[Case of gastric cancer in pregnancy].
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Biomedical subjects
Publications and source records attributed to H Tsuchida.
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Desmopressin (DDAVP), an AVP.V2-receptor agonist, evokes endothelium-dependent relaxation (EDR) due to nitric oxide (NO), EDR factor (EDRF) in the systemic vasculature, and glomerular afferent arterioles via AVP receptor(s). Glyceryl trinitrate (GTN) causes endothelium-independent (nonreceptor-mediated) vasodilation. We elucidated the possible involvement of EDRF in early non-insulin-dependent diabetes mellitus (NIDDM) and glomerular hyperfiltration (GHF) by DDAVP and GTN infusions. Patients with advanced DM nephropathy (DM.Np) (n = 7) were also examined. DDAVP and GTN decreased the mean blood pressure in DM with GHF (DM + GHF) and without GHF (DM-GHF) greater than that in normal subjects (N), without any difference in the heart rate changes in any group. Plasma levels of cGMP, a cellular messenger of NO, were significantly increased by DDAVP and GTN with a similar increment in each group. DDAVP caused a significant increase in urinary cGMP excretion in each group with a similar increment in each group. However, it caused a transient increase in creatinine clearance only in DM + GHF although GTN did not, and an exaggerated excretion of urinary albumin in early NIDDM, especially in DM+GHF, without a change in beta 2-microglobulin excretion. In contrast, in DM.Np GTN caused a decrease in blood pressure and an increase in plasma cGMP levels, but DDAVP did not. In conclusion, in peripheral vasculature and kidney, an enhanced sensitivity of vascular smooth muscle to NO is present in early NIDDM. The exaggerated dilation of glomerular afferent arterioles by preferentially produced NO in in situ, which causes a rise in PGC, might be partly responsible for the glomerular hyperfiltration and subsequently the increase in the glomerular protein permeation of DM+GHF. However, in peripheral blood vessels of DM.Np EDR is impaired. Thus, EDR seems to change with the development of NIDDM.
The effect of the short-term administration of beraprost sodium, an analogue of prostaglandin I2 (PGI2), on the function of vascular endothelial cells and platelet in non-insulin-dependent diabetes mellitus (NIDDM) patients was investigated. Seven nonobese NIDDM patients with microalbuminuria were recruited for this study. They received a dose of 20 micrograms of beraprost sodium three times daily for 1 month. Before and after this treatment, various factors concerning functions of vascular endothelial cells and platelet were measured. Treatment with PGI2 analogue caused a decrease in basal levels of plasma lipoprotein (a) from 16.8 +/- 5.3 to 13.2 +/- 4.4 mg/dL (p < 0.05), immunoreactive-(i)endothelin from 2.4 +/- 0.3 to 1.6 +/- 0.2 pg/mL, and i-thrombomudulin from 9.3 +/- 3.7 to 7.9 +/- 3.0 FU/L, respectively, and caused a significant increase in basal plasma i-tissue type plasminogen activator (tPA) from 5.3 +/- 0.7 to 8.3 +/- 1.5 ng/mL (p < 0.01). This treatment also increased maximum response of i-tPA induced by desmopressin infusion. Platelet aggregation due to ADP was inhibited in five of six patients after this treatment. In conclusion, treatment with PGI2 analogue caused a decrease in the presumed promoting factors of angiopathy such as lipoprotein (a) and endothelin and an increase in the protecting endothelial factor of angiopathy, tissue type plasminogen activator in patients with NIDDM. And immunoreactive thrombomodulin levels which reflect the vascular endothelial cell injury tended to decrease with the treatment. Therefore, it is suggested that this treatment preserves the vascular endothelial function in diabetes.
We examined 24 patients with osteochondritis dissecans of the humeral capitellum to determine the results of nonoperative treatment. The average age of the patients at the initial examination was 13.3 years (range, 11 to 16). All the patients were advised to stop heavy use of the elbow for 6 months. At the last examination, at a mean follow-up period of 5.2 years, 4 patients (17%) had no residual elbow pain, 7 (29%) had pain only with heavy activities, and 13 (54%) had pain with activities of daily living. Final radiographs were obtained for 15 lesions, of which 3 lesions were assessed as healed, 3 as improved, and 9 as not improved. Five of 11 lesions in the early stage and all 4 advanced lesions failed to show radiographic improvement. These results suggest that osteochondritis dissecans of the capitellum has only a slight tendency to heal, and that instability can cause failure of the lesion to heal.
Standard polytetrafluoroethylene (PTFE) grafts (30-microns internodal distance, ID) (ST grafts), high-porosity PTFE grafts (90 microns ID) (HP grafts), high-porosity PTFE grafts preclotted with autogenous blood (BHP grafts), and high-porosity PTFE grafts presealed with fibrin glue (FHP grafts) were implanted in both common carotid and femoral arteries of 18 dogs. Of the three high-porosity groups, the FHP graft showed the shortest bleeding time. Seromas and/or hematomas occurred as follows: ST grafts 1, HP grafts 7 (P < .05 vs ST), BHP grafts 5 and 2 with FHP grafts. Fibrin glue was observed in all histological sections of 1-week samples, but by 4 weeks it was almost totally absorbed. No endothelialization (ET) was measurable at 2 weeks. By 4 weeks ET extended for a short distance from each anastomosis and there were no significant differences between the four graft groups. At 18 weeks, the HP, BHP, and FHP grafts showed a significant increase in ET compared with the ST graft (P < .01) but there were no significant differences between the three types of high-porosity graft. The differences in patency rates and neointimal thicknesses did not reach statistical significance. High-porosity PTFE grafts showed superior endothelialization in dogs; however, the enlarged ID of PTFE grafts increased intraoperative bleeding and postoperative seroma formation. Fibrin glue sealant controlled bleeding through the graft wall without affecting graft healing, but its sealant effect was not enough to prevent late fluid leakage.
Highly porous PTFE arterial prostheses form endothelium more extensively than the low-porosity grafts in clinical use, but are subject to seroma formation. PTFE vascular grafts were modified to produce a highly porous inner layer (inner layer 60 or 90 microns, outer layer 20 microns). The effect of this modified, composite design on the histology of graft healing was investigated. Twenty-five modified and 25 control grafts, each 4 mm in diameter by 5 cm in length, were implanted into carotid and femoral arteries of dogs. No late seroma formation was observed. After 12 and 18 weeks, the neointima of the grafts was examined by light microscopy and scanning electron microscopy. At 2- and 4-mm distances from the proximal and distal anastomoses, intimal thickness of the control grafts was 238.7 and 96.1 microns, respectively; for the modified grafts it was 236.2 and 202.8 microns at 18 weeks. Thus, the neotinima of modified grafts was thicker than that of control grafts when measured at 4 mm from the anastomoses. Neointimal coverage was less extensive in the control grafts than in modified grafts (26.8 +/- 6.1% vs. 58.8 +/- 13.2%; p < .05). Smooth muscle cells were seen on light-microscopy to penetrate the highly porous inner layer; on scanning electron microscopy, the PTFE fibrils appeared to anchor the neointima of the modified graft. The results suggest that modified PTFE grafts with an inner surface of 60 or 90 microns internodal distance have enhanced formation and anchoring of neointima while remaining impervious to blood.
From November 1986 to January 1993, 97 wrinkled ePTFE prosthetic vascular grafts were implanted in 90 peripheral arterial reconstructions for 87 patients with arteriosclerosis obliterans (ASO) (79 men and 8 women). Grafts used in this series were 54 Vitagraft and 33 Technograft. Initial results for a period of as long as 6 years are summarized here. Forty-four (45.3%) grafts were implanted anatomically, and the remaining were extra-anatomically routed. The mean age of patients in the anatomic bypass group was 64.7 years, and that of patients in the other group was 71.4 years. Twenty-three (43.3%) grafts in the extra-anatomic group were anastomosed sequentially. Mean follow-up periods for each group were 32.4 months and 30.9 months, respectively. None of nine late deaths during the follow-up period was graft related. There was one primary obstruction in the anatomic group; in the extra-anatomic groups, primary graft occlusion occurred in four grafts. In addition, one perigraft seroma and one pseudoaneurysm requiring surgical repair were seen. Cumulative event free ratio for this group was 80.8% at 72 months. These results reveal that the wrinkled ePTFE graft is clinically applicable to arterial reconstruction for ASO with satisfactory long-term patency, even in extra anatomic sequential bypasses.