Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-CD3 monoclonal antibodies induce the proliferation of human T-cells in vitro and activate specific and nonspecific cytolysis by human T-cell clones and human peripheral blood lymphocytes. In vivo administration of anti-CD3 prevents tumor growth of a UV-induced mouse fibrosarcoma. We conducted a phase I trial to determine the toxicity and immunomodulatory properties of low doses of anti-CD3 in 36 patients with cancer. In 23 patients, anti-CD3 was given i.v. over 3 h at 1, 10, 30, and 100 mcg/patient. Five other patients received anti-CD3 at 30 mcg by i.v. bolus. Patients were treated every 3 days for a total of four doses. An additional eight patients received anti-CD3 daily for 14 days at 3 mcg by i.v. bolus, 3-h infusion, or 24-h infusion. Dose-limiting toxicity was headache. Headache was often accompanied by signs and symptoms of meningeal irritation leading to performance of a lumbar puncture in nine patients. The opening pressure was usually elevated, and six patients had a cerebrospinal fluid lymphocytosis with an elevated protein. Increased levels of interleukin 6 were identified in the cerebrospinal fluid. The maximum tolerated dose by 3-h infusion was 30 mcg. There were no objective tumor responses. There was a dose-related increase in the number of peripheral blood lymphocytes expressing the T-cell activation antigen CD69 (Leu 23), but no changes were seen in CD25 (interleukin 2 receptor) expression, and no changes were observed in the serum levels of the soluble interleukin 2 receptor. Even at these low doses of anti-CD3, 8 of 16 patients tested developed human anti-mouse antibodies.
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PMID:Anti-CD3 monoclonal antibody treatment of patients with CD3-negative tumors: a phase IA/B study. 153 72

The clinical profile of cluster headache, in Italy better known as "Horton's histaminic headache" is described. The Author makes an inventory of all pathogenetic theories about this excruciating pain syndrome that strikes men more than women. On the basis of findings of the Author and his School over a ten-year period, there is a "periodic lack of immunitary oversee". The salient points of various stages of this study are: low frequency of HLA-B14 antigen with, in contrast, high frequency of the HLA-DR5 antigen of the major histocompatibility system. The HLA B18 antigen of the same major histocompatibility system has been found in patients who respond to lithium therapy. A lack of the HLA-B18 antigen has been found in cluster headache patients who are "non-responders" to lithium therapy. Low titers of antibody response in the pain free periods of these subjects, and high titers in the painful periods has also been found in the serum of cluster headache patients; the lack of alpha 1-antitrypsin in basal conditions; increase of IgE (PRIST) values in painful periods; high titers of C1qSp and KgBt circulating immuno-complexes. The cellular immunity studies of the patients showed an increase of the leukocyte subpopulations Leu7+ and Leu M3+. Besides, the natural killer function that contributes to the defense-mechanism against viral disease, was very low. High titers of anti-herpes simplex 1 and 2 viruses and anti-Epstein-Barr virus have been found in cluster headache patients and in a few observations of Burkitt's lymphoma with associated cluster headache, studied in Sahel area too.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New findings in cluster headache. 215 Apr 89

In a previous study we demonstrated that cluster headache (CH) patients present an increased Natural Cytotoxic response after incubation of their peripheral blood lymphocytes (PBL) with Interleukin-2 (IL-2). This phenomenon led to an investigation of the phenotypic expression of PBL before and after IL-2 incubation, and of the IL-2 lymphocyte receptor. IL-2 receptor is expressed on T-lymphocytes activated with an high-affinity binding site. The analysis of the function of human IL-2 receptor was facilitated by the production of a specific monoclonal antibody (MAb). This MAb identifies the IL-2 receptors by blocking the binding of radiolabelled IL-2 to T-cells. In addition, we studied the expression of Leu-4, specific for T-cells; of Leu-11b, specific for FC receptor on NK cells; and the Transferrin Receptor, specific for lymphoblasts and monocytes. Twenty-three episodic CH patients were selected for this study. Ten sex and age-matched healthy volunteers were used as the control group. We evaluated the PBL phenotypic expression of cells subsets before incubation with IL-2 (1,000 I.U./ml) and after 72 hours. The following Becton Dickinson MAbs have been used: anti-Leu-4 (CD3), anti-IL-2 receptors (CD25), anti-Transferrin receptor (TFR) and anti-Leu-11b (CD16). Indirect fluorescence with a Becton Dickinson FACS-420 flow cytometer was used to analyze the cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1990 Mar
PMID:Defective expression of IL-2 receptors on peripheral blood lymphocytes from patients with cluster headache. 233 78

Twenty-six malignant lymphomas involving the central nervous system were studied. Eleven were primary (P) and 15 were systemic (S). Eight cases (3 P, 5 S) occurred in immunocompromised patients. Age at presentation in immunocompromised patients was typically younger than in the nonimmunocompromised patients. Presenting complaints of central nervous system involvement included headache, seizures, personality changes, memory lapses, ataxia, cranial nerve symptoms, and impaired consciousness. Cerebrospinal fluid involvement was seen only in 3 S cases. In 8 of the P cases, the diagnosis was first established at autopsy; in 6 of the S cases, central nervous system involvement was first documented at autopsy. Survival was longer in treated patients than in those who received no therapy (5 months in P cases and 9.3 months in S cases; 2.3 months without therapy). Regardless of therapy, the average survival of immunocompromised patients was 2.4 months. The majority of cases were multifocal. Of the P cases, 1 was of low histologic grade, 9 were of intermediate grade, and 1 was of high grade. Of the S cases, 5 were of low grade, 9 were of intermediate grade, and 1 was of high grade. Immunophenotypic studies were performed on formalin-fixed, paraffin-embedded tissue with antisera against common leukocyte antigen (all reactive), B-cell markers (L26, MB2, LN1, and LN2), T-cell markers (UCHL1 and MT1), Leu-M1, Leu-7, and HLA-DR (LN3). Two S cases were of T-cell phenotype; all others were of B-cell derivation. Eleven cases were HLA-DR positive (all of B-cell phenotype). One T-cell lymphoma was reactive for Leu-7. All cases were nonreactive for Leu-M1. All cases in immunosuppressed patients and all P cases were of B-cell phenotype.
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PMID:Central nervous system lymphomas. Immunohistochemical and clinicopathologic study of 26 autopsy cases. 252 37

Recombinant interleukin-2 (rIL-2) (NSC# 600664; Hoffmann-La Roche, Inc., Nutley, NJ) was studied in a phase I clinical trial in 33 patients with advanced, measureable cancer of the colon or malignant melanoma, Eastern Cooperative Oncology Group (ECOG) performance status O-1, and no prior chemotherapy or radiotherapy. The goal of the study was to identify a dose and schedule of IL-2 to generate maximal immune modulation with tolerable toxicity. Such a regimen might allow the addition of other treatment modalities and/or prolonged treatment duration in later trials. Each patient received IL-2 as a continuous 24-hour infusion once weekly for 4 weeks and then twice weekly for 4 weeks. Five treatment groups received from 10(3) U/m2 to 3 x 10(7) U/m2 per 24-hour infusion. The maximal tolerated dose was 3 x 10(7) U/m2/d twice weekly. Patients treated twice weekly at 1 x 10(7) and 3 x 10(7) U/m2/d had immune modulation in terms of lymphocytosis, eosinophilia, increased natural killer (NK) activity, and elevated numbers of peripheral blood mononuclear cells expressing CD16, OKT10/Leu-17, and Leu-19 surface markers. Endogenous generation of peripheral blood lymphokine-activated killer (LAK) activity was demonstrated by lysis of NK-resistant Daudi targets, in patients treated at 3 x 10(7) U/m2/d. Biochemical and hematological abnormalities were moderate and reversible. Clinical toxicity included hypotension, myalgia, arthralgia, stomatitis, fever, fatigue, nausea, headache, chills, diarrhea, and oliguria at high doses. Cardiovascular toxicity was tolerable for most patients and reversed after IL-2 was stopped. Two of six melanoma patients at 3 x 10(7) U/m2/d achieved partial responses by the end of the eighth week. This IL-2 schedule appears to produce potentially clinically useful immune enhancement with tolerable toxicity.
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PMID:A phase I clinical trial of recombinant interleukin-2 by periodic 24-hour intravenous infusions. 278 32

Nine patients with chronic hepatitis type B were treated with recombinant interleukin 2 (rIL-2). Side effects were limited to low-grade fever and headache, which were transient and tolerable for the patients. Seven normal volunteers and nine patients with chronic active hepatitis were administered by one bolus of 500 units of rIL-2. Acute effects of rIL-2 administration on lymphoid cells included a rapid decrease in lymphocytes, especially in cytotoxic T cells and natural killer cells. These acute effects resolved within 24 hours. There was no difference in the changes of immunological parameters between normal volunteers and patients. The same effects were seen during 28 days of rIL-2 administration. The number of lymphocytes and CD4 positive cells was increased after rIL-2 administration for 28 days (P less than 0.01). Natural killer cell activity, especially that of CD16+ and Leu-7- cells was also increased (P less than 0.05). These effects may favour the elimination of virus-infected hepatocytes.
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PMID:Immunologic effects on peripheral lymphoid cells from patients with chronic hepatitis type B during administration of recombinant interleukin 2. 297 35

Both complement (C) and neutrophils (PMN) are activated in critically ill patients. To evaluate the role of endotoxin in this response, we studied C activation products and PMN cell surface receptors in seven normal subjects before and after endotoxin (USRef 20 U/kg) or saline solution administered on separate occasions. By 4 hours, with endotoxin only, all subjects had myalgia, headache, an increase in body temperature and heart rate, and leukocytosis that returned to normal by 24 hours. At the same time, PMN cell surface receptors for the complement opsonin C3b increased, as measured by indirect immunofluorescence, rising to 251 +/- 44% of baseline by 4 hours (p less than 0.01) and remaining elevated at 24 hours (237 +/- 16%, p less than 0.01). PMN receptors for iC3b increased to 308 +/- 49% of baseline by 4 hours (p less than 0.02) and returned to normal by 24 hours. There was no change in plasma of C3a desArg, C4a desArg, and C5a desArg (4 hours: mean C3a: 153.4 +/- 11.5 ng/ml versus 176.2 +/- 16.2 ng/ml for saline solution, p = ns; C4a: 159.6 +/- 32 ng/ml versus 151.4 +/- 21 ng/ml, p = ns; C5a: undetectable). To confirm the lack of C activation, we examined PMN chemotaxis (CTX) to C5a for any impairment caused by prior in vivo exposure to C5a. CTX to C5a was unaffected (4 hours: 109% +/- 22% of normal versus 114% +/- 10% for saline solution, p = ns). PMN CTX to formyl-methionyl-leucine-phenylalanine and PMN phagocytosis and killing of S. aureus were also unaffected by endotoxin. Thus, a single dose of endotoxin produced a subjective febrile illness and precipitated sustained PMN activation as indicated by increased PMN cell surface complement receptor number in the absence of C activation.
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PMID:A single dose of endotoxin activates neutrophils without activating complement. 330 97

The A 3243 G mutation of the mitochondrial tRNA(Leu) gene was found to segregate with maternally inherited diabetes mellitus, sensorineural deafness, hypertrophic cardiomyopathy, or renal failure in a large pedigree of 35 affected members in four generations. Presenting symptoms almost consistently involved deafness and recurrent attacks of migraine-like headaches, but the clinical course of the disease varied within and across generations. The A 3243 G mutation has been previously reported in association with the mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode syndrome (MELAS) and with diabetes mellitus and deafness. To our knowledge, however, hypertrophic cardiomyopathy is not a common feature in people with the A 3243 G mutation and renal failure has not been hitherto reported in association with this mutation. The present observation gives additional support to the variable clinical expression of mtDNA mutations in humans.
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PMID:Point mutation of the mitochondrial tRNA(Leu) gene (A 3243 G) in maternally inherited hypertrophic cardiomyopathy, diabetes mellitus, renal failure, and sensorineural deafness. 747 62

A 16-year-old female presented with clinical, morphologic and molecular features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Her early development was normal. Starting from the age of 14 years, she experienced recurrent episodes of headaches, with vomiting, seizures, transient right hemiparesis and decreased visual acuity. Computed tomographic brain scans revealed calcification in the bilateral basal ganglia. Biopsied specimens from her left biceps brachii and rectus femoris muscles revealed ragged-red fibers and strong succinate dehydrogenase-reactive blood vessels. Electron microscopy revealed paracrystalline inclusions in muscle mitochondria. Analysis of mitochondrial DNA (mtDNA) from blood, hair follicles and muscle specimens showed an A to G point mutation at nucleotide position 3,243 in the transfer RNA(Leu(UUR)). The proportion of mutant mtDNA in the patient's blood was 43%, in hair follicles 62% and in muscle 82%. The patient was followed up for 4 years and had progressive mental deterioration and died of an episode of status epilepticus. This patient and 5 other MELAS patients reported in Taiwan are compared.
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PMID:Heteroplasmic mitochondrial DNA mutation in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. 761 32

The clinical manifestations and mitochondrial DNA (mtDNA) mutations in a Taiwanese family with a female proband exhibiting mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes syndrome are reported. Clinically, the proband had a stroke-like episode with right hemiparesis, hemianopsia and mental dysfunction as well as short stature, hearing impairments, and elevated lactate levels. Brain magnetic resonance images showed multiple increased signal intensities over the left frontal, parietal and temporal areas. There were no ragged-red fibers, but paracrystalline inclusion bodies were shown in the muscle biopsies under electron microscopic examination. A deficiency of NADH-CoQ reductase was also found in biochemical studies of the muscles. The family survey revealed no abnormal findings except for headache and episodic vomiting in her mother. The molecular analysis of mtDNA disclosed a mutation from A to G at the nucleotide pair 3243 of the mitochondrial transfer RNA(Leu) gene in the blood, hair follicles and/or muscle of the maternal relatives. A characteristic finding of the MELAS family is variation of percentage of mutated mtDNA in various tissues and individuals. However, a higher proportion of mutated mtDNA was noted in the proband than that in the asymptomatic or oligosymptomatic family members. From the data, the variable clinical phenotypes in this MELAS family can be explained at least partly, by the different proportions of mutant mtDNA in the target tissues of the proband and maternal relatives.
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PMID:MELAS syndrome: correlation between clinical features and molecular genetic analysis. 788 36


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