Association Between Ferroptosis and Central Nervous System Diseases and A Review of Traditional Chinese Medicine Intervention / 中国实验方剂学杂志

Central nervous system （CNS） is a sophisticated system subject to complex regulation， which dominates the high-level neural activities of the human body. Due to its complex physiological structure and refined regulatory mechanism covering a variety of diseases， CNS is the place where many chronic， refractory and rare diseases occur. Nerve cell is the basic unit of CNS， and its dysfunction and death is the root cause of CNS diseases. Ferroptosis is a new form of programmed cell death proposed in recent years， and has been proved to be closely related to the production and development of multiple CNS diseases. Traditional Chinese medicine （TCM）， including Chinese herbs， acupuncture and moxibustion， and massage， has shown unique advantages in the treatment of CNS diseases for a long time. A large number of studies have demonstrated that TCM participates in the regulation of CNS diseases via regulating ferroptosis and shows a good research prospect. This paper summarized the characteristics of ferroptosis and discussed the association between ferroptosis and CNS diseases in pathological mechanism. We also reviewed the regulation of various CNS diseases by different TCM interventions through ferroptosis， providing references for TCM to participate in the treatment of CNS diseases properly in the future.

FLASH Binds p53 and Enhances its Transcriptional Activity / 中国生物化学与分子生物学报

As an important transcription factor, the tumor suppressor protein p53 is involved in multiple biological processes such as cell cycle regulation, cell division, cell senescence and DNA repair The functional roles of p53 under various physiological conditions are inseparable from the assistance of many cofactors, which can regulate the protein modification, cellular sub-localization, and protein stability of p53 Therefore, the identification of p53-binding protein(s) has important biological significance for further understanding the signal transduction network of p53 in vivo. In the present study, a novel p53-binding protein, FADD-like interleukin-1β-converting enzyme associated huge protein (FLASH) was identified through a yeast two-hybrid screen The protein-protein interaction and the structural basis of the interaction between FLASH and p53 was also confirmed by co-immunoprecipitation analysis These studies have shown that p53 can simultaneously interact with both FLASH-N1 (aa 1 ~ 200) and FLASH-C1 (aa 1 534 ~ 1 780) In addition, both of FLASH-N and FLASH-C can interact with the same region of p53 (aa 293 ~ 393) Transcription analysis has revealed that the full length of FLASH and FLASH-M (aa 921 ~ 1533) can enhance the transcription activity of p53 In summary, FLASH can bind to p53 and enhance its transcriptional activity

Effect of TSG on GSK3β，PKA and PP2A of APP/PS1/Tau Triple-transgenic Mice Dementia Model / 中国实验方剂学杂志

Objective:To observe the effect of tetrahydroxy stilbene glycoside （TSG） on the expression of glycogen synthase kinase 3<italic>β </italic>（GSK3<italic>β</italic>）， cyclic adenosine monophosphate-dependent protein kinase （PKA） and Serine/threonine phosphatase 2A（PP2A） in the brain of amyloid precursor protein/presenilin-1/Tau （APP/PS1/Tau） triple-transgenic mice dementia model. Method:A total of forty-five 8-month-old APP/PS1/Tau transgenic mice were randomly divided into model group， positive control group （Huperzine-A， 0.15 mg·kg^-1）， low， medium and high dose TSG groups （TSG， 0.033，0.1，0.3 g·kg^-1）， with 9 mice in each group， and another nine C5B7L/6J mice of the same age were selected as normal control group. After 60 days of intragastric administration， the general structure of hippocampal neurons was observed by hematoxylin-eosin （HE） staining， immunohistochemical （IHC） was used to detect the expression of PKA protein in the brain of mice in each group， the mRNA expression levels of GSK3<italic>β</italic>， PKA and PP2A were detected by real time quantitative reverse transcription polymerase chain reaction （Real-time PCR）， and protein expression levels of GSK3<italic>β</italic> and PP2A were detected by Western blot. Result:Compared with the normal control group， the apoptosis level of neurons in the model group was significantly increased， the protein and mRNA expression levels of GSK3<italic>β</italic> and PKA were significantly increased （<italic>P</italic><0.05， <italic>P</italic><0.01）， and the protein and mRNA expression levels of PP2A were significantly decreased （<italic>P</italic><0.05， <italic>P</italic><0.01）. Compared with the model group， the apoptosis level of neurons in each treatment group was significantly down-regulated， the protein and mRNA expression levels of GSK3<italic>β</italic> and PKA were significantly down-regulated （<italic>P</italic><0.05， <italic>P</italic><0.01）， and the protein and mRNA expression levels of PP2A were significantly increased （<italic>P</italic><0.05， <italic>P</italic><0.01）. Conclusion:The mechanism of TSG in the treatment of Alzheimer's disease （AD） may be related to lowering the transcription and expression of GSK3<italic>β</italic> and PKA， increasing the transcription and expression of PP2A.

Changes of serum galectin-3 and pentraxin-3 levels in CHF patients and their correlation with progno-sis / 心血管康复医学杂志

Objective :To explore changes of serum levels of galectin-3 and pentraxin-3 (PTX-3) in patients with chro-nic heart failure (CHF) and their correlation with prognosis .Methods : A total of 150 CHF patients (CHF group) treated in our hospital and 150 healthy volunteers undergoing physical examination simultaneously (healthy group ) from Jan 2015 to Dec 2015 were enrolled .Serum levels of galectin-3 ,PTX-3 and N-terminal pro brain natriuretic peptide (NT-proBNP) ,left atrial diameter (LAD) ,left ventricular end-diastolic dimension (LVEDd) and left ven-tricular mass index (LVMI) were compared between two groups at enrollment .According to one-year follow-up out-come ,CHF group (12 cases lost ,another 138 cases) was divided into poor prognosis group (n＝36) and good prog-nosis group (n＝102).Spearman linear correlation analysis was used to analyze correlation among serum galectin-3 , PTX-3 levels and poor prognosis of CHF patients .Results :Compared with healthy group ,there were significant rise in serum levels of galectin-3 [ (2-23 ± 0-25) ng／ml vs .(16-61 ± 1-48) ng／ml] ,PTX-3 [ (1-28 ± 0-54) μg／L vs. (3-58 ± 0-52) μg／L] ,NT-proBNP [(223-23 ± 76-28) pg／ml vs.(952-75 ± 85-43) pg／ml] ,LAD ,LVEDd and LV-MI in CHF group , P＝0-001 all.Compared with good prognosis group at enrollment ,there were significant rise in serum levels of galectin-3 [ (18-52 ± 1-91) ng／ml vs.(24-63 ± 2-26) ng／ml] and PTX-3 [ (2-65 ± 0-74) μg／L vs. (3-95 ± 1-05) μg／L] in poor prognosis group , P＝0-001 both .Spearman linear correlation analysis indicated that serum galectin-3 and PTX-3 levels were significant positively correlated with major adverse cardiovascular events in CHF patients ( r＝0-608 ,0-558 , P＝0-001 both).Conclusion :Serum levels of galectin-3 ,PTX-3 and NT-proBNP levels are significant rise and closely related to prognosis of CHF patients ,can be used as auxiliary indexes predicting prognosis and may provide the basis for formulation of target therapy .

Compose a new chapter of cardiopulmonary resuscitation training with Chinese characteristics / 中华危重病急救医学

China's cardiopulmonary resuscitation (CPR) training in the form of a Chinese tutor classes for the training of CPR has spread across the country. It is supported by three Chinese original theoretical systems: "2016 Chinese cardiopulmonary resuscitation expert consensus", "2018 China cardiopulmonary resuscitation training expert consensus", and "Chinese public health guidelines for cardiopulmonary resuscitation". There are five characteristics in the classes, such as the "three analysis" "three-prevention" (precaution, prewarning and early identification),"three-ways" (standardization, diversification and individuation), "three lives" (demutation, transcending and extension),"three dimensional" (time, space and society). Highlighting the Chinese CPR training of the "three training" policy for CPR training (the cultivation of a sound system, the cultivation of scientific guidelines and the cultivation of a healthy culture), the "three training" program of CPR training (training professional skills, training multidimensional and training flexible ), the "three party" direction of CPR training (the application for achievement translation, the precision disseminators and theoretical innovation guides) under the new era background. A new chapter of CPR training with Chinese characteristics was composed.

Anti-prostate cancer effect of roemerine: An experimental study / 中华男科学杂志

Objective@#To investigate the anti-prostate cancer (PCa) effect of roemerine in vitro and in vivo in the mouse model of PCa.@*METHODS@#We detected the effects of roemerine on the proliferation, apoptosis and migration of PCa cells DU145, LNCaP, PC-3 and 22RV1, screened out the sensitive cell line and constructed a tumor-bearing model in mice for verification of the antitumor efficacy of roemerine in vivo.@*RESULTS@#Roemerine inhibited the proliferation and migration of the DU145, LNCaP, PC-3 and 22RV1 cells and induced their apoptosis in different degrees, particularly those of the LNCaP cells. The average tumor weight was less in the roemerine intervention group (［1.99±0.95］ g) than in the control (［2.95±1.04］ g), the least in the high-dose roemerine (30 mg/kg) plus paclitaxel intervention group (［0.90±0.16］ g). The mean heart, liver, and kidney indexes were markedly lower in the roemerine (0.58±0.06, 6.20±0.42 and 1.49±0.33) than in the paclitaxel group (0.66±0.04, 6.99±0.72 and 1.95±0.34), while the mean spleen and thymus indexes were remarkably higher in the former (0.54±0.11 and 0.06±0.01) than in the latter (0.41±0.09 and 0.05±0.01). Pathological staining showed a lower degree of malignancy and metastasis in both the roemerine and the roemerine + paclitaxel intervention group than in the control, as well as a lower degree of visceral injury in the roemerine and roemerine + paclitaxel groups than in the paclitaxel group.@*CONCLUSIONS@#Roemerine has some anti-PCa effect and alleviates adverse reactions in paclitaxel combination administration.

Research progress of hepatocyte necroptosis in liver injuries / 中国药理学通报

Various pathological factors can result in the death of hepatocytes during liver injury. Persistent hepatocyte death initi-ates and aggravates chronic inflammation and fibrosis,ultimately leading to liver cirrhosis and hepatocellular carcinoma. Thus, limiting hepatocyte death is an effective strategy for improving liver injury. Necroptosis is a newly characterized form of cell death,which is highly regulated by signaling pathways and has typical morphological features of necrosis. Increasing evidence indicates that necroptosis plays a key role in drug-induced or im-munological acute liver injuries,and in chronic liver injuries in-cluding alcoholic fatty liver,nonalcoholic fatty liver and liver fi-brosis. This article reviews the recent advances on the hepato-cyte necroptosis in liver injury,providing novel insights into the pathogenesis of liver disease and related therapeutic reagents.

PID1, a new tumor-promoting gene in insulin resistance mediated acceleration of hepatocellular carcinoma development and progression / 中国药理学与毒理学杂志

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) on promotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to inducethe liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells. qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1.Immunoprecipitation was used to determine the receptor of PID1. Chromatin immunoprecipitation (ChIP) was operated to measure the modification of H3K4me3 of PID1 promoter. RESULTS PID1 restriction improved insulin resistance, hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover, PID1 liver- specific protooncogenes via hydrodynamics- based transfection established a primary hepatocellular carcinoma mouse model, induced an immunosuppressive environment, with the reduction of CD3 +, CD4 +, CD8 +T cells, retarded maturation of dendritic cells (DCs), pronounced differentiation of regulatory T cells (Tregs), and recruitment of MDSC. In addition, PID1 overexpression activated proliferation related genes, promoted anti- inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor (EGFR) and activation of downstream MAPK pathway. As such, PID1 exist trimethylation of histone H3 at lysine 4 (H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function. IR accelerates liver cancer development and progression partially dependent on the activation of PID1.

Progress in the study of signal pathways for chronic inflammation-associated pancreatic carcinogenesis / 药学学报

Pancreatic cancer is one of the most lethal and intractable human malignancies with poor prognosis. Chronic pancreatitis is the independent risk factor for pancreatic cancer. Smoking, obesity and family history are the risk factors for chronic inflammation-associated pancreatic carcinogenesis. Recent studies of signal pathways have made a significant progress in our understanding of chronic pancreatitis in pancreatic cancer. This review summarizes recent development in the important signal pathways involved in pancreatic carcino-genesis from chronic pancreatitis.

Clinical Value of Tumor Markers for Determining Cause of Pleural Effusion / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>It is often challenging to distinguish tuberculous pleural effusion (TPE) from malignant pleural effusion (MPE); thoracoscopy is among the techniques with the highest diagnostic ability in this regard. However, such invasive examinations cannot be performed on the elderly, or on those in poor physical condition. The aim of this study was to explore the differential diagnostic value of carbohydrate antigen 125 (CA125), carbohydrate antigen 199 (CA199), carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), and squamous cell carcinoma (SCC) associated antigen in patients with TPE and MPE.</p><p><b>METHODS</b>Using electrochemiluminescence, we measured the concentration of tumor markers (TMs) in the pleural effusion and serum of patients with TPE (n = 35) and MPE (n = 95). We used receiver operating characteristic (ROC) curve analysis to evaluate the TMs and differentiate between TPE and MPE.</p><p><b>RESULTS</b>The cut-off values for each TM in serum were: CA125, 151.55 U/ml; CA199, 9.88 U/ml; CEA, 3.50 ng/ml; NSE, 13.27 ng/ml; and SCC, 0.85 ng/ml. Those in pleural fluid were: CA125, 644.30 U/ml; CA199, 12.08 U/ml; CEA, 3.35 ng/ml; NSE, 9.71 ng/ml; and SCC, 1.35 ng/ml. The cut-off values for the ratio of pleural fluid concentration to serum concentration (P/S ratio) of each TM were: CA125, 5.93; CA199, 0.80; CEA, 1.47; NSE, 0.76; and SCC, 0.90. The P/S ratio showed the highest specificity in the case of CEA (97.14%). ROC curve analysis revealed that, for all TMs, the area under the curve in pleural fluid (0.95) was significantly different from that in serum (0.85; P < 0.001).</p><p><b>CONCLUSIONS</b>TMs in TPE differ significantly from those in MPE, especially when detected in pleural fluid. The combined detection of TMs can improve diagnostic sensitivity.</p>

Effect of Ganoderma Lucidum Polysaccharides Combined with Metformin on Oxidative Stress of Type 2 Diabetic Rats in Vivo / 医药导报

Objective To study the effect of ganoderma lucidum polysaccharides combined with metformin on oxidative stress of type 2 diabetic rats. Methods SD rats were fed with high fat diet for 4 weeks and injected with streptozotocin (30 mg·kg-1 ) to produce type 2 diabetic model. The diabetic rats were randomly divided into diabetes model group, ganoderma lucidum polysaccharides group (600 mg·kg-1 ), metformin group (600 mg·kg-1 ), combination group (ganoderma lucidum polysaccharides 300 mg·kg-1+ metformin 300 mg·kg-1 ), After 12 weeks of treatment, the level of fasting blood glucose was determined, and the activity of superoxide dismutase ( SOD), malondialdehyde ( MDA), catalase ( CAT), glutathione peroxidase (GSH-Px), total cholesterol (TC) and triglyceride (TG) were detected. Results The levels of fasting blood glucose in the treatment groups were significantly lower than that in the diabetes model group (P<0. 01). Furthermore, fasting blood glucose in the combination group was significantly lower than that in ganoderma lucidum polysaccharides group and metformin group (P<0. 01). Compared with diabetes model group, serum TC and TG in the treatment groups were significantly lower (P<0. 05, P<0. 01). Serum TC and TG were significantly lower in the combination group than in ganoderma lucidum polysaccharides group and metformin group (P<0. 05, P<0. 01). Compared with diabetes model group, serum SOD levels in the treatment groups were significantly higher (P<0. 01). Compared with ganoderma lucidum polysaccharides group and metformin group, serum SOD levels in the combination group was significantly higher (P<0. 05). Compared with diabetes group, serum MDA levels in the treatment groups were significantly lower (P<0. 01). Serum MDA in the combination group was significantly lower than that in ganoderma lucidum polysaccharides group and metformin group ( P<0. 05). Compared with diabetes model group, serum CAT and GSH-Px in the treatment groups were significantly higher (P<0. 05, P<0. 01). Serum CAT and GSH-Px in the combination group were significantly higher than those in ganoderma lucidum polysaccharides group and metformin group (P<0. 05). Conclusion Ganoderma lucidum polysaccharides combined with metformin could effectively inhibit oxidantion stress in type 2 diabetic rats. The effect was better than ganoderma lucidum polysaccharides or metformin used alone. The possible mechanism may be related to increased activity of SOD, CAT, GSH-Px in vivo and regulation of dyslipidemia.

Incidence of pleural effusion in patients with pulmonary embolism / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>No data on the incidence of pleural effusion (PE) in Chinese patients with pulmonary embolism are available to date. The aim of the current study was to investigate the frequency of PE in a Chinese population of patients with pulmonary embolism.</p><p><b>METHODS</b>This was a retrospective observational single-center study. All data of computed tomography pulmonary angiography (CTPA) performed over 6-year period on adult patients with clinically suspected pulmonary embolism were analyzed.</p><p><b>RESULTS</b>From January 2008 until December 2013, PE was identified in 423 of 3141 patients (13.5%) with clinically suspected pulmonary embolism who underwent CTPA. The incidence of PE in patients with pulmonary embolism (19.9%) was significantly higher than in those without embolism (9.4%) (P < 0.001). Majority of PEs in pulmonary embolism patients were small to moderate and were unilateral. The locations of emboli and the numbers of arteries involved, CT pulmonary obstruction index, and parenchymal abnormalities at CT were not associated with the development of PE.</p><p><b>CONCLUSIONS</b>PEs are present in about one fifth of a Chinese population of patients with pulmonary embolism, which are usually small, unilateral, and unsuitable for diagnostic thoracentesis.</p>

Immune Regulation of Interleukin-27 in Malignant Pleural Effusion / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Interleukin (IL)-27 has been reported to have anti-proliferate and anti-angiogenic activities on cancer cells. However, the involvement of IL-27 in malignant pleural effusion (MPE) remains unknown. Thus, in this research, we compared the immune functions of IL-27, interferon (IFN)-γ, and IL-17 on lung cancer cells and revealed the regulatory mechanism of IL-27 in MPE.</p><p><b>METHODS</b>The distribution of IL-27 in both MPE and blood was evaluated by enzyme-linked immunosorbent assay and flow cytometry. The expressions of cytokine receptors and the levels of the phosphorylated signal transducer and activator of transcription (STAT) signalings were detected by flow cytometry. As well as the effects of proliferation, apoptosis, migration, and adherent activity of IL-27, IFN-γ, and IL-17 on lung cancer cells were also explored.</p><p><b>RESULTS</b>The expression of IL-27 was increased in MPE when compared with blood (147.3 ± 25.1 pg/ml vs. 100.3 ± 13.9 pg/ml, P = 0.04). IL-27 was noted to suppress both proliferation (18.33 ± 0.21 vs. 27.77 ± 0.88, P = 0.0005) and migration (1.82 ± 0.44 vs. 3.13 ± 0.07, P = 0.04) of A549 cells, but obviously promoted apoptosis of A549 cells (9.47 ± 1.14 vs. 4.96 ± 0.17, P = 0.02) by activating STAT1 signaling. Interestingly, IL-27 played totally opposite effects on A549 cells by activating STAT3 pathway. Moreover, IL-27 exerted different intercellular adherent activities of A549 cells to pleural mesothelial cell monolayer by activating different STAT signalings.</p><p><b>CONCLUSIONS</b>IL-27 might exert an important immune regulation on lung cancer cells in human pleural malignant environment.</p>

Combined detections of interleukin 27, interferon-γ, and adenosine deaminase in pleural effusion for diagnosis of tuberculous pleurisy / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Previous studies reported interleukin-27 (IL-27), interferon-γ (IFN-γ), or adenosine deaminase (ADA) alone plays a helpful role in diagnosing tuberculous pleural effusion (TPE). The present study aims at comparing the diagnostic accuracy of pleural IL-27, IFN-γ, and ADA, and investigate the diagnostic accuracy of the combination of IL-27, IFN-γ, or/and ADA for differentiating TPE from pleural effusions with the other etiologies.</p><p><b>METHODS</b>The concentrations of IL-27, IFN-γ and ADA were simultaneously determined in pleural fluids and sera from 40 patients with TPE; 26 with malignant pleural effusion, seven with infectious pleural effusion, and eight with transudative pleural effusion by enzyme linked immunosorbent assay and colorimetric method. The corresponding biochemical indexs were also simultaneously determined.</p><p><b>RESULTS</b>The concentrations of pleural IL-27 and IFN-γ in the tuberculous group were significantly higher than those in the malignant, infectious, and transudative groups. The concentrations of ADA in TPE were significantly higher than those in MPE or transudative effusions, while much lower than those in infectious effusions. Among these three biomarkers, IL-27 was the most effective for TPE diagnosis, with the cut off value of 900.8 ng/L. IL-27 had a high sensitivity of 95% and specificity of 97.6% for differential diagnosis of TPE from non-TPEs. Combinations of IL-27, IFN-γ and ADA measurements further increased the sensitivity or specificity up to 100%.</p><p><b>CONCLUSIONS</b>Compared to non-TPEs, IL-27, IFN-γ and ADA all simultaneously increased in TPE; and among these three rapid detection methods, IL-27 appeared to be the best for distinguishing tuberculous from non-TPEs, especially from MPE. Combinations of the three markers (IL-27, IFN-γ and ADA) yielded the highest sensitivity and specificity. These findings suggest that the applications of a new biomarker, IL-27, alone or with IFN-γ and ADA, may contribute to more efficient diagnosis strategies in the management of tuberculous pleurisy.</p>

Bioinformatic analysis for structure and function of TCTP from Spirometra mansoni

OBJECTIVE@#To predict structure and function of translationally controlled tumor protein (TCTP) from Spirometra mansoni by bioinformatics technology, and to provide a theoretical basis for further study.@*METHODS@#Open reading frame (ORF) of EST sequence from Spirometra mansoni was obtained by ORF finder and was translated into amino acid residue by DNAclub. The structure domain was analyzed by Blast. By the method of online analysis tools: Protparam, InterProScan, protscale, SignalP-3.0, PSORT II, BepiPred, TMHMM, VectorNTI Suite 9 packages and Phyre2, the structure and function of the protein were predicted and analyzed.@*RESULTS@#The results showed that the EST sequence was Sm TCTP with 173 amino acid residues, theoretical molecular weight was 19 872.0 Da. The protein has the closest evolutionary status with Clonorchis sinensis, Schistosoma mansoni, and Schistosoma japonicum. Then it had no signal peptide site and transmembrane domain. Secondary structure of TCTP contained two α -helices and eight β -strands.@*CONCLUSIONS@#Sm TCTP was a variety of biological functions of protein that may be used as a vaccine candidate molecule and drug target.

Association between dyslipidemia and chronic kidney disease: a cross-sectional study in the middle-aged and elderly Chinese population / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Dyslipidemia, a well-known risk factor for cardiovascular disease, is common in patients with kidney disease. Recent studies discerned that dyslipidemias play a critical role in renal damage progression in renal diseases, but the association between dyslipidemias and chronic kidney disease (CKD) in the general population remains unknown. Thus, we assessed whether the growing prevalence of dyslipidemia could increase the risk of CKD.</p><p><b>METHODS</b>A total of 4779 middle-aged and elderly participants participated in this study. Dyslipidemias were defined by the 2007 Guidelines in Chinese Adults. Incident CKD was defined as albuminuria and/or reduced estimated glomerular filtration rate (eGFR, < 60 ml×min(-1)×1.73 m(-2)). Regression analysis was used to evaluate the association between dyslipidemia and albuminuria/reduced eGFR.</p><p><b>RESULTS</b>Participants with hypercholesterolemia exhibited a greater prevalence of albuminuria and reduced eGFR (10.0% vs. 6.1%, P = 0.001; 4.0% vs. 2.4%, P = 0.028, respectively). Both hypercholesterolemia and low high density lipoprotein cholesterol (HDL-C) were independently associated with albuminuria (odds ratio (OR) 1.49; 95% confidence interval (CI) 1.08 - 2.07 and OR 1.53; 95%CI 1.13 - 2.09, respectively). The multivariable adjusted OR of reduced eGFR in participants with hypercholesterolemia was 1.65 (95%CI 1.03 - 2.65). As the number of dyslipidemia components increased, so did the OR of CKD: 0.87 (95%CI 0.65 - 1.15), 1.29 (95%CI, 0.83 - 2.01), and 7.87 (95%CI, 3.75 - 16.50) for albuminuria, and 0.38 (95%CI 0.21 - 0.69), 1.92 (95%CI 1.14 - 3.25), and 5.85 (95%CI 2.36 - 14.51) for reduced eGFR, respectively.</p><p><b>CONCLUSIONS</b>Our findings indicate that dyslipidemias increase the risk of CKD in the middle-aged and elderly Chinese population. Hypercholesterolemia plays an important role in reducing total eGFR. Both low HDL-C and hypercholesterolemia are associated with an increased risk for albuminuria.</p>

Primary human hepatocyte transplantation in the therapy of hepatic failure: 2 cases report

Liver failure is the end stage of hepatopathy with unfavorable prognosis. In two patients with liver failure, viable primary human hepatocytes, obtained from resected liver tissue of patients with hepatolithiasis, were transplanted into the spleen by interventional therapy through femoral arterial cannula. After transplantation, the patients' clinical symptoms and liver function were significantly improved. However, their bilirubin increased within six days following transplantation. One suffered from hepatic coma and give up treatment and the other patient died fourteen days after transplantation. It is technically safe to treat liver failure by intrasplenic transplantation of adult hepatocytes and the clinical efficacy has been confirmed. How to make transplanted hepatic cells proliferate and functionally survive is the key point to maintain continuous improvement of the recipient's hepatic function.

Changes of protein kinase A expressions in central amygdaloid nuclei during the process of chronic morphine-induced conditioned place aversion in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore neurobiological mechanisms of the withdrawal-induced aversion. The changes of protein kinase A were measured in central amygdaloid nucleic (CeA) of conditioned place aversion (CPA) model rats.</p><p><b>METHODS</b>(1) All 72 male SD rats were divided into three groups, model group (MN group), and control group (MS group and SN group). MN group was injected with morphine,6.5 days, 10 mg/kg, intraperitoneally (ip), twice per day, naloxone injection, 0.3 mg/kg, ip, along with conditioned place aversion training, to develop the CPA model. The MS group was administrated equivalent volume of morphine and saline. Also the SN group was injected with equivalent volume of saline and naloxone. (2) During the process of morphine-induced CPA, the expression of protein kinase A was assayed with immunohistochemistry in the CeA.</p><p><b>RESULTS</b>In the MN group, protein kinase A expressions in the CeA occurred adaptive changes at different points of CPA (P < 0.05). Protein kinase A expressions after establishment(Day7,134.43 +/- 4.481, P < 0.05), and after extinction (Day 13, 141.01 +/- 3.360, P < 0.01), and after reinstatement (Day 14,137.18 +/- 40.330, P < 0.05) were also lower than those before the establishment of the CPA (Day 5, 124.48 +/- 6.722). However, PKA expressions were not significantly different both in MS group (P > 0.05)and SN group (P > 0.05).</p><p><b>CONCLUSION</b>(1) Protein kinase A expression, in turn regulating the aversion expression, in the CeA probably is a key pathway contributing to the development of CPA. (2) The neuroadaptation mediated by protein kinase A may be one of the important molecular underpinnings of CPA.</p>

Cellular sources of interleukin 16 in benign and malignant pleural effusions / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Interleukin 16 (IL-16) can be detected by ELISA in pleural effusion (PE) and its concentration is higher than in serum. This study investigated the cellular sources of IL-16 in PE.</p><p><b>METHODS</b>The samples of PE were collected from 34 patients who were newly diagnosed having PE in the pleural cavity. We performed cell culture to purify the pleural mesothelial cells (PMC), Wright staining to count the purity and immunocytochemical stain to identify the cultured cells. The intracellular IL-16 expression was detected by flow cytometry (FCM). The different cells in PE were first separated by magnetic cell sorting (MCAS) then the separated cells were cultured in RPMI1640 with 10% fetal calf serum (FCS). We extracted the supernatant and detected IL-16 concentration by ELISA. The IL-16 protein was detected by immunohistochemistry and double immunofluorescence staining.</p><p><b>RESULTS</b>The percentages of cells which secreted IL-16 were: CD3(+)CD8(-) cells ((74.27 ± 15.56)%, n = 34); CD3(+)CD8(+) cells ((69.86 ± 18.55)%, n = 34); CD19(+) cells ((45.30 ± 18.77)%, n = 15); CD14(+) cells ((16.91 ± 16.69)%, n = 15); and PMC ((2.05 ± 1.85)%, n = 7). The concentrations of IL-16 in the supernatant from cultured cells were: CD4(+) cells ((102.50 ± 42.51) ng/L, n = 5); CD8(+) cells ((92.58 ± 18.34) ng/L, n = 5); CD19(+) cells ((79.85 ± 5.62) ng/L, n = 5); CD14(+) cells ((58.51 ± 25.38) ng/L, n = 5); and PMC ((18.14 ± 8.37) ng/L, n = 5). In lymphocytes, monocytes/macrophages and PMC, we could observe the cells that expressed IL-16 protein. In paraffin-embedded sections, we also could observe by immunohistochemistry the CD4(+)IL-16(+) cells, CD8(+)IL-16(+) cells, CD19(+)IL-16(+) cells, and CD14(+)IL-16(+) cells.</p><p><b>CONCLUSIONS</b>IL-16 in PE is mainly secreted by T lymphocytes, including CD3(+)CD8(-) cells and CD3(+)CD8(+) cells. CD19(+) cells and CD14(+) cells can also secrete IL-16, but the percentage of PMC that can secrete IL-16 is very low.</p>

Expression difference of cerebral cortex and liver glucocorticoid receptors at protein level following severe closed traumatic brain injury in awake mice / 中华创伤杂志

Objective To study the relationship of expression of central cortex glucocorticoid receptor (GR) at protein level with GR expression in the liver at protein level and with changes of serum cortisol and adrenocorticotropic hormone (ACTH) following severe closed traumatic brain injury (TBI) in mice. Methods Severe TBI was established in awake mice by using a BIM-Ⅲ biomechanical machine. At 0.5, 2, 8, 24, 48 and 72 hours after TBI, the total cytosolic GR in the cortex and liver were detected with Western blotting. Levels of serum ACTH and cortisol were measured by ELISA technique and radio-immunological assay (RIA) respectively. Results The expression of GR both in the cortex and liver were obviously down-regulated at protein levels at 2-72 hours after TBI and increased slowly eight hours after injury. The GR in the liver showed no recovery at 72 hours after injury and that in the cortex was decreased continually at 24 hours after injury. Serum ACTH and cortisol levels were increased markedly compared with control group, when there were two different peaks in the observation curve.Conclusion There is glucocorticoid resistance both in the central and peripheral tissues after severe closed TBI in the awake mice, which changes in a time-dependent manner.