Spread into regional lymph node is the major route of metastasis in cervical cancer. Although lymph node status is not involved in the International Federation of Gynecology and Obstetrics staging system of uterine cervical cancer, the presence or absence of lymph node metastasis provides important information for prognosis and treatment. In this review, we have attempted to focus on the incidence and patterns of lymph node metastasis, and the issues surrounding surgical assessment of lymph nodes. In addition, the preoperative prediction of lymph node status, as well as the intraoperative assessment by sentinel nodes will be reviewed. Finally, lymph node micrometastasis also will be discussed.

Mean platelet volume (MPV) is an early marker of platelet activation. Larger platelets, compared to small ones, increase platelet adhesion and aggregation, and present a higher thrombotic activity. Some studies have explored the association between MPV and the morbidity of portal vein thrombosis (PVT). The aim of this study was to evaluate the predictive effect of MPV in patients with PVT by a meta-analysis. We searched Pubmed, Web of Science, SCOPUS, OVID, CNKI and CBMD from database inception to September 13,2017. Seven studies in accordance with selection criteria were included. The extraction of basic data was independently conducted by two reviewers. The mean difference in MPV between PVT patients and controls were pooled with weighted mean difference (WMD) and 95% confidence interval of 0.88 fl (95% CI: 0.61-1.15). A random-effect model was chosen for an obvious heterogeneity in the pooling (Chi-square=27.12, df=6, P<000l, I²=77.9%). The sources of heterogeneity were from the difference of primary disease of participants and portal vein diameter. Taken together, our results reveal that MPV is a predictive indicator in patients with PVT.

Non-small-cell lung carcinoma (NSCLC) is one of the most frequently diagnosed malignancies worldwide. Previous studies have shown that microRNA-449b (miR-449b) functions as a tumor suppressor in many cancers. However, the role of miR-449b in NSCLC is still unknown. In the present study, miR-449b was significantly downregulated in NSCLC samples and cell lines. Bioinformatics analysis revealed that 3′-UTR region of leucine rich repeat containing G protein-coupled receptor 4 (LGR4) mRNA had putative complementary sequences to miR-449b,which was further confirmed by the luciferase assay. Western blotting showed that restoration of miR-449b in NSCLC cells decreased the expression of LGR4. Interestingly, over-expression of miR-449b inhibited growth and invasion of NSCLC cells in vitro. Furthermore, ectopic expression of LGR4 reversed miR-449b-suppressed proliferation and invasion of NSCLC cells. Therefore, the data of the present study demonstrate that miR-449b inhibits tumor cell growth and invasion by targeting LGR4 in NSCLC.

Copy number aberrations (CNAs) in chromosome arm 8q have been associated with unfavorable clinical outcomes of several cancers and progressive tumor characteristics of hepatocellular carcinoma (HCC). This study was to identify correlation of CNAs in 8q with clinical outcomes of HCC patients, and further screen for differentially expressed genes in outcome-related CNAs. Array comparative genomic hybridization and expression arrays were performed to detect CNAs and expression levels, respectively. The correlations between CNAs in 8q and outcomes were analyzed in 66 patients, with a median follow-up time of 45.0 months (range, 2.6-108.6 months). One hundred and nine cases were further evaluated to identify differentially expressed genes in the potential outcome-related CNAs. Copy number gain in 8q was observed in 22 (33.3%) of the 66 HCC cases. The most recurrent gains (with frequencies >20%) were 8q13.3-21.3,8q21.3-23.3,8q23.3-24.13,8q24.13-24.3, and 8q24.3. Survival analysis showed that 8q24.13-24.3 gain was significantly associated with reduced overall survival (jP=0.010). Multivariate Cox analysis identified 8q24.13-24.3 gain as an independent prognostic factor for poor overall survival (HR=2.47; 95% CI=1.16-5.26; Р=0.019). Apanel of 17 genes within the 8q24.13-24.3 region, including ATAD2,SQLE,PVT1,ASAP1, and NDRG1 were significantly upregulated in HCCs with 8q24.13-24.3 gain compared to those without. These results suggest that copy number gain at 8q24.13-24.3 is an unfavorable prognostic marker for HCC patients, and the potential oncogenes ATAD2,SQLE, PVT1, ASAP1,and NDRG1 within the regional gain, may contribute coordinately to the 8q24.13-24.3 gain-related poor prognosis.

This prospective study was conducted to compare risk factors and pregnancy outcomes between women with complete placenta previa and those with incomplete placenta previa diagnosed in mid-pregnancy. The study was carried out from April 2014 to December 2015, during which 70 patients with complete previa and 113 with incomplete previa between 20⁺⁰ weeks and 25⁺⁶ weeks of gestation were included. Maternal demographics and pregnancy outcomes were compared between the two groups. Comparisons between categorical variables were tested by chi-squared test and those between continuous variables by Student t test. Resolution of previa occurred in 87.43% of the studied women. The mean gestational age at resolution was 32.1±4.4 weeks. Incidence of maternal age ≥35 years and incidence of prior uterine operation ≥3 were high in women with complete previa (28.6% vs 8.8%, P=0.003; 28.6% vs. 8.8%, P=0.003). Resolution of previa occurred less often in complete previa group (74.3% vs. 95.6%, P=0.001). Women with complete previa admitted earlier (37.3±2.0 weeks 38.1±1.4 weeks, P=0.011) and delivered earlier (37.7±1.2 weeks vs. 38.3±1.4 weeks, P=0.025). Maternal age ≥35 years and prior uterine operation ≥3 increase the risk of complete previa in mid-pregnancy. Placenta previa is more likely to persist in women with complete previa than those with incomplete previa diagnosed in midpregnancy. What is more, women with complete previa in mid-pregnancy delivers earlier.

Pregnancy is a critical stimulator of bone mineral resorption. We used to find the MTHFR gene polymorphisms are related with blood lead levels among pregnant women. Pregnancy-stimulated bone turnover may be associated with MTHFR gene polymorphisms too. In this article, we aimed to determine the relationship between MTHFR gene polymorphisms and bone turnover rates among the pregnant women. The participants including pregnant and non-pregnant women were selected and recruited during their routine prenatal or physical examination from July to October in 2012. A total of 1000 participants, including 250 pregnant women in the first, second, and third trimesters and 250 non-pregnant women, were enrolled in the study. Finally, after excluding 27 participants unable to provide blood samples, 973 eligible participants (i.e., 234,249, and 248 pregnant women in the first, second, and third trimesters, respectively, and 242 non-pregnant women) were included in the research. The MTHFR gene 1298CC homozygote carriers were more susceptible to yield higher plasma homocysteine levels than the 1298AA/AC carriers, with standardized coefficients of 0.086 (P<0.05) and 0.104 (P<0.01) of all the participants and the pregnant women, respectively. The MTHFR gene 1793AA homozygote carriers more likely showed higher plasma osteocalcin levels (standardized β=0.091,P<0.01) than the 1793GG/GA carriers among all the subjects. Plasma homocysteine levels were positively correlated with blood lead levels among the participants and the pregnant women with standardized coefficients of 0.320 (P<0.01) and 0.179 (P<0.01), respectively. Plasma osteocalcin levels were positively associated with blood lead levels among pregnant and non-pregnant women with standardized coefficients of 0.084 (P<0.05) and 0.125 (P<0.01), respectively. In conclusion, homocysteine and osteocalcin contents in plasma are associated with the MTHFR gene A1298C polymorphism and blood lead levels among pregnant women. The MTHFR gene A1298C polymorphism-related homocysteine is a possible risk factor for increased blood lead levels among Chinese women.

Studies concerning the association between arsenic exposure and hepatitis B virus (HB V) infection have been lacking. The present study aimed to examine the association between total urinary arsenic (TUA) and infection of HBV. A total of 5186 participants from National Health and Nutrition Examination Survey (NHANES) 2003–2014 were included in the analysis. We used logistic regression to evaluate the association. We defined two measures of TUA. TUAI was the sum of arsenous acid, arsenicacid, monomethylarsonic acid and dimethylarsenic acid. TUA2 was defined as TUA minus arsenobetaine and arsenocholine. The results showed that the weighted overall prevalence of HBV infection was 6.08%. For NHANES 2003–2014, the medians (interquartile range) of TUAI and TUA2 were 5.60 μg/L (3.97–8.09 μg/L) and 4.91 μg/L (2.36–9.11 μg/L), respectively. Comparing the highest quartile to the lowest quartile after multivariable adjustment showed that the odds ratios (ORs) and 95% confidence intervals (CIs) for TUAI and TUA2 were 2.44 (1.40–4.27) and 2.84 (1.60–5.05), respectively. In conclusion, elevated urinary arsenic was associated with the risk of HBV infection. Further studies, especially prospective studies, are needed to confirm the causal relationship between arsenic exposure and HBV infection.

Postpartum hemorrhage (PPH) is one of the most adverse obstetric outcomes. Our aim is to detect the risks of multilevel PPH in different cesarean section (CS) groups [including nulliparous CS with indications, nulliparous CS without indications, repeat cesarean (RC), vaginal birth after cesarean (VBAC), cesarean after vaginal birth (CAVB)]. We conducted a retrospective cohort study, and the data on 127 145 women collected from January 2014 to May 2016 and from 35 tertiary hospitals in Shanxi province, China, were reviewed. Based on the measuring results of PPH, an ordered logistic regression model was used to analyze the adjusted PPH risks for each of the CS groups, and comparisons were drawn between them. Finally, a total of 99 066 nulliparous (77.92%) and 28 079 multiparous (22.08%) women were observed. The number of CS cases was 61 117, and the rate for CS was 48.07%. A total of 10 029 women did not show indications for CS and accounted for 16.41% of the CS parturient, whereas 9103 women underwent a repeated cesarean, with a CS frequency of 14.89%. The number of VBAC cases was 989, whose rate was 9.88% in prior CS women. The number (proportions) of PPH was 3658 (2.88%) in LI (PPH volume: ≥900 and <1500 mL), 520 (0.41%) in 12 (PPH volume: >1500 and <2100 mL), and 201 (0.16%) in L3 (PPH volume: ≥2100 mL). The Ln (n=l, 2,3, etc.) represented the increasing order of PPH severity. In the adjusted results, compared with spontaneous vaginal delivery (SVD) as the reference group, in the adjusted result for nulliparous, there was a decreased PPH risk in CS with indications (OR: 2.32; CI: 2.04–2.62), which was lower than that of CS without indications (OR: 2.50; CI: 2.01–2.96). The highest PPH risk in all subgroups (i.e. nulliparous and multiparous groups) was observed in the RC (OR: 3.61; CI: 3.16–4.17), which was nearly twice higher than that of the VBAC (OR: 1.82; CI: 1.33–2.52). CAVB (OR: 1.03; CI: 0.65–1.62) showed no significant difference with the reference group. Thus, we deemed that CS should be avoided in nulliparous pregnancies unless indicated, to prevent or reduce the rates for the use of RC or VBAC which are high risks of severe PPH to the parturient women.

The clinical outcomes of five groups of infertility patients receiving frozen-thawed, cleavage-stage embryo transfers with exogenous hormone protocols with or without a depot gonadotropin-releasing hormone (GnRH) agonist were assessed. A retrospective cohort analysis was performed on 1003 cycles undergoing frozen-thawed, cleavage-stage embryo transfers from January 1, 2012 to June 31, 2015 in the Reproductive Medicine Center of Wuhan General Hospital of Guangzhou Military Region. Based on the infertility etiologies of the patients, the 1003 cycles were divided into five groups: tubal infertility, polycystic ovary syndrome (PCOS), endometriosis, male infertility, and unexplained infertility. The main outcome was the live birth rate. Two groups were set up based on the intervention: group A was given a GnRH agonist with exogenous estrogen and progesterone, and group B (control group) was given exogenous estrogen and progesterone only. The results showed that the baseline serum hormone levels and basic characteristics of the patients were not significantly different between groups A and B. The live birth rates in groups A and B were 41.67% and 29.29%, respectively (P<0.05). The live birth rates in patients with PCOS in groups A and B were 56.25% and 30.61%,respectively (P<0.05). The clinical pregnancy, implantation and on-going pregnancy rates showed the same trends as the live birth rates between groups A and B. The ectopic pregnancy rate was significantly lower in group A than in group B. We concluded that the live birth rate was higher and other clinical outcomes were more satisfactory with GnRH agonist cotreatment than without GnRH agonist co-treatment for frozen-thawed embryo transfer. The GnRH agonist combined with exogenous estrogen and progesterone worked for all types of infertility tested, especially for women with PCOS.

Increasing evidence has revealed that maternal cytomegalovirus (CMV) infection may be associated with neurodevelopmental disorders in offspring. Potential relevance between the placental inflammation and CMV-related autism has been reported by clinical observation. Meanwhile, abnormal expression of Toll-like receptor 2 (TLR2) and TLR4 in placenta of patients with chorioamnionitis was observed in multiple studies. IL-6 and IL-10 are two important maternal inflammatory mediators involved in neurodevelopmental disorders. To investigate whether murine CMV (MCMV) infection causes alterations in placental IL-6/10 and TLR2/4 levels, we analyzed the dynamic changes in gene expression of TLR2/4 and IL-6/10 in placentas following acute MCMV infection. Mouse model of acute MCMV infection during pregnancy was created, and pre-pregnant MCMV infected, lipopolysaccharide (LPS)-treated and uninfected mice were used as controls. At E13.5, E14.5 and E18.5, placentas and fetal brains were harvested and mRNA expression levels of placental TLR2/4 and IL-6/10 were analyzed. The results showed that after acute MCMV infection, the expression levels of placental TLR2/4 and IL-6 were elevated at E13.5, accompanied by obvious placental inflammation and reduction of placenta and fetal brain weights. However, LPS 50 μg/kg could decrease the EL-6 expression at E13.5 and E14.5. This suggests that acute MCMV infection during pregnancy could up-regulate the gene expression of TLR2/4 in placental trophoblasts and activate them to produce more proinflammatory cytokine IL-6. High dose of LPS stimulation (50 μg/kg) during pregnancy can lead to down-regulation of IL-6 levels in the late stage. Imbalance of IL-6 expression in placenta might be associated with the neurodevelopmental disorders in progeny.

This study aimed to assess the relationship of OAS2 rs739901 5,-flanking C/A polymorphisms with the susceptibility to Enterovirus-71 (EV71) infection. We investigated 294 hand-foot-mouth disease (HFMD) Chinese children with EV71 infection (165 mild cases and 129 encephalitis cases). The improved multiplex ligation detection reaction (iMLDR) technique was used to test the genotypes. In EV71-infected patients, the CA genotype distribution (P=0.007), A allele frequency (OR 1.32,95% CI 1.0–1.7, P=0.034) and CA+AA carriage frequency (P=0.003) of OAS2 rs739901 5′-flanking were obviously elevated as compared with controls, but there were no statistically significant differences between mild cases and encephalitis cases. In EV71-infected patients, the counts of white blood cells (P=0.034) and blood glucose concentrations (P=0.042) were raised in A carriers (CA+AA). Among different genotypes of encephalitis cases, the contents of cerebrospinal fluid (CSF) showed no significant differences. IFN-γ levels in EV71-infected patients were higher than those in controls (mild group vs. control group, P<0.01; encephalitis group vs. control group, P<0.01;). In encephalitis cases, IFN-γ levels were reduced (P<0.05) in A carriers compared to CC genotype, however, there were no significant differences between genotypes CA and AA (P=0.226). These findings suggest that OAS2 rs739901 5′-flanking C/A genetic polymorphisms involve the susceptibility to EV71 infection, and A allele might be a risk factor of the susceptibility to EV-71 infection.

The mechanisms involved in virus-induced severe hepatitis have not been fully elucidated. In this study, we investigated the role of gamma delta T cell receptors (γδ) T cells in the pathogenesis of fulminant viral hepatitis (FVH) induced by murine hepatitis virus strain 3 (MHV-3). The model of FVH was established by intraperitoneal injection of MHV-3 into Balb/cJ mice. The survival days of mice, and the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were examined. The proportions of γδ T cells in blood, spleen and liver, and cytokines secreted by hepatic γδ T cells were analyzed by flow cytometry. The function of hepatic γδ T cells was examined by cytotoxicity assay. Balb/cJ mice died in 3 to 6 days post MHV-3 infection, with severe hepatic necrosis and significant augmentation of serum ALT and AST levels. The proportions of γδ T cells in blood, spleen and liver were significantly increased post MHV-3 infection, while those of the early activating molecule CD69-expressing γδ T cells and productions of cytokines tumor necrosis factor-alpha (TNF-α) and interferon-γ (IFN-γ) increased remarkably in the liver. These highly activated liver γδ T cells were cytotoxic to MHV-3-infected hepatocytes in vitro and this effect of liver γδ T cells against hepatocytes might involve the TNF-α and IFN-γ pathway. These results demonstrated that γδ T cells might contribute to the pathogenesis of MHV-3-induced FVH through the effector cytokines TNF-α and IFN-γ.

The purpose of this study was to evaluate the roles of different housing environments in neurological function, cerebral metabolism, cerebral infarction and neuron apoptosis after focal cerebral ischemia. Twenty-eight Sprague-Dawley rats were divided into control group (CG) and cerebral ischemia group, and the latter was further divided into subgroups of different housing conditions: standard environment (SE) subgroup, individual living environment (IE) subgroup, and enriched environment (EE) subgroup. Focal cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO). Beam walking test was used to quantify the changes of overall motor function. Cerebral infarction and cerebral metabolism were studied by in vivo magnetic resonance imaging and ¹H-magnetic resonance spectra, respectively. Neuron necrosis and apoptosis were detected by hematoxylin-eosin and TUNEL staining methods, respectively. The results showed that performance on the beam-walk test was improved in EE subgroup when compared to SE subgroup and IE subgroup. Cerebral infarct volume in IE subgroup was significantly larger than that in SE subgroup (P<0.05) and EE subgroup (P<0.05) on day 14 after MCAO. NAA/Cr and Cho/Cr ratios were lower in MCAO groups under different housing conditions as compared to those in CG (P<0.05). NAA/Cr ratio was lower in IE subgroup (P<0.05) and higher in EE subgroup (P<0.05) than that in SE subgroup. NAA/ Cr ratio in EE was significantly higher than that in IE subgroup (P<0.05). Cho/Cr ratio was decreased in MCAO groups as compared to that in CG (P<0.05). A significant decrease in normal neurons in cerebral cortex was observed in MCAO groups as compared to CG (P<0.05). The amount of normal neurons was less in IE subgroup (P<0.05), and more in EE subgroup (P<0.05) than that in SE subgroup after MCAO. The amount of normal neurons in EE subgroup was significantly more than that in IE subgroup after MCAO (P<0.05). The ratio of TUNEL-positive neurons in EE was significantly lower than that in SE subgroup (P<0.05) and IE subgroup (P<0.05). Correlation analysis showed that the beam walking test was negatively correlated with NAA/Cr ratio (P<0.05). Cerebral infarct volume was negatively correlated with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.01). The amount of normal cortical neurons was positively correlated with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.05). The TUNEL-positive neurons showed a negative correlation with both NAA/Cr ratio (P<0.01) and Cho/Cr ratio (P<0.01). This study goes further to show that EE may improve neurological functional deficit and cerebral metabolism, decrease cerebral infarct volume, neuron necrosis and apoptosis, while IE may aggravate brain damage after MCAO.

The aim of the present study was to investigate the effect of lipoxin A4 (LXA4) pretreatment on cognitive function of aged rats after global cerebral ischemia reperfusion, and to explore its possible mechanism. Thirty-six aged male Sprague-Dawley rats were randomly divided into three groups (n=2 each): sham-operation group (S group), global cerebral ischemia reperfusion group (I/R group) and LXA4-pretreatment group (L group). The rat model of global cerebral ischemia reperfüsion was established by occlusion of the bilateral common carotid artery with hypotension. The cognitive function of rats was determined by a step-down type passive avoidance test and Morris Water Maze test on the third day after reperfUsion. Rats were sacrificed after Water Maze test and the pathological changes of hippocampal CAI region were observed and the related inflammatory mediators were determined. As compared with S group, the escape latency in I/R group was prolonged from the first day to the fifth day, while that in L group was prolonged from the first day to the third day. The retention time in I/R group and L group in the first quadrant was shortened. The reaction time, frequency of reaction mistake and frequency of escape mistake in I/R group increased, and the latent period shortened. The frequency of escape mistake in L group increased, and the damage in the hippocampal CAI region of I/R group and L group was obvious. The levels of S-100β, TNP-α, IL-lβ, IL-10 and NF-κB in I/R group and L group increased. As compared with I/R group, the escape latency in L group was shortened from the first day to the fifth day, and the retention time in the first quadrant prolonged. The reaction time, frequency of reaction mistake and frequency of escape mistake in L group decreased, and the latent period prolonged. The damage in the hippocampal CAI region of L group was alleviated as well. The levels of S-100β, TNP-α, IL-lβ and NF-κB in L group decreased, and those of IL-10 increased. It can be concluded that LXA4 pretreatment can improve the cognitive function in aged rats after global cerebral ischemia reperfusion probably by inhibiting the inflammatory reaction.

Mechanical ventilation (MV) with large tidal volumes can increase lung alveolar permeability and initiate inflammatory responses, resulting in ventilator-induced lung injury (VILI). The mechanisms of the injurious effects of MV and the genetic susceptibility remain unclear. VILI-related genes such as cysteine-rich angiogenic inducer 61 (Cyr61) have been demonstrated to play a detrimental role in the aggressive ventilation strategies. In the present study, we investigated the involvement of Cyr61 in the VILI and the underlying mechanism. A549 cells were exposed to cyclic stretch of varying durations and then the mRNA and protein levels of Cyr61 were measured by real-time PCR and Western blotting, respectively. Additionally, after exposure of A549 cells to cyclic stretch for 5 min to 1 h,the expression levels of nuclear factor kappaB (NF-κB) and IL-8 were detected by E L I S A and Western blotting. Thereafter, Cyr61 expression was depressed in A549 cells with the siRNA pGenesil1.1-Cyr61-3 before the cyclic stretch, and IL-8 secretion and the activation of NF-κB pathways were probed by ELISA and Western blotting, respectively. Moreover, A NF-κB inhibitor (PDTC) and an activator (TNF) were used before mechanical stretch. Realtime PCR and ELISA were performed to detect the mRNA and protein of IL-8, respectively. The results showed that the mechanical cyclic stretch led to increased Cyr61 expression at mRNA and protein levels in A549 cells. Additionally, cyclic stretch also mobilized NF-κB from the cytoplasm to the nucleus and increased IL-8 secretion in A549 cells. The inhibition of Cyr61 blocked the NF-κB activation and IL-8 secretion in response to cyclic stretch. Inhibition of NF-κB attenuated the mRNA and protein expression of IL-8 in A549 cells transfected with Cyr61 siRNA. It was suggested that Cyr61/NF-κB signaling pathway mediates the upregulation of IL-8 in response to cyclic stretch in A594 cells. These findings support the hypothesis that Cyr61 plays a critical role in acute lung inflammation triggered by mechanical strain.

The spinal origin of cholestatic itch in experimental obstructive jaundice mouse model remains poorly understood. In this study, the jaundice model was established by bile duct ligation (BDL) in mice, and differential gene expression patterns were analyzed in the lower thoracic spinal cord involved in cholestatic pruritus after BDL operation using high-throughput RNA sequencing. At 21st day after BDL, the expression levels of ENSRNOG00000060523, ENSRNOG00000058405 and ENSRNOG00000055193 mRNA were significantly up-regulated, and those of ENSRNOG00000042197, ENSRNOG00000008478, ENSRNOGOOOOOO19607, ENSRNOG00000020647, ENSRNOG00000046289, Gemin8, Serpina3n and Trim63 mRNA were significantly down-regulated in BDL group. The RNAseq data of selected mRNAs were validated by RT-qPCR. The expression levels of ENSRNOG00000042197, ENSRNOG00000008478, ENSRNOGOOOOOO 19607, ENSRNOG00000020647, ENSRNOG00000046289 and Serpina3n mRNA were significantly down-regulated in BDL group. This study suggested that cholestatic pruritus in experimental obstructive jaundice mouse model is related with in the changes of gene expression profiles in spinal cord.

U-shaped sacral fractures are rare and often difficult to diagnose primarily due to the difficulty in obtaining adequate imaging and the severe associated injuries. These fractures are highly unstable and frequently cause neurological deficits. The majority of surgeons have limited experience in management of U-shaped sacral fractures. No standard treatment protocol for U-shaped sacral fractures has been available till now. This study aimed to examine the management of U-shaped sacral fractures and the early outcomes. Clinical data of 15 consecutive patients with U-shaped sacral fracture who were admitted to our trauma center between 2009 and 2014 were retrospectively analyzed. Demographics, fracture classification, mechanism of injury and operative treatment and deformity angle were assessed. All the patients were treated with lumbopelvic fixation or (and) sacral decompression. EQ-5d score was applied to evaluate the patients’ quality of life. Of the 15 consecutive patients with U-shaped sacral fracture, the mean age was 28.8 years (range: 15–55 years) at the time of injury. There were 6 females and 9 males. The mean followup time was 22.7 months (range: 9 47 months) and mean full weight-bearing time was 9.9 weeks (range: 8–14 weeks). Ten patients received lumbopelvic fixation and sacral decompression, one lombosacral fixation, and 4 merely sacral decompression due to delayed diagnosis or surgery. The post-operation deformity angle (mean 27.87°, and range: 8°–90°) of the sacrum was smaller than that pre-operation (mean 35.67; range: 15–90) with no significance difference noted. At the latest follow-up, all patients obtained neurological recovery with different extents. Visual analogue score (VAS) was reduced from preoperative 7.07 (range: 5–9) to postoperetive 1.93 (range: 1–3). All patients could walk without any aid after treatment. Eight patients were able to care for themselves and undertook some daily activities. Five patients had returned to work foil time. In conclusion, lumbopelvic fixation is an effective method for stabilization of U-shaped sacral fractures with fewer complications developed. Effective reduction and firm fixation are the prerequisite of early mobilization and neurological recovery. Sacral decompression effectively promotes neurological recovery even in patients with old U-shaped sacral fractures.

This study aims to evaluate the clinical outcomes of endoscopic vein harvesting (EVH) for coronary artery bypass grafting (CABG) in obese patients. Totally, 153 obese patients who underwent EVH (n=81) or standard bridging technique (SBT, n=12) in CABG surgery from May 2012 to October 2014 in our hospital were enrolled in this retrospective non-randomized controlled study. The general situation of operation, postoperative complications and short medium-term outcomes were analyzed. The baseline characteristics were similar between these two groups (P>0.05). There were no statistical differences in total operation time (226±28 min vs. 224±30 min, P>0.05), number of damaged vessels (0.12±0.05 vs. 0.16±0.06,P>0.05) and short medium-term outcomes including revascularization rate (1.25% vs. 2.78%, i 0.05), vessel dysfunction rate (11.25% vs. 11.11%,P>0.05) and mortality (0.00% v . 0.00%, P>0.05). Use of EVH was associated with significant reduction of total harvesting time (41 ±6 min vs. 63± 11 min, P<0.05), incision length (4.4±1.1 cm 18.2±4.5 cm, P<0.05) and postoperative lower extremity complications (P<0.05). EVH can reduce the risk of wound complications, whereas does not influence short- and medium-term outcomes in obese patients. It can be considered a reliable procedure of harvesting vessel conduits for obese patients undergoing CABG.

This study examined the effect of saponins from Tupistra chinensis Bak (STCB) on the growth of sarcoma S-180 cells in vitro and in mouse xenografts as well as the underlying mechanisms. Cell proliferation was assessed by MTT assay. Cell cycle distribution was determined by flow cytometry. Sarcoma S-180 tumor-bearing mice were treated with different doses of STCB with 10 μg/mL 5-fluorouracil (5-Fu) as a positive control. The activity of nuclear factor (NF)-κB was detected by gel mobility shift assay. The mRNA level of NF-κB was determined by real-time quantitative RT-PCR. The results showed that in vitro STCB inhibited the growth of S-180 cells in a concentration-dependent manner, which was accompanied by cell cycle arrest at S-phase. In vivo STCB significantly inhibited the growth of S-180 tumor mouse xenografts in a dose-dependent manner with apparent induction of cell apoptosis. Moreover, STCB inhibited the activity of NF-κB p65 and reduced the expression of NF-κB p65 mRNA in mouse xenografts. It was concluded that STCB inhibits the proliferation and cell cycle progression of S-180 cells by suppressing NF-κB signaling in mouse xenografts. Our findings suggest STCB is a promising agent for the treatment of sarcoma.

This study aims to explore the effect and mechanism of Jiao-tai-wan (JTW) on systemic and tissue-specific inflammation and insulin resistance in obesity-resistant (OR) rats with chronic partial sleep deprivation (PSD). OR rats with PSD were orally given JTW and Estazolam for 4 weeks. The amount of food intake and metabolic parameters such as body weight increase rate, fasting plasma glucose (FPG), fasting insulin (FINS), homeostasis model assessment-insulin resistance (HOMA-IR) and plasma inflammatory markers were measured. The expression levels of circadian proteins cryptochrome 1 (Cryl) and cryptochrome 2 (Cry2) in hypothalamus, adipose and liver tissues were also determined. Meanwhile, the mRNA expression of inflammatory markers, activity of nuclear factor kappa B (NF-κB) p65 protein, as well as the expression levels of insulin signaling pathway proteins in hypothalamus, adipose and liver tissues were measured. Additionally, cyclic adenosine 3′, 5′-monophosphate (cAMP) and activity of vasodilator-stimulated phosphoprotein (VASP) in hypothalamus tissue were measured. JTW significantly decreased the body weight increase rate and food intake, ameliorated systemic inflammation and insulin resistance. JTW effectively ameliorated inflammation and increased PI3K/AKT signaling activation in hypothalamus, adipose and liver. Interestingly, all these changes were associated with the up-regulation of circadian gene Cryl and Cry2 protein expression. We also found that in hypothalamus tissue of PSD rats, down-regulation of Cryl and Cry2 activated cAMP/PKA signaling and then led to inflammation, while JTW inhibited this signaling. These results suggested that JTW has the beneficial effect on ameliorating inflammation and insulin resistance in partially sleep-deprived rats by up-regulating Cry expression.

Human tongue cancer (TC) is an aggressive malignancy with a very poor prognosis. There is an urgent need to elucidate the underlying molecular mechanisms involved in TC progression. mRNA expression profiles play a vital role in the exploration of cancer-related genes. Therefore, the purpose of our study was to identify the progression associated candidate genes of TC by bioinformatics analysis. Five microarray datasets of TC samples were downloaded from the Gene Expression Omnibus (GEO) database and the data of 133 TC patients were screened from The Cancer Genome Atlas (TCGA) head and neck squamous cell carcinoma (HNSC) database. The integrated analysis of five microarray datasets and the RNA sequencing data of TC samples in TCGA-HNSC was performed to obtain 1023 overlapping differentially expressed genes (DEGs) in TC and adjacent normal tissue (ANT) samples. Next, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was conducted to enrich the significant pathways of the 1023 DEGs and PI3KAkt signaling pathway (P=0.011) was selected to be the candidate pathway. A total of 23 DEGs with |log2 fold change (FC)| ≥1.0 in phosphatidylinositol 3-kinase-serine/threonine kinase (PI3K-Akt) signaling pathway were subjected to survival analysis of 125 eligible TC samples in TCGA database, indicating increased integrin-α3 gene (ITGA3) expression was significantly associated with poorer prognosis. Taken together, our study suggested ITGA3 may facilitate the development of TC via activating PI3K-Akt signaling pathway.

This study aimed to determine the impact of dentinal tubule orientation on dentin bond strength to provide a reference for clinical cavity preparation in resin-bonded restoration. Patients aged 13–16 years were selected, including 18 males and 21 females. Forty-eight human maxillary first premolars from orthodontic extractions were chosen to prepare the test models with the dentinal tubule orientations perpendicular and parallel to the bonding substrate. The test models in the vertical and parallel groups were divided into three groups: total-etching with 20% phosphoric acid, total-etching with 35% phosphoric acid and self-etching, with the dentinal tubule surfaces bonded with composite resin blocks in each group. After the standard test models of dentinal tubule-composite resin blocks were placed in distilled water and stored at 37°C for 24 h, shearing tests were performed using a universal material testing machine at a crosshead speed of 0.5 mm/min. The bond strength values in the vertical group were 19.33±1.59 MPa for the 20% phosphoric acid group, 21.39±2.34 MPa for the 35% phosphoric acid group, and 16.88±1.54 MPa for the self-etching group. The bond strength values in the parallel group were 24.53±1.99 MPa for the 20% phosphoric acid group, 25.16±2.88 MPa for the 35% phosphoric acid group, and 20.83±1.99 for the self-etching group. After using same total-etching adhesive, the shear bond strength of the parallel group was higher than that of the vertical group, and the difference was statistically significant (P<0.05). Regardless of vertical group or parallel group, the difference in the bond strength value between the total-etching groups and the self-etching group was statistically significant (P<0.05). It was concluded that the dentin bonding substrate which was parallel to the direction of the dentin tubule achieved an improved bond strength; the total-etching adhesives achieved higher bond strengths in dentin bond than the self-etching adhesives.

Renal transplant (RT) recipients have a high risk of developing cardiovascular diseases. However, the effects of renal transplantation on the development of arteriosclerosis have been controversial. The carotid intima-media thickness (СШТ) and diameter (CD) are important indicators of vascular remodeling and arteriosclerosis. In this study, 31 patients with hemodialysis (HD), 31 RT recipients and 84 age- and gender-matched control subjects were enrolled. Their CIMT and CD were measured by ultrasonic radiofrequency tracking, and the linear regression models and Z test were used to identify the progression of arteriosclerosis and the risk factors. Compared with HD group, RT group had significantly lower CIMT and CD. CIMT was found to be associated with age, body weight, resistance index and diastolic velocity, while CD was associated significantly with age, body weight, pulsatility index, end diastolic velocity and diastolic blood pressure (DBP), respectively. The correlation curves between CIMT and age showed the slopes of curves were decreased successively in control, RT and HD groups, and the curves between CD and age showed the slopes were decreased in order of RT > control > HD groups. It was concluded that CIMT and CD were significantly correlated with age in RT and moderately with age in HD patients. RT could reduce the progress of arteriosclerosis in patients with end-stage renal disease.

Genetic variants in glioma tumor suppressor candidate region gene 1 (GLTSCR1) and ATM serine/threonine kinase (ATM) have been associated with various cancer risks. Epidemiological studies also revealed the association of variants of GLTSCR1 and ATM genes with different brain tumors. However, little is known about the relationship between both gene polymorphisms and lung cancer risk. We conducted a Chinese hospital-based case-control study involving 384 lung cancer cases and 387 cancer-free controls. No significant differences in the single polymorphism (GLTSCR1 rs1035938 and ATM rs11212592) association were found in five genetic models (co-dominant, dominant, recessive, over-dominant and log-additive models) (adjusted by smoking duration). Join effect of three SNPs (PPP1R13L rs1970764, CD3EAP rs967591, GLTSCR1 rs1035938) on chromosome 19q13.3 showed that the designated haplotype2 (rs1970764^G-rs967591^A-rs1035938^C) [OR (95% CI)=1.60 (1.11−2.32), P=0.012] and haplotype8 (rs1970764^G-rs967591^G-rs1035938^T) [OR (95% CI)=2.45 (1.17−5.12), P=0.018] were associated with increased risk of lung cancer (adjusted by smoking duration). The analysis of multifactor dimensionality reduction revealed that two 3-way models were the best fit models in analyses of 2 loci (P<0.001) or 4 loci (P=0.015−0.016). The entropy-based analysis indicated the strongest synergistic effect between PPP1R13L rs1970764 and ATM rs11212592 in analysis of four genes. In conclusion, our study suggests that haplotypes consisting of PPP1R13L rs1970764-CD3EAP rs967591-GLTSCR1 rs1035938 on Chr19q13.3, interaction of smoking and GLTSCR1 rs1035938-ATM rs11212592, and synergistic action of PPP1R13L rs1970764 and ATM rs11212592 may associate with lung cancer risk in the Chinese population.

Along with the development of society and the rapid economic growth in the past decades, hypertension and other chronic diseases have become important reasons for people’s poverty caused by illness in China. This study collected a total of 5857 people from 2010 to 2013 randomly from the database of the Medical Insurance Department (MID), including 3229 people in Hubei province and 2628 people in Guangdong province. One-way ANOVA was used to compare the total medical expense, out-of-pocket (OOP) expense and hospital stay between variables. A multiple linear regression analysis was done to identify possible risk factors of total medical expense. The results showed that the average total medical expense per capita was 5709.89 yuan, and the medical expense per capita was 7053.58 and 4555.97 yuan in Guangdong province and Hubei province, respectively. The medical expense of hypertensive inpatients decreased from 7222.32 yuan in 2012 to 4894.66 yuan in 2013. There were no significant differences in medical expenses between different genders of hypertensive patients (P>0.05). People of different ages, provinces, medical insurances and medical institution levels showed significant differences in medical expenses. The government should increase the investment in chronic disease management and treatment in the central and western regions to narrow the gap with the eastern region. Medical insurance fund payment should be improved to ensure the fairness of the use of medical services in different medical insurances. And measures should be taken to encourage chronic patients to visit primary medical institutions to effectively reduce medical expenses.