34 weeks. The clinical data were evaluated. The relations between the pattern of end organ damage and maternal outcomes and perinatal mortality and morbidities were analyzed. Results 71. 70% of all 191 S-PE cases were involved in single organ systemic damage, and the rate was higher than those involved in two or more end organ damage. In those women with single end organ damage, placenta (55. 26%) and liver(15. 79%) were the two main organs concerned in early onset group; while in late onset group they were placental(18. 42% , compared with the early onset group P

The nutritional status in early life have been gradually recognized that it can change the status of development and metabolism of adults.Epidemiological evidence and animal model study have found that low birth weight is the risk factors of adult metabolic syndrome and cardiovascular disease.Insulin resistance is a common pathophysiological basis.Renin-angiotensin system and insulin signaling systems interact to promote the development of insulin resistance.

Administration, Inhalation ; Adrenal Cortex Hormones ; pharmacology ; Asthma ; drug therapy ; metabolism ; Child ; Child, Preschool ; Drug Interactions ; Drug-Related Side Effects and Adverse Reactions ; Female ; Humans ; Male ; Theophylline ; pharmacokinetics ; pharmacology ; Treatment Outcome

Objective To explore the protective effect of selenium, an antioxidant, on fluoride-induced renal injury in rats and find out the optimal level of selenium against fluoride toxicity and its valid molecular target.Methods All 80 male weanling SD rats were randomly divided into 8 groups by body weight as follows: normal control group(drinking tap water), fluoride exposed group (drinking water containing 50 mg/L of NaF), low, middle,high selenium exposed groups(drinking water containing 0.375, 0.750, 1.500 mg/L of Na2SeO3) and low, middle,high Se-fluoride groups (drinking water containing both 50 mg/L NaF and three doses of Na2SeO3 as abovementioned, respectively). After 6 months, the rats were killed then the oxidation level and nuclear factor κB(NF-κB)expression level in kidney were measured. Results The weight of the fluoride exposed group[(695.95 ± 55.89 )g]was significantly deceased than the controls[(782.69 ± 56.12)g, P ＜ 0.01]. Glutathione peroxidase(GSH-Px)activity of fluoride exposed group[(55.86 ± 5.09)U/mgprot] was not significantly different but decreased. Tatal antioxidant capacity (T-AOC) activity in fluoride exposed group [(7.54 ± 1.35)U/mgprot] significantly decreased than the controls[(9.03 ± 0.37 )U/mgprot, P ＜ 0.05]. In addition, a significant increase of malondialdehyde ( MDA )in fluoride exposed group[(3.86 ± 0.31 )mnol/mgprot, P ＜ 0.05] was observed than the controls[(3.14 ± 0.32)nmol/mgprot, P ＜ 0.05]. GSH-Px activity of high Se-fluoride group[(74.99 ± 8.41 )U/mgprot] was significantly higher than the fluoride exposed group[(55.86 ± 5.09)U/mgprot, P ＜ 0.05] and its MDA level[(3.17 ± 0.20)nmol/mgprot] was lower than the fluoride exposed group[(3.86 ± 0.31 ) nmol/mgprot, P ＜ 0.05]. NF-κB expression levels of fluoride group, high selenium group and low Se-fluoride group(0.360 ± 0.015,0.367 ± 0.007,0.376 ± 0.006,respecyively) were obviously increased compared with the controls(0.312 ± 0.022, P ＜ 0.05); it was significantly lower in high Se-fluoride group(0.312 ± 0.005) than in fluoride exposed group(0.360 ± 0.015, P ＜ 0.05). Conclusions Na2SeO3 of 1.5 mg/L is the optimal dose against chronic fluorosis on kidney injury under this experimental condition.NF-κB is likely to be a target molecule of the selenium as an antagonist on fluorosis.

Objective To describe the consistency of three diagnostic criteria for metabolic syndrome(MS) proposed by ATP lI[ in 2005,CDS in 2004 and IDF in 2005 in Chinese.Methods With cluster sampling method,5 494 subjects was selected and studied, and the prevalence of MS was calculated according to three definitions with software SPSS 13.0.Results The crude prevalence of MS in Tongzhou area was 15.8% by IDF(2005) definition,8.5% by CDS(2004) definition and 15.8% by NCEP-ATPⅢ definition,women had higher prevalence than men(P

Isoliquiritigenin (ISL) is an active chalcone compound isolated from licorice. It possesses anti-inflammatory and anti-oxidative activities. In our previous study, we uncovered a great potential of ISL in treatment of type 2 diabetes mellitus (T2DM). Therefore, this study aims to reveal the mechanism underlying the alleviatory effects of ISL on T2DM-induced glycolipid metabolism disorder. High-fat-high-sugar diet (HFD) combined with intraperitoneal injection of streptozotocin (STZ) were used to establish T2DM mice model. All animal experiments were carried out with approval of the Committee of Ethics at Beijing University of Chinese Medicine. HepG2 cells were used in in vitro experiments, and sodium palmitate (SP) was applied to establish insulin resistance (IR) model cells. The effects of ISL on body weight, fasting blood glucose levels, and pathological changes in the livers of mice were examined. Enzyme-linked immune sorbent assay (ELISA) and real-time quantitative PCR (RT-qPCR) were applied to detect the regulatory effects of ISL on key targets involved in glucolipid metabolism. Additionally, molecular docking and analytical dynamics simulation methods were used to analyze the interaction between ISL and key target protein. The results indicate that ISL significantly downregulates the transcriptional levels and inhibits the activities of key enzymes involved in gluconeogenesis, including pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), and fructose-1, 6-bisphosphatase (FBP). It also downregulates the transcriptional and protein levels of hepatocyte nuclear factor 4α (HNF4α) and cAMP response element binding protein (CREB), the two transcriptional factors involved in gluconeogenesis. Thus, ISL inhibits hepatic gluconeogenesis in T2DM mice. In addition, ISL reduces total cholesterol (TC) and triglyceride (TG) levels in the livers of T2DM mice. Moreover, ISL downregulates the mRNA levels of lipogenesis genes and upregulates those of genes involved in fatty acid oxidation, lipid uptake, and lipid export. In conclusion, ISL suppresses hepatic gluconeogenesis, promotes lipolysis, and restrains lipogenesis in T2DM mice, thereby improving the abnormal glycolipid metabolism caused by T2DM.

Isoliquiritigenin (ISL) is a flavonoid compound isolated from licorice. It possesses excellent antioxidant and anti-diabetic activities. This study aims to investigate the molecular mechanism underlying the alleviatory effect of ISL on energy metabolism imbalance caused by type 2 diabetes mellitus (T2DM). 8-week-old male C57BL/6J mice were used in in vivo experiments. The high-fat-high-glucose diet combined with intraperitoneal injection of streptozotocin was applied to establish T2DM animal model. All animal experiments were performed in accordance with the Institutional Guidelines of Laboratory Animal Administration issued by the Committee of Ethics at Beijing University of Chinese Medicine. HepG2 cells were used in in vitro experiments. Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (RT-qPCR) were used to examine the protein and mRNA levels of mitochondrial function-related targets. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) in HepG2 cells were measured by the flow cytometry. Additionally, the molecular docking of ISL and key target proteins was analyzed. It was found that ISL significantly inhibited the activity of mitochondrial respiratory chain complex I and increased the protein levels of uncoupling protein 2 (UCP2) in the livers of mice and HepG2 cells. It also obviously decreased the ROS levels and increased the MMP levels in cultured HepG2 cells. In addition, ISL promoted mitochondrial biogenesis by activating proliferator-activated receptor gamma co-activator 1α (PGC-1α) and enhanced mitophagy by upregulating Parkin. It also improved mitochondrial fusion by increasing the mRNA and protein levels of mitofusin 2 (MFN2). In conclusion, ISL alleviates energy metabolism imbalance caused by T2DM through suppression of excessive mitochondrial oxidative phosphorylation and promotion of mitochondrial biogenesis, mitophagy, and fusion.

Objective To evaluate hemodynamic changes in liver treated by transjugular intrahepatic portosystemic stent-shunt(TIPSS)with hepatic computed tomography(CT)perfusion,Doppler ultrasound and portal vein pressure measurement,as well as the correlation among these methods.Methods Hepatic CT perfusion was performed in 9 cirrhotic patients one week before TIPSS and 72 hours after TIPSS. Intraoperative portal vein pressure was measured before and after portosystemic shunt establish.The follow- up hepatic CT perfusion were carried out in 3 cases at 3 months and 6 months postoperatively.The hemodynamic surveillance by Doppler ultrasound were performed in 48 hours and 3 months after TIPSS for 9 cases,and in 6 months after TIPSS for 6 cases.Two cases underwent venography and portal vein pressure measurement in 6 months after TIPSS treatment.Results The mean of portal vein perfusion(PVP),total hepatic blood flow(THBF),hepatic perfusion index(HPI)and portal vein free pressure(PVFP)before TIPSSwere(0.92?0.18)ml?min~(-1)?ml~(-1),(1.28?0.17)ml?min~(-1)?ml~(-1),(28?8)%,and (23.92?0.86)mmHg,respectively.In 72 hours after TIPSS,the mean of PVP,THBF,HPI and PVFP were(0.21?0.15)ml?min~(-1)?ml~(-1),(0.74?0.18)ml?min~(-1)?ml~(-1),(74 +13)%,and (12.62?1.54)mm Hg,respectively.After treatment,the mean of PVP was(0.49?0.05)ml?min~(-1)? ml~(-1)at 3 months and(0.57?0.03)ml?min~(-1)?ml~(-1)at 6 months,respectively.There was negative correlation between PVP and PVFP before TIPSS(r=0.678,P0.05).Moreover,a signifieant correlation was found between the degree of portal vein pressure decrease and portal vein perfusion decrease(r=0.867,P

OBJECTIVETo investigate the protective effect of Danxuetong injection (DXT, a combination of Danshen and Xueshuantong injections) against testicular ischemia-reperfusion injury following testis torsion/detorsion in rats.

METHODSThirty-two 4-week-old healthy male SD rats were randomly divided into four groups of equal number: sham operation, normal saline, single DXT injection, and successive DXT injection. The rat models of testicular ischemia-reperfusion injury were established by 2-hour 720-degree torsion/detorsion of the unilateral testis. At 6 weeks after modeling, the rats were killed and their testes were harvested for measure- ment of testicular coefficients, sperm counts, sperm motility, and the levels of total anti-oxidative capacity (T-AOC) , superoxide dismutase (SOD) , nitric oxide synthase (NOS) , and malondialdehyde ( MDA) in the testis tissue.

RESULTSCompared with the rats of the normal saline group, those of the single DXT injection and successive DXT injection groups showed significant increases in the testicular coefficient (0.11 ± 0.03 vs 0.35 ± 0.04 and 0.40 ± 0.06, P < 0.05), sperm count ([0.46 ± 0.10] vs [1.44 ± 0.50] and [3.00 ± 1.28] x10(9)/ml, P < 0.05), sperm motility ([13.63 ± 14.04] vs [39.63 ± 5.04] and [76.31 ± 3.67]%, P < 0.05), the activity of SOD (72.76 ± 5.58 vs 116.25 ± 8.83 and 133.20 ± 13.84, P < 0.05), and the level of T-AOC (5.58 ± 1.07 vs 13.34 ± 5.81 and 19.21 ± 5.69, P < 0.05), but a remarkable decrease in the content of MDA (42.38 ± 8.94 vs 20.94 ± 5.65 and 15.02 ± 1.03, P < 0. 05) in the injured testes.

CONCLUSIONDXT can effectively rid the testis tissue of oxygen free radicals, improve sperm count and motility by antioxidation, and protect the testis tissue of prepubertal rats against testicular ischemia-reperfusion injury after testis torsion/detorsion. It also has a protective effect on the contralateral testis, and successive injection has a better effect than single injection of DXT.

Animals ; Antioxidants ; therapeutic use ; Drug Therapy, Combination ; methods ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Male ; Malondialdehyde ; metabolism ; Nitric Oxide Synthase ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Spermatic Cord Torsion ; complications ; therapy ; Superoxide Dismutase ; metabolism ; Testis ; blood supply ; metabolism

BACKGROUNDThere is a difficulty in evaluating the in vivo functionality of individual chondrocytes, and there is much heterogeneity among cartilage affected by osteoarthritis (OA). In this study, in vitro cultured chondrocytes harvested from varying stages of degeneration were studied as a projective model to further understand the pathogenesis of osteoarthritis.

METHODSCartilage of varying degeneration of end-stage OA was harvested, while cell yield and matrix glycosaminoglycan (GAG) content were measured. Cell morphology, proliferation, and gene expression of collagen type I, II, and X, aggrecan, matrix metalloproteinase 13 (MMP-13), and ADAMTS5 of the acquired chondrocytes were measured during subsequent in vitro culture.

RESULTSBoth the number of cells and the GAG content increased with increasing severity of OA. Cell spreading area increased and gradually showed spindle-like morphology during in vitro culture. Gene expression of collagen type II, collagen type X as well as GAG decreased with severity of cartilage degeneration, while expression of collagen type I increased. Expression of MMP-13 increased with severity of cartilage degeneration, while expression of ADAMTS-5 remained stable. Expression of collagen type II, X, GAG, and MMP-13 substantially decreased with in vitro culture. Expression of collagen type I increased with in vitro cultures, while expression of ADAMTS 5 remained stable.

CONCLUSIONSExpression of functional genes such as collagen type II and GAG decreased during severe degeneration of OA cartilage and in vitro dedifferentiation. Gene expression of collagen I and MMP-13 increased with severity of cartilage degeneration.

ADAM Proteins ; ADAMTS5 Protein ; Cartilage ; pathology ; Cell Differentiation ; genetics ; physiology ; Cells, Cultured ; Chondrocytes ; metabolism ; Collagen Type II ; genetics ; Collagen Type X ; genetics ; Glycosaminoglycans ; metabolism ; Humans ; Matrix Metalloproteinase 13 ; genetics ; Osteoarthritis ; genetics ; pathology