Low appendicular skeletal muscle index increases the risk of carotid artery plaque in postmenopausal women with and without hypertension/hyperglycemia: a retrospective study.

BACKGROUND: This study aimed to evaluate whether the low appendicular skeletal muscle index (ASMI) is closely associated with the risk of carotid artery plaque (CAP) in postmenopausal women with and without hypertension/hyperglycemia stratified by body mass index (BMI) categories. METHODS: A total of 2048 Chinese postmenopausal women aged 40-88 years were eventually enrolled in this retrospective study. Skeletal muscle mass was estimated by using segmental multifrequency bioelectrical impedance analysis. ASMI was defined as follows: appendicular skeletal muscle mass(kg)/[height(m)]2. CAP was assessed by B-mode ultrasound. We explored the association between ASMI quartiles or low skeletal muscle mass and the risk of CAP by using multivariate-adjusted logistic regression models. A potential nonlinear relationship was also tested using restricted cubic spline regression. RESULTS: CAP was observed in 289/1074 (26.9%) normal-weight and 319/974 (32.8%) overweight/obese postmenopausal women. Individuals with CAP had significantly lower ASMI values than those without (P < 0.001). The ASMI value also showed a linear relationship with the CAP risk in postmenopausal women stratified by BMI category (Pfor non-linearity > 0.05). In comparison with the highest ASMI quartile, the lowest ASMI quartile was significantly associated with a high risk of CAP development in non-hypertensive individuals with normal weight (odds ratio [OR] = 2.43; 95% confidence interval [CI]: 1.44 ~ 4.12) or overweight/obesity (OR = 4.82, 95% CI: 2.79 ~ 8.33), hypertensive individuals with normal weight (OR = 5.90, 95% CI: 1.46 ~ 11.49) or overweight/obesity (OR = 7.63, 95% CI: 1.62 ~ 35.86), non-hyperglycemic individuals with normal weight (OR = 2.61, 95% CI: 1.54 ~ 4.43) or overweight/obesity (OR = 2.94, 95% CI: 1.84 ~ 4.70), and hyperglycemic individuals with normal weight (OR = 6.66, 95% CI: 1.08 ~ 41.10) or overweight/obesity (OR = 8.11, 95% CI: 2.69 ~ 24.49). Moreover, low skeletal muscle was independently associated with the risk of CAP in postmenopausal women, regardless of the BMI category. CONCLUSION: ASMI was inversely associated with the risk of CAP development in postmenopausal women, especially in patients with high blood sugar and/or hypertension, indicating that skeletal muscle mass maintenance may contribute to prevention of CAP in postmenopausal women.

[Study on the changes in the distribution and chemical states of the hepatic intra-and extra-cellular sodium ion in the rats with severe burns at early stage].

OBJECTIVE: To investigate the changes in the distribution and chemical states of the hepatic intra- and extra-cellular sodium ion in the rats with severe burns, so as to provide guidance for fluid resuscitation at early postburn stage. METHODS: Nineteen adult male Sprague-Dawley (SD) rats were employed in the study and were randomly divided into control (n = 12) and burn (n = 7) groups. The changes in the longitudinal (T1) and transverse (T2) relaxation times of hepatic intra-cellular and extra-cellular sodium in the two groups were studied with 23Na NMR spectroscopy and a shift reagent. RESULTS: After infusion of the shift reagent,the extra-cellular sodium content in rat liver decreased by 17%, with obvious increase in fast T2 component (P < 0.01), indicating an increase in the fraction of Na+ binding sites in the extra-cellular space. The characteristics of relaxation of intra-cellular sodium remained unchanged despite a 57% increment in intra-cellular sodium content. CONCLUSION: The deficiency of sodium as a permeable molecule might be related to the postburn movement of hypertonic sodium from extra-cellular to intra-cellular space. The results indicated that it is reasonable to administer high concentration of sodium in fluid resuscitation during the first 24 postburn hours.

[Role of p38 mitogen-activated protein kinase in the pathogenesis of stress ulcer].

OBJECTIVE: To determine whether the activation of p38 mitogen-activated protein kinase (MAPK) is involved in the pathogenesis of stress ulcer. METHODS: Model of stress ulcer was established with the treatment of rats with water-immersion restraint (WIR) stress. Ulcer index (UI) was macroscopically evaluated as a parameter of gastric mucosal lesions. Expression of phospho- and pan-p38 in gastric mucosa was detected using Western blot analysis. Tumor necrosis factor-alpha (TNF-alpha) and Interleukin 1beta (IL-1beta) gene expressions were analyzed by Northern blot analysis. As indicated in some experiments, rats were pretreated with intravenous injection of the specific p38 MAPK inhibitor CNI-1493 prior to WIR stress and then the changes of UI and TNF-alpha and IL-1beta mRNA expression were examined. RESULTS: The p38 MAPK was persistently activated in the gastric mucosa of rats with WIR stress, with maximal activation after 1 h of stress [(6.8 +/- 3.2) fold of baseline levels, P < 0.01]. Inhibition of p38 MAPK activation with CNI-1493 led to a marked decrease in UI in WIR stress rats. Similarly, the increased gene expression of proinflammatory cytokines TNF-alpha and IL-1beta in gastric mucosa induced by WIR stress were significantly diminished by p38 MAPK inhibition. CONCLUSION: p38 MAPK might have an important role in the pathogenesis of stress ulcer.

Effect of burn injury on relative anaplerosis and gluconeogenesis in rats by 13C magnetic resonance spectrum.

OBJECTIVE: To introduce a safe and specific approach of (13)C magnetic resonance spectrum ((13)C MRS) spectroscopy and investigate the alterations in hepatic anabolism. METHODS: Relative anaplerotic, pyruvate recycling and gluconeogenic fluxes were measured by (13)C MRS isotopomer analysis of blood glucose from rats with 40% body surface area burn injury, and from rats exposed to sham injury. A short chain fatty acid, [U (13)C] propionate which was avidly extracted by the liver, was infused intravenously to deliver (13)C into the citric acid cycle. Proton-decoupled (13)C MRS of deproteinized plasma or extracts of the freeze-clamped liver were used to determine the distribution of (13)C in blood or hepatic glucose. RESULTS: There was no difference in the multiplets detected in the glucose carbon-2 anomer from blood or liver after 45 or 60 minutes of the infusion of the propionate, indicating that steady-state isotopic conditions were achieved. Gluconeogenesis relative to citric acid cycle flux was not altered by burn injury; in both sham and burn groups the rate of glucose production was about equal to flux through citrate synthase. In the sham group of animals, the rate of entry of carbon skeletons into the citric acid cycle was about 4 times than that in the burn group. Similarly, flux through pyruvate kinase (again relative to citrate synthase) was significantly increased after the burn injury. CONCLUSIONS: Since results from analysis of the blood glucose are the same as that of the hepatic glucose, (13)C distribution in the glucose and hepatic metabolism can be assessed based on the (13)C MRS analysis of the blood glucose.

[The role of Kupffer cells on the postburn production of TNFalpha, IL-1beta and IL-6 in severely scalded rats].

OBJECTIVE: To observe the role of Kupffer cells in the postburn production of TNFalpha, IL-1beta and IL-6 in severely scalded rats. METHODS: (1) The production of TNFalpha, IL-1beta and IL-6 from rat Kupffer cells stimulated by burn serum was observed. (2) The postburn change in the expression of cytokine mRNA from rat Kupffer cells was monitored. (3) The change in the plasma cytokine contents in scalded rats was determined after the application of gadolinium chloride, a specific inhibitor of Kupffer cells. RESULTS: Kupffer cells could be stimulated by burn serum to release cytokines TNFalpha, IL-1beta and IL-6. The mRNA expression of TNFalpha, IL-1beta and IL-6 from rat Kupffer cells increased significantly after injury. But the postburn plasma levels of TNFalpha, IL-1beta and IL-6 decreased obviously to 34.71%, 36.99% and 33.7% of those in scalding group, respectively, after the Kupffer cell activity was inhibited. CONCLUSION: The plasma cytokines, i.e. TNFalpha, IL-1beta and IL-6, were primarily produced from Kupffer cells after injury in scalded rats, initiated by TNFalpha, IL-1beta and IL-6 mRNA transcription.