Dietary patterns and the risk of metabolic syndrome in Chinese adults: a population-based cross-sectional study.

OBJECTIVE: Data on dietary patterns in relation to the risk of metabolic syndrome (MetS) in a middle-aged Chinese population are sparse. The present study was performed to determine the major dietary patterns among a population aged 45-59 years and to evaluate their associations with MetS risk in China. DESIGN: Cross-sectional examination of the association between dietary patterns and MetS. Face-to-face interviews were used to assess dietary intake using a validated semi-quantitative FFQ. OR and 95 % CI for MetS were calculated across quartiles of dietary pattern scores using multivariate logistic regression analysis models. SETTING: City of Linyi, Shandong Province, China. SUBJECTS: Adults (n 1918) aged 45-59 years. RESULTS: Three major dietary patterns were identified: traditional Chinese, animal food and high-energy. After adjustment for potential confounders, individuals in the highest quartile of the traditional Chinese pattern had a reduced risk of MetS relative to the lowest quartile (OR=0·72, 95 % CI 0·596, 0·952; P<0·05). Compared with those in the lowest quartile, individuals in the highest quartile of the animal food pattern had a greater risk of MetS (OR=1·28; 95 % CI 1·103, 1·697; P<0·05). No significant association was observed between the high-energy pattern and risk of MetS. CONCLUSIONS: These findings indicate that the traditional Chinese pattern was associated with a reduced risk, while the animal food pattern was associated with increased risk of MetS. Given the cross-sectional nature of our study, further prospective studies are warranted to confirm these findings.

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183.

BACKGROUND/AIMS: Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms which arise from pancreatic islet cells. Recently, lncRNA MEG3 has been reported as a tumor suppressor in variety cancers. This study aimed to reveal the functional effects of MEG3 on pNETs which has not been uncovered previously. METHODS: The expression of MEG3, miR-183, and BRI3 in BON1 cells were altered by transfection with their specific vectors/shRNA, or mimic/inhibitor. Thereafter, cell viability, apoptosis, the protein expressions of cell cycle related factors, and apoptosis associated factors, as well as cell migration and invasion were respectively assessed by typan blue staining, flow cytometry, western blotting, and transwell assay. RESULTS: MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). MEG3 overexpression decreased BON1 cells viability, invasion, migration, but significantly induced apoptosis. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/ß-Catenin signaling in BON1 cells. CONCLUSION: This study demonstrated a tumor suppressive effect of MEG3 in BON1 cells that suppresses tumor cells growth and metastasis. A novel regulatory mechanism has been revealed that modulation of MEG3/miR-183/BRI3 axis may be pivotal in pNET.

[Influence of inhibitors of nitric oxide synthase and L-arginine on the survival rate in a rat model of traumatic shock].

OBJECTIVE: To investigate the influence of inhibitors of nitric oxide synthase (NOS) and L-arginine on the survival rate in a rat model of traumatic shock. METHODS: A rat model of traumatic shock was established by fracturing the posterior limb of the rat. Nomega-nitro-L-arginine-methyl ester (L-NAME, non-selective NOS inhibitor, 10 mg/kg), amino- guanidine (AG, selective inducible nitric oxide synthase (iNOS) inhibitor, 100 mg/kg) and L-arginine (L-Arg, the precursor of nitric oxide (NO) synthesis 100 mg/kg) were injected intravenously during resuscitation,survival time and survival rate were observed. RESULTS: There were no significant changes in survival time and 24-hour survival rate between L-NAME ((23.80+/-9.09) hours and 40 percent) and control group (18.78+/-4.64)hours and 10 percent, both P>0.05); the survival time of AG group (28.72+/-6.25) hours and L-Arg group (30.64+/-8.77) hours prolonged apparently (both P<0.01), and 24-hour survival rate was also increased (both 80 percent, both P<0.01). CONCLUSION: Selective iNOS inhibitor AG and L-Arg exert beneficial effects on after traumatic shock rats.

[L-arginine decreases P-selectin expression in traumatic shock].

OBJECTIVE: To investigate the changes of P-selectin distribution in the vital organs and plasma during traumatic shock and explore the significance of these changes. METHODS: Twenty-four normal SD rats were randomly assigned into 3 groups (n=8), namely traumatic shock group, L-arginine (L-Arg) treatment and control group. The rats in the former 2 groups were subjected to traumatic shock with L-Arg treatment group given 100 mg/kg L-Arg during resuscitation while the other receiving no medication. The control group received only intubation without trauma or phlebotomy. P-selectin expression in the vital organs including the heart, lungs, spleen, liver and small intestine was determined by means of streptavidin-biotin (SABC) immunocytochemical staining technique and serum P-selectin level assayed by enzyme-linked immunosorbent assay. RESULTS: Before traumatic shock, P-selectin was scarcely detected in the vital organs except the lungs, and the serum was positive for P-selectin expression. Four hours after shock, intense P-selectin expression was observed in almost all the vital organs and the serum P-selectin level was significantly higher than that of the control group. In L-Arg treatment group, P-selectin levels were significantly lowered than those of shock group. CONCLUSIONS: P-selectin expression in the vital organs and serum is up-regulated during traumatic shock in rats, possibly due to severe microcirculatory disorder and endothelial dysfunction in this condition. L-Arg may decrease the expression of P-selectin very likely through promoting endothelial NO synthesis.

Effects of TNP-470 on proliferation and apoptosis in human colon cancer xenografts in nude mice.

AIM: To study the effect of TNP-470 on cell growth, proliferation and apoptosis in human colon cancer xenografts in nude mice. METHODS: Human colon cancer xenografts were transplanted into 20 nude mice. Mice were randomly divided into two groups. TNP-470 treated group received TNP-470(30 mg/kg, s.c) every other day and the control group received a sham injection of same volume saline solution. They were sacrificed after 4 weeks and their tumors were processed for histological examination. The expression of proliferating cell nuclear antigen (PCNA) in tumors was detected using immunohistochemical method with image analysis, and apoptosis in tumor cells was measured by TdT-mediated biotinyated-dUTP nick end labeling (TUNEL) staining. RESULTS: Comparing with controls, tumor growth was significantly inhibited in TNP-470 treated group, the inhibitory rate being 54.4 %. Expression of PCNA in tumors of TNP-470 treated group (PI 54.32+/-11.47) was significantly lower than that of control group (PI 88.54+/-12.36), P<0.01. Apoptosis index (AI) of TNP-470 treated group (18.95+/-1.71) was significantly higher than that of control group (7.26+/-1.44), P<0.001, typical morphological change of apoptosis in tumor cells was observed in TNP-470 treated group. CONCLUSION: Besides the anti-angiogenic effects, TNP-470 can inhibit tumor growth by inhibiting the proliferation and inducing apoptosis of tumor cells.

[Therapeutic effect of L-arginine on traumatic shock in rats].

OBJECTIVE: To evaluate the therapeutic effect of L-arginine (L-Arg) on traumatic shock in rats and explore the possible mechanisms. METHODS: Rat models of traumatic shock were established in Sprague-Daulay rats, which were randomly divided into two groups either to receive L-Arg treatment or not. The plasma concentration of endothelin (ET) and oxygen partial pressure in the tissues from the skeletal muscles, liver and small intestine were measured before and after the shock and 1, 3, and 5 h after resuscitation. The hemodynamics of the rats and their survival rates at 12 and 24 h were recorded. RESULTS: The changes of plasma ET levels and oxygen partial pressure in tissues of both groups were statistically significant after traumatic shock (P<0.05). Plasma ET concentration at 5 h after resuscitation was significantly lower in the treatment group than in the non-treatment shock group (P<0.05), while oxygen partial pressure in the liver and small intestine after resuscitation were significantly higher in the treatment group (P<0.05). The survival rates at 12 and 24 h were also significantly different between the 2 groups. CONCLUSION: Adscititious L-Arg can decrease plasma ET levels, improve oxygen partial pressure of internal organs and significantly increase the survival rate of the rats with traumatic shock.

Dynamic changes in serum level of nitric oxide and its mechanisms in rats with traumatic shock.

OBJECTIVE: To investigate the dynamic changes of serum nitric oxide (NO) level and its mechanisms in rats in traumatic shock. METHODS: Rat models of traumatic shock were established by fracturing the posterior limb of the rats. Serum levels of nitrate/nitrite were measured with the method described by Griess. RESULTS: No significant changes in serum NO level took place during traumatic shock. One hour after resuscitation, however, serum NO level first underwent marked decline and then increased to the peak level at 6 h after resuscitation, retaining a high level till 24 h after resuscitation. No obvious changes of serum NO levels were observed in rats without resuscitation. CONCLUSION: Serum NO level does not significantly alter during traumatic shock, while after resuscitation, NO level increases after transient decrease, possibly due to reperfusion injury.