Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a case of non-herpetic acute encephalitis with unilateral temporal cortex lesion revealed by MR imaging and SPECT study. The patient was an eighteen years old woman who developed tonic-clonic seizure after common cold symptom. She was healthy before this episode. Neurological abnormality was only a single convulsion at onset and there was no other abnormal physical and neurological signs except for low grade fever. Electroencephalogram showed spike and slow wave complex of 2 Hz focused on a right posteriotemporal point (T 6) and an MR FLAIR (fluid-attenuated inversion recovery) image revealed a high signal intensity area at right temporal cortex. There was a decrease of cerebral blood flow in the same portion on SPECT study. This lesion was obscure on T1 and T2 MR images. Cerebrospinal fluid showed pleocytosis with normal glucose level and protein concentration. Bacterial and fungal cultures of CSF were negative and a detection of tubercule bacillus by PCR hybridization method was also negative. Although CSF findings suggested viral infection of CNS, virological study could not demonstrate infections of herpes simplex virus type 1, type 2, varicella-zoster virus, cytomegalovirus, measles virus, mumps virus, Japanese encephalitis virus, and influenza virus type A and B. After infusion of acyclovir and antibiotics, the patient was discharged from our hospital without sequelae of encephalitis. EEG was normal at this point and a high intensity area of MR FLAIR image disappeared two months later. SPECT findings were normalized six months later. The encephalitis presenting unilateral temporal cortex lesion without the infection of herpes simplex virus is thought to be very rare. Our case was distinguished from non-herpetic acute limbic encephalitis by an extent of the lesion and clinical manifestations. MR FLAIR image was useful for the detection of the lesion in this case.
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PMID:[A case of non-herpetic acute encephalitis presenting high intensity lesion at unilateral temparal cortex on MR FLAIR image]. 1054 15

A 49-year-old woman, with a two-year-history of multiple screlosis (MS), noticed postural dizziness, intractable hiccups and vomiting. On admission, she had mild quadriparesis, hypesthesia below the C5 level, and a girdle sensation at the T5 and L1 levels. A CSF examination showed slight increases in the protein level (48 mg/dl) and cell count (7/mm3). Brain MRI demonstrated no obvious lesion in the medulla oblongata. The head-up-tilting test showed a decrease in the blood pressure from 105/63 mmHg to 70/55 mmHg. The pulse rate, however, increased from 57/min to 72/min. The cold pressure test also revealed a mild impairement in her blood pressure response. The R-R interval variation (coefficient of variation: CVRR) during normal breathing was 2.58 (normal: > 1.66). The valsalva ratio was 1.84 (normal: 1.4-2.0). The Aschner eye-ball pressure test, the blood pressure response to the injection of epinephrine, and the sweating response to the injection of acetylcholine were all normal. She was thus administered domperidone and chlorpromazine. Only domperidone effectively improved the nausea and vomiting. All symptoms, including orthostatic hypotension, hiccups and vomiting, disappeared about one month after admission. The remission of her symptoms was considered to reflect the natural course of MS. The results of autonomic nervous system function tests and her clinical features suggest that an irritable lesion in the medullary tegmentum, including the nucleus tractus solitarii, most likely caused her symptoms. The above findings indicate that autonomic symptoms, such as orthstatic hypotension, hiccups and vomiting, may sometimes be the only symptoms observed in a relapse of MS.
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PMID:[A case of relapsing multiple sclerosis presenting with only autonomic symptoms including orthostatic hypotension, hiccups and vomiting]. 1061 56

A 36-year-old Japanese woman was admitted to our hospital, because of facial palsy, ophthalmoplegia, cerebellar ataxia, and rhythmic myoclonus of the neck. About a few weeks before admission, she developed symptoms of common cold and general fatigue. Her laboratory data were unremarkable, and her CSF was normal. Serum levels of antibodies to gangliosides were within normal limits. Her MRIs of the brain and neck were normal. Both somatosensory evoked cortical potential study and auditory evoked brainstem response study were normal. She was diagnosed as postinfectious brainstem encephalitis, and the administration of corticosteroid was started. After the treatment, her symptoms improved. To our knowledge, it is rare to see myoclonus to the neck without palatal tremor in patients with brainstem encephalitis.
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PMID:[Rhythmic involuntary movement of the neck in a patient with brainstem encephalitis]. 1065

Beta amyloid peptides are major insoluble constituents of amyloid fibrils in senile plaques and cerebrovascular deposits, both characteristic of Alzheimer disease (AD). Low concentrations of soluble forms of amyloid peptides are also present in normal CSF. We previously demonstrated that the 40 amino acid form of soluble beta-amyloid peptide (sAbeta) is rapidly cleared from rat CSF into blood. Herein we hypothesized that a saturable, outwardly directed flux of this peptide occurs at the blood-brain barrier (BBB) and tested whether supraphysiological (possibly pathological) concentrations of sAbeta could alter the permeability of this barrier to a paracellular tracer, polyethylene glycol (PEG). Using an in vitro model of BBB, we showed that influx and efflux of sAbeta were equal, modest (60%-160% greater than that of PEG), and not saturable. These observations suggest that sAbeta moved across the monolayer by a diffusional process, and not via a transporter. PEG flux was doubled immediately after the luminal concentration of cold sAbeta was raised to 5 microM, and was doubled 150 min after the abluminal concentration of sAbeta was increased to 5 microM. Pathological elevations of sAbeta concentration in plasma or brain interstitial fluid may, therefore, alter the permeability of brain capillaries in vivo.
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PMID:In vitro evidence that beta-amyloid peptide 1-40 diffuses across the blood-brain barrier and affects its permeability. 1074 33

The cell activation depends on T cell antigen receptor binding to antigen plus MHC and costimulation. The binding of CD28, expressed on the T cell surface to B7 (B7-1 or CD80/B7-2 or CD86) present on the antigen--presenting cells (APCs), determines, in several T cell function models, if activation or anergy follows antigenic stimulation. In leprosy, the role of CD80 and CD86 as costimulatory signal in M. leprae-specific cellular immunity has not yet been defined. We investigated the role of B7-CD28 pathway of T cell activation in the in vitro response to M. leprae, following stimulation in the presence of monocytes or dendritic cells (DCs) as APCs. Monocytes were purified, by cold aggregation, from peripheral blood mononuclear leukocytes (PBMC), isolated from leprosy patients. In order to obtain DCs, the monocytes were cultured in the presence of IL-4 and GM-CSF. T cells were purified from PBMC by negative selection with mABs and C'. The phenotype of the cell populations was monitored by FACS. Lymphoproliferative assays were performed with T cells, in the presence of monocytes or DCs. The cells were stimulated by M. leprae in the presence of anti-CD80 antibody (Ab) and/or anti-CD86 antibody (Ab) (Innogenetics). In some experiments Il-10, Il-12 and anti-Il-12 Ab were also added to the culture. We observed a significantly more efficient APC function for DCs when compared to monocytes in T cell in vitro responses to M. leprae. Regardless of the clinical form of Leprosy, the M. leprae-specific immune response was markedly reduced in the presence of anti-CD86 Ab. Il-12 increase the immune response to M. leprae while IL-10 or anti-IL-12 Ab reduce this response when monocytes or DCs were used as APCs.
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PMID:Evaluation of B7-1 (CD80) and B7-2 (CD86) costimulatory molecules and dendritic cells on the immune response in leprosy. 1124 83

Reactive oxygen species (ROS) generated by mitochondrial respiration and other processes are often viewed as hazardous substances. Indeed, oxidative stress, defined as an imbalance between oxidant production and antioxidant protection, has been linked to several neurological disorders, including cerebral ischemia-reperfusion and Parkinson's disease. Consequently, cells and organisms have evolved specialized antioxidant defenses to balance ROS production and prevent oxidative damage. Research in our laboratory has shown that neuronal levels of ascorbate, a low molecular weight antioxidant, are ten-fold higher than those in much less metabolically active glial cells. Ascorbate levels are also selectively elevated in the CNS of anoxia-tolerant reptiles compared to mammals; moreover, plasma and CSF ascorbate concentrations increase markedly in cold-adapted turtles and in hibernating squirrels. Levels of the related antioxidant, glutathione, vary much less between neurons and glia or among species. An added dimension to the role of the antioxidant network comes from recent evidence that ROS can act as neuromodulators. One example is modulation of dopamine release by endogenous hydrogen peroxide, which we describe here for several mammalian species. Together, these data indicate adaptations that prevent oxidative stress and suggest a particularly important role for ascorbate. Moreover, they show that the antioxidant network must be balanced precisely to provide functional levels of ROS, as well as neuroprotection.
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PMID:Brain antioxidant regulation in mammals and anoxia-tolerant reptiles: balanced for neuroprotection and neuromodulation. 1245 80

Like opioid tolerance, neuropathic pain syndrome manifested by hyperalgesia and allodynia responds poorly to opioids. Hitherto, its development is still not clear and its treatment and prevention are still disputable. Pertussis toxin (PTX) which ADP-ribosylates the alpha-subunit of inhibitory guanine nucleotide binding regulatory proteins (Gi/Go), is used to induce morphine tolerance through intrathecal (i.t.) injection. It decreases the antinociceptive effect of opioid receptor agonists, and produces a thermal hyperalgesia as well. With treatment of PTX the inhibitory Gi- and Go-proteins signal transduction is inactivated. Inhibition of the inhibitory system would likely lead to a predominance of the excitatory system. Intrathecal PTX administration has also been suggested as a model for study of the central mechanisms of neuropathic pain. In our previous studies, with intrathecal microdialysis and drug delivery techniques, we correlated the biochemical and pharmacological effects on the behavioral expressions of i.t. PTX-treated rats. Intrathecal PTX administration would induce thermal hyperalgesia in rats, with accompaniments of a prolonged increase in the concentrations of excitatory amino acids (EAAs), glutamate and aspartate, and a decrease in the concentration of the inhibitory amino acid (IAA) glycine in the spinal CSF dialysates. The PTX-induced thermal hyperalgesia peaked between day 2 and 4, but no cold allodynia is observed; i.t. administration of N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosponovaleric acid (D-AP5), glycine and protein kinase C (PKC) inhibitor chelerythrine attenuated the thermal hyperalgesia. The PKC gamma content of both synaptosomal and cytosolic fractions were significantly increased in PTX-treated rats. In contrast, the levels of PKC alpha, beta I, or beta II isozymes in these fractions were unaffected. Infusion of NMDA antagonist D-AP5 prevented both the thermal hyperalgesia and the increase in PKC gamma expression in PTX-treated rats. Similar to our previous report, i.t. PTX reduced morphine's analgesic effect. PKC inhibitor chelerythrine attenuated this reduction of morphine's analgesia, and an inhibition of the morphine-evoked EAAs release was observed in PTX-treated rats as well. Taken together, i.t. PTX-induced neuropathic pain syndrome is accompanied by increasing of EAAs, decreasing of IAA release, and a selective increasing of PKC gamma expression in the spinal cord. Inhibition of PKC not only blocked thermal hyperalgesia, but also reversed the reduction of morphine's analgesic effect in PTX-rats. These results suggest that PTX-induced neuropathic pain syndromes are involved in EAAs, IAAs and PKC alternations.
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PMID:Implications of intrathecal pertussis toxin animal model on the cellular mechanisms of neuropathic pain syndrome. 1476 16

Sub acute sclerosing pan-encephalitis (SSPE) is a slowly progressive inflammatory disorder of the central nervous system. A decline in frequency has been noticed in most of the developed countries, whereas it continues to be high in developing countries. Though a number of studies have been carried out, the exact trend of SSPE is still not clear. Hence the present study was carried out to analyze the trend of SSPE over the past ten years in and around Chandigarh. A total of 205 patients with clinical features suggestive of SSPE were enrolled for the study during Jan'92 to Dec. 2001. Measles specific antibodies were detected in blood and CSF by HAI method. 114 patients were found to be positive for measles specific HAI antibody with a male preponderance. The number of SSPE cases were found to be more during the period 1992-95 in comparison to the next 6 years (p < 0.05). The high incidence of SSPE in our country could be due to improper vaccine coverage, poor cold chain maintenance or circulation of atypical measles virus strain.
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PMID:Changing trend of SSPE over a period of ten years. 1647 5

Cooling has been shown to terminate experimentally induced epileptiform activity in models of epilepsy without causing injury to the cooled brain, suggesting that cooling could represent an approach to seizure control in intractable focal epilepsies. Here we sought to determine the most effective way to apply cooling to abort spontaneous epileptiform discharges in in vitro brain slice models. We induced spontaneous epileptiform activity in rat brain slices by exposure to 4-aminopyridine (4-AP), 4-AP plus bicuculline, and Mg(2+)-free artificial CSF (aCSF) at 28-34 degrees C. Extracellular field recordings were made at hippocampal or neocortical sites. Slice temperature was reduced by perfusion with cold aCSF. Rapid cooling at rates of 2-5 degrees C/s was compared to cooling at slower rates of 0.1-1 degrees C/s. Cooling at both rates reversibly aborted epileptiform discharges in all three models and at all recording sites. With rapid cooling, small temperature drops were highly effective in terminating discharges, an effect that was sustained for as long as the reduced temperature level was maintained. In contrast, slow cooling required much larger temperature drops to inhibit discharges. With slow cooling, absolute temperature drops to 21-22 degrees C caused a 90% reduction in event frequency, but cooling to 14-15 degrees C was required to terminate discharges. We conclude that rapid cooling as effectively aborts discharges in in vitro epilepsy models as does slow cooling, but the magnitude of the temperature change required is less. Practical devices to inhibit seizure activity may only need to induce small temperature drops, if the cooling can be applied sufficiently rapidly.
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PMID:Termination of epileptiform activity by cooling in rat hippocampal slice epilepsy models. 1681 80

Intermittent allergic rhinitis and common cold constitute frequent conditions and show similar clinical symptoms. The purpose of this study was to investigate the pattern of cytokines in the nasal fluid of patients with acute symptoms caused by allergic and viral rhinitis. Nasal secretions were analyzed by immunosorbent assay techniques using a cytokine panel assay and routine ELISA. Allergic patients had significantly higher levels of eosinophil cationic protein (ECP), interleukin (IL)-5, and tryptase. Significantly elevated concentrations of proinflammatory cytokines (IL-1b, IL-6, IL-7, IL-17, interferon [IFN] gamma, and tumor necrosis factor [TNF]-alpha) as well as chemokines for cellular infiltration (IL-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1beta), factors for cellular proliferation (granulocyte colony-stimulating factor [G-CSF] and granulocyte macrophage colony-stimulating factor [GM-CSF]), and elastase were found in viral rhinitis. IL-10 was only detectable in viral rhinitis. IL-4 was significantly higher in patients with viral rhinitis than allergic rhinitis, and IL-5 was significantly elevated in viral rhinitis compared with controls. In viral-triggered rhinitis, we detected a predominantly Th1-type cytokine pattern with potent proinflammatory mediators. Factors reflecting a neutrophil and eosinophil immune response, due to IL-5, IL-8, GM-CSF, ECP, and elastase were shown. Nasal secretions of patients with allergic rhinitis showed highest concentrations of tryptase, IL-5, and ECP, reflecting a mast cell and eosinophil immune response. Nasal secretion levels of IL-4 did not show highest levels in allergic rhinitis but did in viral rhinitis. IL-4 also may play a role in limiting inflammatory processes by inhibiting the production of inflammatory cytokines.
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PMID:Mediators and cytokines in allergic and viral-triggered rhinitis. 1788 11


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