Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Objective To observe the changes of expression of P-glycoprotein (PGP) in the brain of pentylenetetrazole (PTZ)-kindled epileptic mice after 2-chloride adenosine (2-CAdo) stimulation. Methods The C57BL/6 mice (n=40) were randomly divided into three groups: control group (n=8), PTZ group (n=16) and 2-CAdo group (n=16). The epileptic model was established by intraperitoneal injection of PTZ [30 mg/(kg.d)]. The control group were given the same amount of normal saline. The seizures were observed during PTZ kindling (kindling rate, latency time, start time and durations of seizures). After kindled, the 2-CAdo group was continuously injected with 2-CAdo [0.6 mg/(kg.d)] for 2 weeks. The other two groups were injected with normal saline instead. Then, all the mice of these three groups were sacrificed. HE staining was adopted to observe the histopathological changes of cerebral cortex and hippocampus of the mice, and the expression of PGP was detected by immunohistochemistry and Western blotting. Results At the time of seizures, the mice showed whole body tremor, hair erection, apathy, loss of appetite, cage offense and other abnormalities. HE staining showed that the damage of cerebral cortex and hippocampus of the 2-CAdo group was less than that of the PTZ group. Immunohistochemistry and Western blotting showed that the expression of PGP in the cerebral cortex of the 2-CAdo group was significantly lower than that in the control and PTZ groups. In the hippocampus, the expression of PGP in the 2-CAdo and PTZ groups was significantly higher than that in the control group, especially highest in the 2-CAdo group. Conclusion The 2-CAdo can reduce the damage of brain tissue, upregulate the expression of PGP in the hippocampus, and downregulate the expression of PGP in the cerebral cortex.
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PMID:[The 2-chloride adenosine alleviates the damage of brain tissues in pentylenetetrazole-kindled epileptic mice by regulating P-glycoprotein expression]. 2839 20

Narrative Medicine sessions can encourage patients to rediscover personal identity and meaning by telling or writing their stories. We explored this process to improve care and quality of life for brain cancer patients in an academic neuro-oncology program. Brain cancer and its treatments may threaten a patient's quality of life and sense of self in many ways, including impaired cognitive skills, loss of memory, reduced coordination, and limited capacity for self-expression. The impact of symptoms and side effects on quality of life must be evaluated in terms of each patient's identity and may be understood in terms of each patient's story. Insights from Narrative Medicine visits may also be helpful for the treatment team as they seek to assess patient needs, attitudes, and abilities. We provide case-based histories demonstrating applications of Narrative Medicine in the care of patients with brain tumors whose sense of self and quality of life are challenged. The cases include managing frontal lobe syndrome of loss of initiative and pervasive emotional apathy with his wife and young children, regaining a meaningful activity in a patient, re-establishing self-identity in a young woman with ependymoma, and improving spells with coexistent epilepsy and psychogenic non-epileptic seizures (PNES).
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PMID:Narrative Medicine perspectives on patient identity and integrative care in neuro-oncology. 2866 13

True and psychogenic nonepileptic seizures (PNES) go hand in hand. One colors the picture of other. Although it is thought that children carry lower risk for PNES than adults, this may represent the under-diagnosis of this condition in childhood due to few studies on this specific topic. Again, true seizure can be misdiagnosed by dramatic and varied manifestations appearing as psychological phenomena. We report a case of a 9-year-old boy presenting with sudden onset, short lasting, off and on different "melodramatic" episodic behavioral problems with La-Belle' indifference without loss of consciousness, appearing to be of psychogenic origin but finally ended with a diagnosis of temporal lobe epilepsy and responded dramatically with antiepileptics. The goal of this case report is to alert the reader to be cautious about rarer presentations of epilepsy and see each case holistically which may be misguided as PNES.
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PMID:Temporal Lobe Seizures Presenting as Abrupt Clinging Behavior in a Child. 2885 55

We report a hereditary leukodystrophy in Standard Schnauzer puppies. Clinical signs occurred shortly after birth or started at an age of under 4 weeks and included apathy, dysphoric vocalization, hypermetric ataxia, intension tremor, head tilt, circling, proprioceptive deficits, seizures and ventral strabismus consistent with a diffuse intracranial lesion. Magnetic resonance imaging revealed a diffuse white matter disease without mass effect. Macroscopically, the cerebral white matter showed a gelatinous texture in the centrum semiovale. A mild hydrocephalus internus was noted. Histopathologically, a severe multifocal reduction of myelin formation and moderate diffuse edema without inflammation was detected leading to the diagnosis of leukodystrophy. Combined linkage analysis and homozygosity mapping in two related families delineated critical intervals of approximately 29 Mb. The comparison of whole genome sequence data of one affected Standard Schnauzer to 221 control genomes revealed a single private homozygous protein changing variant in the critical intervals, TSEN54:c.371G>A or p.(Gly124Asp). TSEN54 encodes the tRNA splicing endonuclease subunit 54. In humans, several variants in TSEN54 were reported to cause different types of pontocerebellar hypoplasia. The genotypes at the c.371G>A variant were perfectly associated with the leukodystrophy phenotype in 12 affected Standard Schnauzers and almost 1000 control dogs from different breeds. These results suggest that TSEN54:c.371G>A causes the leukodystrophy. The identification of a candidate causative variant enables genetic testing so that the unintentional breeding of affected Standard Schnauzers can be avoided in the future. Our findings extend the known genotype-phenotype correlation for TSEN54 variants.
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PMID:TSEN54 missense variant in Standard Schnauzers with leukodystrophy. 3158 37

Autoimmune Limbic Encephalitis (LE) is a relatively new category of immune-mediated diseases with a wide range of neuropsychiatric symptoms. LE associated with Glutamic Acid Decarboxylase (GAD) antibodies is difficult to diagnose due to its possible atypical presentation with neuropsychiatric and behavioral features. We performed a systematic review of literature and retrieved 21 cases of anti GAD-associated LE with neuropsychiatric signs. Median age at onset was 27 years with a female predominance (81.0 %) and median diagnostic delay of 6 months. Clinical presentation included typical LE symptoms such as anterograde amnesia (95.2 %) and temporal lobe or tonico-clonic seizures (95.2 %). Psychiatric symptoms were described in 61.9 % of patients, presenting as anxiety, depressive symptoms, apathy and behavioral changes. Extra-limbic symptoms were present in 14.3 % of patients. No neoplasia associated was found. Some patients had poor epileptic, cognitive and psychiatric outcomes requiring prolonged immunosuppressive treatment. The description of the neuropsychiatric spectrum of anti-GAD LE and its specificities aims to improve our understanding of this entity, and may lead to earlier diagnosis as well as better outcome.
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PMID:Psychiatric symptoms in anti glutamic acid decarboxylase associated limbic encephalitis in adults: a systematic review. 3302 99

Uraemic encephalopathy (UE) is rarely associated with acute kidney injury or chronic kidney disease in domestic animals, and we now report the first case in a cat. The animal presented with hypothermia, apathy, lethargy, depression, severe dehydration, uraemic breath, elevated serum urea nitrogen and creatine concentrations, and eventual seizures and coma prior to death. Gross necropsy findings included severe bilateral renal scarring, ulcerative stomatitis and glossitis, and uraemic gastropathy. Microscopic lesions of diffuse interstitial fibrosis, multifocal mineralization and lymphoplasmacytic interstitial nephritis were seen in the kidneys. There was symmetrical, bilateral spongy vacuolation of the white matter of the basal nuclei and cerebellum and Alzheimer type II astrocytes in the cerebral cortex and hippocampus. Glial fibrillary acid protein immunolabelling was absent or faint in astrocytes of the cerebral grey matter. UE should be included in the differential diagnosis in animals with chronic kidney disease and neurological signs.
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PMID:Uraemic Encephalopathy in a Persian Cat with Chronic Kidney Disease. 3322 66


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