Preliminary study on AI-assisted diagnosis of bone remodeling in chronic maxillary sinusitis.

OBJECTIVE: To construct the deep learning convolution neural network (CNN) model and machine learning support vector machine (SVM) model of bone remodeling of chronic maxillary sinusitis (CMS) based on CT image data to improve the accuracy of image diagnosis. METHODS: Maxillary sinus CT data of 1000 samples in 500 patients from January 2018 to December 2021 in our hospital was collected. The first part is the establishment and testing of chronic maxillary sinusitis detection model by 461 images. The second part is the establishment and testing of the detection model of chronic maxillary sinusitis with bone remodeling by 802 images. The sensitivity, specificity and accuracy and area under the curve (AUC) value of the test set were recorded, respectively. RESULTS: Preliminary application results of CT based AI in the diagnosis of chronic maxillary sinusitis and bone remodeling. The sensitivity, specificity and accuracy of the test set of 93 samples of CMS, were 0.9796, 0.8636 and 0.9247, respectively. Simultaneously, the value of AUC was 0.94. And the sensitivity, specificity and accuracy of the test set of 161 samples of CMS with bone remodeling were 0.7353, 0.9685 and 0.9193, respectively. Simultaneously, the value of AUC was 0.89. CONCLUSION: It is feasible to use artificial intelligence research methods such as deep learning and machine learning to automatically identify CMS and bone remodeling in MSCT images of paranasal sinuses, which is helpful to standardize imaging diagnosis and meet the needs of clinical application.

Aflatoxin B1-exposed hepatocyte-derived extracellular vesicles: Initiating hepatic stellate cell-mediated liver fibrosis through a p53-Parkin-dependent mitophagy pathway.

Environmental aflatoxin B1 (AFB1) exposure has been proposed to contribute to hepatocellular carcinoma by promoting liver fibrosis, but the potential mechanisms remain to be further elucidated. Extracellular vesicles (EVs) were recognized as crucial traffickers for hepatic intercellular communication and play a vital role in the pathological process of liver fibrosis. The AFB1-exposed hepatocyte-derived EVs (AFB1-EVs) were extracted, and the functional effects of AFB1-EVs on the activation of hepatic stellate cells (HSCs) were explored to investigate the molecular mechanism of AFB1 exposure-induced liver fibrogenesis. Our results revealed that an environment-level AFB1 exposure induced liver fibrosis via HSCs activation in mice, while the AFB1-EVs mediated hepatotoxicity and liver fibrogenesis in vitro and in vivo. AFB1 exposure in vitro increased PINK1/Parkin-dependent mitophagy in hepatocytes, where upregulated transcription of the PARK2 gene via p53 nuclear translocation and mitochondrial recruitment of Parkin, and promoted AFB1-EVs-mediated mitochondria-trafficking communication between hepatocytes and HSCs. The knockdown of Parkin in HepaRG cells reversed HSCs activation by blocking the mitophagy-related AFB1-EVs trafficking. This study further revealed that the hepatic fibrogenesis of AFB1 exposure was rescued by genetic intervention with siPARK2 or p53's Pifithrin-α (PFTα) inhibitors. Furthermore, AFB1-EVs-induced HSCs activation was relieved by GW4869 pharmaceutic inhibition of EVs secretion. These results revealed a novel mechanism that AFB1 exposure-induced p53-Parkin signal axis regulated mitophagy-dependent hepatocyte-derived EVs to mediate the mitochondria-trafficking intercellular communication between hepatocytes and HSCs in the local hepatotoxic microenvironment to promote the activated HSCs-associated liver fibrogenesis. Our study provided insight into p53-Parkin-dependent pathway regulation and promised an advanced strategy targeting intervention to EVs-mediated mitochondria trafficking for preventing xenobiotics-induced liver fibrosis.

Right atrial wall inflammation detected by 18F-FDG PET/CT may be significantly associated with persistent atrial fibrillation: a prospective case-control study.

AIM: Atrial fibrillation (AF) is a progressive disease from paroxysmal to persistent, and persistent AF (PerAF) had worse prognosis. AF has potential link with inflammation, but it is not clear whether PerAF or paroxysmal AF (ParAF) is more closely related to inflammation. On the basis of inhibiting myocardial physiological uptake, 18F-fluorodeoxyglucosepositron emission tomography/computed tomography (18F-FDG PET/CT) is an established imaging modality to detect cardiac inflammation. We aimed to decipher the association between AF and atrial inflammatory activity by 18F-FDG PET/CT. METHODS: Thirty-five PerAF patients were compared to age and sex matched ParAF group with baseline 18F-FDG PET/CT scans prior to radiofrequency catheter ablation (RFCA) in the prospective case-control study. High-fat and low-carbohydrate diet and prolonged fast (HFLC+Fast) was applied to all AF patients before PET/CT. Then 22 AF patients with positive right atrial (RA) wall FDG uptake (HFLC+Fast) were randomly selected and underwent HFLC+Fast+heparin the next day. The CHA2DS2-VASc score was calculated to evaluate the risk of stroke. Clinical data, ECG, echocardiography, and atrial 18F-FDG uptake were compared. RESULTS: PerAF patients had significantly higher probability of RA wall positive FDG uptake and higher SUVmax than ParAF group [91.4% VS. 28.6%, P < 0.001; SUVmax: 4.10(3.20-4.90) VS. 2.60(2.40-3.10), P < 0.001]. Multivariate logistic regression analyses demonstrated that RA wall SUVmax was the independent influencing factor of PerAF (OR = 1.80, 95%CI 1.02-3.18, P = 0.04). In 22 AF patients with RA wall positive FDG uptake (HFLC+Fast), the "HFLC+Fast+Heparin" method did not significantly change RA wall FDG uptake evaluated by either quantitative analysis or visual analysis. High CHA2DS2-VASc score group had higher RA wall 18F-FDG uptake [3.35 (2.70, 4.50) vs, 2.8 (2.4, 3.1) P = 0.01]. CONCLUSIONS: RA wall FDG positive uptake was present mainly in PerAF. A higher RA wall 18F-FDG uptake was an independent influencing factor of PerAF. RA wall FDG uptake based on 18F-FDG PET/CT may indicate pathological inflammation. TRIAL REGISTRATION: http://www.chictr.org.cn , ChiCTR2000038288.

Prenatal exposure to phthalates and polybrominated diphenyl ethers on neonatal health: A birth cohort study in Guangxi, China.

Few epidemiological studies have focused on prenatal phthalates (PAEs) and polybrominated diphenyl ethers (PBDEs) exposure to neonatal health in China. This study aimed to assess the associations between prenatal PAEs and PBDEs exposure and neonatal health in Guangxi, a Zhuang autonomous region of China. Concentrations of 4 PAEs metabolites (mPAEs) and 5 PBDEs congeners were measured in the serum of 267 healthy pregnant women. Birth outcomes and clinical data of neonates were collected after delivery. Mono-(2-Ethylhexyl) phthalate (MEHP) (81.52%) and BDE47 (35.21%) were the mPAEs and PBDEs congeners with the highest detection rate in serum. Prenatal exposures to mono-n-butyl phthalate (MBP), MEHP, and ΣmPAEs were negatively associated with birth weight (BW), birth length (BL), and gestational age (GA). Higher exposures to MBP, MEHP, and ΣmPAEs were associated with an increased odds ratio (OR) for low birth weight (LBW), but exposure to BDE28 exhibited the opposite effect. Moreover, higher exposures to MBP, MEHP, ΣmPAEs, BDE99, and ΣPBDEswere associated with an increased OR for premature birth (PTB) (P < 0.05). In contrast to MBP exposure, BDE28 exposure was associated with a higher OR for neonatal jaundice (NNJ) (P < 0.05). The interaction analysis showed a positive interaction between monoethyl phthalate (MEP) and BDE28 on the risk of NNJ and positive interaction between ΣmPAEs and BDE47 on the risk of NNJ. In addition, there are ethnicity-specific associations of prenatal PBDEs exposure with neonatal health in individuals of Zhuang and Han nationalities, and boy neonates were more sensitive to prenatal PBDEs exposure than girl neonates. The results revealed that prenatal exposure to mPAEs and PBDEs might have adverse effects on neonatal development, and the effects might be ethnicity- and sex-specific.

Multi-omics analysis reveals BDE47 induces depression-like behaviors in mice by interfering with the 2-arachidonoyl glycerol-associated microbiota-gut-brain axis.

2,2',4,4'-tetrabromodiphenyl ether (BDE47) is a foodborne environmental risk factor for depression, but the pathogenic mechanism has yet to be fully characterized. In this study, we clarified the effect of BDE47 on depression in mice. The abnormal regulation of the microbiome-gut-brain axis is evidenced closely associated with the development of depression. Using RNA sequencing, metabolomics, and 16s rDNA amplicon sequencing, the role of the microbiome-gut-brain axis in depression was also explored. The results showed that BDE47 exposure increased depression-like behaviors in mice but inhibited the learning memory ability of mice. The RNA sequencing analysis showed that BDE47 exposure disrupted dopamine transmission in the brain of mice. Meanwhile, BDE47 exposure reduced protein levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT), activated astrocytes and microglia cells, and increased protein levels of NLRP3, IL-6, IL-1ß, and TNF-α in the brain of mice. The 16 s rDNA sequencing analysis showed that BDE47 exposure disrupted microbiota communities in the intestinal contents of mice, and faecalibaculum was the most increased genus. Moreover, BDE47 exposure increased the levels of IL-6, IL-1ß, and TNF-α in the colon and serum of mice but decreased the levels of tight junction protein ZO-1 and Occludin in the colon and brain of mice. In addition, the metabolomic analysis revealed that BDE47 exposure induced metabolic disorders of arachidonic acid and neurotransmitter 2-Arachidonoyl glycerol (2-AG) was one of the most decreased metabolites. Correlation analysis further revealed gut microbial dysbiosis, particularly faecalibaculum, is associated with altered gut metabolites and serum cytokines in response to BDE47 exposure. Our results suggest that BDE47 might induce depression-like behavior in mice through gut microbial dysbiosis. The mechanism might be associated with the inhibited 2-AG signaling and increased inflammatory signaling in the gut-brain axis.

Clinical relevance of serum lipids in the carcinogenesis of oral squamous cell carcinoma.

BACKGROUND: Dyslipidaemia is associated with cancers. However, the specific expression of serum lipids in oral potentially malignant disorders (OPMD) and oral squamous cell carcinoma (OSCC) remains unclear, and it remains unknown whether serum lipids are associated with the development of OPMD and OSCC. This study investigated the serum lipid profiles of OPMD and OSCC patients, and the association of serum lipids with the occurrence of OPMD and OSCC. METHODS: A total of 532 patients were recruited from the Affiliated Hospital of Stomatology, Nanjing Medical University. Serum lipid parameters including total cholesterol (TC), triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A (Apo-A), apolipoprotein B (Apo-B), and lipoprotein (a) (Lpa) were analysed, and clinicopathological data were collected for further analysis. Furthermore, a regression model was used to evaluate the relationship between serum lipids and the occurrence of OSCC and OPMD. RESULTS: After adjusting for age and sex, no significant differences were observed in serum lipid or body mass index (BMI) between OSCC patients and controls (P > 0.05). HDL-C, Apo-A, and Apo-B levels were lower in OSCC patients than in OPMD patients (P < 0.05); HDL-C and Apo-A levels were higher in OPMD patients than in controls (P < 0.05). Furthermore, female OSCC patients had higher Apo-A and BMI values than males. The HDL-C level was lower in patients under 60 years of age than in elders (P < 0.05); and age was related to a higher risk of developing OSCC. Female patients with OPMD had higher TC, HDL-C, and Apo-A levels than males (P < 0.05); OPMD patients over 60 years of age had higher HDL-C than youngers (P < 0.05), whereas the LDL-C level was lower in elders (P < 0.05). The HDL-C and BMI values of the patients with oral leukoplakia (OLK) with dysplasia were more elevated than those of the oral lichen planus group, and the LDL-C, and Apo-A levels in patients with OLK with dysplasia were decreased (P < 0.05). Sex, high HDL-C and Apo-A values were associated with the development of OPMD. CONCLUSION: Serum lipids exhibited certain differences according to the occurrence and development of OSCC; high levels of HDL-C and Apo-A might be markers for predicting OPMD.

Downregulation of SDCBP inhibits cell proliferation and induces apoptosis by regulating PI3K/AKT/mTOR pathway in gastric carcinoma.

Syndecan-binding protein (SDCBP) has been reported to critically process a core role in tumorigenesis. This study was conducted to characterize a novel regulatory network of SDCBP in gastric carcinoma (GC) cells. Our findings indicated that overexpression of SDCBP promoted the proliferation of GC cell and increased proliferating cell nuclear antigen (PCNA) expression. Moreover, the overexpression of SDCBP suppressed the apoptosis of GC cell along with a decrease of Bax/Bcl-2 ratio and induction of PI3K/AKT/mTOR activation. However, knockdown of SDCBP exhibited opposed effects on GC cells. Furthermore, silencing SDCBP significantly inhibited GC cell viability and PCNA expression accompanied with the upregulated cell apoptosis and Bax/Bcl-2 ratio, which was regulated by PI3K/AKT/mTOR signaling pathway. And it was further determined that PI3K inhibitor LY294002, AKT inhibitor Torin1, and mTOR inhibitor MK-2206 suppressed the apoptosis. In conclusion, SDCBP promotes the growth ability of GC by inducing the PCNA expression and inhibiting GC cell apoptosis via inactivation of the PI3K/AKT/mTOR pathway.

Verification of genetic differences and immune cell infiltration subtypes in the neuroblastoma tumour microenvironment during immunotherapy.

BACKGROUND: Improved understanding of the tumour microenvironment (TME) has enabled remarkable advancements in research on cancer progression in the past few years. It is crucial to understand the nature and function of the TME because precise treatment strategies, including immunotherapy, for managing specific cancers have received widespread attention. The immune infiltrative profiles of neuroblastoma (NB) have not yet been completely illustrated. The purpose of this research was to analyse tumour immune cell infiltration (ICI) in the microenvironment of NB. METHODS: We applied the CIBERSORT and ESTIMATE algorithms to evaluate the ICI status of 438 NB samples. Three ICI models were selected, and ICI scores were acquired. Subgroups with high ICI scores determined based on the presence of immune activation signalling pathways had better overall survival. RESULTS: Genes involved in the immunosuppressive heparan sulphate glycosaminoglycan biosynthesis signalling pathway were markedly enriched in the low ICI score subgroup. It was inferred that patients with high ICI NB subtypes were more likely to respond to immunotherapy and have a better prognosis than those of patients with low ICI NB subtypes. CONCLUSION: Notably, our ICI data not only provide a new clinical and theoretical basis for mining NB prognostic markers related to the microenvironment but also offer new ideas for the development of NB precision immunotherapy methods.

Hepatocyte-Derived Prostaglandin E2-Modulated Macrophage M1-Type Polarization via mTOR-NPC1 Axis-Regulated Cholesterol Transport from Lysosomes to the Endoplasmic Reticulum in Hepatitis B Virus x Protein-Related Nonalcoholic Steatohepatitis.

Lipid metabolic dysregulation and liver inflammation have been reported to be associated with nonalcoholic steatohepatitis (NASH), but the underlying mechanisms remain unclear. Hepatitis B virus x protein (HBx) is a risk factor for NASH. Based on metabolomic and transcriptomic screens and public database analysis, we found that HBx-expressing hepatocyte-derived prostaglandin E2 (PGE2) induced macrophage polarization imbalance via prostaglandin E2 receptor 4 (EP4) through in vitro, ex vivo, and in vivo models. Here, we revealed that the M1-type polarization of macrophages induced by endoplasmic reticulum oxidoreductase-1-like protein α (ERO1α)-dependent endoplasmic reticulum stress was associated with the HBx-related hepatic NASH phenotype. Mechanistically, HBx promoted Niemann-Pick type C1 (NPC1)/oxysterol-binding protein-related protein 5 (ORP5)-mediated cholesterol transport from the lysosome to the endoplasmic reticulum via mammalian target of rapamycin (mTOR) activation. This study provides a novel basis for screening potential biomarkers in the macrophage mTOR-cholesterol homeostasis-polarization regulatory signaling pathway and evaluating targeted interventions for HBx-associated NASH.

Palladium-catalyzed dearomative cyclocarbonylation of allyl alcohol for the synthesis of quinolizinones.

An approach for the synthesis of quinolizinone with potential bioactivity has been developed via palladium-catalytic dearomative cyclocarbonylation of allyl alcohol. Diverse quinolizinone compounds could be attained with good efficiencies. A feasible reaction pathway could be a successive procedure of allylation, dearomatization, CO insertion and the Heck reaction.

Sinapic Acid Alleviated Inflammation-Induced Intestinal Epithelial Barrier Dysfunction in Lipopolysaccharide- (LPS-) Treated Caco-2 Cells.

The integrity and permeability of the intestinal epithelial barrier are important indicators of intestinal health. Impaired intestinal epithelial barrier function and increased intestinal permeability are closely linked to the onset and progression of various intestinal diseases. Sinapic acid (SA) is a phenolic acid that has anti-inflammatory, antihyperglycemic, and antioxidant activities; meanwhile, it is also effective in the protection of inflammatory bowel disease (IBD), but the specific mechanisms remain unclear. Here, we evaluated the anti-inflammatory of SA and investigated its potential therapeutic activity in LPS-induced intestinal epithelial barrier and tight junction (TJ) protein dysfunction. SA improved cell viability; attenuated epithelial permeability; restored the protein and mRNA expression of claudin-1, ZO-1, and occludin; and reversed the redistribution of the ZO-1 and claudin-1 proteins in LPS-treated Caco-2 cells. Moreover, SA reduced the inflammatory response by downregulating the activation of the TLR4/NF-κB pathway and attenuated LPS-induced intestinal barrier dysfunction by decreasing the activation of the MLCK/MLC pathway. This study demonstrated that SA has strong anti-inflammatory activity and can alleviate the occurrence of high intercellular permeability in Caco-2 cells exposed to LPS.

A preliminary study on the mechanism of the neurosteroid-mediated ionotropic receptor dysfunction in neurodevelopmental toxicity induced by decabromodiphenyl ether.

The mechanism of neurodevelopmental toxicity of decabromodiphenyl ether (BDE209) remains unclear. Recent evidence suggests that neurosteroids disorders play a vital role in BDE209 induced-neurodevelopmental toxicity. To explore the mechanism of it, pregnant ICR mice were orally gavaged with 0, 225, and 900 mg kg-1 BDE209 for about 42 days. Spatial learning and memory abilities of offspring were tested on postnatal day (PND) 21. Offspring were euthanized at PND26, the neuronal structure, neurosteroids level, and related proteins including neurosteroids synthase, ionotropic receptors and cAMP-response element binding protein (CREB) pathway were evaluated, as well as Ca2+ concentration and the mitochondrial membrane potential (Mmp). Our results showed that BDE209 impaired learning and memory abilities and disrupted neuronal structure. Meanwhile, BDE209 decreased the pregnenolone (PREG), dehydroepiandrosterone (DHEA), progesterone (PROG) and allopregnanolone (ALLO) levels in the serum and brain, as well as the mRNA and protein levels of cholesterol-side-chain cleavage enzyme (P450scc), steroid 17α-hy-droxylase (P450C17), 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and steroid 5α-reductase of type I (5α-R) in the hippocampi. Also, BDE209 suppressed mRNA and protein levels of NR1, NR2A and NR2B subunits of the N-methyl-D-aspartic acid receptor (NMDAR) and α1 subunit of the Gamma-amino butyric acid A receptor (GABAAR), but increased the levels of ß2 and γ2 subunits of the GABAAR in the hippocampi. Moreover, BDE209 increased the Ca2+ concentration and phosphorylation extracellular regulated protein kinases (P-ERK) 1/2 level, but decreased the P-CREB and Mmp level in the hippocampi. These results indicate that BDE209 exposure during pregnancy and lactation is possible to affect learning and memory formation of offspring by the neurosteroid-mediated ionotropic receptors dysfunction.

Global distribution of publications in anesthesiology : A bibliometric analysis from 1999 to 2018.

PURPOSE: Only few studies have analyzed the global distribution of anesthesia research. This study was designed to reveal the current global research status of anesthesiology. METHODS: Articles published between 1999 and 2018 in international journals in the field of anesthesiology were retrieved from the PubMed database. The top 20 ranked countries were identified. The gross domestic product (GDP) of each country was also retrieved to reveal the correlation between research outputs and the economy. The total outputs and outputs per 10 million inhabitants in each country were calculated and compared. To analyze the quality of publications among the top 10 ranked countries, the impact factor (IF), article influence score (AIS), and immediacy index (ImI) were calculated and analyzed. In addition, the keywords of publications were retrieved to conduct co-occurrence analysis in order to determine the research focus in anesthesiology. RESULTS: A total of 112,918 articles were published in 30 selected journals from 1999 to 2018. There was a positive correlation between research outputs and GDP of 10 countries (p < 0.001, r = 0.825). The USA ranked 1st with 21,703 articles, followed by the UK (8393 articles) and Germany (6504 articles). Canada had the highest number of publications per 10 million inhabitants in 2018. The UK had the highest average IF (4.70), average AIS (1.16), and average ImI (1.64) among the 10 countries. The research highlights in the field of anesthesiology included "mechanism and management of pain", "cardiac anesthesia", "pediatric anesthesia and airway management", "analgesia" and "anesthetic agents". CONCLUSION: Regarding quantity trend, the output of global production in anesthesiology increased continuously as the number of articles from the high-output countries showed an increasing trend; however, there was still a gap between developing and developed countries in research quality. High-quality research should be encouraged in developing countries.

Okadaic acid promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells by inhibiting protein phosphatase 2A.

As a specific inhibitor of serine/threonine protein phosphatases, okadaic acid (OA) has been found to be a tumor promoter. However, whether OA plays a role in metastasis of hepatocellular carcinoma (HCC) has not been well elucidated. In this study, Hep3B and HepG2 cells were treated with different doses of OA and the cell viability was determined by CCK8 test. As a result, Hep3B and HepG2 cells showed no obvious cytotoxicity after OA treatment below 20 or 25 nM for 12 or 24 hours. However, wound healing, invasion, and migration abilities of HCC cells were significantly enhanced in the OA-treated groups than those of the control group (P < .05), measured by cell scratching and BD transwell assays. Moreover, we found that the expression of epithelial-mesenchymal transition (EMT)-related key factors was changed upon OA treatment in a dose-dependent manner. In addition, the activity of protein phosphatase 2A (PP2A) in OA-treated cells was also decreased significantly compared with the control cells (P < .05). Interfering of PP2A subunit A or C caused a similar expression change of EMT-related key factors as the OA treatment in HCC cells. Our results suggest that OA promotes the EMT process of HCC cells by inhibiting the activity of PP2A.

MiR-361-5p exerts tumor-suppressing functions in gastric carcinoma by targeting syndecan-binding protein.

MiR-361-5p, a tumor-related microRNA, has been reported to be implicated in the tumorigenesis and progression of diverse types of human malignancies; however, its role in gastric carcinoma remains unclear. This study aimed to explore the biological role of miR-361-5p in gastric carcinoma and clarify the potential mechanisms involved. In the present study, miR-361-5p was found to be significantly downregulated in both gastric carcinoma tissues and cell lines. Functional studies demonstrated that enhanced expression of miR-361-5p suppressed gastric carcinoma cell proliferation in vitro, inhibited tumor growth in vivo, and induced gastric carcinoma cell apoptosis. Moreover, the tumor-suppressing effects of miR-361-5p in gastric carcinoma were abrogated by the miR-361-5p inhibitor treatment. Notably, syndecan-binding protein was downregulated by miR-361-5p via direct binding to its 3' untranslated region in gastric carcinoma cells. Furthermore, syndecan-binding protein expression was discovered to be markedly upregulated and inversely correlated with miR-361-5p expression in gastric carcinoma tissues. Mechanistic studies revealed that restoring the expression of syndecan-binding protein alleviated miR-361-5p-induced inhibitory effects on proliferation of gastric carcinoma cells. Taken together, these findings suggest that miR-361-5p functions as a tumor suppressor in gastric carcinoma by directly targeting syndecan-binding protein and that miR-361-5p might be a novel therapeutic target for gastric carcinoma.

Translocator protein 18 kDa: a potential therapeutic biomarker for post traumatic stress disorder.

Post traumatic stress disorder (PTSD) is widely regarded as a stress-related and trauma disorder. The symptoms of PTSD are characterized as a spectrum of vulnerabilities after the exposure to an extremely traumatic stressor. Considering as one of complex mental disorders, little progress has been made toward its diagnostic biomarkers, despite the involvement of PTSD has been studied. Many studies into the underlying neurobiology of PTSD implicated the dysfunction of neurosteroids biosynthesis and neuorinflammatory processes. Translocator protein 18 kDa (TSPO) has been considered as one of the promising therapeutic biomarkers for neurological stress disorders (like PTSD, depression, anxiety, et al) without the benzodiazepine-like side effects. This protein participates in the formation of neurosteroids and modulation of neuroinflammation. The review outlines current knowledge involving the role of TSPO in the neuropathology of PTSD and the anti-PTSD-like effects of TSPO ligands.

A Gradient-Based Method for Robust SensorSelection in Hypothesis Testing.

This paper considers the binary Gaussian distribution robust hypothesis testing under aBayesian optimal criterion in the wireless sensor network (WSN). The distribution covariance matrixunder each hypothesis is known, while the distribution mean vector under each hypothesis driftsin an ellipsoidal uncertainty set. Because of the limited bandwidth and energy, we aim at seeking asubset of p out of m sensors such that the best detection performance is achieved. In this setup, theminimax robust sensor selection problem is proposed to deal with the uncertainties of distributionmeans. Following a popular method, minimizing the maximum overall error probability with respectto the selection matrix can be approximated by maximizing the minimum Chernoff distance betweenthe distributions of the selected measurements under null hypothesis and alternative hypothesis tobe detected. Then, we utilize Danskin's theorem to compute the gradient of the objective functionof the converted maximization problem, and apply the orthogonal constraint-preserving gradientalgorithm (OCPGA) to solve the relaxed maximization problem without 0/1 constraints. It is shownthat the OCPGA can obtain a stationary point of the relaxed problem. Meanwhile, we provide thecomputational complexity of the OCPGA, which is much lower than that of the existing greedyalgorithm. Finally, numerical simulations illustrate that, after the same projection and refinementphases, the OCPGA-based method can obtain better solutions than the greedy algorithm-basedmethod but with up to 48.72% shorter runtimes. Particularly, for small-scale problems, the OCPGA-based method is able to attain the globally optimal solution.

Effects of maternal exposure to BDE209 on neuronal development and transcription of iodothyronine deiodinase in offspring mice.

The present study investigated the alterations in nerve function and its potential mechanism of offspring result from the decabromodiphenyl ether (BDE209) orally gavage (0, 1.5, and 225 mg/kg.d body weight) in pregnant and lactating mice. Weight gain and litter size of maternal mice and body weight of offspring were examined. Learning and memory abilities of offspring were tested by the Morris water maze experiment. Thyroid hormones (THs) concentrations in peripheral blood of offspring were detected by the chemiluminescence enzyme immunoassay. Relative mRNA expression of type 1 iodothyronine deiodinase (dio1), type 2 iodothyronine deiodinase (dio2), and type 3 iodothyronine deiodinase (dio3) in the livers and brains of offspring were measured by QRT-PCR (quantitative real-time polymerase chain reaction). Protein expression of dio3 in the livers and brains of offspring was measured by Western blot. All indexes of offspring were tested at postnatal day (PND) 21 and PND 60, respectively. As a result, administration of BDE209 decreased weight gain and litter size of maternal mice, and reduced body weight of offspring mice, prolonged escape latency and declined guardant time of offspring in the Morris water maze experiment. Moreover, BDE209 elevated serum levels of total thyroxine (T4), total triiodothyronine (T3), free T4, and free T3 in offspring. In addition, maternal exposure to BDE209 inhibited dio1, dio2, dio3 mRNA expression in the livers of offspring, while elevated dio1 mRNA expression and reduced dio3 mRNA expression in the brains of offspring. BDE209 also inhibited the protein expression of dio3 in the livers and brains of offspring. These results indicate that BDE209 exposure to pregnant and lactating mice can cause disruption in serum THs of offspring by altering mRNA and protein expression of iodothyronine deiodinases, which might consequently result in neurologic impairment of offspring mice.

[Effects of fungi fraction on growth and anti-oxidative activity of Eleutherococcus senticosus].

The present study was conducted to explore the effect of endophytic fungi fraction on growth and anti-oxidative activity of Eleutherococcus senticosus. The growth,yield,contents of MDA,and antioxidant activities were assessed in E. senticosus under five fungi fractions,namely BZ,MH,DT,JS,and XFZ. The results showed that fungi fractions and component significantly affected the growth,low concentration of DT fungi fraction significantly increased the biomass of E. senticosus,reduced the MDA content in cells,and the antioxidant activities of the aqueous extracts were superior to the others. The results indicated that low concentration of DT fungi fraction was the optimum fraction to achieve high yield and quality of E. senticosus.

Inhibition of 5-lipoxygenase represses neutrophils activation and activates apoptosis in pancreatic tissues during acute necrotizing pancreatitis.

Pancreatic glandular necrosis is rapid inflammation of the pancreas and contributes to severe acute pancreatitis in humans. The pathogenesis of pancreatic tissue inflammation during acute pancreatitis is still largely unknown. Recent studies suggest that 5-lipoxygenase (5-LOX) is an essential mediator in modulating cell death pathways in human diseases. In this study, we aimed to evaluate the effects of a 5-LOX inhibitor, zileuton, on tissue apoptosis and neutrophils activation in pancreatic tissues during acute necrotizing pancreatitis (ANP) in a rat model. In this present study, both mRNA and protein levels of 5-LOX are upregulated during ANP and zileuton treatment is shown to repress ANP-induced upregulation of 5-LOX levels. In addition, zileuton treatment is found to repress blood biomarkers of neutrophils activation such as soluble intercellular adhesive molecular 1 (ICAM-1), soluble E-selectin (E-selectin), soluble P-selectin (P-selectin), leukotriene B4 (LTB4), and myeloperoxidase (MPO). Also, zileuton treatment attenuates pancreatic tissue pathology, upregulates caspase-3, downregulates B-cell lymphoma 2 (Bcl-2), and activates tissue apoptosis evaluated by TUNEL staining. Our results show that 5-LOX plays an important role in activating apoptosis and repressing neutrophils activation during ANP. The current study suggests that 5-LOX can be used as a potential target for the treatment of ANP.