Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genetically diabetic db/db mouse is a model of type-2 diabetes, where nephropathy and neuropathy, but not retinopathy were observed. The authors studied the retinas (trypsin digestion technique) of 16 db/db mice and 16 age-matched litter mates (db/m; controls), divided into five age groups. They noted a marked increase in the ratio of endothelial cells to intramural pericytes in diabetic mice compared to controls. This increase resulted from a selective and highly significant loss of pericytes in db/db mice (p less than 0.05). Some strand-like and relatively acellular capillaries were also observed. The db/db mouse may represent an adequate model for studies on the pathogenesis of retinopathy.
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PMID:Studies on the retina of the diabetic db/db mouse. I. Endothelial cell-pericyte ratio. 273 1

The sera of 9 patients with benign IgM paraproteinaemia and chronic sensorimotor neuropathy were tested for reactivity to human peripheral nerves by the indirect immunoperoxidase method. They reacted in very high titre (10(-3)-10(-6) with a cytoplasmic Schwann cell component, and to lesser degree, with peripheral nerve myelin (10(0)-10(-3). The Schwann cell staining was in the form of perinuclear cytoplasmic granules and was only seen with adult nerve. The distribution of the antigen was similar to that of the metachromatically staining Pi-granules of Reich, which accumulate in the peripheral nerves with age. Specific activity was present in the IgM and F(ab)2 fractions and could be absorbed out with peripheral nerve tissue, but not with liver. Reactivity is not a simple function of the IgM level, since many IgM paraproteins do not react. The antibody is species specific and binds to human, but not to any component of rabbit, rat or guinea pig sciatic nerves. Antigenicity is removed by pretreatment of the nerve with chloroform-methanol or periodate, but not protease or trypsin. Reactivity is restored, after periodate treatment, by exposure to sodium borohydride. It is suggested that some IgM paraproteins have a specificity for a myelin glycolipid or glycoprotein, which normally accumulates in the Pi-granules of the Schwann cell cytoplasm as a function of age.
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PMID:IgM paraproteins with immunological specificity for a Schwann cell component and peripheral nerve myelin in patients with polyneuropathy. 618 71

Plasma levels of active and trypsin-activatable inactive renin and catecholamines were measured in 6 diabetic patients with neuropathy (group 1), 8 diabetic patients without neuropathy (group 2) and 8 age-matched normal subjects. The effect of insulin administration on plasma active and inactive renin and plasma catecholamine levels in diabetic patients was also investigated. The levels of inactive renin were calculated as the difference between the levels of total renin after trypsin activation and those of active renin. The levels of plasma catecholamines were determined by the trihydroxyindole method. The levels of active renin were significantly lower and inactive renin was increased slightly in group 1 when compared with controls. Group 1 showed a significant reduction in plasma norepinephrine levels. Group 2 showed slightly reduced active renin, normal inactive renin and normal norepinephrine values. There was no significant difference in the levels of epinephrine between the 3 groups. After insulin injection, active renin levels were increased in groups 1 and 2. The mean increment in active renin levels was less in group 1 than in group 2. Inactive renin levels were slightly decreased in both groups. Significant increases in epinephrine and norepinephrine levels were observed following insulin administration. The mean increment in norepinephrine levels was less in group 1 than in group 2. There was a positive correlation between the mean increment in active renin and in norepinephrine levels in diabetic patients. These results suggest that the impaired conversion of inactive renin into an active form is responsible in part for the low levels of active renin in diabetics with neuropathy.
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PMID:Plasma inactive renin in diabetic patients with neuropathy: a role for the sympathetic nervous system in the conversion in vivo of inactive renin. 635 43

HTLV-1 (human T-cell leukemia virus type I) associated myelopathy (HAM) is a demyelinating disease. We showed that the CSF of patients and heated CSF of normal subjects induce a segmentary demyelination in rat nerves, and potentiate trypsin in vitro. Here we further characterize the neuropathy induced by the CSF of patients. Peroneal nerves injected 5-8 days before with native or heated CSF of patients, besides extensive demyelination, presented proliferation of myelinating and nonmyelinating Schwann cells, axonal sprouting, fine fibres with a few turns of myelin, disarray of nonmedullated bundles, desmosome-like junctions, and coated pits and vesicles in Schwann cells and axons. The normal CSF was innocuous to the nerve in its native form, but after heating, it induced a neuropathy in all, similar to that elicited by the CSF of patients. Our findings indicate that the CSF of HAM patients contains a thermostable pathogen for nerves of the rat; a thermostable pathogen also occurs in the normal CSF although its activity is checked by endogenous thermolabile factors. We suggest that the pathogen present in the CSF of HAM patients participates in the disease.
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PMID:Cerebrospinal fluid of HTLV-1 associated myelopathy patients induces axonal sproutings and Schwann cell proliferation in the rat sciatic nerve. 970 Jun 98

We hypothesized that sera from type 2 diabetic patients with neuropathy contains an autoimmune immunoglobulin that promotes complement-independent, calcium-dependent apoptosis in neuronal cell lines. Neuronal cells were cultured in the presence of complement-inactivated sera obtained from patients with type 2 diabetes with and without neuropathy and healthy adult control patients. Serum from diabetic patients with neuropathy was associated with a significantly greater induction of apoptosis, compared to serum from diabetic patients without neuropathy and controls. In the presence of calcium channel antagonists, induction of apoptosis was reduced by approximately 50%. Pretreatment of neuronal cells with serum from diabetic patients with neuropathy was associated with a significant increase in elevated K+-evoked cytosolic calcium concentration. Serum-induced enhancement in cytosolic calcium and calcium current density was blocked by treatment with trypsin and filtration of the serum using a 100,000-kd molecular weight filter. Treatment with an anti-human IgG antibody was associated with intense fluorescence on the surface of neuronal cells exposed to sera from patients with type 2 diabetes mellitus with neuropathy. We conclude that sera from type 2 diabetic patients with neuropathy contains an autoimmune immunoglobulin that induces complement-independent, calcium-dependent apoptosis in neuronal cells.
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PMID:Serum from patients with type 2 diabetes with neuropathy induces complement-independent, calcium-dependent apoptosis in cultured neuronal cells. 976 38

A 35 kDa protein was purified from rat spinal ganglia and sensory fibers. Combined direct trypsin digest and liquid chromatography ion trap mass spectrometry analysis, the 35 kDa protein was identified as annexin V. We then studied the distribution of serum antibodies to annexin V in patients with peripheral neuropathy. We found serum positive antibodies to annexin V only in some patients with immune-mediated neuropathy. This indicated that humoral immune responses to annexin V might play a role in the pathogenesis of autoimmune sensory neuropathy or sensory neuronopathy.
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PMID:Identification of a 35 kDa protein in rat spinal ganglia and sensory fibers. 1548 86