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OBJECTIVE -Dietary patterns in Western populations have been linked to type 2 diabetes, but the role of diet in Japanese remains unclear. We investigated the association between major dietary patterns and glucose tolerance status as measured by A1C in Japanese adults.RESEARCH DESIGN AND METHODS -The groups of subjects were comprised of 3,243 men and 4,667 women who participated in the baseline survey of an ongoing cohort study on lifestyle-related diseases in Fukuoka, Japan. Dietary patterns were derived by using principalcomponent analysis of the consumption of 49 food items, ascertained by a food-frequency questionnaire. Logistic regression analysis was used to estimate sex-specific odds ratios (ORs) of elevated A1C (Ն5.5%), with adjustment for potential confounding variables.RESULTS -The Westernized breakfast pattern characterized by frequent intake of bread but infrequent intake of rice was inversely related to A1C concentrations (P trend ϭ 0.02 in both men and women); the multivariate-adjusted ORs for the highest versus lowest quintiles were 0.60 (95% CI 0.43-0.84) and 0.64 (0.46 -0.90) for men and women, respectively. The seafood dietary pattern was positively associated with A1C concentrations in men only (P trend ϭ 0.01). Neither the healthy nor high-fat dietary pattern was related to A1C.CONCLUSIONS -A dietary pattern featuring frequent intake of white rice may deteriorate glucose metabolism in Japanese men and women, and the salty seafood dietary pattern may have a similar effect in men.

Accumulating evidence suggests that vitamin D has anticarcinogenic effects. However, it is unclear whether the nutrient is involved in the early stage of colorectal carcinogenesis. We examined the association between circulating vitamin D concentrations and colorectal adenomas in Japanese men. The study subjects comprised 656 cases of colorectal adenomas and 648 controls with normal colonoscopy among male self defense officials receiving a pre-retirement health examination between 1997 and 2004. Plasma or serum levels of 25-hydroxyvitamin D [25(OH)D] were measured using a radioimmunoassay method. Logistic regression analysis was used to obtain odds ratios (OR) and 95% confidence intervals (CI) with adjustment for potential confounding variables. Overall, there was no measurable association between circulating 25(OH)D concentrations and colorectal adenomas. When the analysis was restricted to subjects whose blood was taken during the winter season (November-April), the prevalence odds of colorectal adenomas for the highest versus lowest quartile of 25(OH)D was statistically significantly decreased (OR = 0.58; 95% CI = 0.34-0.99). The reduction was more pronounced for the rectum (OR = 0.22) and distal colon (OR = 0.47) than for proximal colon (OR = 0.70). During the summer season (May-October), higher levels of 25(OH)D were associated with an increased odds of small, but not large, adenomas. The present study adds to evidence that high levels of circulating vitamin D measured during darker season is associated with decreased prevalence of adenomas in the distal sites of the colorectum. (Cancer Sci 2010; 101: 1695-1700 T he protective role of vitamin D has recently drawn much interest in colorectal carcinogenesis.(1-3) Vitamin D has long been known to enhance intestinal absorption of calcium, (3) which has also been associated with decreased risk of colorectal cancer.(4) Natural sources of vitamin D are production in the skin by solar exposure, fish oil, and shiitake mushroom. The hypothesis that vitamin D is protective against colorectal cancer in humans was proposed on the basis of a geographical correlation between sunlight exposure and colon cancer mortality in the USA.(5) Subsequently, cohort and case-control studies have observed a fairly consistent, protective association between vitamin D intake and colon or colorectal cancer, as reviewed comprehensively elsewhere.(1) Furthermore, decreased risk of colon, rectal, or colorectal cancer has been observed in individuals with higher circulating 25(OH)D levels in several prospective studies (6)(7)(8)(9)(10)(11)(12) although not all studies have found such an association.(13) With regard to colorectal adenomas, a wellestablished precursor lesion of colorectal cancer, (14,15) six casecontrol studies have addressed the association with plasma or serum concentrations of 25(OH)D, reporting a protective association for adenoma prevalence (16)(17)(18) and recurrence (19,20) consistently with one exception. (21) Of particular interest is a recent observation that an inve...

Dexmedetomidine, a highly selective alpha(2)-adrenoceptor agonist, is used in combination with local anesthetics for sedation and analgesia. We tested the hypothesis that dexmedetomidine used for sedation alters the convulsive potency of racemic bupivacaine and levobupivacaine in awake, spontaneously breathing rats. In the first experiments, male Sprague-Dawley rats were randomly divided into six groups: bupivacaine with no dexmedetomidine (bupivacaine control; BC), bupivacaine with small-dose dexmedetomidine (BS), bupivacaine with large-dose dexmedetomidine (BL), levobupivacaine with no dexmedetomidine (levobupivacaine control; LC), levobupivacaine with small-dose dexmedetomidine (LS), and levobupivacaine with large-dose dexmedetomidine (LL) (n = 10 for each group). Continuous infusion of dexmedetomidine (Groups BC and LC, 0 microg x kg(-1) x h(-1); Groups BS and LS, 3.6 microg x kg(-1) x h(-1); and Groups BL and LL, 10.8 microg x kg(-1) x h(-1)) was started after bolus injection (Groups BC and LC, 0 microg/kg; Groups BS and LS, 0.5 microg/kg; and Groups BL and LL, 1.5 microg/kg). Fifteen minutes after the start of the dexmedetomidine infusion, continuous infusion of bupivacaine (Groups BC, BS, and BL) or levobupivacaine (Groups LC, LS, and LL) at 1 mg x kg(-1) x min(-1) was started and continued until tonic/clonic convulsions occurred. Dexmedetomidine achieved significantly different sedation levels both in Groups BC, BS, and BL and in Groups LC, LS, and LL (P < 0.05). Convulsive doses of bupivacaine and levobupivacaine were significantly larger in Groups BL and LL than in Groups BC and LC, respectively (P < 0.01 for both). Concentrations of bupivacaine and levobupivacaine in plasma and in brain at the onset of convulsions were also larger in Groups BL and LL than in Groups BC and LC (P < 0.01 for both). In the second experiment, yohimbine (1 mg/kg) administered 10 min before and 5 min after the start of dexmedetomidine infusion completely reversed the sedative effect of dexmedetomidine (bolus 1.5 microg/kg, followed by 10.8 microg x kg(-1) x h(-1)). Convulsive doses and plasma and brain concentrations of bupivacaine and levobupivacaine at the onset of convulsions in rats receiving yohimbine and dexmedetomidine were significantly smaller than in those receiving only dexmedetomidine (P < 0.05 for all) and were similar to those without dexmedetomidine or yohimbine. We conclude that dexmedetomidine used for sedation decreases the convulsive potency of both bupivacaine and levobupivacaine in rats. Alpha(2)-adrenoceptor agonism may be involved in this anticonvulsant potency.

Chronic inflammation has been implicated in colorectal carcinogenesis. Several studies have investigated the relationship between C-reactive protein (CRP), a biomarker of inflammation, and colorectal cancer and adenomas, resulting in inconsistent findings. The present study examined the relationship between circulating levels of high-sensitivity CRP and colorectal adenomas. The study subjects comprised 646 cases of colorectal adenoma and 635 controls of normal total colonoscopy among men receiving a preretirement health examination at two hospitals of the Self Defense Forces. Statistical adjustment was made for cigarette smoking, alcohol use, body mass index, physical activity, and other potential confounders. The multivariate-adjusted geometric means showed no measurable differences between adenoma cases and controls, but were higher among cases with larger adenomas (trend P = 0.03). Likewise, although the prevalence odds of colorectal adenomas did not differ according to CRP levels as categorized at the 30th, 60th, and 90th percentiles in the controls, higher levels of CRP were associated with a statistically significant increase in the prevalence odds of large adenomas (³5 mm), but not of small adenomas (<5 mm). The multivariate-adjusted odds ratios of large adenomas for the lowest to highest categories of CRP were 1.00 (referent), 1.81 (95% confidence interval 1.17-2.80), 1.61 (95% confidence interval 1.03-2.52), and 2.21 (95% confidence interval 1.28-3.84), respectively (trend P = 0.01). A positive association between CRP and prevalence odds of large adenomas was not modified by either smoking or overweight. These findings suggest that inflammation is linked to the growth of colorectal adenomas. (Cancer Sci 2009; 100: 709-714) C hronic inflammation has been implicated in carcinogenesis. (1,2) Inflammatory cytokines are considered to promote carcinogenesis by inducing oxidative DNA damage, stimulating cell proliferation and angiogenesis, and inhibiting apoptosis.(1,2) Particular interest has been drawn to the role of inflammation in colorectal carcinogenesis. Chronic inflammatory bowel diseases are known to confer increased risk of colorectal cancer, (3,4) and use of aspirin or non-steroidal anti-inflammatory drugs has consistently been related to reduced risk of colorectal adenomas and cancer in observational and intervention studies.(5-8) Recently, several prospective studies have investigated the relationship between C-reactive protein (CRP), a biomarker of inflammation, and colorectal cancer risk, resulting in inconsistent findings. (9)(10)(11)(12)(13)(14)(15)(16) An increased risk of colorectal cancer associated with increased concentrations of CRP was first reported in the CLUE II study. (9) A positive association between CRP and colorectal caner risk was replicated in three subsequent studies, (10)(11)(12) but no such association was observed in four other studies. (13)(14)(15)(16) One of the latter studies even suggested a decreased risk associated with high concentrations of CRP. (13) Results are al...

The authors determined that serotonin-reduced rats were predisposed to tramadol-induced seizures, and that serotonin concentrations were negatively associated with seizure thresholds. Moreover, serotonin receptor antagonism precipitated seizure manifestation, indicating that tramadol-induced seizures are distinct from serotonin syndrome.

SummaryWe performed a randomised controlled double-blinded study of patients having laparoscopic colectomy with bilateral transversus abdominis plane block plus rectus sheath block, comparing a control group receiving 80 ml levobupivacaine 0.2% in saline with a dextran group receiving 80 ml levobupivacaine 0.2% in 8% low-molecular weight dextran. Twenty-seven patients were studied in each group. The mean (SD) maximum plasma concentration of levobupivacaine in the control group (1410 (322) ng.ml À1) was higher than the dextran group (1141 (287) ng.ml À1 ; p = 0.004), and was reached more quickly (50.6 (30.2) min vs 73.2 (24.6) min; p = 0.006). The area under the plasma concentration-time curve from 0 min to 240 min in the control group (229,124 (87,254) ng.min.ml À1 ) was larger than in the dextran group (172,484 (50,502) ng.min.ml À1; p = 0.007). The median (IQR [range]) of the summated numerical pain rating score at rest during the first postoperative 24 h in the control group (16 (9-20 [3-31]) was higher than in the dextran group (8 (2-11 [0-18]); p = 0.0001). In this study, adding dextran to levobupivacaine decreased the risk of levobupivacaine toxicity while providing better analgesia.