Voltage-gated sodium (Nav) channels are critical players in the generation and propagation of action potentials by triggering membrane depolarization. Mutations in Nav channels are associated with a variety of channelopathies, which makes them relevant targets for pharmaceutical intervention. So far, the cryoelectron microscopic structure of the human Nav1.2, Nav1.4, and Nav1.7 has been reported, which sheds light on the molecular basis of functional mechanism of Nav channels and provides a path toward structure-based drug discovery. In this review, we focus on the recent advances in the structure, molecular mechanism and modulation of Nav channels, and state updated sodium channel blockers for the treatment of pathophysiology disorders and briefly discuss where the blockers may be developed in the future.

As a rapidly progressing field in oncology, the adoptive transfer of T cells that have been genetically modified with chimeric antigen receptors (CARs) has shown striking efficacy in the management of hematological malignancies and has been reported in a number of clinical trials. Of note, CAR T cell therapy has shown extraordinary potential, especially in relapsed/refractory patients. However, there are still challenges regarding the further development of this strategy, spanning from engineering and manufacturing issues, to limited applications, to accompanying toxicities. In this review, we will summarize the general knowledge of this novel method, including receptor composition, applications, adverse events and challenges. Additionally, we will propose several comprehensive recommendations.

Malaria remains a global health problem. The relationship between Plasmodium spp. and the gut microbiota as well as the impact of Plasmodium spp. on the gut microbiota in vertebrate hosts is unclear. The aim of the current study was to evaluate the effect of blood-stage Plasmodium parasites on the gut microbiota of mice. The gut microbiota was analyzed by 16S rRNA sequencing and bioinformatic analyses at three stages. The gut microbiota changed during the three phases: the healthy stage, the infection stage, and the cure stage (on the 9th day after malarial elimination). Moreover, the gut microbiota of these infected animals did not recover after malaria infection. There were 254 operational taxonomic units (OTUs) across all three stages, and there were unique strains or OTUs at each stage of the experiment. The percentages of community abundance of 8 OTUs changed significantly (P<0.05). The dominant OTU in both the healthy mice and the mice with malaria was OTU265, while that in the cured mice was OTU234. In addition, the changes in OTU147 were the most noteworthy. Its percentage of community abundance varied greatly, with higher values during malaria than before malaria infection and after malaria elimination. These results indicated that the external environment influenced the gut microbiota after host C57BL/6 mice were infected with blood-stage P. berghei ANKA and that the same was true during and after elimination of blood-stage P. berghei ANKA. In addition, we could not isolate OTU147 for further study. This study identified gut microbiota components that were reconstructed after infection by and elimination of blood-stage P. berghei ANKA in host C57BL/6 mice, and this process was affected by P. berghei ANKA and the external environment of the host.

Licorice, one of the most widely used medicinal herbs in East Asia, has effects such as anti-inflammation, antioxidant, and detoxifying. This study aimed to evaluate the protective effect of licorice on brucine-induced nephrotoxicity. Sprague Dawley rats were administered with brucine intraperitoneally for 7 consecutive days with or without treatment with licorice. The content of blood urea nitrogen and creatinine in serum, the activities of superoxide dismutase and content of glutathione, malonaldehyde in kidney tissue were detected. Hematoxylin-eosin staining was employed to observe the histopathological changes of kidney. The expression and phosphorylation levels of protein were evaluated by Western blotting and immunohistochemical analysis. The results illustrated that treatment with licorice extracts (LE) significantly protected against the brucine-induced nephrotoxicity by reducing the content of blood urea nitrogen and serum creatinine, attenuating pathologic damage. The unbalance of oxidative stress was repaired by LE via increasing the level of glutathione, promoting the activities of superoxide dismutase and decreasing the content of malonaldehyde. In addition, LE overturned the influence of brucine on apoptosis-related protein and signal transducer and activator of transcription-3 (STAT3) activation. Taken together, these data demonstrate that licorice may attenuate brucine-induced nephrotoxicity via inactivation of oxidative stress and mitochondrial-mediated apoptosis pathway. More importantly, the renoprotective effects may be mediated, at least partly, by preventing the activation of STAT3 protein.

Absent in melanoma 2 (AIM2) inflammasome is a crucial link bridging the innate host defense and the subsequent adaptive immunity when activated by exogenous double stranded DNA (dsDNA). Through establishing models of disseminated murine cytomegalovirus (MCMV) infection in BALB/c and C57BL/6 mice, we evaluated dynamic expression of AIM2 inflammasome components and its relationship with pathological damage and viral replication, trying to figure out whether AIM2 inflammasome is related to the chronic mechanism of MCMV. BALB/c and C57BL/6 mice were sacrificed on day 0, 1, 3, 7, 14 and 28 post infection. Expression levels of AIM2, pro-caspase-1, caspase-1 p20, pro-IL1β and mature IL1β in primary peritoneal macrophages (PMs) and spleens were detected by Western blotting. Contents of IL18 in the serum were detected by ELISA. Pathological examinations of livers were performed, and mRNA levels of MCMV glycoprotein B (gB) in salivary glands also assessed. Results showed that expression levels of AIM2 in PMs and spleens of C57BL/6 mice increased on day 3, even continued to day 28; caspase-1 p20 and mature IL1β increased on day 7, 14 and 28; the persistently high expression of IL18 in the serum started on day 1, showing a double peak curve. As for BALB/c mice, expression of AIM2 in PMs increased on day 1 and day 7, while contents of AIM2 in spleens increased on day 1 and day 3; caspase-1 p20 and mature IL1β merely increased 7 days fter infection. Thereafter, expression levels of AIM2, caspase-1 p20, mature IL1β and IL18 were limited; the duration of AIM2 inflammasome activation in BALB/c mice was much shorter than that in C57BL/6 mice. The severer pathological damage and more viral replications in BALB/c mice further proved the deficient antiviral immunity to MCMV. In conclusion, the activation of AIM2 inflammasome in BALB/c mice was short-lived, which is quite possibly related to the chronicity of MCMV infection.

This study aimed to assess whether genetic variants of dendritic cell-associated C-type lectine-1 (Dectin-1), Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 (MyD88) influence the susceptibility to pulmonary invasive fungal disease (IFD) in patients with acute myeloid leukemia (AML) from a Chinese Han population. Eight single nucleotide polymorphisms (SNPs) of Dectin-1 (rs16910526, rs3901533, and rs7309123), TLR2 (rs5743708), TLR4 (rs4986790 and rs4986791) and MyD88 (rs4988453 and rs4988457) in the genomic DNA of 172 adult AML patients were genotyped. Pulmonary IFD was diagnosed as proven or probable according to the 2008 European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group (EORTC/MSG) consensus guidelines. SNPs that were significant in the univariate analysis were further analyzed using the multiple logistic regression analysis to determine their association with the occurrence of pulmonary IFD. The mRNA expression of Dectin-1 was detected according to the genotype by quantitative realtime PCR (qRT-PCR), and the correlation of this expression with the occurrence of pulmonary IFD in AML patients was analyzed. Two Dectin-1 intron SNPs (rs3901533 and rs7309123) were found to be significantly associated with the susceptibility to pulmonary IFD in AML patients in a Chinese Han population. Significant associations were noted between pulmonary IFD and Dectin-1 rs3901533 dominant model (G/T+G/G vs. T/T, OR: 2.158; 95% CI: 1.109–4.2, P=0.02), Dectin-1 rs3901533 G allele (OR: 2.201; 95% CI: 1.206–4.019, P=0.01), or Dectin-1 rs7309123 C allele (OR: 1.919; 95% CI: 1.047–3.518, P=0.03). There were no significant associations between pulmonary IFD and the remaining Dectin-1 SNPs (rs16910526), TLR2 (rs5743708), TLR4 (rs4986790 and rs4986791) or MyD88 (rs4988453 and rs4988457). In conclusion, two Dectin-1 SNPs (rs3901533 and rs7309123) are associated with increased susceptibility to pulmonary IFD in AML patients in a Chinese Han population.

The activation of the Wnt/β-catenin signaling pathway in oval cells after liver injury is implicated in hepatocarcinogenesis. Diwu Yanggan capsule is a Chinese herbal medicine that has been used for treating liver disorder. The present study aimed to examine the mechanism by which Diwu Yanggan inhibits liver carcinogenesis, and the involvement of the Wnt/β-catenin signaling pathway. Diwu Yanggan capsule was administered to 2-acetaminofluorene/partial hepatectomy (2-AAF/PH) rats, a murine model of liver injury. The biomarkers of oval cells and key proteins in the Wnt/β-catenin signaling pathway were assessed on postoperative day 8, 10, 14, 17, 19 and 22. The results showed that treatment with Diwu Yanggan was associated with reduced expression of oval cell and stem cell biomarkers in the 2-AAF/PH animals. The expression pattern of key proteins in the Wnt/β-catenin pathway was altered in Diwu Yanggan-treated animals, indicating that the Diwu Yanggan treatment accelerated the activation of the Wnt/β-catenin pathway in the initial stage and contributed to its deactivation in the later stage. Histological findings indicated that hepatocyte proliferation was suppressed in Diwu Yanggan-treated animals, compared with untreated 2-AAF/PH animals. Taken together, Diwu Yanggan capsule may reduce the risk of hepatocarcinogenesis by modulating the Wnt/β-catenin signaling pathway.

The aim of the present study was to observe the protective effects of α-lipoic acid (ALA) on vascular injury in rats with hyperuricemia (HUA). The ALA treatment groups (10, 30 and 90 mg/kg, respectively) were administered with ALA via gavage for 2 weeks. Subsequently, the levels of blood urea nitrogen (BUN), creatinine (CREA), uric acid (UA), total cholesterol (TC), high density lipoprotein-C (HDL-C) and low density lipoprotein-C (LDL-C) were measured; the activities of glutathione peroxidase (GSH-Px), catalase (CAT), malonaldehyde (MDA), superoxide dismutase (SOD) and xanthine oxidase (XOD) were also determined. The thoracic aorta of rats in each experimental group was observed under a light microscope; ultrastructural analysis was performed. SOD and CAT protein contents were investigated by Western blotting. The results revealed that: i) Compared with the model group, the levels of UA were decreased in the ALA groups and the levels of BUN, CREA, TC, and LDL-C decreased in the 30 and 90 mg/kg ALA groups (P<0.05); ii) compared with the model group, the activities of GSH-Px, SOD and XOD were increased and the levels of MDA were reduced in the 90 mg/kg ALA group (P&lt;0.05); and iii) in the model and 10 mg/kg ALA groups, edema and shedding were observed in endothelial cells. Compared with the model and 10 mg/kg ALA groups, the 30 and 90 mg/kg ALA groups exhibited fewer swollen endothelial cells. In summary, the results of the present study indicated that HUA resulted in vascular oxidative stress injury and decreased the activity of antioxidative enzymes, which leads to endothelial cell damage and vascular lesions. ALA may serve as a therapeutic agent for the treatment of HUA-induced endothelial dysfunction.

The molecular mechanisms underlying the development of intrahepatic cholangiocarcinoma (ICC) are not clear yet. In this study, we investigated the involvement of Notch1 in the development of ICC. The cDNA microarray analysis showed that Notch1 expression was higher in ICC tissues than in normal biliary epithelial cells. Stable transfection of Notch1 receptor intracellular domain (NICD1) by hydrodynamic tail vein injection induced ICC formation in mice. Western blotting confirmed that Notch1 signaling was activated in human ICC cell lines and mouse ICC tissues. Silencing Notch1 with specific short interfering RNA (siRNA) inhibited the proliferation of ICC cells. Flow cytometry and Western blotting indicated that apoptosis was induced in Notch1-silenced ICC cells compared with controls. Additionally, Notch1 silencing was associated with the inhibition of hairy and enhancer of split-1 (Hes1) and activation of the phosphatase and tensin homolog (PTEN)/p53 pathway. Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.

Diabetic cardiomyopathy (DCM) is one of the major heart complications of diabetic patients. Hydrogen sulfide (H₂S) is now recognized as an important signaling molecule and has been shown to attenuate the development of diabetic cardiomyopathy. However, the underlying mechanisms linking H₂S and the development of DCM have not been fully elucidated. In the present study, we therefore sought to explore the role and mechanism of H₂S in the pathogenesis of DCM by establishing high glucose-induced injury model in neonatal rat cardiomyocytes (NRCMs) and H9c2 cells. Using cystathionine gamma-lyase (CSE) overexpression and CSE interference vectors transfection, the cell viability, cell apoptosis. and oxidative stress were determined and compared between the treatment of high glucose induction and exgenous NaHS administration. Meanwhile, the relationship between the CSE/H₂S system and Wnt/beta-catenin pathway was analyzed and discussed in the high glucose-induced cardiomyocytes. Our results indicated that H₂S played an important protective role in high glucose-induced apoptosis and oxidative stress in cardiomyocytes, as shown by the decreased reactive oxygen species and malondialdehyde levels, and the increased activities of superoxide dismutase, catalase and glutathione peroxidase. Moreover, H₂S could attenuate the Wnt/β-catenin signalling pathway and up-regulate the expression of haem oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1) in the diabetic myocardium cells. Together, these results demonstrated that H₂S could attenuate high glucose-induced myocardial injury in rat cardiomyocytes by suppressing Wnt/β-catenin pathway.

Acupuncture is an alternative therapy for tinnitus in clinical practice. The mechanism by which acupuncture can alleviate tinnitus is still unknown. Autonomic nervous system was reported to be responsible for tinnitus. The aim of this study was to explore the effect of acupuncture on autonomic balance in adult tinnitus patients. Thirty patients were randomly assigned into either the deep acupuncture (DA) group or the shallow acupuncture (SA) group. Each patient received 6 acupuncture sessions (a–f phase) over three weeks. Measures of heart rate variability and Tinnitus Handicap Inventory (THI) were obtained at baseline and after the sixth acupuncture session in all patients. The results showed that the low frequency/high frequency (LF/HF) pattern was increased at b–f phase until the sixth acupuncture session when compared with that at the first acupuncture session in DA group. However, it continuously increased at b–f phase in SA group even at the sixth acupuncture session, which was not significantly different from that at the first acupuncture session. The decrease in THI in DA group was greater than that in SA group after 3-week treatment (P=0.043). Our preliminary study suggests three-week deep acupuncture can improve tinnitus symptoms in adult tinnitus patients, which may be related to the regulation of autonomic nervous system balance.

MiRNAs are integral for maintaining immune homeostasis and self-tolerance. In this study, qPCR analyses were performed to determine which miRNAs play an important role in wound healing. Next, an experiment in a model of wound healing was performed, and histology, mRNA expression and T-cell subpopulations in wound tissue were analyzed. The accelerated experiments were performed by local injection of either rIL-17A and/or rIL-9 after wound healing. In vitro, the differentiation of Th17/Th9 in miR-155^+/+ or miR-155^−/− mice was investigated, and the target genes of miR155 were analyzed. From our findings, miR-155^−/− in mice promoted wound healing and weakened T cell-mediated inflammation, especially in IL-17/IL-9, and less severe skin fibrosis developed in the mice. rIL-17A and/or rIL-9 could exacerbate inflammatory injury and delay wound healing. We also demonstrated that miR-155^−/− led to a defect in the differentiation of Th17/Th9 in vitro, and this effect of IL-17/IL-9 might be related to the expression of C-maf, which is a target gene of miR155. MiR-155 regulated IL-17/IL-9-related inflammation in wound healing and might be a potential therapeutic target to attenuate the inflammatory response in wound tissue and promote the closure of wound injuries.

Shenqi Fuzheng injection (SFI) has been confirmed to be able to alleviate brain injury in mice. This study examined the brain-protective effect of SFI on patients after cranial radiation. Lung cancer patients with brain metastasis were randomly assigned to two groups. The SFI group received cranial radiation in combination with SFI. The control group received cranial radiation alone. The changes in cognitive function were evaluated pre- and post-radiation against the Mini-Mental State Exam (MMSE), Montreal Cognitive Assessement (MoCA), Zung Self-Rating Depression Scale (SDS) and Zung Self-Rating Anxiety Scale (SAS). The changes in inflammatory factors, such as TGF-β1, TNF-α and IL-10, were also detected before, during and after radiation (15Gy/5F). The results showed that 6 months after cranial radiation, the total scores on the MMSE and MoCA scales of the patients decreased, especially memory ability. The control group experienced a more evident decline, the memory ability being the greatest. TGF-β1 and TNF-a increased shortly after radiation and decreased one month later, and the change was more conspicuous in SFI group than in control group. IL-10 increased after radiation and stayed at a high level one month later in both groups, the level being higher in the SFI group than in the control group. Our study indicated that cognitive functions, especially memory ability, were impaired after cranial radiation. SFI could alleviate radiation-induced brain injury by regulating inflammatory factors.

The purpose of this study was to investigate the presence of endolymphatic hydrops (EH) in both affected and unaffected ears of patients with pantonal unilateral idiopathic sudden sensorineural hearing loss (ISSNHL) using three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging (3D-FLAIR MRI) and further evaluate the significance of EH in this disorder. Twenty-seven ISSHL patients were enrolled in this study. 3D-FLAIR MRI was performed 24 h after intratympanic injection of gadolinium-diethylenetriaminepentaacetic acid (Gd-DPTA). The incidences of EH in the affected ears and contralateral unaffected ears were compared and the correlations of EH with vertigo or prognosis were analyzed using the Chi-square test. The results showed that the incidence of EH was 68.0% (17/25) in the affected ears and 34.8% (8/23) in the unaffected ears. There was a statistically significant difference between affected ears and unaffected ears in regard to the incidence of EH (P&lt;0.05). There were no significant correlations of EH with vertigo (P=1.000) or with prognosis (P=0.359) in the affected ears. In conclusion, there is EH in the inner ear of patients with pantonal ISSNHL; EH is not related to vertigo, a concomitant symptom of ISSNHL, and the prognosis of this condition. The presence of EH may be a secondary reaction following the impairment of the inner ears with pantonal ISSNHL.

This study aims to explore the expression of stanniocalcin 2 (STC2) gene in breast cancer and its clinical significance. Female patients with breast cancer from Zhongnan Hospital of Wuhan University admitted during March 2014 to October 2014 were enrolled in this study. All the tissues used in this experiment included 50 cases of breast cancer tissues and corresponding 50 cases of paracancer normal breast tissues with complete patients’ information. The real-time quantitative polymerase chain reaction (qPCR) was applied to detect the expression of STC2 gene in 50 cases of breast cancer and paracancer normal breast tissues. The results showed that the expression level of STC2 gene in 50 cases of breast cancer tissues was significantly higher than that in paracancer normal breast tissues (P&lt;0.001). The expression of STC2 gene was correlated with lymph node metastasis, distant metastasis, TNM stage and histological grade (P&lt;0.001). The expression level of STC2 gene was significantly higher in breast cancer tissues with higher expression of Ki-67 (P&lt;0.001). The expression level of STC2 gene was significantly higher in estrogen receptor (ER) positive breast cancer tissues than in ER negative ones (P&lt;0.001). However, different groups of age, pathological type, tumor size, PR expression and human epidermal growth factor receptor-2 (HER2) expression did not show significant differences in STC2 expression (P&gt;0.05). In conclusion, the abnormal overexpression of STC2 gene may play a role in the development and progression of breast cancer, and it can be used as an independent metastasis and prognostic factor of breast cancer. In addition, STC2 gene probably promotes the development and metastasis of breast cancer by interacting with estrogen and ER, and it may become a new direction for breast cancer endocrine therapy.

Parenchymal neurocysticercosis is the most common form of neurocysticercosis in the central nervous system (CNS), which mainly causes epilepsy and usually responses well to routine medications. However, there are appreciable cases of relapses refractory to medical treatment. We investigated microsurgical treatment of epilepsy with parenchymal neurocysticercosis. Nine cases of epilepsy caused by parenchymal neurocysticercosis from 2002 to 2018 were analyzed retrospectively. Cysts in 7 cases were completely removed. No case died of operation and no new dysfunction of the nervous system was observed after surgery. Among the other 9 cases, 8 cases became seizure-free or controlled by medicine according to the postoperative follow-up for 6 months to 9 years. One case was lost for follow-up. It was suggested that epilepsy with parenchymal neurocysticercosis can usually be controlled after routine medications. However, surgery is still indicated in some cases and careful microsurgery is associated with satisfactory clinical outcomes in appropriately selected cases.

This study explored the feasibility of employing computer-aided design (CAD) and 3 dimensional (3D)-printed personalized guide plate for the mini-invasive percutaneous internal screw fixation of fractured scaphoid. The study consisted of two parts: (1) experimentation on upper limbs from corpses and (2) preliminary clinical application. Corpse experiments involved upper limbs of 6 adult corpses. The specimens of upper limbs were subjected to plain CT scan. Then the CT data were input into computer to conduct 3D reconstruction of wrist region. The direction and depth of the guide wire and screw were designed on the basis of the principle that screw should lie at the center of scaphoid and the long axis of the screw should be aligned with that of the scaphoid. The carpal bone model and the guide plate were designed and 3D-printed. By using the guide plates, the guide wire was placed and the cannulated compression screw was inserted. The wrist region was examined by X-ray and CT to observe the location of the screw in the scaphoid. The scaphoid was longitudinally excised to grossly observe the location and evaluate the result of screw insertion. For clinical application, the guide plate was employed in 4 patients with fresh scaphoid fracture using the aforementioned operative technique. Our results showed that, in the 6 corpse limbs, the guide plate well fitted the skin surface and the guide wire and screw were accurately put in place in one session. X-ray examination and gross observation confirmed that the screw was satisfactorily positioned and the result met the requirements of the preoperative design. For 4 patients, the guide wire and screw were all precisely inserted into place in one session. The operation time and X-ray exposure times were apparently reduced. The imaging examination exhibited satisfactory results and the hand functioned well. It was concluded that the operative guide plate used for the mini-invasive percutaneous internal screw fixation of fractured scaphoid not only can assist in accurate placement of screw but also shorten operation time and reduce insertion and X-ray exposure times, thereby reducing the radiation injury and damage to the substance and the blood circulation of carpal bone. Its use can also improve the learning curve of surgeons.

Embryo implantation is a complicated physiological process tightly regulated by multiple biological molecules including growth factors. Transforming growth factor-betas (TGF-βs) and their most specific signal transduction factors, Smads, are expressed in the endometrium during the window of implantation. Recent researches indicated that Smad dependent TGF-β signaling may play an important role in the process of embryo implantation. In this study, we measured the expression of TGF-β1, TGF-β receptor type I (TβRI), Smad3 and p-Smad3 in the endometrium of mice and observed their elevation on day 4, 5 and 6 of pseudopregnancy. Then we administrated a specific Smad3 inhibitor (Sis3) into the uterine cavity of mice on day 3 of pregnancy. The results showed a reduction in insulin-like growth factor-1 (IGFBP-1) expression and the decreased number of implanted embryo after the administration. In addition, Sis3 was found to reduce the IGFBP-1 secretion in decidualized endometrial stromal cells. Taken all together, our findings demonstrated that TGF-β/Smad3 signaling is involved in the process of embryo implantation.

Human beings are increasingly exposed to phthalates, which are a group of chemicals used to make plastics more flexible and harder to break, and simultaneously ingesting abundant food emulsifiers via daily diet. The purpose of this study was to investigate the effect of the food emulsifier glycerin monostearate (GMS) on male reproductive toxicity caused by di(2-ethylhexyl) phthalate (DEHP, one of the phthalates) and explore the underlying mechanism. Thirty male Sprague-Dawley rats were randomly divided into control group, DEHP group and DEHP+GMS group. Rats in the DEHP group and DEHP+GMS group were orally administered with 200 mg/kg/d DEHP with or without 20 mg/kg/d GMS. After 30 days of continuous intervention, it was found that the serum testosterone level was significantly lowered in DEHP group and DEHP+GMS group than that in control group (P&lt;0.01). The serum testosterone level and the relative testis weight were significantly decreased in the DEHP+GMS group as compared with those in the DEHP group and control group (P&lt;0.05). More spermatids were observed to be shed off in DEHP+GMS group than in DEHP group. The expression levels of cell cycle checkpoint kinase 1 (Chk1), cell division cycle gene 2 (Cdc2), and cyclin-dependent kinase 2 (CDK2) were down-regulated in DEHP group, and this tendency was more significant in DEHP+GMS group (P&lt;0.05 or P&lt;0.01). There was no significant difference in the P-glycoprotein (P-gp) expression between DEHP group and control group. However, P-gp was markedly down-regulated in DEHP+GMS group (P&lt;0.01). The results indicated that the food emulsifier GMS aggravated the toxicity of DEHP on male reproduction by inhibiting the cell cycle of testicular cells and the expression of P-gp in testis tissues.

Pancreatic fistula (PF) remains the most frequent complication after pancreaticoduodenectomy (PD). This study was undertaken to explore the risk factors of postoperative PF following PD and discuss the management of PF in our center. A single-center respective study, involving 241 patients who underwent PD between September 2015 and June 2018, was conducted. Differences in the demographic data, preoperative, intraoperative and postoperative variables between the group with PF [International Study Group on Pancreatic Surgery (ISGPS) grade B/C] and the group without PF (no PF and ISGPS grade BL) were evaluated. The diagnosis and grading of PF were in strict accordance with ISGPS. Risk factors were analyzed by univariate analysis and multivariate logistic regression analysis. The results showed that postoperative PF occurred in 50 (20.7%) of the patients; 25 (10.4%) patients had a PF type BL, 46 (19.1%) patients developed a PF type B and 4 (1.6%) had a PF type C. Univariate analysis showed that fasting blood glucose (P=0.02), pancreatic texture (P&lt; 0.001) and pancreatic duct diameter (P=0.01) were correlated with PF. Multivariate logistic regression analysis identified one independent risk factor for postoperative PF: soft pancreatic texture (OR=3.251, P=0.002). Among the cases, there were three postoperative deaths, giving a 60-day hospital mortality rate of 1.2% (3/241), and the mortality related to PF was 4.0% (2/50). One of the patients died from multiple organ failure caused by postoperative abdominal hemorrhage. In conclusion, soft pancreatic texture is an independent risk factor for PF. Surgeons should be well aware of this risk factor when performing a PD.

Gestational hypertension (GH) is a common complication during pregnancy. GH is regarded as a potential public health challenge for pregnant women and infants. Limited evidence has linked ambient air pollution to an increased GH risk. However, most of the studies were conducted in developed countries, with inconsistent results obtained. The present study was performed to explore whether exposure to particulate matters with an aerodynamic diameter &lt; 2.5 (PM_2.5) and ozone (O₃) was related to elevated odds of GH in a Chinese population. This population-based cohort study involved 38 115 pregnant women in Wuhan, China. All information was collected from the Wuhan Maternal and Child Health Management Information System, using standardized quality control. The daily air pollutant data for PM_2.5 and O₃ were obtained from the 20 monitoring stations of the Wuhan Environmental Monitoring Center during 2014. The nearest monitor approach was applied to individual exposure assessment of PM_2.5 and O₃ for each participant. After adjusting for major confounders and other air pollutants, a 10 µg/m³ increase in PM_2.5 and O₃ concentrations was found to correlate to a 1.14-fold [95% confidence interval (95% CI): 1.09, 1.20] and a 1.05-fold (95% CI: 1.02, 1.07) increase in GH risk, respectively. Additionally, stronger relationships between GH risk and PM_2.5 and O₃ exposure were observed in women who conceived in winter and summer, respectively. These findings suggest that air pollutants may contribute to the development of GH.

High incidence of patellofemoral pain and patellofemoral joint osteoarthritis was found following anterior cruciate ligament (ACL) reconstruction. The unstability of patellofemoral joint might be an important contribution factor. This study was designed to define the relationship between the unstability of patellofemoral joint and quadriceps femoris atrophy. Twenty patients underwent MRI scan before ACL reconstruction and every two weeks after surgery, until 12 weeks. The merchant’s patellar congruence angle, lateral inclination angle, and quadriceps femoris muscle cross-sectional area were measured and the relationship between the changes of angles and the ratio of quadriceps femoris atrophy was studied by multiple regression analysis. Significant quadriceps femoris atrophy was observed after ACL reconstruction during the follow-up period of 12 weeks. The merchant’s patellar congruence angle and lateral inclination angle significantly changed after surgery. The alterations of the merchant’s patellar congruence angle were significantly correlated with the atrophy ratio of vastus medialis (coefficient=−15.76) and vastus lateralis (coefficient=8.35) during the follow-up period of 12 weeks. The alterations of lateral inclination angle were significantly correlated with the atrophy ratio of vastus medialis (coefficient=20.62), vastus lateralis (coefficient=−11.38) and rectus femoris (coefficient=−0.469) during the follow-up period 12 weeks. To sum up, ACL reconstruction can alleviate the dysfunction of patellofemoral joint to a certain extent. But, the unbalanced atrophy of quadriceps femoris once again destroyed the stability of patellofemoral joint following the operation, which might be one cause of patellofemoral joint pain and early onset of osteoarthritis after ACL reconstruction. So, rehabilitation training that focuses on quadriceps femoris especially the vastus medialis shortly following operation is suggested.