE3, NBC1, AQP1 and OAT.

K

Gentamicin

gentamicin

gentamicin

Gentamicin

creatinine

creatinine

sodium

K

gentamicin

Gentamicin

K

Nephropathy

nephropathy

nephropathy

Gentamicin

Nephropathy

Gentamicin

nephropathy

Gentamicin

nephropathy

gentamicin

Nephropathy

gentamicin

nephropathy

gentamicin

nephropathy

gentamicin

Nephropathy

gentamicin

nephropathy

gentamicin

nephropathy

Gentamicin

Nephropathy

Gentamicin

nephropathy

Gentamicin

nephropathy

gentamicin

Nephropathy

gentamicin

nephropathy

gentamicin

nephropathy

Gentamicin

Nephropathy

Gentamicin

nephropathy

Gentamicin

nephropathy


Input: Longitudinal association of alcohol use with HIV disease progression and psychological health of women with HIV. We evaluated the association of alcohol consumption and depression, and their effects on HIV disease progression among women with HIV. The study included 871 women with HIV who were recruited from 1993 - 1995 in four US cities. The participants had physical examination, medical record extraction, and venipuncture, CD4 + T - cell counts determination, measurement of depression symptoms (using the self - report Center for Epidemiological Studies - Depression Scale), and alcohol use assessment at enrollment, and semiannually until March 2000. Multilevel random coefficient ordinal models as well as multilevel models with joint responses were used in the analysis. There was no significant association between level of alcohol use and CD4 + T - cell counts. When participants were stratified by antiretroviral therapy (ART) use, the association between alcohol and CD4 + T - cell did not reach statistical significance. The association between alcohol consumption and depression was significant (p < 0. 001). Depression had a significant negative effect on CD4 + T - cell counts over time regardless of ART use. Our findings suggest that alcohol consumption has a direct association with depression. Moreover, depression is associated with HIV disease progression. Our findings have implications for the provision of alcohol use interventions and psychological resources to improve the health of women with HIV.

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

alcohol

HIV disease

depression

HIV disease

depression

Depression

depression

Depression

depression

depression

HIV disease

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

Depression

alcohol

depression

alcohol

depression


Input: Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine - induced status epilepticus. BACKGROUND: Neuroinflammation occurs after seizures and is implicated in epileptogenesis. CCR2 is a chemokine receptor for CCL2 and their interaction mediates monocyte infiltration in the neuroinflammatory cascade triggered in different brain pathologies. In this work CCR2 and CCL2 expression were examined following status epilepticus (SE) induced by pilocarpine injection. METHODS: SE was induced by pilocarpine injection. Control rats were injected with saline instead of pilocarpine. Five days after SE, CCR2 staining in neurons and glial cells was examined using imunohistochemical analyses. The number of CCR2 positive cells was determined using stereology probes in the hippocampus. CCL2 expression in the hippocampus was examined by molecular assay. RESULTS: Increased CCR2 was observed in the hippocampus after SE. Seizures also resulted in alterations to the cell types expressing CCR2. Increased numbers of neurons that expressed CCR2 was observed following SE. Microglial cells were more closely apposed to the CCR2 - labeled cells in SE rats. In addition, rats that experienced SE exhibited CCR2 - labeling in populations of hypertrophied astrocytes, especially in CA1 and dentate gyrus. These CCR2 + astroctytes were not observed in control rats. Examination of CCL2 expression showed that it was elevated in the hippocampus following SE. CONCLUSION: The data show that CCR2 and CCL2 are up - regulated in the hippocampus after pilocarpine - induced SE. Seizures also result in changes to CCR2 receptor expression in neurons and astrocytes. These changes might be involved in detrimental neuroplasticity and neuroinflammatory changes that occur following seizures.

pilocarpine

pilocarpine

pilocarpine

pilocarpine

pilocarpine

status epilepticus

Neuroinflammation

seizures

neuroinflammatory

status epilepticus

SE

SE

SE

SE

Seizures

SE

SE

SE

hypertrophied

SE

SE

Seizures

neuroinflammatory

seizures

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE

pilocarpine

SE


Input: Metallothionein induction reduces caspase - 3 activity and TNFalpha levels with preservation of cognitive function and intact hippocampal neurons in carmustine - treated rats. Hippocampal integrity is essential for cognitive functions. On the other hand, induction of metallothionein (MT) by ZnSO (4) and its role in neuroprotection has been documented. The present study aimed to explore the effect of MT induction on carmustine (BCNU) - induced hippocampal cognitive dysfunction in rats. A total of 60 male Wistar albino rats were randomly divided into four groups (15 / group): The control group injected with single doses of normal saline (i. c. v) followed 24 h later by BCNU solvent (i. v). The second group administered ZnSO (4) (0. 1 micromol / 10 microl normal saline, i. c. v, once) then BCNU solvent (i. v) after 24 h. Third group received BCNU (20 mg / kg, i. v, once) 24 h after injection with normal saline (i. c. v). Fourth group received a single dose of ZnSO (4) (0. 1 micromol / 10 microl normal saline, i. c. v) then BCNU (20 mg / kg, i. v, once) after 24 h. The obtained data revealed that BCNU administration resulted in deterioration of learning and short - term memory (STM), as measured by using radial arm water maze, accompanied with decreased hippocampal glutathione reductase (GR) activity and reduced glutathione (GSH) content. Also, BCNU administration increased serum tumor necrosis factor - alpha (TNFalpha), hippocampal MT and malondialdehyde (MDA) contents as well as caspase - 3 activity in addition to histological alterations. ZnSO (4) pretreatment counteracted BCNU - induced inhibition of GR and depletion of GSH and resulted in significant reduction in the levels of MDA and TNFalpha as well as the activity of caspase - 3. The histological features were improved in hippocampus of rats treated with ZnSO (4) + BCNU compared to only BCNU - treated animals. In conclusion, MT induction halts BCNU - induced hippocampal toxicity as it prevented GR inhibition and GSH depletion and counteracted the increased levels of TNFalpha, MDA and caspase - 3 activity with subsequent preservation of cognition.

Metallothionein

carmustine

metallothionein

MT

ZnSO (4)

MT

carmustine

BCNU

BCNU

ZnSO (4)

BCNU

BCNU

ZnSO (4)

BCNU

BCNU

glutathione

glutathione

GSH

BCNU

MT

malondialdehyde

MDA

ZnSO (4)

BCNU

GSH

MDA

ZnSO (4)

BCNU

BCNU

MT

BCNU

GSH

MDA

cognitive dysfunction

deterioration of learning and short - term memory

deterioration of learning

deterioration of learning and short - term memory

tumor

necrosis

toxicity

carmustine

deterioration of learning and short - term memory

carmustine

deterioration of learning and short - term memory

carmustine

deterioration of learning and short - term memory

carmustine

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

BCNU

deterioration of learning and short - term memory

carmustine

deterioration of learning

carmustine

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

BCNU

deterioration of learning

carmustine

cognitive dysfunction

carmustine

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction

BCNU

cognitive dysfunction


Input: Fatal carbamazepine induced fulminant eosinophilic (hypersensitivity) myocarditis: emphasis on anatomical and histological characteristics, mechanisms and genetics of drug hypersensitivity and differential diagnosis. The most severe adverse reactions to carbamazepine have been observed in the haemopoietic system, the liver and the cardiovascular system. A frequently fatal, although exceptionally rare side effect of carbamazepine is necrotizing eosinophilic (hypersensitivity) myocarditis. We report a case of hypersensitivity myocarditis secondary to administration of carbamazepine. Acute hypersensitivity myocarditis was not suspected clinically, and the diagnosis was made post - mortem. Histology revealed diffuse infiltration of the myocardium by eosinophils and lymphocytes with myocyte damage. Clinically, death was due to cardiogenic shock. To best of our knowledge this is the second case of fatal carbamazepine induced myocarditis reported in English literature.

carbamazepine

carbamazepine

carbamazepine

carbamazepine

carbamazepine

fulminant eosinophilic

hypersensitivity

myocarditis

drug hypersensitivity

hypersensitivity

myocarditis

hypersensitivity

myocarditis

hypersensitivity

myocarditis

cardiogenic shock

myocarditis

carbamazepine

cardiogenic shock

carbamazepine

cardiogenic shock

carbamazepine

cardiogenic shock

carbamazepine

cardiogenic shock

carbamazepine

cardiogenic shock

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

myocarditis

carbamazepine

fulminant eosinophilic

carbamazepine

fulminant eosinophilic

carbamazepine

fulminant eosinophilic

carbamazepine

fulminant eosinophilic

carbamazepine

fulminant eosinophilic

carbamazepine

hypersensitivity

carbamazepine

drug hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

drug hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

drug hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

drug hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

drug hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity

carbamazepine

hypersensitivity


Input: Neuropsychiatric behaviors in the MPTP marmoset model of Parkinson' s disease. OBJECTIVES: Neuropsychiatric symptoms are increasingly recognised as a significant problem in patients with Parkinson' s disease (PD). These symptoms may be due to' sensitisation' following repeated levodopa treatment or a direct effect of dopamine on the disease state. The levodopa - treated MPTP - lesioned marmoset was used as a model of neuropsychiatric symptoms in PD patients. Here we compare the time course of levodopa - induced motor fluctuations and neuropsychiatric - like behaviors to determine the relationship between duration of treatment and onset of symptoms. METHODS: Marmosets were administered 1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine (2. 0 mg / kg s. c.) for five days, resulting in stable parkinsonism. Levodopa (15 mg / kg and benserazide, 3. 75 mg / kg) p. o. b. i. d, was administered for 30 days. Animals were evaluated for parkinsonian disability, dyskinesia and on - time (motor fluctuations) and neuropsychiatric - like behaviors on Day 0 (prior to levodopa) and on Days 1, 7, 13, 27 and 30 of treatment using post hoc DVD analysis by a trained rater, blind to the treatment day. RESULTS: The neuropsychiatric - like behavior rating scale demonstrated high interrater reliability between three trained raters of differing professional backgrounds. As anticipated, animals exhibited a progressive increase in levodopa - induced motor fluctuations, dyskinesia and wearing - off, that correlated with the duration of levodopa therapy. In contrast, levodopa - induced neuropsychiatric - like behaviors were present on Day 1 of levodopa treatment and their severity did not correlate with duration of treatment. CONCLUSIONS: The data suggest that neuropsychiatric disorders in PD are more likely an interaction between levodopa and the disease state than a consequence of sensitisation to repeated dopaminergic therapy.

MPTP

levodopa

dopamine

levodopa

MPTP

levodopa

1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine

Levodopa

benserazide

levodopa

levodopa

levodopa

levodopa

levodopa

levodopa

Parkinson' s disease

Parkinson' s disease

PD

neuropsychiatric symptoms

PD

neuropsychiatric - like behaviors

parkinsonism

parkinsonian disability

dyskinesia

neuropsychiatric - like behaviors

neuropsychiatric - like behavior

dyskinesia

neuropsychiatric - like behaviors

neuropsychiatric disorders

PD

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

Levodopa

dyskinesia

Levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

MPTP

parkinsonian disability

MPTP

parkinsonian disability

1 - methyl - 4 - phenyl - 1, 2, 3, 6 - tetrahydropyridine

parkinsonian disability


Input: Contrast medium nephrotoxicity after renal artery and coronary angioplasty. BACKGROUND: Renal dysfunction induced by iodinated contrast medium (CM) administration can minimize the benefit of the interventional procedure in patients undergoing renal angioplasty (PTRA). PURPOSE: To compare the susceptibility to nephrotoxic effect of CM in patients undergoing PTRA with that of patients submitted to percutaneous coronary intervention (PCI). MATERIAL AND METHODS: A total of 33 patients successfully treated with PTRA (PTRA group, mean age 70 + / - 12 years, 23 female, basal creatinine 1. 46 + / - 0. 79, range 0. 7 - 4. 9 mg / dl) were compared with 33 patients undergoing successful PCI (PCI group), matched for basal creatinine (1. 44 + / - 0. 6, range 0. 7 - 3. 4 mg / dl), gender, and age. In both groups postprocedural (48 h) serum creatinine was measured. RESULTS: Postprocedural creatinine level decreased nonsignificantly in the PTRA group (1. 46 + / - 0. 8 vs. 1. 34 + / - 0. 5 mg / dl, P = NS) and increased significantly in the PCI group (1. 44 + / - 0. 6 vs. 1. 57 + / - 0. 7 mg / dl, P < 0. 02). Changes in serum creatinine after intervention (after - before) were significantly different between the PTRA and PCI groups (- 0. 12 + / - 0. 5 vs. 0. 13 + / - 0. 3, P = 0. 014). This difference was not related to either a different clinical risk profile or to the volume of CM administered. CONCLUSION: In this preliminary study patients submitted to PTRA showed a lower susceptibility to renal damage induced by CM administration than PCI patients. The effectiveness of PTRA on renal function seems to be barely influenced by CM toxicity.

Contrast medium

contrast medium

CM

CM

creatinine

creatinine

creatinine

creatinine

creatinine

CM

CM

CM

nephrotoxicity

Renal dysfunction

nephrotoxic

renal damage

toxicity

Contrast medium

nephrotoxicity

Contrast medium

Renal dysfunction

Contrast medium

nephrotoxic

Contrast medium

renal damage

contrast medium

nephrotoxicity

contrast medium

Renal dysfunction

contrast medium

nephrotoxic

contrast medium

renal damage

CM

nephrotoxicity

CM

Renal dysfunction

CM

nephrotoxic

CM

renal damage

CM

nephrotoxicity

CM

Renal dysfunction

CM

nephrotoxic

CM

renal damage

CM

nephrotoxicity

CM

Renal dysfunction

CM

nephrotoxic

CM

renal damage

CM

nephrotoxicity

CM

Renal dysfunction

CM

nephrotoxic

CM

renal damage

CM

nephrotoxicity

CM

Renal dysfunction

CM

nephrotoxic

CM

renal damage


Input: Medical and psychiatric outcomes for patients transplanted for acetaminophen - induced acute liver failure: a case - control study. BACKGROUND: Acetaminophen - induced hepatotoxicity is the most common cause of acute liver failure (ALF) in the UK. Patients often consume the drug with suicidal intent or with a background of substance dependence. AIMS AND METHODS: We compared the severity of pretransplant illness, psychiatric co - morbidity, medical and psychosocial outcomes of all patients who had undergone liver transplantation (LT) emergently between 1999 - 2004 for acetaminophen - induced ALF (n = 36) with age - and sex - matched patients undergoing emergent LT for non - acetaminophen - induced ALF (n = 35) and elective LT for chronic liver disease (CLD, n = 34). RESULTS: Acetaminophen - induced ALF patients undergoing LT had a greater severity of pre - LT illness reflected by higher Acute Physiology and Chronic Health Evaluation II scores and requirement for organ support compared with the other two groups. Twenty (56%) acetaminophen - induced ALF patients had a formal psychiatric diagnosis before LT (non - acetaminophen - induced ALF = 0 / 35, CLD = 2 / 34; P < 0. 01 for all) and nine (25%) had a previous suicide attempt. During follow - up (median 5 years), there were no significant differences in rejection (acute and chronic), graft failure or survival between the groups (acetaminophen - induced ALF 1 year 87%, 5 years 75%; non - acetaminophen - induced ALF 88%, 78%; CLD 93%, 82%: P > 0. 6 log rank). Two acetaminophen - induced ALF patients reattempted suicide post - LT (one died 8 years post - LT). CONCLUSIONS: Despite a high prevalence of psychiatric disturbance, outcomes for patients transplanted emergently for acetaminophen - induced ALF were comparable to those transplanted for non - acetaminophen - induced ALF and electively for CLD. Multidisciplinary approaches with long - term psychiatric follow - up may contribute to low post - transplant suicide rates seen and low rates of graft loss because of non - compliance.

acetaminophen

Acetaminophen

acetaminophen

acetaminophen

Acetaminophen

acetaminophen

acetaminophen

acetaminophen

acetaminophen

acetaminophen

acetaminophen

acetaminophen

acute liver failure

hepatotoxicity

acute liver failure

ALF

ALF

ALF

chronic liver disease

CLD

ALF

ALF

ALF

CLD

ALF

ALF

CLD

ALF

ALF

ALF

CLD

acetaminophen

hepatotoxicity

Acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

Acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

hepatotoxicity

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

Acetaminophen

acute liver failure

Acetaminophen

acute liver failure

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

Acetaminophen

acute liver failure

Acetaminophen

acute liver failure

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

Acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

acute liver failure

acetaminophen

acute liver failure

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF

acetaminophen

ALF


Input: Studies of synergy between morphine and a novel sodium channel blocker, CNSB002, in rat models of inflammatory and neuropathic pain. OBJECTIVE: This study determined the antihyperalgesic effect of CNSB002, a sodium channel blocker with antioxidant properties given alone and in combinations with morphine in rat models of inflammatory and neuropathic pain. DESIGN: Dose response curves for nonsedating doses of morphine and CNSB002 given intraperitoneally alone and together in combinations were constructed for antihyperalgesic effect using paw withdrawal from noxious heat in two rat pain models: carrageenan - induced paw inflammation and streptozotocin (STZ) - induced diabetic neuropathy. RESULTS: The maximum nonsedating doses were: morphine, 3. 2 mg / kg; CNSB002 10. 0 mg / kg; 5. 0 mg / kg CNSB002 with morphine 3. 2 mg / kg in combination. The doses calculated to cause 50% reversal of hyperalgesia (ED50) were 7. 54 (1. 81) and 4. 83 (1. 54) in the carrageenan model and 44. 18 (1. 37) and 9. 14 (1. 24) in the STZ - induced neuropathy model for CNSB002 and morphine, respectively (mg / kg; mean, SEM). These values were greater than the maximum nonsedating doses. The ED50 values for morphine when given in combination with CNSB002 (5 mg / kg) were less than the maximum nonsedating dose: 0. 56 (1. 55) in the carrageenan model and 1. 37 (1. 23) in the neuropathy model (mg / kg; mean, SEM). The antinociception after morphine (3. 2 mg / kg) was increased by co - administration with CNSB002 from 28. 0 and 31. 7% to 114. 6 and 56. 9% reversal of hyperalgesia in the inflammatory and neuropathic models, respectively (P < 0. 01; one - way analysis of variance - significantly greater than either drug given alone). CONCLUSIONS: The maximum antihyperalgesic effect achievable with nonsedating doses of morphine may be increased significantly when the drug is used in combination with CNSB002.

morphine

sodium

sodium

morphine

morphine

carrageenan

streptozotocin

STZ

morphine

morphine

carrageenan

STZ

morphine

morphine

carrageenan

morphine

morphine

neuropathic pain

neuropathic pain

pain

inflammation

diabetic neuropathy

hyperalgesia

neuropathy

neuropathy

hyperalgesia

neuropathic

streptozotocin

diabetic neuropathy

STZ

diabetic neuropathy

STZ

diabetic neuropathy

streptozotocin

hyperalgesia

streptozotocin

hyperalgesia

STZ

hyperalgesia

STZ

hyperalgesia

STZ

hyperalgesia

STZ

hyperalgesia

carrageenan

inflammation

carrageenan

inflammation

carrageenan

inflammation

carrageenan

hyperalgesia

carrageenan

hyperalgesia

carrageenan

hyperalgesia

carrageenan

hyperalgesia

carrageenan

hyperalgesia

carrageenan

hyperalgesia


Input: Heparin - induced thrombocytopenia: a practical review. Heparin - induced thrombocytopenia (HIT) remains under - recognized despite its potentially devastating outcomes. It begins when heparin exposure stimulates the formation of heparin - platelet factor 4 antibodies, which in turn triggers the release of procoagulant platelet particles. Thrombosis and thrombocytopenia that follow comprise the 2 hallmark traits of HIT, with the former largely responsible for significant vascular complications. The prevalence of HIT varies among several subgroups, with greater incidence in surgical as compared with medical populations. HIT must be acknowledged for its intense predilection for thrombosis and suspected whenever thrombosis occurs after heparin exposure. Early recognition that incorporates the clinical and serologic clues is paramount to timely institution of treatment, as its delay may result in catastrophic outcomes. The treatment of HIT mandates an immediate cessation of all heparin exposure and the institution of an antithrombotic therapy, most commonly using a direct thrombin inhibitor. Current " diagnostic " tests, which primarily include functional and antigenic assays, have more of a confirmatory than diagnostic role in the management of HIT. Special attention must be paid to cardiac patients who are often exposed to heparin multiple times during their course of treatment. Direct thrombin inhibitors are appropriate, evidence - based alternatives to heparin in patients with a history of HIT, who need to undergo percutaneous coronary intervention. As heparin remains one of the most frequently used medications today with potential for HIT with every heparin exposure, a close vigilance of platelet counts must be practiced whenever heparin is initiated.

Heparin

Heparin

heparin

heparin

heparin

heparin

direct thrombin inhibitor

heparin

Direct thrombin inhibitors

heparin

heparin

heparin

heparin

thrombocytopenia

thrombocytopenia

HIT

Thrombosis

thrombocytopenia

HIT

HIT

HIT

thrombosis

thrombosis

HIT

HIT

HIT

HIT

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

HIT

Heparin

thrombocytopenia

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

HIT

Heparin

thrombocytopenia

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

Heparin

Thrombosis

Heparin

thrombosis

Heparin

thrombosis

Heparin

Thrombosis

Heparin

thrombosis

Heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis

heparin

Thrombosis

heparin

thrombosis

heparin

thrombosis


Input: Abductor paralysis after botox injection for adductor spasmodic dysphonia. OBJECTIVES / HYPOTHESIS: Botulinum toxin (Botox) injections into the thyroarytenoid muscles are the current standard of care for adductor spasmodic dysphonia (ADSD). Reported adverse effects include a period of breathiness, throat pain, and difficulty with swallowing liquids. Here we report multiple cases of bilateral abductor paralysis following Botox injections for ADSD, a complication previously unreported. STUDY DESIGN: Retrospective case series. METHODS: Patients that received Botox injections for spasmodic dysphonia between January 2000 and October 2009 were evaluated. Patients with ADSD were identified. The number of treatments received and adverse effects were noted. For patients with bilateral abductor paralysis, age, sex, paralytic Botox dose, prior Botox dose, and course following paralysis were noted. RESULTS: From a database of 452 patients receiving Botox, 352 patients had been diagnosed with ADSD. Of these 352 patients, eight patients suffered bilateral abductor paralysis, and two suffered this complication twice. All affected patients were females over the age of 50 years. Most patients had received treatments prior to abductor paralysis and continued receiving after paralysis. Seven patients recovered after a brief period of activity restrictions, and one underwent a tracheotomy. The incidence of abductor paralysis after Botox injection for ADSD was 0. 34%. CONCLUSIONS: Bilateral abductor paralysis is a rare complication of Botox injections for ADSD, causing difficulty with breathing upon exertion. The likely mechanism of paralysis is diffusion of Botox around the muscular process of the arytenoid to the posterior cricoarytenoid muscles. The paralysis is temporary, and watchful waiting with restriction of activity is the recommended management.

paralysis

adductor spasmodic dysphonia

adductor spasmodic dysphonia

ADSD

throat pain

paralysis

ADSD

spasmodic dysphonia

ADSD

paralysis

paralysis

ADSD

paralysis

paralysis

paralysis

paralysis

ADSD

paralysis

ADSD

paralysis

paralysis

botox

Botox

Botox

Botox

Botox

Botox

Botox

Botox

Botox

Botox

botox

adductor spasmodic dysphonia

botox

adductor spasmodic dysphonia

botox

ADSD

botox

ADSD

botox

ADSD

botox

ADSD

botox

ADSD

botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

adductor spasmodic dysphonia

Botox

adductor spasmodic dysphonia

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD

Botox

ADSD


Input: Mitochondrial impairment contributes to cocaine - induced cardiac dysfunction: Prevention by the targeted antioxidant MitoQ. The goal of this study was to assess mitochondrial function and ROS production in an experimental model of cocaine - induced cardiac dysfunction. We hypothesized that cocaine abuse may lead to altered mitochondrial function that in turn may cause left ventricular dysfunction. Seven days of cocaine administration to rats led to an increased oxygen consumption detected in cardiac fibers, specifically through complex I and complex III. ROS levels were increased, specifically in interfibrillar mitochondria. In parallel there was a decrease in ATP synthesis, whereas no difference was observed in subsarcolemmal mitochondria. This uncoupling effect on oxidative phosphorylation was not detectable after short - term exposure to cocaine, suggesting that these mitochondrial abnormalities were a late rather than a primary event in the pathological response to cocaine. MitoQ, a mitochondrial - targeted antioxidant, was shown to completely prevent these mitochondrial abnormalities as well as cardiac dysfunction characterized here by a diastolic dysfunction studied with a conductance catheter to obtain pressure - volume data. Taken together, these results extend previous studies and demonstrate that cocaine - induced cardiac dysfunction may be due to a mitochondrial defect.

Mitochondrial impairment

cardiac dysfunction

cardiac dysfunction

cocaine abuse

left ventricular dysfunction

mitochondrial abnormalities

mitochondrial abnormalities

cardiac dysfunction

diastolic dysfunction

cardiac dysfunction

mitochondrial defect

cocaine

MitoQ

cocaine

cocaine

oxygen

ATP

cocaine

cocaine

MitoQ

cocaine

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction

cocaine

cardiac dysfunction


Input: Trimethoprim - induced immune hemolytic anemia in a pediatric oncology patient presenting as an acute hemolytic transfusion reaction. A 10 - year - old male with acute leukemia presented with post - chemotherapy anemia. During red cell transfusion, he developed hemoglobinuria. Transfusion reaction workup was negative. Drug - induced immune hemolytic anemia was suspected because of positive direct antiglobulin test, negative eluate, and microspherocytes on smear pre - and post - transfusion. Drug studies using the indirect antiglobulin test were strongly positive with trimethoprim and trimethoprim - sulfamethoxazole but negative with sulfamethoxazole. The patient recovered after discontinuing the drug, with no recurrence in 2 years. Other causes of anemia should be considered in patients with worse - than - expected anemia after chemotherapy. Furthermore, hemolysis during transfusion is not always a transfusion reaction.

Trimethoprim

trimethoprim

trimethoprim - sulfamethoxazole

sulfamethoxazole

hemolytic anemia

acute leukemia

anemia

hemoglobinuria

hemolytic anemia

anemia

anemia

hemolysis

Trimethoprim

hemolytic anemia

Trimethoprim

hemolytic anemia

trimethoprim

hemolytic anemia

trimethoprim

hemolytic anemia


Input: Blockade of endothelial - mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin - induced diabetic nephropathy. OBJECTIVE: A multicenter, controlled trial showed that early blockade of the renin - angiotensin system in patients with type 1 diabetes and normoalbuminuria did not retard the progression of nephropathy, suggesting that other mechanism (s) are involved in the pathogenesis of early diabetic nephropathy (diabetic nephropathy). We have previously demonstrated that endothelial - mesenchymal - transition (EndoMT) contributes to the early development of renal interstitial fibrosis independently of microalbuminuria in mice with streptozotocin (STZ) - induced diabetes. In the present study, we hypothesized that blocking EndoMT reduces the early development of diabetic nephropathy. RESEARCH DESIGN AND METHODS: EndoMT was induced in a mouse pancreatic microvascular endothelial cell line (MMEC) in the presence of advanced glycation end products (AGEs) and in the endothelial lineage - traceble mouse line Tie2 - Cre; Loxp - EGFP by administration of AGEs, with nonglycated mouse albumin serving as a control. Phosphorylated Smad3 was detected by immunoprecipitation / Western blotting and confocal microscopy. Blocking studies using receptor for AGE siRNA and a specific inhibitor of Smad3 (SIS3) were performed in MMECs and in STZ - induced diabetic nephropathy in Tie2 - Cre; Loxp - EGFP mice. RESULTS: Confocal microscopy and real - time PCR demonstrated that AGEs induced EndoMT in MMECs and in Tie2 - Cre; Loxp - EGFP mice. Immunoprecipitation / Western blotting showed that Smad3 was activated by AGEs but was inhibited by SIS3 in MMECs and in STZ - induced diabetic nephropathy. Confocal microscopy and real - time PCR further demonstrated that SIS3 abrogated EndoMT, reduced renal fibrosis, and retarded progression of nephropathy. CONCLUSIONS: EndoMT is a novel pathway leading to early development of diabetic nephropathy. Blockade of EndoMT by SIS3 may provide a new strategy to retard the progression of diabetic nephropathy and other diabetes complications.

streptozotocin

angiotensin

streptozotocin

STZ

STZ

STZ

diabetic nephropathy

type 1 diabetes

nephropathy

diabetic nephropathy

diabetic nephropathy

fibrosis

diabetes

diabetic nephropathy

diabetic nephropathy

diabetic nephropathy

fibrosis

nephropathy

diabetic nephropathy

diabetic nephropathy

diabetes complications

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy

STZ

diabetic nephropathy


Input: Cytostatic and anti - angiogenic effects of temsirolimus in refractory mantle cell lymphoma. Mantle cell lymphoma (MCL) is a rare and aggressive type of B - cell non - Hodgkin' s lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor. Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression - free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well - limited fibrotic areas, compatible with post - necrotic tissue repair, were found after 6 - month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti - angiogenic effects. This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy.

temsirolimus

temsirolimus

temsirolimus

temsirolimus

temsirolimus

temsirolimus

temsirolimus

temsirolimus

temsirolimus

mantle cell lymphoma

Mantle cell lymphoma

MCL

B - cell non - Hodgkin' s lymphoma

MCL

MCL

tumor

tumor

tumor

tumor

necrotic

tumor

tumor

MCL

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic

temsirolimus

necrotic


Input: Syncope caused by hyperkalemia during use of a combined therapy with the angiotensin - converting enzyme inhibitor and spironolactone. A 76 year - old woman with a history of coronary artery bypass grafting and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The concentration of serum potassium was high, and normal sinus rhythm was restored after correction of the serum potassium level. The cause of hyperkalemia was considered to be several doses of spiranolactone, an aldosterone antagonist, in addition to the long - term intake of ramipril, an ACE inhibitor. This case is a good example of electrolyte imbalance causing acute life - threatening cardiac events. Clinicians should be alert to the possibility of hyperkalemia, especially in elderly patients using ACE / ARB in combination with potassium sparing agents and who have mild renal disturbance.

Syncope

hyperkalemia

myocardial infarction

loss of consciousness

bradycardia

hyperkalemia

hyperkalemia

hyperkalemia

renal disturbance

angiotensin

spironolactone

potassium

potassium

spiranolactone

aldosterone

ramipril

potassium

potassium

bradycardia

potassium

bradycardia

potassium

bradycardia

spironolactone

hyperkalemia

spironolactone

hyperkalemia

spironolactone

hyperkalemia

spironolactone

hyperkalemia

spiranolactone

hyperkalemia

spiranolactone

hyperkalemia

spiranolactone

hyperkalemia

spiranolactone

hyperkalemia

ramipril

hyperkalemia

ramipril

hyperkalemia

ramipril

hyperkalemia

ramipril

hyperkalemia


Input: Diffuse skeletal pain after administration of alendronate. BACKGROUND: Osteoporosis is caused by bone resorption in excess of bone formation, and bisphosphonates, are used to inhibit bone resorption. Alendronate, a biphosphonate, is effective for both the treatment and prevention of osteoporosis in postmenopausal women. Side effects are relatively few and prominently gastrointestinal. Musculoskeletal pain may be an important side effect in these patients. We presented a patient admitted to our out - patient clinic with diffuse skeletal pain after three consecutive administration of alendronate. CONCLUSION: We conclude that patients with osteoporosis can report pain, and bisphosphonate - related pain should also be considered before ascribing this complaint to osteoporosis.

pain

Osteoporosis

osteoporosis

Musculoskeletal pain

pain

osteoporosis

pain

pain

osteoporosis

alendronate

bisphosphonates

Alendronate

biphosphonate

alendronate

bisphosphonate

alendronate

pain

alendronate

pain

alendronate

pain

alendronate

pain

Alendronate

pain

Alendronate

pain

Alendronate

pain

Alendronate

pain

alendronate

pain

alendronate

pain

alendronate

pain

alendronate

pain


Input: Cerebrospinal fluid penetration of high - dose daptomycin in suspected Staphylococcus aureus meningitis. OBJECTIVE: To report a case of methicillin - sensitive Staphylococcus aureus (MSSA) bacteremia with suspected MSSA meningitis treated with high - dose daptomycin assessed with concurrent serum and cerebrospinal fluid (CSF) concentrations. CASE SUMMARY: A 54 - year - old male presented to the emergency department with generalized weakness and presumed health - care - associated pneumonia shown on chest radiograph. Treatment was empirically initiated with vancomycin, levofloxacin, and piperacillin / tazobactam. Blood cultures revealed S. aureus susceptible to oxacillin. Empiric antibiotic treatment was narrowed to nafcillin on day 4. On day 8, the patient developed acute renal failure (serum creatinine 1. 9 mg / dL, increased from 1. 2 mg / dL the previous day and 0. 8 mg / dL on admission). The patient' s Glasgow Coma Score was 3, with normal findings shown on computed tomography scan of the head 72 hours following an episode of cardiac arrest on day 10. The patient experienced relapsing MSSA bacteremia on day 9, increasing the suspicion for a central nervous system (CNS) infection. Nafcillin was discontinued and daptomycin 9 mg / kg daily was initiated for suspected meningitis and was continued until the patient' s death on day 16. Daptomycin serum and CSF trough concentrations were 11. 21 ug / mL and 0. 52 ug / mL, respectively, prior to the third dose. Lumbar puncture results were inconclusive and no further blood cultures were positive for MSSA. Creatine kinase levels were normal prior to daptomycin therapy and were not reassessed. DISCUSSION: Daptomycin was initiated in our patient secondary to possible nafcillin - induced acute interstitial nephritis and relapsing bacteremia. At a dose of 9 mg / kg, resultant penetration of 5% was higher than in previous reports, more consistent with inflamed meninges. CONCLUSIONS: High - dose daptomycin may be an alternative option for MSSA bacteremia with or without a CNS source in patients who have failed or cannot tolerate standard therapy. Further clinical evaluation in patients with confirmed meningitis is warranted.

daptomycin

methicillin

daptomycin

vancomycin

levofloxacin

piperacillin

tazobactam

oxacillin

nafcillin

creatinine

Nafcillin

daptomycin

Daptomycin

Creatine

daptomycin

Daptomycin

nafcillin

daptomycin

meningitis

bacteremia

meningitis

weakness

pneumonia

acute renal failure

cardiac arrest

bacteremia

infection

meningitis

interstitial nephritis

bacteremia

bacteremia

meningitis

nafcillin

interstitial nephritis

Nafcillin

interstitial nephritis

nafcillin

interstitial nephritis


Input: The role of nitric oxide in convulsions induced by lindane in rats. Lindane is an organochloride pesticide and scabicide. It evokes convulsions mainly trough the blockage of GABA (A) receptors. Nitric oxide (NO), gaseous neurotransmitter, has contradictor role in epileptogenesis due to opposite effects of L - arginine, precursor of NO syntheses (NOS), and L - NAME (NOS inhibitor) observed in different epilepsy models. The aim of the current study was to determine the effects of NO on the behavioral and EEG characteristics of lindane - induced epilepsy in male Wistar albino rats. The administration of L - arginine (600, 800 and 1000 mg / kg, i. p.) in dose - dependent manner significantly increased convulsion incidence and severity and shortened latency time to first convulsion elicited by lower lindane dose (4 mg / kg, i. p.). On the contrary, pretreatment with L - NAME (500, 700 and 900 mg / kg, i. p.) decreased convulsion incidence and severity and prolonged latency time to convulsion following injection with a convulsive dose of lindane (8 mg / kg, i. p.). EEG analyses showed increase of number and duration of ictal periods in EEG of rats receiving l - arginine prior to lindane and decrease of this number in rats pretreated with L - NAME. These results support the conclusion that NO plays a role of endogenous convulsant in rat model of lindane seizures.

nitric oxide

lindane

Lindane

GABA

Nitric oxide

NO

L - arginine

NO

L - NAME

NO

lindane

L - arginine

lindane

L - NAME

lindane

l - arginine

lindane

L - NAME

NO

lindane

convulsions

convulsions

epilepsy

epilepsy

convulsion

convulsion

convulsion

convulsion

convulsive

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures

Lindane

convulsions

Lindane

convulsions

Lindane

convulsion

Lindane

convulsion

Lindane

convulsion

Lindane

convulsion

Lindane

convulsive

Lindane

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures

lindane

convulsions

lindane

convulsions

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsion

lindane

convulsive

lindane

seizures


Input: Long - term oral galactose treatment prevents cognitive deficits in male Wistar rats treated intracerebroventricularly with streptozotocin. Basic and clinical research has demonstrated that dementia of sporadic Alzheimer' s disease (sAD) type is associated with dysfunction of the insulin - receptor (IR) system followed by decreased glucose transport via glucose transporter GLUT4 and decreased glucose metabolism in brain cells. An alternative source of energy is d - galactose (the C - 4 - epimer of d - glucose) which is transported into the brain by insulin - independent GLUT3 transporter where it might be metabolized to glucose via the Leloir pathway. Exclusively parenteral daily injections of galactose induce memory deterioration in rodents and are used to generate animal aging model, but the effects of oral galactose treatment on cognitive functions have never been tested. We have investigated the effects of continuous daily oral galactose (200 mg / kg / day) treatment on cognitive deficits in streptozotocin - induced (STZ - icv) rat model of sAD, tested by Morris Water Maze and Passive Avoidance test, respectively. One month of oral galactose treatment initiated immediately after the STZ - icv administration, successfully prevented development of the STZ - icv - induced cognitive deficits. Beneficial effect of oral galactose was independent of the rat age and of the galactose dose ranging from 100 to 300 mg / kg / day. Additionally, oral galactose administration led to the appearance of galactose in the blood. The increase of galactose concentration in the cerebrospinal fluid was several times lower after oral than after parenteral administration of the same galactose dose. Oral galactose exposure might have beneficial effects on learning and memory ability and could be worth investigating for improvement of cognitive deficits associated with glucose hypometabolism in AD.

galactose

streptozotocin

glucose

glucose

glucose

d - galactose

d - glucose

glucose

galactose

galactose

galactose

streptozotocin

STZ

galactose

STZ

STZ

galactose

galactose

galactose

galactose

galactose

galactose

galactose

cognitive deficits

dementia

Alzheimer' s disease

memory deterioration

cognitive deficits

cognitive deficits

cognitive deficits

glucose hypometabolism

AD

glucose

Alzheimer' s disease

glucose

AD

glucose

Alzheimer' s disease

glucose

AD

glucose

Alzheimer' s disease

glucose

AD

d - glucose

Alzheimer' s disease

d - glucose

AD

glucose

Alzheimer' s disease

glucose

AD

streptozotocin

Alzheimer' s disease

streptozotocin

AD

streptozotocin

Alzheimer' s disease

streptozotocin

AD

STZ

Alzheimer' s disease

STZ

AD

STZ

Alzheimer' s disease

STZ

AD

STZ

Alzheimer' s disease

STZ

AD

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

streptozotocin

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

STZ

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

d - galactose

cognitive deficits

d - galactose

cognitive deficits

d - galactose

cognitive deficits

d - galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits

galactose

cognitive deficits