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

Department of molecular basis of semiotics was organized in 1986. The main task of the department was to work out new approaches in estimation of the state of immune and blood system at the tissue, cell and molecular levels, using biochemical, biophysical and molecular biology techniques. There are several main directions of scientific investigations at the department. Most informational methods were collected in "immunological portrait" for differential diagnostic and complex investigation of the immune system of autoimmune patients. This group of techniques was used to study changes in the immune system of Kievites after the Chernobyl disaster. A decrease of complement and thymic serum activity was detected. Antibodies against nuclear components appeared in 20% of donors. And a higher of circulating immune complex of low molecular weight was observed. Low level of thymic serum activity in blood of autoimmune patients with rheumatoid arthritis, lupus erythematosus, diabetes, herpes and other depends on the appearance of zinc-independent timuline inhibitor less then 2000 D. Another kind of thymic hormone inhibitors was detected in thymectomized adult mice. Its effect disappears when zinc added in blood rather due to competition for lymphocyte surface receptors timuline and its inactive analogue than other mechanism. Therapeutic effect of UV irradiation of patients' blood was shown to be closely connected with the changes in thymic serum activity in respect to stabilization of thymic hormone/inhibitor ratio. The immunochemical techniques were used to detect and investigate tumor-associated chromatin antigens in human and animal tumor cells. Antigens not found in normal tissues were detected when using rabbit antibodies against chromatin of rat hepatocarcinoma and human colon and carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Department of the molecular bases of semiotics]. 757 Oct 65

A catastrophic complication after total knee arthroplasty (TKA) is rupture of the patellar tendon. Several techniques for treatment have been described, including cast immobilization with or without operative repair, the use of a semitendinosus, fascia lata, or hamstring tendon autogenous graft, the use of a Dacron 4-mm vascular graft (U.S. Catheter and Instrument, Glen Falls, NY), the use of bovine xenograft and even transplantation of an entire allograft extensor mechanism. Treatment results of patellar tendon rupture after TKA can be discouraging. Altered tissue quality secondary to connective tissue diseases, diabetes, rheumatoid arthritis, lupus erythematosus, secondary hyperparathyroidism, or concurrent steroid medications contributes to poor results. Additionally, no one treatment has provided consistent clinical success. Successful treatment of a patient with a ruptured patellar tendon after TKA using the bone-patellar tendon-bone allograft commonly used for anterior cruciate ligament reconstruction is reported.
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PMID:Use of patellar allograft to reconstruct a patellar tendon-deficient knee after total joint arthroplasty. 767 3

The authors define pro-thrombotic states as conditions associated with a high frequency of thrombosis; this association is based on pathogenetic or simply clinical and epidemiological relationships. Thrombophilic states have well-defined, specific causes: antithrombin III, protein C and S and similar deficiencies for inherited thrombophilias, and lupus anticoagulant, antiphospholipid antibodies for the acquired forms. Another identifiable group is made up of several conditions predisposing to thrombosis (CPT) characterized by less specific and multiple mechanisms (e.g. malignancy, inflammatory bowel disease, nephrotic syndrome, diabetes, obesity, etc.). These conditions may induce thrombosis by themselves or contribute to its clinical onset in patients with true thrombophilic states. This is especially the case for patients who are taking contraceptive drugs, are pregnant, have undergone surgery or trauma. The term hypercoagulability states is by no means equivalent to either thrombophilia or CPT. In fact, hypercoagulability may be defined as "activation of blood coagulation" in the presence of specific markers such as fibrinopeptide A and prothrombin fragment F1 + 2. Hypercoagulability is therefore a laboratory rather than a clinical condition and can be a transient feature appearing during certain phases of thrombophilia or CPT. Lastly, conditions involving the presence of hemostatic risk factors for atherothrombosis are simply terms used to describe a statistical-epidemiological relationship between certain hemostatic variables (fibrinogen, factor VII, PAI, etc.) involving the risk of cardiovascular morbidity and mortality but not necessarily indicating a hypercoagulability state.
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PMID:Pro-thrombotic states and their diagnosis. 800 87

Microalbuminuria in the general population is associated with recognized risk factors for cardiovascular disease such as hypertension, hyperglycemia, hyperinsulinemia, and hyperlipidemia; and it is an independent predictor of subsequent cardiovascular mortality in hypertensive, diabetic, and elderly populations. Although different methods have been used for measuring and expressing urinary albumin excretion and a variety of cutoff levels have been used for defining microalbuminuria, prevalence of microalbuminuria appears to be higher in non-Europeans (8%-28%) than in Europeans (2%-10%). However, because of the large within-individual variability of urinary albumin excretion and the relatively low prevalence of microalbuminuria, large studies are required to detect statistically significant associations between albuminuria and cardiovascular risk factors. Evidence presented here supports the proposition that microalbuminuria represents a marker of cardiovascular disease risk in nondiabetic individuals as well as diabetic individuals. Moreover, because of a high sensitivity of the test and because albuminuria is a concomitant of many forms of renal disease, microalbuminuria also has a role in detecting patients with renal involvement associated with essential hypertension, lupus erythematosus, women with pre-eclampsia, and subjects with unsuspected primary and secondary nephropathies.
J Diabetes Complications
PMID:Epidemiology of microalbuminuria in the general population. 808 51

There is now increasing evidence that the hormonal form of vitamin D, 1,25(OH)2D3, is involved in the regulation of the immune system. Local production of the hormone in various infectious diseases can benefit the immune environment. 1,25(OH)2D3 exerts most of its actions only after it has bound to its specific nuclear receptor. These receptors are present in monocytes and activated lymphocytes. The hormone inhibits lymphocyte proliferation and immunoglobulin production in a dose-dependent fashion. It also blocks the accumulation of the mRNAs for IL-2, IFN-gamma and GM-CSF. It interferes with T helper cell (Th) function, reducing Th-induction of immunoglobulin production by B-cells and inhibits the passive transfer of cellular immunity by Th in vivo. The steroid hormone promotes suppressor cell activity and inhibits the generation of cytotoxic and NK cells. The expression of Class II antigen by lymphocytes and monocytes is also affected. In vivo, 1,25(OH)2D3 is particularly effective in preventing auto-immune diseases such as experimental auto-immune encephalomyelitis, murine lupus, and diabetes in NOD mice. Synthetic analogues of vitamin D3 that bind to receptors but have no hypercalcemic effect in vivo have recently been developed for therapeutic use.
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PMID:[Vitamin D and the immune system]. 809 May 62

During intrauterine life the health conditions of the fetus are closely related to those of the mother. Hence, maternal diseases and especially endocrine-metabolic unbalances may have a negative impact on the fetus. Major maternal pathologies include: diabetes, hyperthyroidism, hypothyroidism, phenylketonuria, lupus erythematosus, epilepsy and antiepileptic drugs.
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PMID:Maternal diseases and congenital malformations. 812 74

Gestational diabetes resistant to insulin therapy occurring in association with insulin receptor antibodies has not been reported previously. A patient developed diabetes mellitus at 21 weeks' gestational age and had a previous history of thrombotic thrombocytopenia purpura, then in remission. She developed life-threatening diabetic ketoacidosis that was severely resistant to insulin treatment despite the usage of adjunct therapy, including plasmapheresis, and intravenous cyclophosphamide and steroids. She also had lupus nephropathy. Termination of the pregnancy at 22 weeks' gestation resulted in a rapid resolution of both the diabetes and lupus nephropathy.
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PMID:Gestational diabetes mellitus with profound insulin resistance. A case report. 816 28

The work presented in this review suggests that in human and murine type I diabetes, defective MHC class I expression on APC is linked to autoimmunity. The defect in self-antigen presentation is present on prediabetic and diabetic APC, and this presumably delivers abnormal or lack of signals to T cells to allow self tolerance. Since most autoimmune diseases have strong genetic linkage to MHC class II region, our recent results additionally demonstrating low MHC class I expression on lymphoid cells in a diversity of autoimmune diseases (hypothyroidism, rheumatoid arthritis, lupus, etc.) suggest that this pathway of abnormal class I presentation of self epitopes may be important for tolerance to many tissue-specific antigens (40). Certainly, the unanswered genetic questions will address the role of the specific genes controlling self-antigen presentation through MHC class I followed by T-cell education to self.
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PMID:Mechanisms of autoimmunity in type I diabetes. 844 41

In the gastroenterological diagnostic armamentarium, dysphagia is considered as an important symptom for diseases of the esophagus. Concerning the history of illness, symptoms such as retrosternal pain and heartburn are often associated with gastroesophageal reflux disease. Morphological changes of the mucosa can be diagnosed by flexible endoscopy and radiographic examinations. Investigation with 24-h pH monitoring, manometry, and pharmacological tests is necessary for the diagnosis of functional disorders. Additionally, dysphagia can be associated with multiple internal diseases, including muscular diseases such as dermatomyositis, progressive systemic sclerosis, as well as lupus erythematosus. Difficulties in swallowing associated with hypo- and hyperthyroidism can also be interpreted as muscular lesions. Metabolic disorders such as alcoholism, and diabetes mellitus can be the cause of dysphagia. Increasing importance in the differential diagnosis of dysphagia is attached to infections of the upper GI tract. Especially in immunocompromised patients, infections of Candida albicans, mycobacterias, herpes, varicella zoster, and cytomegaloviruses can produce dysphagia and odynophagia. The differential diagnosis of the "angina-like chest pain" has to differentiate between cardiac disease and a noncardiac genesis. Therefore, besides the cardiac diagnostic investigation, endoscopy, radiography, and manometry are often indicated.
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PMID:The gastroenterologist's approach to dysphagia. 846 28

The CD4 molecule represents a major functional T-cell surface molecule, defining an important T-cell subset, which also is expressed on monocyte, dendritic, and Langerhans cells. Various in vivo studies have demonstrated its implication in various steps of physiological T-cell activation: 1. CD4 interacts with its physiological ligand, the class II molecules, thus increasing the affinity of the conjugation between CD4+CD(3+)-TCR+ and class II+ antigen-presenting cells. 2. Through CD4, the signal transduction machinery is stimulated via its association with p56lck. In addition, CD4 has proved to be the receptor for gp120, the surface glycoprotein of HIV, that allows the virus to penetrate the CD4+ T cells and monocytes. Based on in vitro studies in various animal models, CD4 mAbs have proved to be efficient in the prevention and/or therapy of a variety of immunologically based diseases: 1. When injected early in the prodromic phase of autoimmune diseases (AID) such as diabetes, either delay or prevention is achieved with or without maintenance after therapy. 2. These mAbs have proved to be self-tolerogenic, thus allowing prolonged in vivo therapy and suppression of immunogenicity of mAb of a distinct specificity. In humans, CD4 mAbs are, or could be, used and evaluated in AID (lupus, diabetes, rheumatoid arthritis, etc.), transplantation, leukemias and lymphomas expressing CD4, and, finally, in AIDS patients, in whom CD4 mAbs can block HIV-CD4 binding and deliver a negative signal to T cell, thus blocking T-cell activation and HIV transcription. CD4 mAbs at least provide evidence that the CD4 molecules are suitable for immunomodulation and could be the target for a new pharmacological antagonist.
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PMID:Therapeutic applications of anti-CD4 antibodies. 847 11


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