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)

Based on the results of quantitative isotope ventriculography (QIV) a group of 25 patients was divided into 17 hydrocephalic and 8 non- or doubtfully hydrocephalic patients. An atrio-ventricular shunt (A-V shunt) was inserted in all 25 patients. Eight of the hydrocephalic patients improved or became well, while nine hydrocephalic patients were unchanged, worse or dead at the time of follow-up. These nine patients suffered either from severe brain damage, chronic alcoholism over several years, arterial hypertension, severe diabetes, or acute meningo-encephalitis caused by a virus infection. None of the eight non- or doubtfully hydrocephalic patients improved after the operation. From this it was concluded that QIV is of considerable diagnostic value in acquired hydrocephalus.
 ...
PMID:Acquired hydrocephalus VI. The influence of some competitive diseases in the treatment of acquired hydrocephalus. 31 65

Viral infections have been implicated in the induction of diabetes mellitus in man and laboratory animals. Since virus-specific immunofluorescence (FA) is detectable in hamster pancreas during the acute phase of Venezuelan encephalitis (VE), experiments were designed to correlate pathologic and virologic events with metabolic studies in VE-infected hamsters. Golden Syrian hamsters were inoculated s.c. in groups of four to 12 with 100,000 plaque-forming units (PFU) of the vaccine strain (TC-83) of VE or 1,000 PFU of the virulent Trinidad strain of VE. Ultrastructurally, during Trinidad infection, mature virions were associated with the cell surfaces and within pancreatic beta cells in contrast to absence of virus-related changes in TC-83-infected hamsters. Virus-specific-FA was noted in islet cells and acinar cells of Trinidad-infected hamsters. VE growth curves demonstrated viral replication in pancreas with both strains. Although ultrastructural and FA changes were much more prominent in Trinidad-infected hamsters in contrast to TC-83-infected hamsters during the first few days of illness, the rapid lethality of the Trinidad-infected group necessitated performing all metabolic studies in TC-83-strain-infected hamsters. Accordingly, for the metabolic studies, glucose tolerance tests (GTT) using 2 mg. or 5 gm./kg. glucose i.p. were performed in groups of hamsters acutely infected two days earlier with the TC-83 vaccine strain and in 24-day and 90-day convalescent hamsters after TC-83 vaccine strain. Samples were obtained for glucose and immunoreactive insulin (IRI) determinations. Glucose intolerance occurred in hamsters in each of the infected groups given 5 gm./kg. glucose except for the 90-day convalescent TC-83 group. Severely decreased IRI responses occurred in the 24-day and 90-day convalescent TC-83 hamsters following both 2- and 5-gm./kg. glucose. Pancreatic IRI content in 24-day convalescent TC-83 hamsters was within normal limits, suggesting a defect in IRI release from the beta cells at this stage of convalescence.
Diabetes 1976 Jul
PMID:Virus-induced pancreatic disease by Venezuelan encephalitis virus. Alterations in glucose tolerance and insulin release. 77 26

Postmortem examination of 21 patients showed a vacuolar myelopathy resembling that associated with the acquired immunodeficiency syndrome. Underlying diseases included six cases of leukemia or lymphoma, five of carcinoma, three of systemic lupus erythematosus, two of chronic lung disease, and one each of cadaveric renal transplant, cirrhosis, diabetes, hemophagocytic syndrome, and viral encephalitis. Fourteen patients were on long-term steroid therapy and 10 of these also had immunosuppressive chemotherapy. No patient had the acquired immunodeficiency syndrome, although one received blood transfusions in 1978. Signs and symptoms consistent with myelopathy included paraparesis in seven patients, ataxia in one, and bilateral extensor plantar reflexes in one. Microscopic examination showed vacuolation in spinal cord white matter primarily located in posterior and lateral columns. Lipid-laden macrophages and axonal changes were proportional to the severity of the vacuolation, which was severe in five patients, moderate in 10, and mild in six. Eight patients had coexistent viral diseases elsewhere in the central nervous system, but viral-associated antigens or genomic material was not found in regions of vacuolated spinal cord white matter. Although the etiology of these myelopathies is unknown, their association with immune suppression and coexistent viral infection of the central nervous system suggests that an opportunistic viral infection may be important.
 ...
PMID:Idiopathic myelopathies with white matter vacuolation in non-acquired immunodeficiency syndrome patients. 186 65

B10.BR, DBA/2, and BALB/c by J mice were infected with Trypanosoma brucei rhodesiense (Lou Tat clone 1). Subsequent infection with the D variant of encephalomyocarditis virus (EMC-D) resulted in no diabetes or encephalitis, even in the susceptible DBA/2 and BALB/c by J strains. Low levels of circulating interferon (IFN) were detected in trypanosome-infected mice at the time of EMC-D infection. All strains were severely immunosuppressed as a result of trypanosome infection, as evidenced by decreased virus-specific neutralizing antibody titers, compared to virus-infected controls. We attempted to simulate some aspects of T.b. rhodesiense infection in B10.BR mice by pretreating mice with cyclophosphamide and IFN prior to EMC-D infection. Immunosuppression by cyclophosphamide greatly enhanced the pathogenesis of EMC-D, while IFN protected against the diabetogenic effect of this virus. Our results indicate that: (i) T.b. rhodesiense infection inhibited EMC-D-induced diabetes, (ii) this inhibition was not due solely to the immunosuppression generated by the trypanosome infection, and (iii) IFN generated by the trypanosome infection could play some protective role in the inhibition of EMC-D-induced diabetes by trypanosome infection.
 ...
PMID:Trypanosoma brucei rhodesiense infection in mice prevents virus-induced diabetes: possible role of interferon and immunological mechanisms. 243 62

We describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease beginning between age 21-40 years should be called "young onset Parkinson's disease." Twenty percent of such patients in our series had at least one first- or second-degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called "juvenile parkinsonism." All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.
 ...
PMID:Young onset Parkinson's disease. 350 66

Adult male ICR Swiss mice develop diabetes mellitus when infected with the D variant of encephalomyocarditis virus. It was determined that the disease syndrome caused by the virus in this mouse strain is dependent upon the age of the animals. Mice younger than 7 weeks developed lethal encephalitis, whereas those past this age developed diabetes. The susceptibility of young mice to the diabetogenic effects of encephalomyocarditis virus was enhanced by testosterone.
 ...
PMID:Virus-induced diabetes mellitus in ICR Swiss mice is age dependent. 630 84

In mice, Mengovirus produces a fatal encephalitis. Plaque purification of the virus resulted in the isolation of a clone (Mengo- 2T ), which in addition to encephalitis caused diabetes. Microscopic examination of pancreases from infected mice revealed necrosis in the islets of Langerhans and infiltration of inflammatory cells. By immunofluorescence viral antigens were found in the islets, and radioimmunoassays demonstrated a substantial decrease in pancreatic immunoreactive insulin. Studies on susceptibility among inbred strains of mice showed that whereas the D variant of encephalomyocarditis virus caused diabetes only in SJL/J mice, Mengo- 2T caused diabetes in strains of mice resistant to encephalomyocarditis-induced diabetes (i.e., CBA/J, C3H/HeJ, CE/J, AKR/J, C57BL/6J). The ability of Mengo- 2T to induce diabetes in encephalomyocarditis-resistant mice was found to be due to the greater capacity of Mengo- 2T as compared to the D variant of encephalomyocarditis virus to replicate in and destroy the islets of these animals. Although Mengo- 2T and the D variant of encephalomyocarditis virus are antigenically indistinguishable by hyperimmune sera, our studies show that these viruses have different host ranges and tissue tropisms .
 ...
PMID:Virus-induced diabetes mellitus: mengovirus infects pancreatic beta cells in strains of mice resistant to the diabetogenic effect of encephalomyocarditis virus. 632 99

This review summarizes those neurological diseases which are accompanied by a drooping of the upper lid, due to weakness of the m. levator palpebrae or m. tarsalis respectively. After connatal ptosis with or without involvement of other bulbar muscles the different types of muscular dystrophies are mentioned. Myositis, disturbances of potassium regulation and myasthenia gravis are other causes of ptosis. Diseases involving the oculomotor nerve (aneurysm, upper herniation, cavernous sinus thrombosis, orbital cavity processes, superior orbital fissure syndrome) may lead to associated ptosis. Metabolic disturbances, such as diabetes mellitus, Wernicke's encephalopathy and botulism may be accompanied by ptosis. Infectious diseases such as polyneuritis, meningitis or encephalitis can lead to ptosis. Sympatholytic ptosis is due to diseases of the central or peripheral course of the sympathetic nerve from the diencephalon via the cervical medulla, the neck, internal carotid artery to the superior orbital fissure. This type of ptosis is usually accompanied by miosis and often by sweating loss on the same side.
 ...
PMID:[Ptosis in the differential diagnosis of neurologic diseases]. 640 79

Although diabetes mellitus is generally subclassified into either of two categories, insulin-dependent (type I) and non-insulin-dependent (type II), the heterogeneity of its clinical expressions, genetics, and etiologies may make a clear distinction in classification difficult. Evidence to date for the involvement of viruses in the etiology of the disease has involved only type I diabetes. However, clinical data derived from the subtle chronicity of type II diabetes, the lack of pathological alterations in the pancreas in some patients with type II diabetes, and animal and human studies with Venezuelan encephalitis virus and rubella virus suggest a possible role for viruses in the pathogenesis of non-insulin-dependent diabetes.
 ...
PMID:Viruses may be etiologic agents for non-insulin-dependent (type II) diabetes. 668 70

Autoimmune inflammatory diseases, including many human arthritides, cause significant morbidity and mortality. The control of their immunological aspects is central to management of the diseases and usually involves drugs that are, in the immunological sense, non-specific in their effects. The efficacy of such drugs may be limited, and they may have side-effects so serious that if immunologically specific means were available to control these diseases, there would be significant benefits. Immunological specificity is carried only by antibodies, T cell receptors, MHC molecules and, of course, antigen. Based upon the experimental outcome of inducing systemic specific immunological unresponsiveness-the so-called oral tolerance effect-by feeding antigens, several groups have investigated the effects on experimental autoimmune diseases of delivering autoantigens across gastric and respiratory mucosal surfaces. Three forms of arthritis, those induced by type II collagen, adjuvant and oil, respectively, have been examined in this way, and the results from these studies show that disease can be specifically prevented or ameliorated. In parallel, examination of experimental encephalitis and uveitis, as examples of neurological diseases, and diabetes in the NOD mouse, have produced the same results. This review discusses the results of these experimental studies and draws out their common features. The uniform finding is that T cells are made hyporesponsive, and that the most likely mechanism is one of active suppression mediated through the selective activation of T cells, of either CD4+ or CD8+ phenotype, that make cytokines which in turn can suppress pathological T cells responsible for the disease lesions. There are many unanswered questions concerning optimal dosage regimes, routes and vehicles for antigen delivery and antigen pharmacokinetics that need to be answered if the promising results of early human trials are to be exploited with benefit. At the fundamental level, the full identity of the cell type, or types, responsible for the tolerance, most likely to be active peripheral suppression, is still elusive. Given the complexity of disease processes in the different situations that have been examined, it is likely that no one mechanism applies in all, and that therefore different therapeutic approaches will need to be tailored accordingly.
 ...
PMID:Oral tolerance in the control of experimental models of autoimmune disease. 766 Jun 85


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