Antihypertensive and antioxidant effects of dietary black sesame meal in pre-hypertensive humans.

BACKGROUND: It has been known that hypertension is an independent risk factor for cardiovascular disease (CVD). CVD is the major cause of morbidity and mortality in developed and developing countries. Elevation of blood pressure (BP) increases the adverse effect for cardiovascular outcomes. Prevention of increased BP plays a crucial role in a reduction of those outcomes, leading to a decrease in mortality. Therefore, the purpose of this study was to investigate the effects of dietary black sesame meal on BP and oxidative stress in individuals with prehypertension. METHODS: Twenty-two women and eight men (aged 49.8 ± 6.6 years) with prehypertension were randomly divided into two groups, 15 subjects per group. They ingested 2.52 g black sesame meal capsules or placebo capsules each day for 4 weeks. Blood samples were obtained after overnight fasting for measurement of plasma lipid, malondialdehyde (MDA) and vitamin E levels. Anthropometry, body composition and BP were measured before and after 4-week administration of black sesame meal or a placebo. RESULTS: The results showed that 4-week administration of black sesame meal significantly decreased systolic BP (129.3 ± 6.8 vs. 121.0 ± 9.0 mmHg, P < 0.05) and MDA level (1.8 ± 0.6 vs. 1.2 ± 0.6 µmol/L, P < 0.05), and increased vitamin E level (29.4 ± 6.0 vs. 38.2 ± 7.8 µmol/L, P < 0.01). In the black sesame meal group, the change in SBP tended to be positively related to the change in MDA (R = 0.50, P = 0.05), while the change in DBP was negatively related to the change in vitamin E (R = -0.55, P < 0.05). There were no correlations between changes in BP and oxidative stress in the control group. CONCLUSIONS: These results suggest the possible antihypertensive effects of black sesame meal on improving antioxidant status and decreasing oxidant stress. These data may imply a beneficial effect of black sesame meal on prevention of CVD.

Synovial fluid adenosine deaminase activity to diagnose tuberculous septic arthritis.

There are reports of a correlation between high adenosine deaminase (ADA) levels in body fluid and tuberculosis (TB) infection, but none have evaluated synovial fluid ADA and TB arthritis. The objectives of this study were to determine the proper cut-off level for synovial fluid adenosine deaminase (SF-ADA) and the sensitivity and specificity of SF-ADA to diagnose TB arthritis. Between January 2006 and December 2007, SF-ADA were determined using the modified Giusti's method on patients over 15 years of age with clinically suspected TB arthritis or having an unknown etiology of their arthritis. Synovial fluid culture for TB was performed in all patients as a gold standard test. Forty cases were included in the study, with a female to male ratio of 1.7:1 and a mean age of 52.3 +/- 17.4 years (range, 16-80). The median duration of symptoms was 60 days. The prevalence of TB arthritis was 16.7% (6 cases) while the remaining cases were rheumatoid arthritis (8), non-TB bacterial septic arthritis (3), and miscellaneous (23). The mean SF-ADA levels in patients with TB arthritis and non-TB arthritis were 35.7 +/- 10.4 (range, 20-51) and 15.4 +/- 9 (range, 2-34) U/1, respectively. The cut-off value for the diagnosis of TB arthritis was 31 U/1, with a sensitivity of 83.3% (95% CI 35.9-99.6), a specificity of 96.7% (95% CI 82.8-99.9) and an agreement Kappa of 0.8 (p < 0.001). SF-ADA levels higher than 31 U/1 were highly correlated with a diagnosis of TB arthritis, with a high sensitivity and specificity. SF-ADA may be considered as a less invasive and time-consuming diagnostic tool for TB arthritis.

Estimation of plasma small dense LDL cholesterol from classic lipid measures.

Calculated low-density lipoprotein cholesterol (cLDL-C) may differ from direct measurement (dLDL-C), and this difference may depend on presence of small, dense LDL (sdLDL) particles in addition to variation in triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C) concentrations. The presence of such dependence would offer a simple means to estimate sdLDL. We studied dependence of sdLDL on cLDL-C, dLDL-C, and other variables. We measured the levels of glucose, creatinine, total cholesterol, TG, HDL-C, and dLDL-C using standardized methods in 297 samples. For sdLDL cholesterol (sdLDL-C), a novel homogeneous assay was used. The cLDL-C was calculated using the Friedewald formula for 220 subjects after excluding for liver or renal disease. Using stepwise regression analysis identified non-HDL-C, cLDL-C, and dLDL-C as significant variables (P < .001; R(2) = 0.88). The regression equation was as follows: sdLDL-C (mg/dL) = 0.580 (non-HDL-C) + 0.407 (dLDL-C) - 0.719 (cLDL-C) - 12.05. The sdLDL-C concentration can be estimated from non-HDL-C, dLDL-C, and cLDL-C values. Identification of a simple, inexpensive marker for sdLDL particles provides a cost-effective method for screening cardiovascular disease risk.

Endogenous oxalogenesis after acute intravenous loading with ethylene glycol or glycine in rats receiving standard and vitamin B6-deficient diets.

OBJECTIVES: The effect on endogenous oxalate synthesis of acute intravenous loading with ethylene glycol or glycine was investigated in rats on a standard or a vitamin B6-deficient diet. METHODS: Twenty-four male Wistar rats weighing approximately 180 g were randomly divided into ethylene glycol and glycine groups of 12 animals each. These groups were further divided into two subgroups of six animals each that were fed either a standard or a vitamin B6-deficient diet for 3 weeks. Animals of these two subgroups received an intravenous infusion of 20 mg (322.22 micromol) of ethylene glycol or 100 mg (1332.09 micromol) of glycine, respectively. Urine samples were collected just before intravenous infusion of each substance and at hourly intervals until 5 h after receiving the infusion. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. RESULTS: Urinary oxalate and glycolate excretion was significantly increased after ethylene glycol administration. Significant differences between the control and vitamin B6-deficient groups were found. In contrast, there were only small changes of oxalate and glycolate excretion after glycine administration. Recovery of the given dose of ethylene glycol as oxalate in 5-h urine was 0.31% and 7.15% in the control and vitamin B6-deficient groups, respectively, whereas recovery of glycolate was 0.68% and 7.22%, respectively. CONCLUSIONS: Ethylene glycol loading has a significant effect on urinary oxalate excretion in both normal and vitamin B6-deficient rats, whereas glycine loading only has a small effect. Oxalate and glycolate excretion after ethylene glycol loading were respectively 23-fold and 11-fold higher in vitamin B6-deficient rats than in controls.

Oxalate synthesis from hydroxypyruvate in vitamin-B6-deficient rats.

We studied the effects of an intravenous hydroxypyruvate load on endogenous oxalogenesis in rats receiving a standard diet or a vitamin-B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet or a vitamin-B6-deficient diet for 3 weeks. Then the animals received an intravenous infusion of 100 mg/ml (960.6 micromol/ml) of hydroxypyruvate slowly over 10 min. Urine samples were collected just before hydroxypyruvate infusion and at hourly intervals until 5 h afterward. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Hourly urinary oxalate excretion peaked within 2 h, while urinary glycolate excretion peaked at 1 h, after the hydroxypyruvate load in both control and vitamin-B6-deficient rats. Both urinary oxalate and glycolate excretion were higher in vitamin-B6-deficient rats than in control rats. Infusion of hydroxypyruvate increased the 5-h urinary oxalate and glycolate excretion to 0.68% (6.56 micromol) and 0.53% (5.10 micromol) of the administered dose (mol/mol), respectively, in the control rats, while oxalate and glycolate excretion, respectively, increased to 2.43% (23.36 micromol) and 0.79% (7.59 micromol) of the dose in the vitamin-B6-deficient rats. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin-B6-deficient rats than in the control rats. In conclusion, a hydroxypyruvate load increased endogenous oxalate synthesis in control rats, and its synthesis was even greater in vitamin-B6-deficient rats. Vitamin B6 deficiency also resulted in significant hypocitraturia.

Cerebrospinal fluid adenosine deaminase activity for the diagnosis of tuberculous meningitis in adults.

We studied adenosine deaminase (ADA) activity in cerebrospinal fluid (CSF) of 16 cases of tuberculous meningitis, 4 cases of cryptococcal meningitis, 5 cases of bacterial meningitis, 12 cases of eosinophilic meningitis, 26 cases of aseptic meningitis, 6 cases of carcinomatous meningitis and 108 cases with normal CSF. The mean CSF ADA values for the different groups were: 39.44 +/- 41.46, 13.00 +/- 7.43, 34.20 +/- 40.81, 3.17 +/- 4.82, 10.03 +/- 9.23, 8.67 +/- 13.60, and 2.58 +/- 2.90 U/I, respectively. Comparing the ADA activity between patients with tuberculous meningitis and non-tuberculous meningitis, the receiver-operating characteristic (ROC) curve identified a CSF ADA level of 15.5 U/I as the best cut-off value to differentiate between the two, with a sensitivity of 75% and a specificity of 93%, with an area under the curve of 0.92. When tuberculous meningitis was compared with aseptic and carcinomatous meningitis, the ROC curve identified a CSF ADA level of 19.0 U/I as the best cut-off value for differentiation, with a sensitivity of 69% and a specificity of 94%, with an area under the curve of 0.83. The level of CSF ADA may be useful as a complementary tool in the early diagnosis of tuberculous meningitis.

Anti-p53 antibodies and p53 protein expression in cholangiocarcinoma.

BACKGROUND/AIMS: Mutations of p53 are found in the majority of human malignancies. The accumulated mutant p53 can be detected in tumor sections by immunohistochemical methods. The abnormal accumulation of the defective p53 protein can induce the host to develop anti-p53 antibodies in sera of cancer patients. This study aimed to investigate the presence of anti-p53 antibodies in sera of patients with cholangiocarcinoma and to evaluate the correlation between such antibodies and p53 protein accumulation. METHODOLOGY: The presence of serum anti-p53 antibodies in 49 patients with cholangiocarcinoma was determined by ELISA kit (Pharma Cell, France). Immunohistochemical detection of p53 protein expression was examined in available tissue samples of 36 patients. RESULTS: Serum anti-p53 antibodies were detected in 6 of 49 patients with cholangiocarcinoma (12.2%). Immunostaining of p53 was found in 15 of 36 patients (41.6%) and 4 of these 15 patients (26.7%) were positive for anti-p53 antibodies. The association between anti-p53 antibodies and p53 protein expression was statistically significant (P=0.023). No correlation was found between the presence of anti-p53 antibodies and sex, age, histological grade, site and stage of tumor (P>0.05). CONCLUSIONS: The majority of serum anti-p53 antibodies detected in cholangiocarcinoma were specifically associated with the accumulation of p53 protein in tumor tissues. However, antibody generation against the p53 protein is a relatively uncommon event in cholangiocarcinoma.