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)

Infectious disease of the spine is infrequently seen in the rehabilitation setting. We examined retrospectively 26 patients with spinal infections admitted to the rehabilitation centre over a 6-year period to determine the demographic characteristics, clinical features and outcome after rehabilitation. Their ages ranged from 24 to 83 years (mean = 56.4); 65.4% were males. The infection was due to pyogenic bacteria in 14 patients (53.8%) and Mycobacterium tuberculosis in 12 (46.2%). Staphylococcus aureus was the causative agent in 69% of those with pyogenic infections. A history of diabetes mellitus was present in 35.7% of the pyogenic group but in only 8.3% of the tuberculous group. Localised back pain, fever and neurological deficits were the typical clinical manifestations. The most common site of infection was the thoracic region. Surgery was performed on 24 patients and all received prolonged courses of antibiotics. All but three patients completed the rehabilitation programme. The motor score for the lower limbs and the modified Barthel scores for activities of daily living (ADL) and mobility improved significantly (P < 0.05) for both pyogenic and tuberculous groups. The amounts of improvement achieved were not significantly different between the pyogenic and tuberculous groups except for ADL. Age, gender and the presence of diabetes mellitus did not appear to significantly affect the neurological or functional outcome in our study population. The majority of patients (87.5%) were discharged to their own homes.
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PMID:Infectious disease of the spine: outcome of rehabilitation. 967 Mar 88

Long chain fatty acids (LCFAs) are an important source of energy for most organisms. They also function as blood hormones, regulating key metabolic functions such as hepatic glucose production. Although LCFAs can diffuse through the hydrophobic core of the plasma membrane into cells, this nonspecific transport cannot account for the high affinity and specific transport of LCFAs exhibited by cells such as cardiac muscle, hepatocytes, and adipocytes. Transport of LCFAs across the plasma membrane is facilitated by fatty acid transport protein (FATP), a plasma membrane protein that increases LCFA uptake when expressed in cultured mammalian cells [Schaffer, J. E. & Lodish, H. F. (1994) Cell 79, 427-436]. Here, we report the identification of four novel murine FATPs, one of which is expressed exclusively in liver and another only in liver and kidney. Both genes increase fatty acid uptake when expressed in mammalian cells. All five murine FATPs have homologues in humans in addition to a sixth FATP gene. FATPs are found in such diverse organisms as Fugu rubripes, Caenorhabditis elegans, Drosophila melanogaster, Saccharomyces cerevisiae, and Mycobacterium tuberculosis. The function of the FATP gene family is conserved throughout evolution as the C. elegans and mycobacterial FATPs facilitate LCFA uptake when overexpressed in COS cells or Escherichia coli, respectively. The identification of this evolutionary conserved fatty acid transporter family will allow us to gain a better understanding of the mechanisms whereby LCFAs traverse the lipid bilayer as well as yield insight into the control of energy homeostasis and its dysregulation in diseases such as diabetes and obesity.
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PMID:A family of fatty acid transporters conserved from mycobacterium to man. 967 28

NOD mice spontaneously develop autoimmune diabetes. One of the manipulations that prevent diabetes in NOD mice is infection with mycobacteria or immunization of mice with mycobacteria-containing adjuvant. Infection of NOD mice with Mycobacterium avium, done before the mice show overt diabetes, results in permanent protection of the animals from diabetes and this protective effect is associated with increased numbers of CD4+ T cells and B220+ B cells. Here, we investigate whether the M. avium-induced protection of NOD mice from diabetes was associated with changes in the expression of Fas (CD95) and FasL by immune cells, as well as alterations in cytotoxic activity, interferon-gamma (IFN-gamma) and IL-4 production and activation of T cells of infected animals. Our data indicate that protection of NOD mice from diabetes is a Th1-type response that is mediated by up-regulation of the Fas-FasL pathway and involves an increase in the cytotoxicity of T cells. These changes are consistent with induction by the infection of regulatory T cells with the ability of triggering deletion or anergy of peripheral self-reactive lymphocytes that cause the autoimmune disease of NOD mice.
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PMID:Mechanisms of Mycobacterium avium-induced resistance against insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice: role of Fas and Th1 cells. 993 49

Fifteen isolates of Mycobacterium kansasii in Showa University Fujigaoka Hospital between 1982 and 1995 were investigated. Comparing by gender, 13 were isolated from male patients and only two were isolated from female patients. The average of cases was 48 years old and 14 out of 15 cases (93%) were isolated from respiratory tract specimens. The rate of the smear- and culture-positives was 64%, which was significantly higher than that (26%) of M. avium complex (p < 0.01 by chi 2 test). All 4 isolates were susceptible to rifampicin (10 micrograms/ml) by drug susceptibility testing using Ogawa egg medium, and only 1 was resistant to ethambutol (2.5 micrograms/ml). Seven out of 10 patients whose medical record was available were diagnosed as pulmonary infection with M. kansasii. Two out of 4 patients with primary infection type had underlying diseases such as diabetes mellitus and leukemia, while the remaining two patients did not have any underlying disease. Two out of 3 patients with secondary infection type had a medical history of tuberculosis and the remaining 1 patient had infected pulmonary cyst. Such as Pseudomonas aeruginosa, Enterobacter aerogenes and Flavobacterium spp., and Branhamella catarrhalis, associated with M. kansasii, bacteria more than 10(7) cfu/ml were isolated from the sputa of 3 patients with leukemia, infected pulmonary cyst and post-tuberculosis, respectively. M. kansasii, Stenotrophomonas maltophilia (10(7) cfu/ml) and Candida albicans were detected from the sputum of 1 patient with nephrosis, for which steroid (predonin) and antibiotics (piperacillin and latamoxef) were administrated, however, this patient was not diagnosed as a case of M. kansasii infection. These findings suggest the fact that M. kansasii inhabits among compromised hosts of a city hospital.
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PMID:[Evaluation of Mycobacterium kansasii isolates from a clinical laboratory in a city hospital]. 1006 52

The incidence of tuberculosis in The Kingdom of Saudi Arabia remains high. The objective of this study is to determine the prevalence of Tuberculosis among haemodialysis patients, since they are highly susceptible to this infection. A retrospective study, over a 5-year period, was carried out in the Renal Units of two large hospitals in Jeddah. Diagnosis was established by Ziehl Neelsen microscopy and culture of specimens on Lowenstein-Jensen media, radiological and histological examinations. Tuberculosis was diagnosed in 17 of 210 patients on hemodialysis. Pulmonary tuberculosis was present in 10 cases and tuberculous lymphadenitis in 8 cases. One patient had both pulmonary and lymph node involvement while another one had both pulmonary and peritoneal tuberculosis. Mycobacterium tuberculosis was diagnosed in sputum in 5 cases, by lymph node histopathology in 5 cases, and combined radiological and clinical evidence in the remaining patients. The Mantoux test was positive in 9 (60%) cases. Eight patients were diabetics (47%) and there appears to be some association of tuberculosis with diabetes in patients on dialysis. Treatment with first-line anti-tuberculosis agents was continued for 6-18 months. Fourteen (82%) patients were completely cured while 3 showed clinical improvement only. The study showed that successful therapy of tuberculosis in this group of dialysis patients could be achieved but high index of suspicion is required to recognize the unusual presentation in this group of patients so that early diagnosis can be achieved and prompt treatment instituted. Diabetic patients presenting for dialysis, in areas with high endemicity for tuberculosis, chemoprophylaxis with anti-tuberculosis agents should be considered.
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PMID:Tuberculosis in active dialysis patients in Jeddah. 1008 47

Non-obese diabetic (NOD) mice spontaneously develop autoimmune insulin-dependent diabetes mellitus (IDDM). Infection of the animals with mycobacteria, or immunization with mycobacteria-containing adjuvant, results in permanent protection of NOD mice from diabetes and we have recently reported that the phenomenon is associated with increased numbers of interferon-gamma-producing T cells, possessing increased cytotoxic activity, and also with augmented numbers of activated immunoglobulin M-positive (IgM+) B cells. Here, we have investigated whether protection of NOD mice from IDDM was associated with changes on costimulatory pathways of T and B cells, namely CD28/CTLA-4-B7 and CD40-CD40 ligand (CD40L) and we also further characterized protective T helper (Th) cells with regards to the expression of the differentiation markers CD45RB and CD38. We report that Th cells involved in diabetes vaccination of NOD mice by mycobacterial infection seem to belong to CD45RBlo CD38+ phenotype. The protective effect of Mycobacterium avium infection is also associated with increased CD40L and CTLA-4- expressing Th cells and with the generation of a CD40- IgG+ B cells. Our data are consistent with induction by mycobacterial infection of regulatory CD45RBlo CD38+ Th cells with the ability to trigger deletion or anergy of peripheral self-reactive lymphocytes, with shutting down of IgG+ B-cell response. They also implicate a role for IgG+ B cells in the autoimmune aggression of the endocrine pancreas of NOD mice.
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PMID:A role for CD45RBlow CD38+ T cells and costimulatory pathways of T-cell activation in protection of non-obese diabetic (NOD) mice from diabetes. 1023 47

The nonobese diabetic (NOD) mouse, a model of spontaneous insulin-dependent diabetes mellitus (IDDM), fails to express surface MHC class II I-Eg7 molecules due to a deletion in the E alpha gene promoter. E alpha-transgenic NOD mice express the E alpha E beta g7 dimer and fail to develop either insulitis or IDDM. A number of hypotheses have been proposed to explain the mechanisms of protection, most of which require peptide binding to I-Eg7. To define the requirements for peptide binding to I-Eg7, we first identified an I-Eg7-restricted T cell epitope corresponding to the sequence 4-13 of Mycobacterium tuberculosis 65-kDa heat shock protein (hsp). Single amino acid substitutions at individual positions revealed a motif for peptide binding to I-Eg7 characterized by two primary anchors at relative position (p) 1 and 4, and two secondary anchors at p6 and p9. This motif is present in eight of nine hsp peptides that bind to I-Eg7 with high affinity. The I-Eg7 binding motif displays a unique p4 anchor compared with the other known I-E motifs, and major differences are found between I-Eg7 and I-Ag7 binding motifs. Analysis of peptide binding to I-Eg7 and I-Ag7 molecules as well as proliferative responses of draining lymph node cells from hsp-primed NOD and E alpha-transgenic NOD mice to overlapping hsp peptides revealed that the two MHC molecules bind different peptides. Of 80 hsp peptides tested, none bind with high affinity to both MHC molecules, arguing against some of the mechanisms hypothesized to explain protection from IDDM in E alpha-transgenic NOD mice.
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PMID:A peptide binding motif for I-Eg7, the MHC class II molecule that protects E alpha-transgenic nonobese diabetic mice from autoimmune diabetes. 1035 80

We revised retrospectively 30 cases of Spontaneous Infectious Spondylodiskitis (SIS) in adults, diagnosed between 1986 and 1997. The mean age of the patients was 68.8 years; 56.7% were males. The identifiable causes were infectious endocarditis 13 (43.3%); tuberculosis 7 (23.3%); urinary tract infection 4 (13.3%); bacteremia with focus 2 (6.7%) and without focus 2 (6.7%). The cause was not identified in other 2 cases (6.7%). Infections were due to pyogenic bacteriae in 19 (63.3%); tuberculosis 6 (20%) and unknown 5 (16.7%). All patients had localized pain, 70% fever, 36.7% irradiated pain and 23.3% paraparesis. Fever was more frequent in patients with pyogenic etiology than in those with tuberculous SIS (p = 0.004). Blood cultures were positive in 70.4%. Percutaneous aspiration of the disc was performed in 13 patients; cultures were positive in 7. Causal germs were Streptococcus spp. 33.3%; Mycobacterium tuberculosis 20%; Staphylococcus spp. 16.6%; Escherichia coli 6.6%; Pseudomonas aeruginosa 6.6%. There was no bacteriological recovery in 5 (16.7%). Localization was lumbar in 18 (60%), dorsal in 8 (26.6%) and cervical in 4 (13.3%). X-ray of the spine was positive in 63.3% of the cases. Technetium scan in 90.5%, CT in 85.7% and MRI in 100% of cases in which it was carried out. All patients received antibiotic treatment with a median duration of 6 weeks for pyogenic SIS and one year for tuberculous SIS. Eighty three percent required immobilizing brace and 10% surgery for stabilization. Thirty six percent of patients presented complications, most of them related to the causal disease. There was a statistically significant association between mortality and diabetes.
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PMID:[Spontaneous infectious spondylodiscitis in adults. Analysis of 30 cases]. 1041 91

NOD mice spontaneously develop autoimmune diabetes; disease onset in females of our colony of NOD mice usually takes place around the 4th month of age. Diabetes of NOD mice can be modulated by different stress protocols, even though these animals were shown to be resistant to the effects of glucocorticoids on their lymphocytes. We have recently found that the early host inflammatory response to mycobacteria can be strongly modified by stress, the autoimmunity-prone NOD and NZB/W mice being particularly affected. These mice show reduced numbers of granulocytes in the inflammatory cavity after exposure to stress. Mycobacterium avium is an opportunistic agent that is responsible for disseminated infections seen in AIDS patients. Here, we investigated whether the early immune response to M. avium was altered by stress in NOD mice and we compared the stress response of these mice with a non-autoimmune strain, BALB/c mice. The effects of stress on infected BALB/c mice, which like AIDS patients are susceptible to M. avium infection, offers experimental evidence that M. avium infection, if coupled with stress of the host, may accelerate loss of T helper cells. In contrast, in NOD mice, stress or infection significantly increased the number of cells of the thymuses of the animals. Data obtained with NOD mice support the previously reported resistance of NOD mice lymphocytes to glucocorticoids and suggest that there are two distinct signalling pathways involved in the response of NOD lymphocytes to these stress hormones: one leading to apoptosis and the other mediating glucocorticoid inhibition of activation-induced cell death.
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PMID:NOD mice are resistant to depletion of thymic cells caused by acute stress or infection. 1043 83

The causes of unsatisfactory result of treatment in 125 patients with pulmonary tuberculosis and diabetes mellitus (DM) are presented. In every patient were revealed 2-4 and more nonfavourable factors, influencing the chemotherapy inefficacy. The main of them are: the severity of the DM course and of its complications, the patient's noncompliance of the treatment, the spreading of tuberculosis, the resistance of the tuberculosis Mycobacterium to preparations.
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PMID:[Causes of ineffective chemotherapy of pulmonary tuberculosis in patients with diabetes mellitus]. 1058 90


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