Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Class II major histocompatibility complex molecules are critical in both normal and abnormal immune responses. Both in mice and in humans, these molecules have been implicated in the development of various diseases, including insulin-dependent diabetes mellitus and systemic lupus erythematosus. The MRL/lpr mouse strain spontaneously develops a lupus-like illness with features that include anti-DNA antibodies, glomerulonephritis, and early death. We evaluated the structure of class II molecules from these mice, to investigate for unique sequences that might contribute to autoimmunity. Utilizing the polymerase chain reaction, we sequenced the second exons from the I-A and I-E genes of MRL/lpr and MRL-+/+ mice. We found that at the nucleotide level, there are several changes between MRL class II genes and the previously sequenced "k" haplotype, but at the protein level, they are identical. Furthermore, by comparing the sequences of class II genes from several strains of autoimmune mice, we found that there are conserved amino acids in the third hypervariable region of the I-E beta chain which may be important in the development of autoimmunity.
 ...
PMID:Sequence of class II major histocompatibility complex genes from MRL mice. Conserved amino acids in the I-E beta chains from autoimmune mice. 195 19

Several studies have demonstrated abnormalities of T cell regulation of Epstein-Barr virus-induced B cell activation in systemic autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematous, and systemic sclerosis. However, a normal suppressive peripheral T cell function was observed in Graves' disease. To investigate whether this abnormality is a common feature to other autoimmune diseases, we studied T cell regulation of Epstein-Barr virus induced B cell activation in 15 newly diagnosed type 1 (insulin dependent) diabetes mellitus patients and 10 normal control subjects. Peripheral B lymphocytes infected with Epstein-Barr virus were cultured for 20 days in the presence or absence of autologous T cells at different ratios (1:1 and 1:4). IgM and IgG secretions into the supernatants were determined using an enzyme-linked immunosorbent assay. The extent of suppression when T cells were added, as measured by a suppression ratio, was not significantly different in type 1 (insulin dependent) diabetes mellitus patients and normal subjects. We conclude that in type 1 (insulin dependent) diabetes mellitus, the autoimmune reactivity is not dependent upon a generalized suppression defect. It can be hypothesized, therefore, that in type 1 diabetes mellitus as well as in Graves' disease, a local or organ specific suppressor deficit may induce the autoimmune phenomena.
 ...
PMID:Normal suppressive T cell function of Epstein-Barr virus induced B cell activation in type 1 (insulin dependent) diabetes mellitus. 196 82

The availability of alternative therapies for many health problems is a well-documented historical fact. Alternative therapies are generally understood to be those therapies outside of the usually accepted medical therapies for disease processes, such as cancer, arthritis, diabetes, psoriasis, lupus, and AIDS. Some other descriptive terms utilized include questionable, unproven, dubious, unorthodox, and unconventional. These alternative therapies vary from active involvement in promotion of one's own health (exercise, diet) to quackery. In today's society, with emphasis on self-involvement with individual health, metabolic therapies have become the most widely practiced alternative therapy. In an antiestablishment, anti-intellectual climate, with an increasingly mobile, rootless population, alternative therapies are in somewhat of a renaissance. Some confusion exists regarding clinical trials and alternative therapies in the general population and in the noninvolved health profession. Various studies indicate that from 10% to 50% of cancer patients use some alternative therapy, with national expenditures ranging as high as $10 billion annually. Better-educated patients with higher-than-average income are more likely to choose alternative therapies and are frequently supported by a physician in this choice. Most cancer patients continue under a physician's care and continue usual therapy while pursuing alternative methods. Approximately 5% of cancer patients abandon appropriate therapy and pursue potentially harmful alternative methods. A variety of sociomedical questions are brought forth by studies of the use of alternative therapies. A great need for public and professional education regarding this subject is evident.
 ...
PMID:Alternative therapies, 1990. An overview. 200 79

A patient had acquired perforating dermatosis and suffered from renal disease, diabetes mellitus, and lupus vulgaris. Histologic and immunohistochemical studies revealed that the bulk of the coarse granular basophilic material being extruded by transepidermal elimination was of nuclear origin obviously derived from polymorphonuclear leukocytes that were particularly abundant in an early, nonperforated lesion. At the lower boundary of the material being eliminated transepidermally, leukocytes were seen to accumulate, to undergo pyknosis and karyorrhexis, and to transform into nuclear debris. As a minor component, the material contained collagen fibers with altered staining qualities and, in an early lesion, elastic fibers. We speculate that accumulation, disintegration, and enzyme release from polymorphonuclear leukocytes may represent an important, hitherto disregarded driving force in transepidermal elimination. Lysosomal enzymes may later be responsible for the alteration of staining properties in collagen fibers, the degradation of elastic fibers, and for opening up the transepidermal route by impairing intercellular keratinocyte cohesion.
 ...
PMID:Acquired perforating dermatosis. Transepidermal elimination of DNA material and possible role of leukocytes in pathogenesis. 202 88

There are a number of mechanisms which cooperate to produce and maintain T-cell tolerance. First, and perhaps most important, is the clonal deletion in the thymus of T cells with high affinity for self antigens. However, to ensure that a wide repertoire of T cells is available in the periphery to combat foreign antigens, the threshold of clonal deletion may be set low enough so that T cells whose TCR's have sub-threshold affinity for self antigens mature and migrate to the periphery. T cells which recognize self antigen-derived peptides not expressed or presented in the thymus will also fail to be deleted. For those self-reactive T cells which are not deleted in the thymus, other mechanisms may produce tolerance, including an undefined alteration of signalling pathways which produces clonal anergy, and lowering the avidity of the TCR for its ligand by downregulating coreceptor and accessory molecules. Active suppression of T-cell responses in another well-described phenomenon whose mechanism is undefined. From our observations with the model systems discussed here, we have observed three distinct mechanisms by which T-cell tolerance can be circumvented, allowing autoimmune phenomena to occur. These mechanisms may have relevance for different types of autoimmune diseases seen in humans. In gld mice, the autoimmune disease seems to be related to a global defect in T-cell differentiation and function, which allows for the expansion of autoimmune B cells. While we showed that clonal deletion of V beta-bearing T cells is appropriate in certain cases, aberrant lymphokine secretion by the abnormal T cells or disruption of immune system regulation are most probably responsible for allowing autoantibody production. While human lupus erythematosis shares much of the pathology of lpr and gld mice, there is no expansion of T cells with a similar phenotype in human lupus. There are environmental factors which must play a role in the development of human lupus, since the incidence of the disease does not follow an absolute genetic pattern. The escape from clonal deletion and subsequent reactivation of autoimmune T cells which we observed in V beta 8.1 TCR-transgenic mice can be a model for human autoimmune diseases such as multiple sclerosis and type I diabetes, in which T cells are directed against a specific autoantigen. According to this model, susceptibility loci for autoimmune disease such as the MHC would function by producing different repertoires of T cells which in some cases could gain autoreactivity following activation.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Mechanisms of autoimmunity in the context of T-cell tolerance: insights from natural and transgenic animal model systems. 215 Apr 1

The murine alloantigen, Ly-6C, is found on 45% of bone marrow cells, 25% of splenocytes and 15% of lymph node cells in all inbred strains of mice tested, with the exception of NOD, NZB and ST. In these three strains, Ly-6C expression can be detected on only 5% of bone marrow cells and not at all on cells from spleen or lymph node. NOD and NZB, which are models for the autoimmune diseases, diabetes and lupus, respectively, also exhibit a depressed syngeneic mixed lymphocyte reaction. Southern blot analysis reveals a restriction fragment length polymorphism involving the Ly-6C gene which is unique to these three strains. Cloning of the affected genomic segment from the NOD mouse indicates the presence of an interruption in the flanking region of the Ly-6C gene at a point 475 bp upstream of the transcription initiation site and the consequent separation of distal 5' sequences from the body of the gene by at least 10 kb. Inspection of the recombination borders reveals a set of inverted copies of a mouse repetitive R element. Transfection of the Ly-6C genes from NOD and BALB/c into a murine carcinoma line indicates relative functional impairment of the NOD gene, thus paralleling performance in vivo.
 ...
PMID:A recombination event in the 5' flanking region of the Ly-6C gene correlates with impaired expression in the NOD, NZB and ST strains of mice. 216 72

The NOD mouse is a model of human juvenile type I diabetes mellitus. As in humans and in the BB rat model, the development of diabetes in NOD mice is accompanied by evident manifestations of cell-mediated and humoral autoimmunity. Beside autoantibodies directed at putative islet cell antigens, NOD sera contain antibodies with specificity for lymphocyte cell-surface determinants. Here we demonstrate that these anti-lymphocyte antibodies have the same characteristics of target cell specificity, of isotype, and of temperature reactivity, as do natural thymocytotoxic autoantibodies (NTA) from lupic NZB mice, or from mice undergoing polyclonal B cell activation. We also demonstrate that the thymocytotoxic activity of NOD sera is not due to cross-reactive anti-insulin antibodies. Biochemical characterization of the determinants recognized by these anti-lymphocyte antibodies reveals two membrane-associated proteins of 28 and 33 kD, partially similar to the two peptides recognized by NTA from NZB mice (30 and 33 kD). Altogether, these results suggest that NOD mice develop manifestations of polyclonal B cell activation similar to those observed in lupus-prone mice. The relationship of these anomalies with the organ-specific pancreatic disease remains to be properly evaluated.
 ...
PMID:Natural thymocytotoxic autoantibodies in non-obese diabetic (NOD) mice: characterization and fine specificity. 239 10

In the period from 1980-86 we obtained 51 strains of Listeria from meningitis in adults for serotyping and phage-typing. Ten strains were associated with meningitis and 3 with septicaemia of immunocompromised patients. They suffered from leukaemia, diabetes, Hodgkin's disease, alcoholism, lupus erythematodes. The lethality rate in these patients was 70%, in other patients with meningitis 30%. Phage typing has shown that 4b strains were often determined by the phage-code 00010 and similar codes. This phage-pattern might be specific for meningitis strains. The immunocomprised patient is especially endangered in taking up listeriae from the environment, but it must also be in consideration that listeriae may easy gain access from the gut into the vessels.
 ...
PMID:Listeria-meningitis and -septicaemia in immunocompromised patients. 251 62

Primary pulmonary cryptococcal granuloma is not common in Sichuan. The diagnosis of this disease is difficult to make because the patient has no characteristic symptoms and the chest X-ray findings of the mass are not easily differentiated from carcinoma of the lung. The incidence of this disease is apparently increasing. Pulmonary cryptococcosis may be disseminated hematogenously to the meninges and cryptococcal meningitis is very difficult to treat. If the pulmonary lesion is localized, the patient's general condition is good with no evidence of systemic lupus erythematosis, diabetes, leukemia or lymphoma, partial resection of the lung is indicated. But, if the patient has a history of recent cryptococcal meningitis, surgery must be deferred. Four cases of primary pulmonary cryptococcal granuloma have been treated surgically supplemented with medical therapy in the First Affiliated Hospital from 1986 to 1987. Follow-up of more than one year showed good results in each case.
 ...
PMID:[Surgical treatment of primary pulmonary cryptococcal granuloma--report of 4 cases]. 259 37

During a survey period of 28 years a total of 449 patients suffering respectively from pemphigus, systemic lupus erythematous and chronic nephritis was admitted to the hospital. Of the 286 patients who received glucocorticoid treatment 28 were found to have steroid diabetes (9.8%). The incidences of steroid diabetes in these diseases were as follows: pemphigus 20% (7/35), systemic lupus erythematous 12.5% (14/112), chronic nephritis 5% (7/139). Two thirds of the diabetic subjects appeared asymptomatic, while the remainder showed polydipsia and polyuria. Renal glucosuria was seen in 3 cases and hyperosmolar hyperglycemia in 4. Blood glucose level in 10 out of the 21 remaining cases was 8.9 +/- 1.5 mmol/L and in the other 11 cases 14.8 +/- 2.4 mmol/L. Generally, the treatment of steroid diabetes is not intricate. Satisfactory improvement was seen in about 80% of the patients if a strict line of therapy against primary diabetes was oriented. In this series 18 patients did well under the treatment either with reduction of steroid or with use of oral hypoglycemic agents or insulin or both. Their blood glucose levels returned to normal and urine sugar disappeared rapidly. Four of the 5 deaths were caused by their primary diseases. One died of pemphigus complicated with infection and shock exhibiting an ante mortem blood glucose level as high as 31.7 mmol/L, obviously hyperosmolar status being the predisposing factor. Due to the fact that most of the steroid diabetic patients were clinically asymptomatic, delayed or misbranded diagnosis was not infrequently seen.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Steroid diabetes: an analysis of 28 cases]. 280 46


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>