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Objectives To compare the levels of serum pepsinogen (PG) in patients with gastric cancer (GC), patients with atrophic gastritis (AG), and healthy donors. Also, we explored the clinical value of PG detection for the diagnosis and treatment of GC. Methods The PG level in peripheral blood from patients and heathy donors was determined using an Abbott automatic chemiluminescence instrument. The study included 117 patients with GC confirmed by gastroscopy and histopathology, of whom 13 patients had cancer at stage I, 47 at stage II, 41 at stage III, and 16 at stage IV. The AG group included 122 patients, and the control group had 120 healthy donors. The relationship between serum PG levels and the occurrence and development of GC, as well as the evaluation of the clinical value of diagnostic tests based on serum PG detection, were investigated by receiver operating characteristic (ROC) curve analyses. Results Pepsinogen I (PGI) levels gradually decreased from the control group, the AG group, and the GC group. PGI exhibited high diagnostic value for GC (area under the curve [AUC], 0.834; cutoff, 51.2 ng/mL, sensitivity, 81.7%; specificity, 68.4%), PGII (AUC, 0.587; cutoff value, 13.05 ng/mL; sensitivity, 65.8%; specificity, 53.8%), and PGR (AUC, 0.752; cutoff, 5.65; sensitivity, 54.2%; specificity, 87.2%). The occurrence of GC was negatively correlated with serum levels of PGI (B = −0.054; OR = 0.947; 95% confidence interval [CI], 0.925–0.970; P Conclusions The combined detection of PGI, PGII, and PGR has important clinical value for the screening, prevention, and diagnosis of GC and could allow for earlier detection, diagnosis, and treatment of GC.

We conducted a cross-sectional study investigating community-dwelling older population to determine association between immunoscenescence marker, inflammatory cytokines and frailty. Frailty status was classified with 33-item modified frailty index and latent class analysis was applied to explore the latent classes (subtypes) of frailty. In multivariable analysis, higher Tfh2 cells were associated with a higher risk of frailty [1.13(1.03–1.25)] in females, but a lower risk of cognitive and functional frail [0.92(0.86–0.99)] and physiological frail [0.92(0.87–0.98)]. Additionally, a greater risk of multi-frail and physiological frail correlated with low Tfh1 [0.77(0.60–0.99); 0.87(0.79–0.96)] and Tfh17 cells [0.79(0.65–0.96); 0.86(0.78–0.94)], respectively. Higher B cells were associated with decreased frailty/pre-frailty both in females [0.89(0.81–0.98)] and males [0.82(0.71–0.96)], but did not correlate with frailty subtypes. Regarding inflammatory markers, participants in the TGF-β 2nd quartile showed a decreased risk of pre-frailty/frailty in females [0.39(0.17–0.89)] and psychological frail [0.37(0.16–0.88)], compared with those in the top tertile. Moreover, we found participants in the 2nd tertile for IL-12 levels showed a decreased risk of physiological frail [0.40 (0.17–0.97)]. Our study highlights the importance of Tfh cell subsets and inflammatory markers in frailty in a sex-specific manner, particularly in terms of frailty subtype.

In order to explore frailty subtypes and find their associated risk factors, we conducted cross-sectional surveys of 5,341 seniors aged 60 and over in China using the Frailty Index (FI) scale. We identified four frailty subtypes, namely multi-frail, cognitive and functionally frail, psychologically frail and physiologically frail. Old age and low education level were the common risk factors among the four subtypes. Being widowed, divorced or unmarried was a risk factor for multi-frail, cognitive and functionally frail and psychologically frail, and male sex was a protective factor against cognitive and functionally frail and psychologically frail subtypes. Having a harmonious relationship with family was a protective factor against multi-frail, and fewer visits to the elderly by their children was a risk factor for psychologically frail. Dissatisfaction with their housing was a risk factor for cognitive and functionally frail, psychologically frail and physiologically frail, and a pension being the main source of income was a risk factor for cognitive and functionally frail and psychologically frail. Exercising every day was a protective factor against multi-frail and cognitive and functionally frail, and a lower level of physical activity was a risk factor for all four frailty subtypes. Our findings confirm the heterogeneity of frailty and suggest that different frail elderly individuals need more targeted care interventions.

Objective To evaluate the association between extra-long interpregnancy interval and adverse perinatal outcomes. Methods A retrospective cohort study on women experiencing their second delivery between 2017 and 2018 in a maternal and child health hospital was conducted to evaluate the association between the extra-long interpregnancy interval (IPI) and adverse perinatal outcomes. IPI ≥180 months was defined as extra-long IPI. Logistic regression analysis was performed to explore the adverse perinatal outcomes in different IPI groups, and compared with the predicted risks at 24–59, 60–119, 120–179, and 180-month IPI, with the 12–23-month interval serving as a reference. Results After adjusting for all possible confounding factors, there was an increased risk of premature rupture of membranes (aOR 1.83, 95% CI 1.13–2.97 and aOR 3.30, 95% CI 1.40–7.74) in the IPI of 60–119 and 120–179 months among women with age-appropriate maternity. However, the effects of extra-long IPI on adverse perinatal outcomes did not significantly differ among women with advanced maternal age. Conclusions These results indicate that long IPI (60–179 month) is an independent risk factor for premature rupture of membranes. Extra-long IPI (≥180 months) was not associated with an increase in major morbidity, but extra-long IPI often coexists with advanced age, so we still need to pay attention to the maternal risk factors associated with extra-long IPI.

BackgroundNoonan syndrome (NS), a genetically heterogeneous disorder, presents with hypertelorism, ptosis, dysplastic pulmonary valve stenosis, hypertrophic cardiomyopathy, and small stature. Early detection and assessment of NS are crucial to formulating an individualized treatment protocol. However, the diagnostic rate of pediatricians and pediatric cardiologists is limited. To overcome this challenge, we propose an automated facial recognition model to identify NS using a novel deep convolutional neural network (DCNN) with a loss function called additive angular margin loss (ArcFace).MethodsThe proposed automated facial recognition models were trained on dataset that included 127 NS patients, 163 healthy children, and 130 children with several other dysmorphic syndromes. The photo dataset contained only one frontal face image from each participant. A novel DCNN framework with ArcFace loss function (DCNN-Arcface model) was constructed. Two traditional machine learning models and a DCNN model with cross-entropy loss function (DCNN-CE model) were also constructed. Transfer learning and data augmentation were applied in the training process. The identification performance of facial recognition models was assessed by five-fold cross-validation. Comparison of the DCNN-Arcface model to two traditional machine learning models, the DCNN-CE model, and six physicians were performed.ResultsAt distinguishing NS patients from healthy children, the DCNN-Arcface model achieved an accuracy of 0.9201 ± 0.0138 and an area under the receiver operator characteristic curve (AUC) of 0.9797 ± 0.0055. At distinguishing NS patients from children with several other genetic syndromes, it achieved an accuracy of 0.8171 ± 0.0074 and an AUC of 0.9274 ± 0.0062. In both cases, the DCNN-Arcface model outperformed the two traditional machine learning models, the DCNN-CE model, and six physicians.ConclusionThis study shows that the proposed DCNN-Arcface model is a promising way to screen NS patients and can improve the NS diagnosis rate.

Background: The hemoglobin glycation index (HGI) has been proposed as a marker to quantify inter-individual variation in hemoglobin glycosylation. However, whether HGI is associated with an increased risk of diabetic complications independent of glycated hemoglobin (HbA1c) remains unclear. This meta-analysis aimed to determine the association between HGI and the risk of all cause mortality and composite cardiovascular disease (CVD).Methods: PubMed, and EMBASE databases were searched for related studies up to March 31, 2021. Observational studies reported associations between HGI levels and composite CVD and all cause mortality were included for meta-analysis. A random effect model was used to calculate the hazard ratios (HRs) and 95% confidence intervals (CI) for higher HGI.Results: A total of five studies, comprising 22,035 patients with type two diabetes mellitus were included for analysis. The median follow-up duration was 5.0 years. After adjusted for multiple conventional cardiovascular risk factors, an increased level of HGI was associated with a higher risk of composite CVD (per 1 SD increment: HR = 1.14, 95% CI = 1.04–1.26) and all cause mortality (per 1 SD increment: HR = 1.18, 95% CI = 1.05–1.32). However, when further adjusted for HbA1c, the association between HGI and risk of composite CVD (per 1 SD increment of HGI: HR = 1.01, 95% CI = 0.93–1.10) and all cause mortality (per 1 SD increment of HGI: HR = 1.03, 95% CI = 0.96–1.10) became insignificant.Conclusions: High HGI was associated with an increased risk of composite CVD and all cause mortality after adjustment for multiple conventional cardiovascular risk factors. However, the association was mainly mediating by the level of HbA1c.

In a recently published paper in Cardiovascular Diabetology, Sinha et al. (Association of fasting glucose with lifetime risk of incident heart failure: the Lifetime Risk Pooling Project. Cardiovasc Diabetol. 2021;20(1):66) reported that prediabetes (defined as a fasting plasma glucose concentration of 100–125 mg/dL) was associated with a higher lifetime risk of heart failure in middle-aged White adults and Black women, with the association attenuating in older Black women. This study provides important evidence that the risk of heart failure is increased in people with a fasting plasma glucose concentration as low as 100 mg/dL, supporting the definition of prediabetes according to the American Diabetes Association guideline. The study also strongly supports the notion that prediabetes should be regarded not only as a high-risk state for the development of diabetes but also as a risk factor for cardiovascular morbidity.

Background Sepsis is a severe condition characterised by the body’s systemic inflammatory response to infection. The specific sepsis-related biomarkers should be used in clinical diagnosis, therapeutic response monitoring, rational use of antibiotics, and prognosis (risk stratification), etc. Results In this study, we investigated the expression level of Decoy Receptor 3 (DcR3) and the mechanism of high expression in sepsis patients. Septic cell model experiments were performed by treating human umbilical vein endothelial cells (HUVECs) and Jurkat cells with lipopolysaccharide (LPS), lipoteichoic acid (LTA) and zymosan, respectively. SP600125, SB203580 and ammonium pyrrolidinedithiocarbamate (PDTC) were used to inhibit JNK1/2, p38MAPK and NF-κB signalling pathways in septic cell model, respectively. These results showed that DcR3 levels were higher in sepsis group than control. DcR3 mRNA and protein levels in HUVECs were increased following treatment with LPS, LTA and zymosan, and also increased in Jurkat cells treated by LPS, but not by LTA or zymosan. When HUVECs were treated with the NF-κB inhibitor PDTC, DcR3 expression was decreased compared with controls. However, SP600125 and SB203580 had no effect on DcR3 mRNA or protein levels. Conclusions The results indicated that DcR3 secretion proceeded through the NF-κB signalling pathway in HUVECs.

Background An estimated 5–10 % of healthy vaccinees lack adequate antibody response following receipt of a standard three-dose hepatitis B vaccination regimen. The cellular mechanisms responsible for poor immunological responses to hepatitis B vaccine have not been fully elucidated to date. Methods There were 61 low responders and 56 hyper responders involved in our study. Peripheral blood samples were mainly collected at D7, D14 and D28 after revaccinated with a further dose of 20 µg of recombinant hepatitis B vaccine. Results We found low responders to the hepatitis B vaccine presented lower frequencies of circulating follicular helper T (cTfh) cells, plasmablasts and a profound skewing away from cTfh2 and cTfh17 cells both toward cTfh1 cells. Importantly, the skewing of Tfh cell subsets correlated with IL-21 and protective antibody titers. Based on the key role of microRNAs involved in Tfh cell differentiation, we revealed miR-19b-1 and miR-92a-1 correlated with the cTfh cell subsets distribution and antibody production. Conclusions Our findings highlighted a decrease in cTfh cells and specific subset skewing contribute to reduced antibody responses in low responders.

Around 5–10% of healthy vaccinees lack or produce an inadequate antibody response following receipt of a standard hepatitis B vaccination regimen. Studying immune response to hepatitis B vaccination could promote researches of immunological events contributing to this poor response. To address this, we investigated follicular helper T (Tfh) cells and firstly demonstrated similar kinetics between circulating Tfh (cTfh) cells and Tfh cells derived from mice spleen after hepatitis B vaccination. And cTfh cells were positively associated with anti-HBs at one week after vaccination (D7). Furthermore, we found PBMCs stimulated by HBsAg showed preferential activation of CXCR3(−) Tfh cells subsets in vitro. The expression of transcription factor BCL6 in CD4(+) T cell significantly differed between D7 and four weeks after vaccination (D28). However, dynamic curve of CD19(+) B cells tended to rise then fall but no significant trends were observed. Our findings revealed a decrease in cTfh cells and subset skewing contribute to reduced antibody responses in immune response to hepatitis B vaccination, which indicated the importance of Tfh cell in facilitating the optimization of vaccine efficacy.

Objectives This study aimed to investigate the factors affecting the quantity of DNA and RNA extractable from human formalin-fixed paraffin-embedded (FFPE) tissues stored for different lengths of time. Methods We randomly selected 20 FFPE specimens harvested from hysteromyoma patients with uterine fibroids during 2010, 2015, and 2017 at the Department of Pathology, Jiading District Central Hospital Affiliated Shanghai University of Medicine and Health Sciences. DNA and RNA extractions were performed using a DNA/RNA FFPE kit. DNA and RNA concentrations and their OD260/OD280 ratios were determined by a NanoDrop 2000 spectrophotometer. The human β-globin gene and aldehyde dehydrogenase-2 (ALDH2) gene were amplified from nucleic acids using a LightCycler 480 Real-Time PCR System, and PCR amplification products were electrophoresed on 1% agarose gels. Results Specimens that were stored for longer showed more degradation and a reduced concentration of DNA and RNA after nucleic acid extraction. However, there was no significant difference in DNA or RNA purity. β-globin and ALDH2 genes could be amplified from more than 99% of specimens. Conclusion We found that FFPE tissues stored for longer had a reduced quantity of extractable DNA and RNA. However, these tissues could be used for the analysis of some small target genes.

Objectives The purpose of this paper was to synthesize 4-amino-1,2,4-triazole Schiff base derivative and to evaluate its antitumor activity. Methods 2,4,6-Tris (4-formylphenoxy)-1,3,5-triazine was synthesized by nucleophilic substitution with reaction of p -hydroxybenzaldehyde with cyanuric chloride. Then, the intermediate was reacted with 1,2,4-triazole to form 4-amino-1,2,4-triazole Schiff base derivative by reduction and ammonification of aldehydes. The 4-amino-1,2,4-triazole Schiff base derivative was characterized by infrared spectroscopy, nuclear magnetic resonance, and elemental analyses. Finally, the anticancer effect of 4-amino-1,2,4-triazole Schiff base derivative was evaluated by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay on a lung adenocarcinoma cell line (A549) and a human hepatoma cell line (Bel7402). Results The product synthesized in this study was confirmed to be 4-amino-1,2,4-triazole Schiff base derivative, and it significantly suppressed the proliferation of cancer cell lines in a dose-dependent manner. Conclusions We successfully prepared 4-amino-1,2,4-triazole Schiff base derivative and verified its antitumor activity.

The activation of Janus kinase 1 (JAK1) has been reported to occur in non-small cell lung cancer (NSCLC), activating the JAK/signal transducers and activators of transcription cascade. However, the association between JAK1 activation and the prognostic value in NSCLC remains unclear. The present study initially investigated the association between expression of the activated form of JAK1 (p-JAK1) and prognosis in patients with NSCLC. A cohort of 142 resected primary NSCLC tissue samples, including 74 adenocarcinoma (ADCC) and 68 squamous cell carcinoma samples, were analyzed. p-JAK1 expression status was determined by immunohistochemistry. Evaluation of epidermal growth factor receptor (EGFR) gene amplification by fluorescence in situ hybridization was subsequently performed in 74 ADCC samples. The prognostic significance of p-JAK1 expression and EGFR gene amplification were evaluated with univariate and multivariate survival analyses. Compared with normal lung tissue, p-JAK1 expression level was significantly increased in NSCLC (P

Background Sepsis causes nutritional substrate malabsorption; hence, preventing gut barrier problems and improving the nutritional status in sepsis is a compelling issue. Aims We tested whether ghrelin administration affects peptide transporter 1 (PepT1) activity in the intestinal epithelium of rats with sepsis. Methods Sixty male Sprague-Dawley rats were randomly divided into sham-operated, sepsis, and ghrelin-treated groups. The cecum of sham-operated rats was separated after laparotomy without ligation and perforation. Sepsis group rats underwent cecal ligation and puncture (CLP). Mucosal specimens were used for immunohistochemstry, real-time PCR, and western blotting to detect PepT1 distribution, and mRNA and protein expression levels, respectively. TNF-α, IL-1β, and ghrelin levels were estimated in serum and intestinal mucosal tissue by ELISA. High-performance liquid chromatography was used to measure PepT1 uptake by the epithelial cells. Moreover, survival, body weight, and food intake of the rats were recorded during the 7-day treatment period. Results All rats in the sham-operated group survived, and 80% of rats in the sepsis group died within 7d of CLP. Treatment with ghrelin attenuated the CLP-induced body weight loss, intestine mucosa damage, and the survival rate was better. In addition, ghrelin attenuated increases in TNF-α and IL-1β production. The expressions of PepT1 mRNA and protein were higher in ghrelin-treated group rats than in sepsis rats. Moreover, the uptake function of PepT1 was better in ghrelin-treated group rats. Conclusion Ghrelin treatment can reduce the inflammatory response and greatly upregulate the physiological function of PepT1 in intestinal epithelial cells of rats with sepsis.

A possible correlation between liver cancer pain and the hypoxia-inducible factor (HIF)-1 and vascular endothelial growth factor (VEGF) expression levels was examined. From January, 2015 to January, 2016, 30 patients suffering from liver cancer with pain, 30 patients with liver cancer without pain and 30 hepatitis patients with pain were enrolled in the study. Pain level was evaluated by visual analogue scale (VAS), the expression levels of HIF-1 and VEGF mRNA were determined by RT-PCR and the expression levels of HIF-1 and VEGF proteins were examined by ELISA. Before intervention, the VAS in the hepatitis group was significantly higher than that of the liver cancer pain group. However, after intervention the VAS in the two groups was reduced. HIF-1 and VEGF mRNA expression levels in the liver cancer pain group were significantly higher than those in the liver cancer group before and after intervention. The expression levels of HIF-1 and VEGF mRNA in the hepatitis group were the lowest. The expression levels of HIF-1 and VEGF mRNA in the liver cancer pain group considerably increased after intervention. The expression levels of HIF-1 and VEGF mRNA in the other two groups showed no changes before or after intervention. Before and after the intervention, VAS in the liver cancer pain group was positively correlated to the expression levels of HIF-1 and VEGF. Thus, pain occurrence and the pain level in liver cancer patients were correlated with the expression levels of HIF-1 and VEGF. As the regular three-step medicine analgesic ladder is ineffective in these cases, verification of HIF-1 and VEGF expression levels may be considered the new target for pain release.

This study investigated sulfamethoxazole (SMX) biodegradation and nitrogen conversion by Achromobacter sp. JL9 using different carbon and nitrogen sources. Results showed that SMX and sodium acetate could be co-metabolized as carbon sources for bacterial growth and nitrogen conversion with highest removal efficiencies of 82.44%, 80.2%, and 79.45% for NH4+-N, NO3--N, and SMX, respectively. Strain JL9 was able to utilize SMX as its sole nitrogen source for growth, with an SMX biodegradation efficiency of 63.10%. In addition, carbon and nitrogen balance analyses showed that approximately 35.31% and 63.22% of carbon and nitrogen, respectively, were lost as gaseous products. Finally, medium toxicity gradually decreased during the carbon and nitrogen dependence experiments. This study, thus, suggests that carbon and nitrogen play vital roles in SMX biodegradation and biotoxicity reduction.

Chronic hepatitis B (CHB) is associated with the development of hepatocellular carcinoma (HCC). Decoy receptor 3 (DcR3) is a tumor necrosis factor receptor that promotes tumor cell survival by inhibiting apoptosis and interfering with immune surveillance. Previous studies showed that DcR3 was overexpressed in HCC cells and that short hairpin RNA (shDcR3) sensitizes TRAIL-resistant HCC cells. However, the expression of DcR3 during hepatitis B virus (HBV) infection has not been investigated. Here, we demonstrated that DcR3 was overexpressed in CHB patients and that DcR3 upregulation was positively correlated with the HBV DNA load and liver injury (determined by histological activity index, serum alanine aminotransferase level, and aspartate aminotransferase level). We found that hepatitis B virus X protein (HBx) upregulated DcR3 expression in a dose-dependent manner, but this increase was blocked by NF-κB inhibitors. HBx also induced the activation of NF-κB, and the NF-κB subunits p65 and p50 upregulated DcR3 by directly binding to the DcR3 promoters. Inhibition of PI3K significantly downregulated DcR3 and inhibited the binding of NF-κB to the DcR3 promoters. Our results demonstrate that the HBx induced DcR3 expression via the PI3K/NF-κB pathway; this process may contribute to the development of HBV-mediated HCC.

Background Cardiovascular complications, especially myocardial infarctions (MIs), are the leading mortality cause in diabetic patients. The transplantation of stem cells into damaged hearts has had considerable success as a treatment for MI, although whether antidiabetic drugs affect the therapeutic efficacy of stem cell transplantation is still unknown. This study aims to understand whether and how metformin, one of the first-line drugs used to treat type 2 diabetes mellitus (T2DM), induces mesenchymal stromal cell (MSC) apoptosis and dampens their cardioprotective effect after transplantation into infarcted hearts. Methods A mouse MI model was generated via permanent ligation of the left anterior descending (LAD) coronary artery. MSCs with or without metformin treatment were transplanted after MI in diabetic mice. Echocardiography was used to assess cardiac function and determine cardiac remodeling, and TTC staining was performed to evaluate infarction size. A mouse gavage model was performed to evaluate bone marrow MSCs for flow cytometry assay. Results Metformin dampened MSC therapeutic efficacy, which increased infarct size and restricted functional cardiac recovery. Specifically, metformin induced the activation of AMP-activated protein kinase (AMPK)-mediated apoptosis through the inhibition of S6K1-Bad-Bcl-xL cell survival signaling, resulting in the upregulated expression of apoptosis-associated proteins and increased MSC apoptosis. Accordingly, counteracting AMPK attenuated metformin-induced apoptosis in MSCs and partially restored their cardioprotective effects in diabetic mice with MI. Furthermore, a decrease in peripheral blood MSCs was found in patients with T2DM who had a metformin medication history. Conclusions Our results highlight an unexpected adverse effect of metformin-induced MSC apoptosis through AMPK-mediated mTOR suppression, which is attenuated by an AMPK inhibitor. Moreover, AMPK inhibition may be a novel strategy for enhancing the effectiveness of stem cell therapy after MI in diabetes. Electronic supplementary material The online version of this article (10.1186/s13287-018-1057-0) contains supplementary material, which is available to authorized users.

This study investigated whether bioaugmentation improves sulfamethoxazole (SMX) degradation and nitrogen removal in the Moving Bed Biofilm Reactor (MBBR) system. The effects of the C/N ratio on SMX degradation and nitrogen removal were also evaluated. Using MBBR system operation experiments, the bioaugmented reactor was found to perform more effectively than the non-bioaugmentation reactor, with the highest SMX, nitrate-N, and ammonia-N removal efficiencies of 80.49, 94.70, and 96.09%, respectively. The changes in the sulfonamide resistance genes and bacterial communities were detected at various operating conditions. The results indicate that the diversity of the bacterial communities and the abundance of resistance genes were markedly influenced by bioaugmentation and the C/N ratio, with Achromobacter among the dominant genera in the MBBR system. The bio-toxicity of samples, calculated as the inhibition percentage (IP) toward Escherichia coli, was found to decrease to non-toxic ranges after treatment.

The urotensin II/urotensin receptor (UII/UT) system can mediate inflammatory liver injury in acute liver failure (ALF); however; the related mechanism is not clear. In this study, we confirmed that lipopolysaccharide/D-galactosamine (LPS/D-GalN) induced up-regulation of liver interferon regulatory factor 3 (IRF3) in ALF mice, whereas the UT antagonist urantide inhibited the up-regulated liver IRF3. LPS stimulation induced IRF3 transcription and nuclear translocation and promoted the secretion of interleukin-6 (IL-6), interferon (IFN)-β, and IFN-γ in Kupffer cells (KCs); these effects in LPS-stimulated KCs were inhibited by urantide. Knockdown of IRF3 using an adenovirus expressing an IRF3 shRNA inhibited IFN-β transcription and secretion as well as tumor necrosis factor (TNF)-α and IL-1β secretion from LPS-stimulated KCs; additionally, IL-10 transcription and secretion were promoted in response to LPS. However, LPS-stimulated TNF-α and IL-1β mRNA was not affected in the KCs. The IRF3 shRNA also did not have a significant effect on the NF-κB p65 subunit and p38MAPK protein phosphorylation levels in the nuclei of LPS-stimulated KCs. Therefore, IRF3 expression and activation depended on the signal transduction of the UII/UT system, and played important roles in UII/UT-mediated immune inflammatory injury in the liver but did not affect NF-κB and p38 MAPK activity.

MicroRNAs (miRNAs or miRs) are small, non-coding RNA molecules that play significant roles in numerous diseases. However, there is limited information regarding the plasma expression of miRNAs in patients with primary biliary cirrhosis (PBC) as well as the potential role of miRNAs in the development of PBC. miRNA microarray analysis was performed using plasma obtaind from three patients with PBC and three healthy controls. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to confirm the differential expression of miRNAs in the plasma and peripheral blood mononuclear cells (PBMCs) isolated from 20 patients with PBC, 20 patients with chronic hepatitis B (CHB) and 20 healthy controls. These miRNAs in PBMCs and plasma were validated by linear regression analyses. The T cell subset frequency was analyzed by flow cytometry. Correlations between altered miRNA expression and the frequency of the T cell subsets were determined by linear regression analyses. The co-expression of miRNAs and IL-17A was examined using fluorescence in situ hybridization (FISH) and immunohistochemistry. The microarray analysis identified sixteen miRNAs that were differentially expressed. Four miRNAs were validated by RT-qPCR. The expression pattern of miR-572 and miR-92a in the PBMCs correlated with the expression pattern in plasma. We also found that miR-92a expression closely correlated with the frequency of a subset of IL-17-producing T helper cells (Th17), and that miR-92a was co-expressed with IL-17A in patients with PBC. Taken together, these findings revealed that plasma from patients with PBC has a unique miRNA expression profile. Moreover, miR-92a may play an important role in the pathogenesis of PBC by regulating Th17 cell differentiation.

The pharmaceutical industry produces large volumes of low C/N ratio wastewater that is difficult to treat. In this study, we isolated Achromobacter sp. JL9 with high efficiency for sulfamethoxazole degradation and nitrogen conversion in low C/N ratio pharmaceutical wastewater. The SMX biodegradation and nitrogen removal ratio were 92.4% (nitrate-N), 86.7% (ammonia-N), 89.4% (total nitrogen), and 90.4% (SMX). The reaction kinetics and reaction rate constant were C/N ratio-, SMX concentration-, and dissolved oxygen concentration-dependent, and the highest reaction rate constant for SMX biodegradation was 0.0384 min−1. Gaseous compounds analysis and Nap gene amplification analysis by gas chromatography (GC) and polymerase chain reaction (PCR), respectively, showed N2 as an end product during nitrogen conversion. Moreover, toxicity assays were conducted by the inhibition percentage (PI) and agar well diffusion methods. The toxicity of the medium gradually decreased, falling within the nontoxic range after 96 h. The present study showed that biological technologies could be an effective, economical, and environmentally friendly remediation against pharmaceutical pollutants.

Functional dyspepsia (FD) is a widely prevalent gastrointestinal disorder throughout the world, whereas the efficacy of current treatment in the Western countries is limited. As the symptom is equivalent to the traditional Chinese medicine (TCM) term “stuffiness and fullness,” FD can be treated with Zhi-zhu Wan (ZZW) which is a kind of Chinese patent medicine. However, the “multi-component” and “multi-target” feature of Chinese patent medicine makes it challenge to elucidate the potential therapeutic mechanisms of ZZW on FD. Presently, a novel system pharmacology model including pharmacokinetic parameters, pharmacological data, and component contribution score (CS) is constructed to decipher the potential therapeutic mechanism of ZZW on FD. Finally, 61 components with favorable pharmacokinetic profiles and biological activities were obtained through ADME (absorption, distribution, metabolism, and excretion) screening in silico. The related targets of these components are identified by component targeting process followed by GO analysis and pathway enrichment analysis. And systematic analysis found that through acting on the target related to inflammation, gastrointestinal peristalsis, and mental disorder, ZZW plays a synergistic and complementary effect on FD at the pathway level. Furthermore, the component CS showed that 29 components contributed 90.18% of the total CS values of ZZW for the FD treatment, which suggested that the effective therapeutic effects of ZZW for FD are derived from all active components, not a few components. This study proposes the system pharmacology method and discovers the potent combination therapeutic mechanisms of ZZW for FD. This strategy will provide a reference method for other TCM mechanism research.

Background HOXB9 is a homeobox transcription factor which plays an important role in carcinoma development. This protein has been shown to inhibit cancer cell proliferation. However, the mechanisms that underpin HOXB9-mediated inhibition of cellular proliferation remain to be elucidated. Methods In this study, two gastric cancer cell lines, SGC7901 and MKN45, were transfected with plasmids pLVX-HOXB9 and shHOXB9. These transfections resulted in the over-expression of the HOXB9 gene in the SGC7901/HOXB9 cells and knockdown of the HOXB9 gene in the MKN45/shHOXB9 cells. Results Over-expression of the HOXB9 gene in the SGC7901/HOXB9 cells caused an increase in the apoptotic rate and a concomitant reduction in metastatic ability compared with the knocked-down MKN45/shHOXB9 cells. Moreover, a reduction in the expression of the phosphorylated-Akt protein was observed in the SGC7901/HOXB9 cells, while an increase in expression of the same protein was observed in the MKN45/shHOXB9 cells. We also observed that HOXB9 mediated a reduction in both NF-κB and N-cadherin and Snail protein expression. Conversely, HOXB9 caused an increase in the expression of E-cadherin. Conclusions In summary, this study reports that HOXB9 can suppress both phosphorylated-Akt expression and NF-κB activity. The latter phenomenon affects Snail protein expression and the inhibition of gastric carcinoma proliferation.

PepT1 can transport bacterial oligopeptide products and induce intestinal inflammation. Our aim was to investigate the mechanism of the small intestine injury induced by bacterial oligopeptide product muramyl dipeptide (MDP) which is transported by PepT1. We perfused the jejunum with a solution with or without MDP, or with a solution of MDP + Gly-Gly and explored the degree of inflammation to determine the role of PepT1–Nod2 signaling pathway in small intestine mucosa. MDP perfusion induced inflammatory cell accumulation and intestinal damage, accompanied by an increase in mucosal Nod2 and Rip2 transcript expression. NFκB activity and inflammatory cytokine expression, including serum levels of TNF-α, IL-1β, and IL-6, increased in the MDP group compared to the controls; these effects were reversed by perfusion of the nutritional dipeptide Gly-Gly. MDP can be transported through PepT1, causing inflammatory damage in the rat small intestine. Nod2–Rip2–NFκB signaling involved in the small intestinal inflammatory injury caused by MDP which is transported through PepT1.

Lanostane-type triterpenoids, inotolactones A and B, a drimane-type sesquiterpenoid, inotolactone C, and five known terpenoids 6β-hydroxy-trans-dihydroconfertifolin, inotodiol, 3β,22-dihydroxyanosta-7,9(11),24-triene, 3β-hydroxycinnamolide, and 17-hydroxy-ent-atisan-19-oic acid, were isolated from the submerged culture of chaga mushroom, Inonotus obliquus. Their structures were characterized by spectroscopic methods, including MS and NMR (1D and 2D) spectroscopic techniques. Inotolactones A and B, examples of lanostane-type triterpenoids bearing α,β-dimethyl, α,β-unsaturated δ-lactone side chains, exhibited more potent alpha-glucosidase inhibitory activities than the positive control acarbose. This finding might be related to the anti-hyperglycemic properties of the fungus and to its popular role as a diabetes treatment. In addition, a drimane-type sesquiterpenoid and an atisane-type diterpenoid were isolated from I. obliquus.

This study aimed to determine the clinical, psychological features, and quality of life in Chinese fibromyalgia (FM) patients who fulfilled the American College of Rheumatology (ACR) 2010 FM classification criteria at initial diagnosis. A cross-sectional study was carried out in the Chinese People's Liberation Army (PLA) General Hospital. A hundred and seven Chinese FM patients (86 females, 21 males) were included. Eighty-six patients completed the questionnaires. Descriptive, differences, and correlation analyses were performed. The results showed that Chinese FM patients started their diseases at a median age of 37 years, with a male-to-female ratio of 1:4.1. Most patients were diagnosed about 2 years after symptoms onset. Nearly 60 % (59.81%) patients had less than college education, 58.88% did not have a full-time job, and 41.12% had low-back pain. Out of 86 patients, 58 (67.4%) had anxiety and 75 (87.2%) had depression. FM patients had poor quality of life in each aspect and deficient social support. The level of pain for the past 7 days was strongly correlated with patient global impression of severity (PGI-S; r = 0.651, p

Web application has been widely used. So it is urgent to test the security of Web application efficiently to resist various attacks. In this paper, key technologies (detecting framework with plugin, discovering unknown vulnerability and building detection tools integrated by user-defined) are absolutely researched. No matter Web application is running or not, the platform can be dramatically able to discover the vulnerability efficiently to insure their security.

A finite-element mechanical model is established aiming at the features of telescopic suspension arm of dirt-removing crane in practice, such as that there exist many compound modes, the range of variation in lifting weight is big, etc. The strength, stiffness and stability of suspension arm is calculated and optimized based on ANSYS (software). The result of conventional design, which is checked and revised, tallies with the measured value relatively and may provide valuable reference for the design of suspension arm, which is to some extent significant to prolonging the fatigue life of cranes.

Chronic infection with hepatitis B virus (HBV) plays a significant role in hepatocellular carcinoma development. To investigate the effect of hepatitis B virus X protein (HBx) on inflammatory cytokines of human T cell, a eukaryotic expression vector, HBx-pEGFP-C1, was constructed and transfected into the Jurkat human T-cell line. Jurkat cells were transfected transiently using Lipofectamine 2000 and activated by phytohemagglutinin (PHA). Interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), IL-4, IL-10, IL-13, and IL-14 mRNA was measured. The results showed that the vector HBx-pEGFP-C1 was successfully constructed, and HBx was expressed in Jurkat cells. Compared with a control group, mRNA of IL-1β and TNF-α was significantly elevated in the HBx-pEGFP-C1 group (p < 0.05), while IL-4, IL-10, IL-13, and IL-14 mRNA was decreased (p < 0.05). Therefore, transient overexpression of HBx promoted PHA-induced pro-inflammatory cytokine secretion and repressed anti-inflammatory cytokine secretion in human T cells.

Aimed at exploring the mechanism of acupuncture therapy, we develop functional brain networks using electroencephalogram (EEG) data, and use the methods cluster coefficient to analyze the functional networks. We develop the following result: during the acupuncture, the structure of network becomes tighter, the relativity grows stronger and the structure of the networks becomes complex. Our conclusion is that acupuncture is able to affect the firing properties of the central nervous system, and make the information transmission in the brain functional sections stronger.

Inflammatory and immune responses, as well as melatonin secretion, are affected by circadian regulation. Abnormal circadian rhythm of melatonin release has been reported to be associated with the later stages of sepsis; however, its role in the early stages of sepsis is unclear. We studied 11 septic and 11 non-septic patients in our intensive care unit (ICU). Peripheral blood was drawn at 4-h intervals on the first day, beginning at 2:00 p.m., over a total period of 24 h. Plasma levels of melatonin, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) were measured by radioimmunoassay or enzyme-linked immunosorbent assay (ELISA). Messenger RNA levels of circadian genes Cry-1 and Per-2 were analyzed using quantitative real-time PCR. Results show the circadian rhythm of melatonin secretion was altered in the early stages of sepsis. The melatonin secretion acrophase occurred earlier in septic patients at 6:00 p.m., compared with at 2:00 a.m. in non-septic ICU patients. Compared with the non-septic group, both Cry-1 and Per-2 expression were significantly decreased while TNF-α and IL-6 expression were significantly increased in septic patients [TNF-α, 64.1 (43.6-89.1) vs. 11.4 (10.4-12.5) ng/ml; IL-6, 41.2 (35.7-50.8) vs. 19.1 (16-136.7) ng/ml; median (range), both P=0.04]. The peak concentrations of TNF-α and IL-6 were shown to be in concordance with the rhythm of melatonin secretion. The circadian rhythm of melatonin secretion and circadian gene expression were altered in the early stages of sepsis, which likely led to the changes in pro-inflammatory cytokine release. These findings shed light on the potential link between circadian rhythm and the progression of early-stage sepsis.

Hepatitis B virus (HBV) infection is a global public health problem, because patients with chronic hepatitis B (CHB) may progress to liver cirrhosis and eventually evolve into hepatocellular carcinoma. Decoy receptor 3 (DcR3) is a soluble receptor of the tumor necrosis factor receptor superfamily, and has been implicated in anti-apoptotic and anti-inflammatory pathways. In this study, we explored the clinical value of serum DcR3 in predicting the active status of CHB in hepatitis B e antigen-negative patients (active HBeAg (-) CHB), which was determined with ELISA. The serum level of DcR3 in active HBeAg (-) CHB patients (1.92 ± 0.68 ng/ml) was higher than that in healthy controls (0.80 ± 0.25 ng/ml, p < 0.0001) and that in inactive status of HBeAg (-) CHB (inactive hepatitis B surface antigen carrier, HBsAg-IaC) patients (0.95 ± 0.26 ng/ml, p < 0.0001). DcR3 level was correlated with HBV DNA level (r = 0.819, p < 0.0001) and alanine transaminase level (ALT, r = 0.704, p < 0.0001) in active HBeAg (-) CHB patients. The area under the Receiver Operating Characteristics curve of DcR3 for detecting the active status of HBeAg (-) CHB patients was 0.914 (95% confidence interval, 0.851-0.977). The optimal cut-off value for DcR3 to predict active HBeAg (-) CHB was 1.22 ng/ml, which had a sensitivity of 87.5% and a specificity of 84.4%. These results suggest that serum DcR3 level may be useful for detecting HBeAg (-) CHB in the active stage, which requires medical treatment.

Background Ghrelin is a hormone that protects against hypoxic injury of cardiac cells by inducing autophagy, but the role of autophagy in sepsis remains unclear. This study aimed to evaluate whether ghrelin could enhance autophagy in rats with intestinal sepsis. Methods The cecal ligation and perforation (CLP) method was used to induce sepsis in Sprague-Dawley rats. The rats were assigned to four groups: normal group, sham-operated group, sepsis group, and Ghrelin-treated group. Sera and small intestinal tissues were collected from all groups. The sepsis was evaluated by histological analysis, and autophagy of small intestinal epithelial cells was assessed by electron microscopy, immunofluorescence, and biochemical methods. Results The expression of autophagy-associated proteins such as LC3, Atg 7 and Beclin 1 increased by 8 h post-CLP and declined to basal levels by 12 h post-CLP. The expression of LC3, Atg 7 and Beclin 1 in Ghrelin-treated rats was higher than that in rats with sepsis. Furthermore, compared to rats with sepsis, Ghrelin-treated rats showed significantly reduced intestinal mucosa injury at 20 h post-CLP. Conclusion Autophagy is induced in the early stages of sepsis. Ghrelin could enhance the autophagy of intestinal epithelial cells in rats with sepsis and protect the small intestinal epithelium against sepsis-induced injury.

CD36, a scavenger receptor, plays an important role in the progression of atherosclerosis through its interaction with oxidized low-density lipoprotein (ox-LDL). Porphyromonas gingivalis (P. gingivalis, Pg) has been shown to promote macrophage-derived foam cell formation by affecting the expression of CD36. However, the regulatory role of CD36 in macrophages infected with Pg remains largely unknown. Therefore, the aim of the present study was to explore the molecular mechanism of Pg induced CD36 expression in macrophages. Our results showed that Pg promoted ox-LDL uptake by macrophages and the formation of foam cells. Pg infection increased CD36 mRNA and protein levels in ox-LDL-untreated macrophages. Moreover, small interferon RNA (siRNA) targeting CD36 significantly reduced foam cell formation induced by Pg. Additionally, Pg stimulated nuclear translocation of p65, which directly bound to the promoters of CD36 to facilitate its transcription. Inhibition of p65, NF-κB or ERK1/2 blocked Pg-induced CD36 production; whereas, overexpression of NF-κB subunits p65 and p50 upregulated CD36. Furthermore, Ras inhibitors significantly attenuated ERK1/2 activation and CD36 expression. Taken together, the data indicated that stimulation of the ERK/NF-κB pathway by Pg led to transactivation of the CD36 promoters, thereby upregulating CD36 expression in the infected macrophages. These findings may help design new treatment strategies in atherosclerosis.

Background: Osteotomy of the fibula is a common orthopedic procedure performed for various indications, including harvesting fibula for grafting purposes. The effect of fibular osteotomy and need for tibiofibular syndesmotic fixation fusion at different levels on tibiotalar joint is matter of debate. We performed a biomechanical analysis of the impact of fibular osteotomies at different levels and whether the fixation of distal tibiofibular joint mitigates instability caused by the osteotomy. Materials and Methods: Six lower limb specimens from fresh adult cadavers were used to prepare leg-foot models. The specimens were assigned to six status according to the level of osteotomy and whether fixation of distal tibiofibular joint was performed or not. Each specimen was then loaded axially to 700 N by the material testing machine, and the tibiotalar joint contact area and peak pressure were measured using an electronic pressure sensor. Results: The contact area and the pressure of tibiotalar joint showed significant changes when compared to the normal specimen . All osteotomy specimens had a decreased tibiotalar contact area and an increased peak pressure. This positively correlated with proximity of level of osteotomy to the lateral malleolus. Conclusions: Through this study, we found that fibular osteotomy had an adverse effect in terms of decreasing the contact surface of tibiotalar joint that led to increased peak pressure in the joint. However, bone fusion and screw fixation of the distal tibiofibular joint reduced these adverse effects.

Objective: To investigate the stability and three-dimensional movements of the atlantoaxial joint after artificial atlanto-odontoid joint (AAOJ) arthroplasty. Method: Ten sets of AAOJ implanted in bony specimens from 10 adults were used to test the pull-out strength of the atlas-axis components with a MTS858 Mini Bionix machine. Another twelve human cadaveric specimens including C0-C4 were used to evaluate the three-dimensional movements of C1-C2 under five different conditions in sequence, that is, the complete specimen, anterior decompression, posterior transarticular screws fixation, AAOJ arthroplasty and fatigue test. Result: There were significant differences between atlas and axis components in the maximum pull-out strength and trajectory length, however the yield length was not significantly different. The maximum pull-out strength of the atlas and axis was positively correlated with trajectory length (r1= 0.880, P 0.05), but the ROM in flexion-extension and lateral bending was significantly smaller compared with the specimens which underwent anterior decompression (P < 0.05). No abrasion and abnormal mobilization were observed after 2000 cycles of flexion, extension, lateral bending and axial rotation in the fatigue test. Conclusions: The self-designed AAOJ has excellent biomechanical performance, and AAOJ arthroplasty can restore excellent instant stability and preserve the movement of the atlantoaxial joint.

Objective: To investigate the effects of hibernation drugs on early wound sepsis in severely scalded rats. Methods: Sprague-Dawley rats inflicted 30% TBSA deep thickness were randomly divided into A (immediate resuscitation) and B (immediate resuscitation and lytic cocktail). After infusion of 108 CFU/ml Pseudomonas aeruginosa in the wound on third postburn day, survival was compared between two groups. Local tissue samples and plasma were collected and the plasma level of IL-2 mRNA, IL-4 mRNA, IL-10 mRNA, and IFN-γ mRNA were assayed by fluorescence PCR. Results: Compared with Group A, host survival significantly increased (0.663 ± 0.026, P

Purpose Unbalanced inflammatory response and lymphocyte apoptosis is associated with high mortality in septic patients. Decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor superfamily, is an anti-inflammatory and anti-apoptotic factor. Recently, DcR3 expression was found to be increased in septic patients. This study evaluated the therapeutic effect and mechanisms of DcR3 on cecal ligation and puncture (CLP)-induced sepsis in mice. Methods C57BL/6 mice were subjected to CLP-induced polymicrobial sepsis. DcR3 Fc was intravenously injected 30 min before and 6 h after CLP. Bacterial clearance, cytokine production, histology, lymphocyte apoptosis and survival were evaluated. Furthermore, we investigated the systemic effects of DcR3 in in vitro lymphocyte apoptosis regulation. Results Our results demonstrated that DcR3 protein treatments significantly improved survival in septic mice (p

Aim: To evaluate the efficacy and safety of diacerein in patients with knee osteoarthritis (OA). Methods: A total of 223 patients fulfilling the American College of Rheumatology criteria for knee OA were enrolled in this 17-week, randomized, double-dummy, diclofenac-controlled trial, with diacerein dosages of 100 mg/day and diclofenac sodium administered at 75 mg/day. Result: After 12 weeks of treatment, the total efficacy rates of patient/physician global assessment in diacerein and diclofenac groups were 65.4%/61.6% and 61.2%/61.2% respectively (P > 0.05). In the intent-to-treat population, the primary criterion (visual analogue scale [VAS] assessment of pain on walking 20 m) was significantly superior (P 0.05). Mild-to-moderate gastrointestinal disorders were the most frequent adverse events. Conclusion: Diacerein was shown to be as effective as diclofenac sodium in treating patients with knee OA, coupled with a carry-over effect. Diacerein was generally well tolerated, with a good safety profile. No severe adverse events were occurred.

Supplemental Digital Content is available in the text, Background: Postoperative nausea and vomiting (PONV) is a frequent complication in postoperative period. The aim of this article was to evaluate the effect of dexmedetomidine on PONV. Method: RevMan 5.3 software was applied for performing statistic analysis. Twenty-four trials with 2046 patients were included. Results: The PONV of the dexmedetomidine group was significantly lower compared with the placebo group (0.56, 95% CI: 0.46, 0.69). Subgroup analysis further confirmed the effect of dexmedetomidine (irrespective of administration mode) (P

AIM: To investigate urotensin-II (UII) and its effects on tumor necrosis factor (TNF)-α and interleukin (IL)-1β in early acute liver failure (ALF). METHODS: We investigated the time-dependent alteration in UII levels and its effects on TNF-α and IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF. RESULTS: After lipopolysaccharide/D-galactosamine challenge, UII rose very rapidly and reached a maximal level 0.5 h, and the level remained significantly elevated after 2 h (P < 0.05). Six hours after challenge, UII began to degrade, but remained higher than at 0 h (P < 0.05). Pretreatment with urantide, an inhibitor of the UII receptor, suppressed the degree of UII increase in liver and blood at 6 h after challenge (P < 0.05 vs paired controls). In addition, liver and blood TNF-α increased from 1 to 6 h, and reached a peak at 1 and 2 h, respectively; however, IL-1β did not rise until 6 h after challenge. Urantide pretreatment inhibited the degree of TNF-α and IL-1β increase following downregulation of UII post-challenge (all P < 0.05). CONCLUSION: UII plays a role in the pathogenesis and priming of ALF by triggering an inflammatory cascade and driving the early release of cytokines in mice.

In the present study, we aimed to develop and validate a rapid and sensitive, Alu-based real-time PCR method for the detection of circulating cell-free DNA (cfDNA). This method targeted repetitive elements of the Alu reduplicative elements in the human genome, followed by signal amplification using fluorescence quantification. Standard Alu-puc57 vectors were constructed and 5 pairs of specific primers were designed. Valuation was conducted concerning linearity, variation and recovery. We found 5 linear responses (R1–5=0.998–0.999). The average intra- and inter-assay coefficients of variance were 12.98 and 10.75%, respectively. The recovery was 82.33–114.01%, with a mean recovery index of 101.26%. This Alu-based assay was reliable, accurate and sensitive for the quantitative detection of cfDNA. Plasma from normal controls and patients with myocardial infarction (MI) were analyzed, and the baseline levels of cfDNA were higher in the MI group. The area under the receiver operating characteristic (ROC) curve for Alu1, Alu2, Alu3, Alu4, Alu5 and Alu (Alu1 + Alu2 + Alu3 + Alu4 + Alu5) was 0.887, 0.758, 0.857, 0.940, 0.968 and 0.933, respectively. The optimal cut-off value for Alu1, Alu2, Alu3, Alu4, Alu5 and Alu to predict MI was 3.71, 1.93, 0.22, 3.73, 6.13 and 6.40 log copies/ml. We demonstrate that this new method is a reliable, accurate and sensitive method for the quantitative detection of cfDNA and that it is useful for studying the regulation of cfDNA in certain pathological conditions. Alu4, Alu5 and Alu showed better sensitivity and specificity for the diagnosis of MI compared with cardiac troponin I (cTnI), creatine kinase MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH). Alu5 had the best prognostic ability.

We present a case report of a patient with Sjogren’s syndrome accompanied with interstitial cystitis. A 64-year-old woman complained of dry mouth for 21 years, recurrent swelling and pain on the right parotid in 2000, and urinary irritation symptoms in the past 2 years. Several courses of different types of antibiotics could not relieve her urinary irritation symptoms. Bladder hydraulic dilatation had only transient effects. Urine sediment contained neither erythrocytes nor leukocytes, and urine cultures yielded no growth. However, increased γ-globulin, positive antinuclear antibodies, and anti-SS-A and anti-SS-B antibodies were detected. Histopathological data of labial salivary glands showed three foci of numerous mononuclear cells. Cystoscopy revealed redness, edema, angiectasis, and extensive ecchymosis of the mucosal surface and several small floating cruor entities in the bladder. Urinary bladder biopsy specimens revealed the absence of urothelium and edematous lamina propria and submucosa, with diffuse or multiple focal chronic inflammatory cell infiltration. Based on these findings, she was diagnosed with Sjogren’s syndrome accompanied with interstitial cystitis. Therapy with corticosteroids relieved the symptoms significantly.

To explore the relationship of Pi-deficiency syndrome in TCM with the change of serum high density lipoprotein (HDL) in blood lipid metabolic disorder.Sixty-eight patients with confirmed coronary heart disease (CHD) were selected for TCM syndrome typing into Pi-deficiency (PD) group and non-Pi-deficiency (NPD) group. Routine blood lipids and serum lipoprotein electrophoretogram (SLPG) were determined in all patients to analyze the total content of HDL and its relative contents of sub-components HDL(1-5), as well as their relation with PD syndrome. Besides, a healthy control group (62 cases) was set up.The level of serum HDL-C was lowered, SLPG abnormality rate increased in the patients with CHD, with total HDL and the relative contents of subcomponent HDL(1) and HDL(3) significantly lower than those in the healthy control group (P0.01). The total HDL, HDL(1) and HDL(3) in the PD group were also lower than those in the NPD group (P0.05, P0.01).Serum HDL and its sub-components showed a definite relation with TCM PD syndrome type, therefore, further exploring the granular specificity of HDL and its sub-components as well as their influence on reverse cholesterol transport (RCT) may hopefully provide clues for developing RCT regulatory Chinese new drugs and for CHD prevention and treatment.