A novel soft surimi gel with functionality prepared using alcalase for people suffering from dysphagia.

In this study, effects of alcalase on physical properties, pepsin digestibility, and antioxidative activity in the heat-induced surimi gel were investigated to develop a novel gel product for people with dysphagia. The heat-induced gelation profile of surimi showed that alcalase activity was maximized at approximately 37 °C. The surimi gel attained an appropriate texture for people with dysphagia, when a combination of 0.3-0.5% alcalase and two-step heating at 37 °C and 90 °C was used. Adding alcalase effectively promoted proteolysis, resulting in softening of the gel. Furthermore, the gel with 0.5% alcalase showed improved pepsin digestibility, when heated at 37 °C and 90 °C. Its antioxidative activity was enhanced by adding 0.5% alcalase. Therefore, a combination of 0.5% alcalase and the two-step heating at 37 °C and 90 °C was useful in improving the physical and functional properties of the surimi gel for people with dysphagia.

High serum high-sensitivity C-reactive protein concentrations are associated with relative cardiac sympathetic overactivity during the early morning period in type 2 diabetic patients with metabolic syndrome.

Sympathetic activation is associated with metabolic syndrome (MS) and increased risk of cardiovascular disease. The aim of this study was to investigate whether cardiac autonomic activity or sympathovagal balance, as estimated by a 24-hour power spectral analysis of heart rate variation, is associated with serum concentrations of high-sensitivity C-reactive protein (hs-CRP), a sensitive predictor for cardiovascular events, in type 2 diabetic patients with and without MS. We studied 104 type 2 diabetic patients (50 female and 54 male). The diagnosis of MS was based on the National Cholesterol Education Program Adult Treatment Panel III criteria. Based on the serum hs-CRP, diabetic patients were also divided into 3 groups: low risk (CRP < 1.0 mg/L), moderate risk (1.0 < or = CRP < or = 3.0), and high risk (CRP > 3.0). Heart rate variation was determined automatically every 5 minutes over 24 hours using an ambulatory Holter electrocardiographic recording. Power spectral analysis of the R-R intervals was performed by fast Fourier transformation. Low frequency (LF, both sympathetic and parasympathetic activities), high frequency (HF, pure parasympathetic activity), and the ratio of LF to HF, an index of sympathovagal balance, were used as indices of cardiac autonomic activity. Blood concentrations of hs-CRP, interleukin 6, and plasminogen activator inhibitor 1 were higher in diabetic patients with than in those without MS (P < .0001, P = .0056, and P < .0001, respectively). Both the 24-hour mean LF and the LF-to-HF ratio were also significantly higher in diabetic patients with than in those without MS (P = .0397 and P = .0483, respectively). The LF-to-HF ratio at 6:00 am was significantly higher in diabetic patients with a high CRP concentration than in those with a low or moderate CRP concentration (P < .001 and P < .01, respectively). Only urinary albumin and hs-CRP were independent factors predicting the LF-to-HF ratio at 6:00 am in diabetic patients. In conclusion, type 2 diabetic patients with MS have elevated markers of inflammation and evidence of cardiac sympathetic predominance. High serum concentrations of hs-CRP are associated with relative cardiac sympathetic overactivity during the early morning in type 2 diabetic patients.

Comparison of serum high-molecular weight (HMW) adiponectin with total adiponectin concentrations in type 2 diabetic patients with coronary artery disease using a novel enzyme-linked immunosorbent assay to detect HMW adiponectin.

Adiponectin (Acrp30), an adipocyte-derived protein, exists in serum as a trimer, a hexamer, and a high-molecular weight (HMW) form, including 12-18 subunits. Because HMW adiponectin may be biologically active, we measured it in serum using a novel enzyme-linked immunosorbent assay (ELISA) confirmed by gel filtration chromatography that the ELISA detected mainly adiponectin with 12-18 subunits, and we compared HMW with total adiponectin concentration in patients with type 2 diabetes. We next investigated the relationship between serum HMW and coronary artery disease (CAD) in 280 consecutive type 2 diabetic patients, including 59 patients with angiographically confirmed CAD. Total adiponectin was measured in serum by a commercially available ELISA. Like serum total adiponectin, HMW adiponectin correlated positively with HDL cholesterol and negatively with triglyceride, insulin sensitivity, creatinine clearance, and circulating inflammatory markers. Total and HMW adiponectin were significantly higher in women than in men, as was the HMW-to-total adiponectin ratio. Serum HMW and the HMW-to-total adiponectin ratio were significantly lower in men with than without CAD (P < 0.05, respectively). In women, the ratio, but neither total nor HMW adiponectin, tended to be lower when CAD was present. In conclusion, determination of HMW adiponectin, especially relative to total serum adiponectin, is useful for evaluating CAD in type 2 diabetic patients.

Profound reduction in T-helper (Th) 1 lymphocytes in peripheral blood from patients with concurrent type 1 diabetes and Graves' disease.

Type 1 diabetes likely is mediated by T-helper (Th) 1 lymphocytes, while Graves' disease may involve Th2 predominance. We investigated the balance between Th1 and Th2 cells and between Th1- and Th2-associated chemokine receptor expression on peripheral lymphocytes in subjects including patients with coexisting type 1 diabetes and Graves' disease. Peripheral blood mononuclear cells of all subjects were examined by flow cytometry for intracellular cytokines (IFN-gamma for Th1; IL-4 for Th2) and expression of the chemokine receptors CXCR3 (Th1-associated) and CCR4 (Th2-associated). Plasma concentrations of interferon-inducible protein (IP)-10, a CXCR3 ligand, and thymus and activation-regulated chemokine (TARC), a CCR4 ligand, were measured by enzyme-linked immunosorbent assays. IFN-gamma producing-T lymphocytes were significantly fewer in patients with coexisting type 1 diabetes and Graves' disease (12.4 +/- 6.8%, n = 6) than in healthy control subjects (19.9 +/- 4.1%, n = 6; P < 0.01) or patients with type 2 diabetes (19.1 +/- 4.5%, n = 5; P < 0.05). We found no significant difference in IFN-gamma-producing T lymphocytes between healthy controls and patients with only type 1 diabetes (n = 8) or Graves' disease (n = 5). Plasma IP-10 concentrations were significantly higher in patients with coexisting type 1 diabetes and Graves' disease than in control subjects (106.3 +/- 30.48 vs. 66.7 +/- 25.3 pg/ml, P = 0.0343). Considering only patients with type 1 diabetes alone, duration of diabetes correlated positively with IFN-gamma-producing T lymphocytes (r = 0.773, P = 0.0242) and the ratio of CXCR3 to CCR4 receptor expression (r = 0.947, P = 0.0004). In conclusion, Th1-associated T lymphocytes were fewer in peripheral blood from patients having both type 1 diabetes and Graves' disease than in those with either disease alone. Numbers of peripheral Th1 lymphocytes increased with increasing time from onset of type 1 diabetes in patients with type 1 diabetes alone.

Metabolic syndrome accompanied by hypercholesterolemia is strongly associated with proinflammatory state and impairment of fibrinolysis in patients with type 2 diabetes: synergistic effects of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor.

OBJECTIVE: To determine whether plasma concentrations of thrombin-activatable fibrinolysis inhibitor (TAFI) in patients with type 2 diabetes were associated with components of metabolic syndrome (MS), including high-sensitivity C-reactive protein (hs-CRP), plasminogen activator inhibitor (PAI)-1, and LDL cholesterol. RESEARCH DESIGN AND METHODS: We studied 136 consecutive patients with type 2 diabetes. Diagnosis of MS was diagnosed by current criteria. Hypercholesterolemia (HC) was defined as serum LDL cholesterol >140 mg/dl (3.6 mmol/l) or treatment with a statin. For comparisons, diabetic patients were divided into four groups: those with no MS and no HC (n = 38), with MS but not HC (n = 39), with no MS but with HC (n = 26), and with both MS and HC (n = 33). RESULTS: Considering all patients with type 2 diabetes, plasma PAI-1 was strongly associated with MS components such as BMI, triglyceride, alanine aminotransferase, a homeostasis model assessment of insulin resistance, and hs-CRP. Plasma TAFI only correlated positively and independently with LDL cholesterol. Plasma concentrations of plasmin-alpha2-antiplasmin complex (PAP), a measure of fibrinolytic activity in blood, showed a significant negative correlation with plasma PAI-1 but not TAFI. Diabetic patients with both MS and HC had the highest serum hs-CRP concentrations and the lowest plasma PAP concentrations. CONCLUSIONS: LDL cholesterol is a main determinant of plasma TAFI in patients with type 2 diabetes. Coexistence of MS and HC synergistically accelerates inflammation and impairment of fibrinolysis via elevated concentrations of both TAFI and PAI-1, which inhibit fibrinolysis.

Pharmacokinetic interaction with digoxin and glucocorticoids in rats detected by radio-immunoassay using a novel specific antiserum.

We previously prepared a more specific antiserum (Antiserum-I) to digoxin (Dx) compared with commercially available anti-Dx antiserum (Antiserum-II), clinically used in the therapeutic drug monitoring of Dx. The aims of this study are to compare Dx disposition kinetics by radio-immunoassay (RIA) using Antiserum-I and Antiserum-II, and evaluate the drug-drug interaction with Dx and glucocorticoids in rats. When Dx metabolites were added to rat serum containing Dx, the recovery ratios using Antiserum-I showed 100 to 110% and were remarkably lower than those using Antiserum-II. In rats, serum concentration-time courses of Dx after a single i.v. or p.o. administration of Dx (0.017 mg/kg) by RIA using Antiserum-I were much lower than those using Antiserum-II. The area under the concentration-time course of Dx was significantly lower than that using Antiserum-II and the total body clearance values were significantly higher, while an obvious change of bioavailability was not observed. When using Antiserum-I, rats twice and six times pretreated with dexamethasone (75 mg/kg/day, i.p.) and prednisolone (69 mg/kg/day, i.p.), respectively, showed significant change of the pharmacokinetic parameters of Dx compared with the control rats. In contrast, using Antiserum-II, it took three and nine times of pretreatment with dexamethasone and prednisolone, respectively, to significantly change the parameters of Dx. In conclusion, these results demonstrate that Antiserum-I is very useful not only to more precisely monitor serum Dx levels, but also to determine earlier the drug-drug interaction with glucocorticoids than Antiserum-II.