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)

Previous studies showed that resolution of brain oedema may occur by clearance into the CSF. The present study was performed to measure quantitatively the amount of oedema clearance in cold-induced oedema in cats. In order to determine the minute amounts of oedema fluid entering the CSF the oedema fluid was labelled with a high concentration of an extracellular marker (S35-sodium-thiosulphate). Ventriculo-cisternal perfusion was used to collect the marker in the cisternal outflow. By using the assumption that oedema fluid has the same marker concentration as the plasma, the distribution profile of extracellular space as well as the clearance rate of oedema into CSF could be computed. Oedema and thiosulphate space were most pronounced in the white matter underlying the cortical cold injury. The values then declined progressively with the distance from the lesion towards the ventricle. Oedema fluid clearance into the ventricular CSF at 24 hours following the cold injury amounted to 0.8-1.2 microliter/min or 1.15 ml/day. These data support the assumption that this may be one of the main mechanisms of the resolution of vasogenic brain oedema.
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PMID:Dynamics of formation and resolution of vasogenic brain oedema. I. Measurement of oedema clearance into ventricular CSF. 727 Feb 63

A case report of psychomotor status was presented. A 51-year-old male caught a cold and had a high fever at the end of September, 1979. On October 7th, he had a visual hallucination followed by a generalized seizure. After hospitalization he went through several fits of automatism. On October 15th, he was seized with automatism status in which the seizures were repeated every 25 minutes and there was no recovery of consciousness between the seizures. Although an intravenous injection of diazepam interrupted this status, on October 17th he showed subclinical seizure status on the EEG during which automatism traces were rarely found. By the medication of carbamazepine and clonazepam, he improved gradually. CT-scan revealed the disappearance of the right sylvian fissure and CSF showed findings of viral encephalitis. Consequently, he was considered to have been suffering from temporal lobe encephalitis and shown an episode of psychomotor status with automatisms and automatism traces during which typical automatism status was observed as well.
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PMID:Psychomotor status induced by temporal lobe encephalitis. 728 56

A human cytotoxic-T-lymphocyte (CTL) line capable of killing autologous tumor (AuTu) cell targets was established from peripheral-blood lymphocytes of a patient with squamous-cell carcinoma of the tongue. The cultured CTL were CD3+CD8+CD11b-HLA-DR+T cell receptor (TCR) alpha/beta+. When tested in 4-hr 51Cr-release assays against various lines of squamous-cell carcinoma of the head and neck (SCCHN) and a variety of non-squamous human tumor and normal cell targets, the CTL were found to lyse the autologous SCCHN cell line (PCI-50) and 7 allogeneic SCCHN lines: PCI-1, -2, -4A, -4B, -13, -30 and -38. Of these tumor cell lines, PCI-13, -30 and -38 shared HLA-A2 locus with the AuTu, PCI-50, while PCI-4A and -4B shared HLA-B44 with AuTu. Lysis of AuTu (A2+B44+), PCI-13 (A2+B44-) and PCI-4B (A2- B44+) by the CTL was efficiently inhibited by monoclonal antibodies (MAbs) to CD3, CD8, TCR alpha/beta or the major-histocompatibility-complex (MHC)-class-I antigens. MAbs to HLA-A2 antigens inhibited lysis of PCI-50 or PCI-13 targets by the CTL. In cold-target inhibition assays, unlabeled PCI-4B or PCI-13 cells inhibited CTL lysis of AuTu targets. The CTL incubated in the presence of the HLA-A2+ SCCHN PCI-50 or -13, but not an HLA-A2+ gastric carcinoma, produced TNF-alpha, IFN-gamma and GM-CSF. The CTL were tested for their TCR V beta gene expression by polymerase chain reaction (PCR). At week 10 in culture, the time of the highest AuTu cytotoxicity mediated by the CTL line, V beta 6 was expressed by 26% of T cells. Three clones, obtained by limiting dilution from 10-week CTL and selected for high cytotoxicity against AuTu, were found to be V beta6+. Further analysis of the specificity of these clones indicated lytic activity against PCI-13 (A2+B44-), but not PCI-4B (A2-B44+) targets. In 16-week cultures, which retained AuTu cytotoxicity as well as V beta 6 expression, TCR V beta 2 was also expressed at high frequency (29%), and AuTu-reactive clones were found to be V beta 2+. Our results indicate that at least 2 different CTL populations (V beta 6+ and V beta 2+) are able to recognize SCCHN-associated antigen(s) and that the V beta 6+ T cells are HLA-A2 restricted, while V beta 2+ T cells may be HLA-B44 restricted.
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PMID:HLA restriction and T-cell-receptor V beta gene expression of cytotoxic T lymphocytes reactive with human squamous-cell carcinoma of the head and neck. 816 88

A 3D simulation procedure has been developed to generate simulated PET brain images from MRI data. MRI slices were segmented into gray matter, white matter, CSF structures, and assigned with radionuclide distributions. Projections through these regions were generated according to physical characteristics of a positron tomograph, including 3D sampling and resolution, attenuation, scatter, randoms, and counting statistics. The projection data were then reconstructed by filtered backprojection. The procedure was validated with a cold spot phantom. Simulated PET images for cerebral blood flow or metabolism are presented, along with a brief discussion of some applications and limitations.
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PMID:3D simulation of PET brain images using segmented MRI data and positron tomograph characteristics. 830 11

Highly purified progenitors (including erythroid [BFU-E], granulo-monocytic [CFU-GM], multipotent [CFU-GEMM] progenitors, as well as multipotent progenitors with self-renewal capacity [CFU-B]) express high-affinity growth factor receptors (GFRs), with prevalent interleukin-3 receptors (IL-3Rs) (2,700/cell), a > or = 10-fold lower number of IL-6Rs (145/cell) and granulocyte-macrophage colony-stimulating factor receptors (GM-CSFRs) (300/cell), and a barely detectable level of erythropoietin (Ep) receptors (75/cell). Hematopoietic growth factor (HGF) dosages inducing peak clonogenetic effects are associated with partial/subtotal occupancy of the homologous HGF receptor (HGFR). Cross-reactivity between GFRs and heterologous GFs (including IL-6, IL-3, GM-CSF, Ep, and the kit ligand [KL]) was explored by competition experiments on purified progenitors with radiolabeled and excess cold HGFs at +4 degrees C. No cross-reaction was observed between IL-6R, IL-3R, EpR, and the heterologous GFs, whereas the GM-CSFR showed cross-reactivity with IL-3 and, to a lesser extent, KL. Modulation of GFRs was examined after 18 or 40 hours of incubation with GF(s) at 37 degrees C, followed by ligand-binding assay at 20 degrees C. IL-6, IL-3, GM-CSF, and Ep induce a marked down-modulation of their own receptors. Interestingly, each GF induces the transactivation of the R(s) for the "distal" GF(s): (1) IL-6 induces transactivation of IL-3R, but not of GM-CSFR/EpR; (2) IL-3 causes a rapid upmodulation of GM-CSFR/EpR ("pure" progenitors treated with IL-3 show upmodulation of GM-CSFR alpha-chain mRNA by reverse transcriptase-polymerase chain reaction); whereas (3) GM-CSF induces the transactivation of the EpR. This chain upmodulation of HGFRs may underlie the synergistic interactions between the HGFs in clonogenetic culture. It is emphasized that KL does not induce upmodulation of the other GFRs. Finally, Ep, GM-CSF, and IL-3 do not modulate the expression of the "proximal" HGFRs (ie, GM-CSFR/IL-3R/IL-6R, IL-3R/IL-6R, and IL-6R, respectively). These results allow insight into the cellular basis of hematopoiesis, ie, the complex and coordinate interactions between HGFs and their receptors. They are compatible with a model of cascade transactivation via upmodulation of GFRs in the initial key steps of hematopoietic differentiation, whereby the action of each GF enhances the effect of the distal GF(s) by a multistep chain-potentiation mechanism.
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PMID:Cascade transactivation of growth factor receptors in early human hematopoiesis. 845 93

Meningococcal meningitis has been recognised as serious problem for almost 200 years. In Africa the disease occurs in epidemics periodically during the hot and dry weather in the "meningitis belt" and in east Africa, which is outside this belt the epidemics tend to occur during the cold and dry months. The infection is mainly transmitted from person to person by nasopharyngeal carriers in crowded places like refugee camps and army barracks. The rural/urban migration, the basic structural conditions of housing in squatter settlements and slums together with an overcrowded transport system have also contributed to the transmission of meningococcal meningitis. The earlier treatment of meningococcal meningitis was by the way of repeated CSF drainage. The first important advance in the treatment was intrathecal injection of antimeningococcal serum. A major break through in the treatment was the introduction of sulphonamides which was the preferred treatment until emergence of resistance to sulphonamides in mid 1960's. Penicillin remains the drug of choice currently. Mass immunisation of selected communities using polyvalent A and C polysaccharide vaccine is a useful control measure. Chemoprophylaxis is generally not recommended during epidemics. Given the current population densities and rural/urban migration together with financial constraints, future epidemic in Kenya may be more explosive unless strict surveillance programmes are maintained.
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PMID:Meningococcal meningitis. 862 60

The functional role of N-methyl-D-aspartic acid (NMDA) glutamate receptors in the real-time regulation of single electrical pulse (1 p)-stimulated endogenous dopamine release was investigated in slices of rat caudate putamen using fast cyclic voltammetry at a carbon fibre electrode. In the presence of Mg2+, 20 microM NMDA had a weak effect on background signals but did not affect 1 p-stimulated dopamine release. Removal of Mg2+ increased the background and doubled 1 p-stimulated dopamine release. In the absence of Mg2+, 20 microM NMDA caused a transient "release" of dopamine and decreased the background signal. The 1 p-stimulated dopamine release was subsequently reduced. In the presence of 1 microM (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), superfusion with 20 microM NMDA did not cause a transient "release" of dopamine, and 1 p-stimulated dopamine release was not subsequently attenuated. In the presence of 1 microM tetrodotoxin, 1 p-stimulated dopamine release was abolished, but 20 microM NMDA still caused a transient "release" of dopamine. Removal of Ca2+ from the artificial CSF abolished 1 p-stimulated dopamine release and resulted in a decline in the baseline but did not affect dopamine "release" when 20 microM NMDA was added. The dopamine release-inducing effect of 20 microM NMDA was less pronounced in sites in the caudate putamen where dopamine release increased with frequency of electrical stimulation (hot spots) than in sites where there was little frequency-dependent dopamine release (cold spots). Subsequent 1 p-stimulated dopamine release was less attenuated in cold spots than in hot spots. We conclude that in the absence of Mg2+, NMDA induces release of dopamine by acting at CPP-sensitive NMDA receptors in a Ca(2+)-independent manner. This transient release depletes dopamine from a storage site from which dopamine is released by 1 p electrical stimulation. These real-time observations of the effects of NMDA on electrical stimulus-independent and -dependent dopamine release may explain the apparently conflicting observations of the effects of NMDA on dopamine release made in previous studies. They also indicate that dopamine release and storage are heterogeneous at different sites in the rat caudate putamen.
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PMID:Real-time effects of N-methyl-D-aspartic acid on dopamine release in slices of rat caudate putamen: a study using fast cyclic voltammetry. 876 69

Interferon-gamma inducing factor (IGIF) is a recently identified cytokine also called interleukin-1gamma (IL-1gamma) or interleukin-18 (IL-18). Its biological activity is pleiotropic, and, so far, it has been shown to induce interferon-gamma production in Th1 cells, to augment the production of granulocyte-macrophage-CSF, and to decrease that of interleukin-10 (IL-10). We first detected newly synthesized IGIF mRNA by differential display in the adrenal gland of reserpine-treated rats and then isolated two transcripts by reverse transcription polymerase chain reaction. They were identified as rat IGIF on the basis of the high homology with mouse: 91% at both the nucleotide and the amino acid level. Subsequently, we investigated the effects of stress on IGIF mRNA levels and found that acute cold stress strongly induced IGIF gene expression. In situ hybridization analysis showed that IGIF is synthesized in the adrenal cortex, specifically in the zona reticularis and fasciculata that produce glucocorticoids. The presence of IGIF mRNA was also detected in the neurohypophysis although induction by stress was not significant. Our results call for more attention to the role of the adrenal gland as a potential effector of immunomodulation and suggest that IGIF itself might be a secreted neuroimmunomodulator and play an important role in orchestrating the immune system following a stressful experience.
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PMID:Induction of interferon-gamma inducing factor in the adrenal cortex. 899 96

Allergic rhinitis involves an early phase, largely mediated through mast cells, and a late phase which involves cellular infiltration and mediator release. In the early phase, mast cells release mediators as a result of antigen cross-linking adjacent immunoglobulin E molecules bound to mast cell surfaces. This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis--sneezing, itching, rhinorrhoea and congestion. The late phase of the allergic response (hours after challenge) involves infiltration of the nasal epithelium by eosinophils, basophils, monocytes and T-lymphocytes, which release leukotrienes, kinins, histamine and a host of other mediators. The most important part of the late-phase response is probably mediated via the production of cytokines (IL-4, IL-5, IL-6, IL-8, GM-CSF and RANTES) by mast cells, TH2 lymphocytes or epithelial cells. The infiltration of tissues by cells normally present only in the blood is brought about by the production of adhesion molecules, such as VCAM-1 and E-selectin, which cause circulating eosinophils, basophils and T-lymphocytes to adhere to endothelial cells before moving through the endothelium into the tissue (diapedesis). Neuronal reflexes also play a role in the allergic response, both by mediating local responses to mediators and possibly playing a part in the activation of T-lymphocytes. The allergic response has also been shown to be less intense in a hot, humid environment, and more marked in a cold, dry environment, possibly due to changes in osmolality of the nasal surface fluid. Similar factors may play a role in the aetiology of non-allergic rhinitis.
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PMID:Pathophysiology of perennial allergic rhinitis. 921 57

An 18-year-old female had common cold and insomnia in early March 1987. Later, abnormal speech and behavior, emotional incontinence, anorexia and consciousness disturbance appeared. On March 19, she was admitted to our hospital in semi-comatose state. Myoclonus-like movement on hands was observed, and epileptic attacks with tonic and clonic convulsions occasionally occurred. There were no neurological findings that suspected cerebral focal lesions. The respiration was assisted through tracheal intubation. Laboratory examinations showed inflammatory reactions (CRP+2, WBC 10,600) and transient high levels serum CK (6,215 IU). As she had bradycardia (30-40/min) with complete AV block on ECG, the pacemaker was implanted. The complication of myocarditis was suspected. EEG showed bilateral slow waves (3-6Hz), dominantly in frontal areas. Brain CT and CSF examinations were normal. After the combined administration of ara-A, dexamethasone and anti-convulsant, the consciousness level was recovered within a month. The serum antibody against coxsackie virus B4 alone was significantly increased. We concluded that coxsackie virus B4 caused acute encephalitis with mental symptoms and myocarditis with AV block. Recently, cytomegalovirus was reported to be the causative virus in a young female with non-HSV encephalitis who showed mental symptoms with good prognosis, but coxsackie virus B4 should also be considered as one of the causative viruses.
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PMID:[Coxsackie virus B4 encephalitis in a young female who developed mental symptoms, and consciousness disturbance, and completely recovered]. 959 14


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