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Two-dimensional electronic-vibrational spectroscopy was used to investigate the ultrafast photoinduced dynamics of betaine-30 in methanol-d4 solution. Our study reveals three vibrational modes (1330, 1350 and 1370 cm-1) are strongly coupled to the back charge transfer process.

Recent studies suggested that estrogen-induced cardiovascular protection might be mediated by an increased synthesis of vascular nitric oxide (NO). In this study, we investigated the effects of isoflavones with weak estrogenic activity on blood pressure and vascular NO actions in ovariectomized strokeprone spontaneously hypertensive rats. Female stroke-prone spontaneously hypertensive rats (n = 32; 15 wk old) were divided into four groups. Groups 1 and 2 were fed the standard diet and groups 3 and 4 were fed daidzein (D)- and genistein (G)-mixed standard diets, respectively (0.16 mmol/100 g standard diet). At age 19 wk, group 1 (Sham) was sham-operated and groups 2 (ovx), 3 (ovx + D) and 4 (ovx + G) were ovariectomized. All rats were killed at age 22 wk and their thoracic aortae were checked for vascular NO release indirectly by precontracting aortic rings with prostaglandin [F.sub.2[Alpha]] and by observing the effect on tone changes induced by N-monomethyl-L-arginine, an L-arginine analog that competes for NO synthase and inhibits NO formation. Systolic blood pressure and urinary NO metabolites were measured before and after surgery. Before surgery, systolic blood pressure and urinary NO metabolites did not differ among all groups. After surgery, however, systolic blood pressure was significantly lower (P [is less than] 0.01) and urinary NO metabolites were significantly higher (P [is less than] 0.05) in ovx + D than in ovx. Basal release of NO in ovx + D was significantly higher than that in ovx (P [is less than] 0.005). These results indicate that daidzein attenuates the development of hypertension by accelerating vascular NO production. This new result supports the several epidemiologic and animal study findings suggestive of a possible cardiovascular protective effect of soy intakes.

Background:In its 1997 Guideline for Diagnosis and Treatment of Hyperlipidemia in Japanese Adults and subsequent revisions, the Japan10 Atherosclerosis Society (JAS) recommends serum lipid management goals (SLMGs) based on a coronary heart disease (CHD) risk classification. A literature search revealed that the status of lipid-lowering therapy based on the current JAS recommendations in Japan has not been assessed.Objective:The aim of this study was to evaluate the efficacy of current lipid-lowering 10 regimens, and to provide the best possible therapeutic strategies for patients with hyperlipidemia by identifying risk factors for the development of CHD, based on the current JAS recommendations.Methods:This multicenter, retrospective study was conducted using data 10 from patients under the care of physicians at 12,500 randomly selected institutions across Japan. Physicians received a survey concerning lipid-lowering therapy, on which each physician provided data from 10 consecutive adult patients with hyperlipidemia who had been prescribed lipid-lowering therapy for at least 3 months before the survey was administered, and who were undergoing routine follow-up on an outpatient basis. Physicians provided patients' demographic and clinical data, including JAS-defined CHD risk classification coronary risk factors and pre- and posttreatment (after >/=3 months) serum lipid levels, and the types and dosages of drugs in patients' current and prior treatment regimens. These data were used to assess the efficacy of lipid-lowering regimens and rates of patients achieving the SLMGs recommended by the JAS.Results:A total of 2540 physicians participated in the survey, and data from 10 24,893 Japanese patients (mean [SD] age, 65.8 [10.5] years) with hyperlipidemia were included in the study. Patients with familial hyperlipidemia (845/24,893 [3.4%]) were excluded from most of the analyses, leaving 24,048 patients with primary hyperlipidemia. The most prevalent coronary risk factors included age (21,902 [91.1%]), hypertension (14,275 [59.4%]), diabetes mellitus type 2 and/or impaired glucose tolerance (6346 [26.4%]), and smoking (3841 [16.0%]). A total of 20,948 patients (87.1%) had a CHD risk classification of B (ie, >/=1 coronary risk factor but no history of CHD). At the time of the survey, the lipid-lowering regimens of 22,080 patients (91.8%) included a statin. The rates of achievement of SLMGs were as follows: total cholesterol (TC), 12,659/23,840 patients (53.1%); low-density lipoprotein cholesterol (LDL-C), 14,025/22,121 (63.4%); high-density lipoprotein cholesterol, 19,702/21,279 (92.6%); and triglycerides (TG), 14,892/ 23,569 (63.2%). TC and LDL-C goals were achieved by most patients (>/=61.1%) in risk categories A, B1, and B2 (ie, 0-2 coronary risk factors; low to moderate risk) but by a low percentage of patients (/=3 coronary risk factors or history of CHD; high risk). In the high-risk group (n = 10,515), the TC goal was achieved by 4059 patients (38.6%). The TC and LDL-C goals were achieved by significantly higher percentages of patients prescribed atorvastatin (5133/7928 [64.7%] and 5487/7426 [73.9%], respectively) compared with the rates of patients prescribed any other statin at the recommended starting doses (all, P < 0.05).Conclusions:The results of this study of Japanese patients undergoing lipid-lowering 10 therapy for the prevention of CHD, prescribed based on the recommendations in the JAS guideline, suggest insufficient reduction of TC, LDL-C, and TG in patients at high risk for CHD and the need for more aggressive lipid-lowering therapy in such patients. [ABSTRACT FROM AUTHOR]

Current studies have indicated both positive and negative roles for the hepatocyte growth factor (HGF)/c-met receptor signaling system in tumor development. Recently, we have shown that HGF has the capacity to induce both growth inhibition and programmed cell death in aflatoxin-transformed (AFLB8) rat liver epithelial cells. Using the same cell line, we have now investigated a potential mechanism for HGF-induced apoptosis. Immunoblot analysis of bcl-2 gene family member (bax, bcl-2, bclX-s/l) expression showed no correlation with HGF treatment, suggesting that HGF-mediated apoptosis is bax independent. Following HGF treatment retinoblastoma protein (pRB) was present in the hypophosphorylated state. HGF treatment increased cyclin A, cyclin G1 and nuclear transcriptional factor (NFκB) protein expression. However, electrophoretic mobility shift analysis showed that NFκB activity decreased with HGF treatment. Under these apoptotic conditions, c-Jun N-terminal kinase (JNK1) and extracellular signal-regulated kinase (ERK2) were activated with lower level activation of ERK2, while no involvement of phosphatidylinositol-3 kinase was observed. Epidermal growth factor (EGF) was not protective, and actually induced cells to undergo apoptosis to a level similar to that of HGF alone or EGF/HGF in combination. These results suggest the possibility of cross-talk between HGF/c-met and EGF/EGFR signaling pathways, and the involvement of JNK1 induction in HGF-mediated apoptotic cell death. [ABSTRACT FROM PUBLISHER]

Ultrastructural and immunohistochemical studies of the small intestine are described in a Japanese patient with alpha heavy chain disease who had a history of colonic ulcers. Endoscopic examinations revealed multiple gastric erosion, duodenal ulcer, and a thickened, cobblestone-like pattern composed of small nodules in the duodenum and jejunum, which was similar in appearance to Crohn's disease. An electron microscopic study showed that the numerous, infiltrated cells in the jejunal lamina propria were matured plasma cells with atypical structure of the organelles. These plasma cells had alpha heavy chain protein devoid of light chain. Although secretory component was demonstrated normally in the epithelial cells by immunofluorescent methods, no association of this component with alpha heavy chain protein could be observed in any of the plasma and epithelial cells of this case. These facts suggest the absence of secretory alpha chain or secretory IgA, and a deficiency of the mucosal secretory immune system in this patient. [ABSTRACT FROM PUBLISHER]

Biopsies of the external and sphincter taken from 24 male patients with haemorrhoids were subjected to examination using histochemical techniques. Fibre size (type 1 mean: 33 micrometers +/- 11.0 SD and type 2 mean: 47.9 micrometers +/- 15.0 SD) was increased when compared with control subjects. The distribution of muscle fibre types in these patients showed markedly greater type 1 fibre predominance (92%) than in control subjects. These abnormalities of the external sphincter did not show any clear relationship with age, degree of haemorrhoidal change, length of history of haemorrhoids, history of straining or of constipation, or perineal descent; however, increasing length of history up to 10 years was associated with increasing type 1 fibre predominance. We suggest that the external and sphincter in patients with haemorrhoids is in a state of increase tonic contraction, which causes work induced muscle hypertrophy and may contribute to increased resting pressure in the anal canal in patients with haemorrhoids. [ABSTRACT FROM PUBLISHER]