Hyperinsulinaemia and blood pressure in patients with insulinoma.
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Biomedical subjects
Publications and source records attributed to T Kodama.
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We examined immunofluorescent staining and corneal sensitivity in 25 control subjects (25 eyes) with normal corneas, six patients (eight eyes) with possible herpes simplex keratitis, and 44 patients (48 eyes) with corneal lesions (recurrent erosion, superficial punctate keratitis, marginal ulcer, and follicular keratoconjunctivitis) in whom herpes simplex keratitis was not suspected. On immunofluorescent staining, all 25 control subjects had negative reactions, all eight eyes suspected of having herpes simplex keratitis had positive reactions, and 11 (23%) of the 48 eyes not suspected of having herpes simplex keratitis had positive reactions; the remaining 37 eyes had negative reactions. Of the 11 eyes not suspected of having herpes simplex keratitis but that had positive reactions on immunofluorescent staining, nine had recurrent erosions and the remaining two eyes had superficial punctate keratitis. Of the eight eyes with possible herpes simplex keratitis, seven (88%) had decreased corneal sensitivity. Of the 11 eyes not suspected of having herpes simplex keratitis but that had positive reactions on immunofluorescent staining, eight (73%) had decreased corneal sensitivity. Of the 37 eyes not suspected of having herpes simplex keratitis that had negative reactions on immunofluorescent staining, 11 (30%) had decreased corneal sensitivity.
Normotriglyceridemic abetalipoproteinemia is a rare familial disorder characterized by an isolated deficiency of apoB-100. We have previously reported a patient with this disease, who had normal apoB-48 but no apoB-100. To elucidate the genetic abnormalities in this family, we studied the linkage of apoB gene using three genetic markers. The proband and her affected brother showed completely different apoB gene alleles, suggesting that the apoB gene itself is not related to this disorder in this family. By contrast, an American case had a point substitution in the apoB gene generating an in-frame stop codon. These results indicate that this disorder can be caused by defect(s) of either an apoB gene or other genes.
A rare case of anomalous arrangement of the pancreaticobiliary ductal system without dilatation of the biliary tract (AAPBDS without DBT) associated with mucosal dysplasia of the biliary duct is described herein. A 53 year old male with a long history of diarrhea and right upper abdominal pain was diagnosed as having AAPBDS without DBT by endoscopic retrograde cholangiopancreatography and other examinations. Excision of the gallbladder and biliary duct with a Roux-en-Y hepatico-jejunostomy was performed and subsequent pathological examination of the surgical specimens showed mucosal hyperplasia of the gall-bladder and mucosal dysplasia of the biliary duct. Considering the dysplastic changes of the biliary duct as seen in our case, and the high incidence of AAPBDS without DBT developing into carcinoma of the biliary duct, being 12.2 per cent, we suggest that pancreaticobiliary ductal diversion with excision of the gallbladder and biliary duct should also be performed for AAPBDS without DBT. However, further pathological investigations concerning the excised biliary duct in AAPBDS without DBT will be need to be carried out.
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We studied the effects of salt loading on glucose tolerance, blood pressure, and albuminuria in rats with mild non-insulin-dependent diabetes mellitus (NIDDM). Two-day-old male Wistar Kyoto (WKY) rats were injected intraperitoneally (IP) with either 75.0 mg/kg streptozotocin (STZ) or vehicle as control. Salt loading was performed as 1% NaCl of drinking solution from 4 weeks until 12 weeks of age (estimated sodium intake: control, 3.14 +/- 0.28 mEq/d in tap-water group, 11.9 +/- 0.95 mEq/d in salt-loaded group; NIDDM, 2.93 +/- 0.16 mEq/d in tap-water group, 12.0 +/- 2.59 mEq/d in salt-loaded group). Oral glucose tolerance, glycosylated hemoglobin (GHb), and pancreatic insulin content at 12 weeks did not differ between the salt-loaded group and tap-water group in both NIDDM and control rats. Urinary sodium excretion was increased in salt-loaded groups of control and NIDDM rats, but systolic blood pressure did not differ among the groups (control, 151 +/- 6 mm Hg in tap-water group, 150 +/- 3 mm Hg in salt-loaded group; NIDDM, 152 +/- 3 mm Hg in tap-water group, 157 +/- 2 mm Hg in salt-loaded group). Urinary albumin excretion was significantly increased in salt-loaded groups (1,790 +/- 272 micrograms/d in control, 1,617 +/- 174 micrograms/d in NIDDM rats) compared with tap-water groups (691 +/- 75 micrograms/d in control, P less than .05; 616 +/- 69 micrograms/d in NIDDM rats, P less than .001), irrespective of STZ injection, but endogenous creatinine clearance was not different among the groups. Furthermore, renal growth was more greatly increased in salt-loaded groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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Right anterior caudocranial oblique (RACCO) projections were evaluated for transarterial portography with digital subtraction angiography. For RACCO projection, the image intensifier was tilted 25 degrees caudally and 30 degrees to the patient's right with the patient in the supine position. The abnormal findings imaged in 20 patients were analyzed by types of abnormalities and their locations in the portal venous systems by comparing RACCO and PA projections. The RACCO view was superior to the PA projection for demonstrating either encasements or tumor thrombi in relatively proximal segments of the portal venous branches. Two encasement lesions and a tumor thrombus were imaged only on the RACCO projection. However, the RACCO projection had no definite advantage over the PA view for showing encasements or tumor thrombi in the distal segmental branches. The RACCO projection was superior to the PA view for demonstrating defects in the hepatograms of some hepatic segments (S5 and S8). We concluded that the RACCO view is extremely useful and is indicated for angiographic work-ups of hepatic or biliary lesions when abnormalities are suspected in proximal portal venous branches.
We studied the pathogenesis of cyclosporine-induced hypomagnesemia in five patients with nephrosis. Serum magnesium concentrations and urinary excretion of magnesium were reduced by the therapy. In contrast, the magnesium concentrations in mononuclear blood cells were increased. We conclude that short-term use of cyclosporine induces an intracellular shift of magnesium and causes hypomagnesemia.
Gel-filtered human platelets exerted lytic activity on autologous red blood cells (RBC) when they were coincubated at 37 degrees C with platelet-activating agents, such as thrombin, collagen, ADP, LPS or PMA in the absence of plasma. Lysis of activated platelets themselves did not occur during the incubation period examined. Morphological observations showed that RBC exposed to thrombin-activated platelets were fragmented and/or transformed into spherocytes. This haemolytic reaction by thrombin-activated platelets did not occur at 4 degrees C, or in the presence of agents which inhibited glycolysis or elevated intracellular levels of cAMP, indicating that energy-dependent and cAMP-regulated platelet metabolism was required for this reaction. When platelets and RBC were incubated in the same vessel, but were prevented from coming into direct cell to cell contact by means of a membrane barrier, their cytotoxicity was reduced but not eliminated completely. No cytotoxic activity against RBC was detected in platelet-free supernatants obtained by centrifugation after activation of platelets with thrombin. On the contrary, activated and washed platelets retained the activity. These observations suggested that the cytotoxic activity was carried by some diffusible and easily inactivated factors, which were continuously produced and liberated from activated platelets. Cyclo-oxygenase inhibitors inhibited the haemolytic activity of thrombin-activated platelets, suggesting a role for some products of platelet-cyclo-oxygenase pathway in platelet-mediated haemolysis. These results provide the first evidence for a direct role of activated platelets in mediation of RBC-damage in the absence of any plasma factors.
Strain SY1, identified as a Corynebacterium sp., was isolated on the basis of the ability to utilize dibenzothiophene (DBT) as a sole source of sulfur. Strain SY1 could utilize a wide range of organic and inorganic sulfur compounds, such as DBT sulfone, dimethyl sulfide, dimethyl sulfoxide, dimethyl sulfone, CS2, FeS2, and even elemental sulfur. Strain SY1 metabolized DBT to dibenzothiophene-5-oxide, DBT sulfone, and 2-hydroxybiphenyl, which was subsequently nitrated to produce at least two different hydroxynitrobiphenyls during cultivation. These metabolites were separated by silica gel column chromatography and identified by nuclear magnetic resonance, UV, and mass spectral techniques. Resting cells of SY1 desulfurized toluenesulfonic acid and released sulfite anion. On the basis of these results, a new DBT degradation pathway is proposed.
Macrophage-tropic virus variants evolved during the course of infection of individual rhesus monkeys with cloned, non-macrophagetropic simian immunodeficiency virus. Specific changes in the envelope gene (env) were found to be primarily responsible for the dramatic increase in the ability of the virus to replicate in macrophages. Cloned viruses differing at nine amino acid positions in env exhibited a more than 100-fold difference in replicative capacity for primary cultures of rhesus monkey alveolar macrophages. At least five of the nine amino acid changes contributed to macrophage tropism. These determinants were distributed across the full length of env, including both the gp120 and gp41 products of the env gene. Furthermore, the emergence of macrophagetropic variants in vivo was associated with specific pathologic manifestations in which the macrophage is the major infected cell type. Thus, major determinants of macrophage tropism reside in env, they can be complex in nature, and the presence of macrophage-tropic virus variants in vivo can influence the disease course and disease manifestations.
In order to establish a technique for successful adrenal tissue autotransplantation, we conducted an experimental study with rats, in which we investigated the effects of the total amount of grafted tissue and the size of each graft piece. Three 'amount' factor levels (1/4 of a gland and 1 and 2 glands) and two 'size' factor levels (1-mm3 fragments and a paste-like mince) were studied. The total amount of grafted adrenal tissue affected the amount of steroid secreted. Autografting of 1/4 of a gland resulted in corticosterone secretion at the normal basal level, but grafting of more than 1 gland enabled the rats to withstand stress better. The take of the grafts with the two different size levels did not differ.
We examined retrospectively a total of 171 patients (236 eyes) who had undergone extracapsular cataract extraction (ECCE) with or without intraocular lens implantation (IOL). The best and practically corrected visual acuities were determined 6 months after surgery. Practically corrected visual acuity of the ECCE group was significantly worse than that of ECCE plus IOL group of patients who had undergone unilateral cataract surgery. In patients who had undergone bilateral surgery, visual improvement was almost optimal in both groups. With regard to practically corrected visual acuity, ECCE plus IOL was the preferable procedure for elderly patients who had had unilateral cataract.
To clarify the role of oxygen radicals in the mucus metabolism of the gastrointestinal tract, the effect of oxygen radicals on the activity of glucosamine synthetase, the rate-limiting enzyme of mucus synthesis, was investigated using homogenate derived from rat gastric mucosa. The simultaneous addition of both xanthine and xanthine oxidase caused a significant inhibition of the enzyme activity, and this decrease was counteracted by catalase, but not by superoxide dismutase. Hydrogen peroxide also caused a significant decrease in the enzyme activity; and this effect of hydrogen peroxide was counteracted by catalase and dithiothreitol, but not by mannitol, dimethyl sulfoxide and reduced glutathione. The inhibition of glucosamine synthetase activity by oxygen radicals is considered to be caused by the oxidation of sulfhydryl groups of the enzyme molecule. The present results also suggest that oxygen radicals in the gastrointestinal tract may induce the suppression of a protective mechanism of the gastric mucosa by inhibiting glucosamine synthesis activity.
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