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ObjectiveTo analyze the criminal behavior characteristics of alcohol-related crime offenders and explore the relationship between criminal behavior characteristics and criminal responsibility capacity. MethodsBasic information, alcohol use information, psychiatric symptoms before and after the crime, criminological behavioral characteristics and conclusion of judicial evaluation were collected. ResultsThe drinking history of the chronic alcoholism group 25.0 (13.3~30.0) years was significantly longer than that of the acute alcoholism group 1.2 (0~14.3) years. In the chronic alcoholism group, 85.0% drank alcohol at least once a day, 52.5% had morning or bedtime drinking habits, and 92.5% drank mainly alone. Violent crimes accounted for 57.6%. Delirium existed in 52.5% of the chronic alcoholics' mental state at the time of the crime, and 84.6% of the acute alcoholics' mental state was hazy. In the chronic alcoholism group, 42.5% committed the crime with pathological motive, and in the acute alcoholism group, 69.2% committed the crime with realistic motive. Acute alcoholism group 96.2% were assessed as complete criminal responsibility capacity, and chronic alcoholism group 50.0% were assessed as complete criminal responsibility capacity. ConclusionCompared with acute alcoholism offenders, chronic alcoholics had a longer drinking duration, more frequency drinking, and obvious morning drinking or bedtime drinking habits. The nature of alcoholism crime cases was mostly violent. Compared with the chronic alcoholism group, the acute alcoholism group had highly selective motives for committing crimes and were mostly rated as complete criminally responsibility.
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Objective To explore the intervention effects of lentinan on sodium arsenite (SA) induced hepatotoxicity in mice. Methods Healthy male C57BL/6 mice were used as experimental subjects and divided into 4 groups, namely control group, SA treatment group, lentinan intervention + SA exposure group, and lentinan intervention control group. The mice were given oral SA (10.0 mg/kg.bw, once every other day) for 14 days, and then the liver tissues and serum samples were collected. Hematoxylin-eosin (HE) was used to evaluate the characteristics of hepatic pathological damage. Enzyme-linked immunosorbent assay (ELISA), Flow Cytometry (FC) and Western-blotting (WB) were used to detect the levels of hepatic function, oxidative stress, CD4+ type 17 helper T cells (Th17), and inflammatory cytokines. Results Compared with the control group, the arsenic exposure group showed obvious hepatic pathological injury and increased levels of serum ALT (8.78±0.76 vs 5.47±0.49) and AST (12.42±1.87 vs 7.14±0.57), FC experiments showed that the Th17 content in liver tissues increased (67.70±4.94 vs 7.36±1.50), and ELISA showed that the antioxidant GSH content decreased (593.40±23.25 vs 730.94±30.81), and the levels of MDA (74.56±7.63 vs 49.90±6.42) and proinflammatory cytokines IL-17A (162.48±10.75 vs 118.53±7.92) and IL-1β (512.50±24.78 vs 462.48±22.15) increased in hepatic tissues (P < 0.05). Compared with the arsenic exposure group, the lentinan showed a significant antagonistic effect after intervention (P < 0.05). Compared to SA exposure group, WB analysis showed that compared with the arsenic exposure group, the expression levels of IL-17A (0.47±0.08 vs 0.89±0.11) and NLRP3 inflammasome (0.80±0.09 vs 1.09±0.16) in the liver tissues of the lentinan intervention group were significantly decreased (P < 0.05). Conclusion Lentinan alleviates SA-induced hepatic injury in mice, which may be mediated through the inhibition of Th17-IL-17A inflammatory signaling.
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Male reproductive infections are known to shape the immunological homeostasis of the testes, leading to male infertility. However, the specific pathogenesis of these changes remains poorly understood. Exosomes released in the inflammatory microenvironment are important in communication between the local microenvironment and recipient cells. Here, we aim to identify the immunomodulatory properties of inflammatory testes-derived exosomes (IT-exos) and explore their underlying mechanisms in orchitis. IT-exos were isolated using a uropathogenic Escherichia coli (UPEC)-induced orchitis model and confirmed that IT-exos promoted proinflammatory M1 activation with increasing expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in vitro. We further used small RNA sequencing to identify the differential miRNA profiles in exosomes and primary testicular macrophages (TMs) from normal and UPEC-infected testes, respectively, and identified that miR-155-5p was highly enriched in IT-exos and TMs from inflammatory testes. Further study of bone marrow derived macrophages (BMDMs) transfected with miR-155-5p mimic showed that macrophages polarized to proinflammatory phenotype. In addition, the mice that were administrated IT-exos showed remarkable activation of TM1-like macrophages; however, IT-exos with silencing miR-155-5p showed a decrease in proinflammatory responses. Overall, we demonstrate that miR-155-5p delivered by IT-exos plays an important role in the activation of TM1 in UPEC-induced orchitis. Our study provides a new perspective on the immunological mechanisms underlying inflammation-related male infertility.
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Humanos , Masculino , Ratones , Animales , Orquitis , Escherichia coli Uropatógena/metabolismo , MicroARNs/metabolismo , Exosomas/metabolismo , Macrófagos/metabolismo , Fenotipo , Infertilidad Masculina/metabolismoRESUMEN
With the growing demand of personalized medicine for children, it is especially important to develop medicines for children. In this study, using metoprolol tartrate as model drug, we developed 3D printed chewable tablets suitable for children with automated dosage distribution using semi-solid extruded (SSE) 3D printing technology. Based on the quality by design concept, this study prepared a semi-solid material with good printability using gelatin as the substrate, constructed 3D models and printed tablets with the aid of computer-aided design. The printing parameters were optimized and determined as follows: print temperature of 35-37 ℃, print speed of 25 mm·s-1, fill rate of 15%, and number of outer profile layers of 2. Subsequently, the printing process and the quality uniformity of the tablets were verified, and a linear relationship between the dose and the number of model layers was obtained. Finally, 3D printed chewable tablets were superior in terms of appearance, dose accuracy and compliance compared with traditional split-dose commercially available tablets. In this study, 3D printed metoprolol tartrate chewable tablets with good performance were successfully prepared to address the personalized medication needs of pediatric patients.
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With the discussion on the origins and the evolution of Star Twelve Points, combined with ancient astronomical stellar map, it is realized that the three-dimensional spatial diagram of Star Twelve Points can be approximately regarded as a Big Dipper map from the side view. Under the direction of image thinking, the function of Big Dipper was compared with the function of Star Twelve Points. Furthermore, according to "the opening-closing-pivoting" theory in and the theory of " cycle in round" proposed by , the mechanisms of Star Twelve Points on adjusting functional activities of and the movement of viscera-meridian--blood is elaborated, providing a new idea for acupuncture clinical treatment of miscellaneous diseases.
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Autoimmune diseases are primary immune diseases in which autoreactive antibodies or sensitized lymphocytes destroy and damage tissue and cellular components, resulting in tissue damage and organ dysfunction. Helper T cells may be involved in the pathogenesis of autoimmune diseases under certain conditions. This review summarizes recent research on the role of helper T cells in autoimmune diseases from two aspects, helper T cell-mediated production of autoantibodies by B cells and helper T cell-induced activation of abnormal lymphocytes, and provides ideas for the treatment of autoimmune diseases. The abnormal expression of helper T cells promotes the differentiation of B cells that produce autoantibodies, which leads to the development of different diseases. Among them, abnormal expression of Th2 cells and T follicular helper cells is more likely to cause antibody-mediated autoimmune diseases. In addition, abnormal activation of helper T cells also mediates autoimmune diseases through the production of abnormal cytokines and chemokines. Helper T cells play an essential role in the pathogenesis of autoimmune diseases, and a full understanding of their role in autoimmune diseases is helpful for providing ideas for the treatment of autoimmune diseases.
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Objective The imbalance of glucagon secretion plays an important role in the development of diabetes. The newly discovered ACE2/Ang(1-7)/Mas pathway is an vital branch of the RAS system and has regulatory effects on islet function, but its effect on glucagon secretion is still unknown. The article aimed to investigate the effect and possible mechanisms of AVE0991, a Mas receptor agonist on glucagon secretion of diabetic db/db mice. Methods A tolal of 30 db/db mice were randomized to AVE group and model group (n=15), and their age-matched nondiabetic db/m mice were selected as the normal group (n=15). The mice in AVE group were treated with AVE0991 20mg/kg/d and those in model group were treated with placebo via gavage for 6 weeks. The metabolic indicators were measured every week. After 6 weeks of treatment, intraperitoneal glucose tolerance test (IPGTT) and islet perifusion were performed to evaluate glucagon release kinetics in vivo and vitro. Double-label immunofluoresence assay was adoppted to assess the content of α and β cells. Moreover, qRT-PCR and western blot were employed to detect the GCK expression in islets. Results The fasting blood sugar[(19.1±0.8)mmol/L] and glucose tolerance [(14.1±0.5) mU/L]of AVE group were significantly lower than those of the model group[(25.3±3.0)mmol/L,(17.3±1.8)mU/L](P<0.05) and still higher than those of normal group[(6.3±0.5)mmol/L,(5.7±0.3)mU/L](P<0.05). At the 30, 60, and 120 min after IPGTT, the blood glucose level and glucagon level in AVE group were lower than model group, but still higher than the normal group (P<0.05). During low glucose perfusion, the glucagon secretion level of the islets of normal group [(20.6±0.5 pmol/L)] was lower than that of model group [(29.1±0.7) pmol/L)] and AVE group [(27.6±0.8) Pmol/L], and the difference was statistically significant (P<0.05). During high glucose perfusion, there was a statistically significant difference in glucagon level between AVE group and model group at 30 and 60 min(P<0.05). Semi-quantitative analysis showed that the islet α-cell content of model group [(3.3±0.7) mg] was significantly higher than that of normal group [(1.2±0.3) mg] (P<0.05), and the β cell content [(2.4±0.6) mg] was significantly lower than that of normal group [(4.8±0.3) mg] (P<0.05); While compared with the model group, the islet α-cell content [(1.8±0.4) mg] decreased significantly (P<0.05) and the β-cell content [(4.2±0.5) mg] increased significantly in AVE group (P<0.05). The expression levels of GCK mRNA and protein in model group were lower than those in normal group (P<0.05). Conclusion Activation of Mas receptors can improve glucose metabolism by reducing the secretion of glucagon after glucose load in db/db diabetic mice. The mechanism may be related to the decrease of islet α cell content and the increase of islet GCK expression.
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Objective:To investigate the activity of nitric oxide synthase (NOS) and α-smooth actin (α-SMA) in rat penile smooth muscle tissue of rats with alcoholic erectile dysfunction (ED). The effects of protein gene 43 (connexin43, Cx43) and transforming growth factor β1 (TGF-β1) mRNA and protein expressions provide an experimental basis for the clinical application of Gegensan in the treatment of alcoholic ED. Method:SD rats were randomly divided into five groups:normal group, model group, and low,medium,high-dose Gegensan groups (5,10,20 g·kg-1). Except the normal group, the other groups were administered with drugs after alcohol intervention for 30 min at 15 mL·kg-1·d-1. Colorimetric assay was used to detect NOS activity in the penile smooth muscle tissue of alcoholic ED rats. Quantitative real-time fluorescence polymerase chain reaction(Real-time PCR) and Western blot were used to detect α-SMA, Cx43, TGF-β1 mRNA and protein expressions in smooth muscle tissue of alcoholic ED rats. Result:Compared with the normal group, the expressions of NOS, α-SMA and Cx43 mRNA and protein in the penile smooth muscle of the model group decreased significantly (Pβ1 mRNA and protein increased significantly (Pβ1 mRNA expression, and α-SMA mRNA and protein expressions in the penis tissue of rats with alcoholic ED were significantly up-regulated (PConclusion:Gegensan has an obvious protective effect on the structure of penile smooth muscle of alcoholic ED rats. The specific mechanism may be related to the regulation of NOS activity and a-SMA, Cx43 and TGF-β1 mRNA and protein expressions.
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Aim To investigate the effect of Jinguishenqi decoction on renal podocyte apoptosis in db/db diabetic mice and the underlying mechanism. Methods Six weeks old db/db diabetic mice were randomly divided into three groups; saline group, Jinguishenqi decoction group, metformin positive control group, and male db/m mice as normal control group. The animals were sacrificed at 18 weeks old, urinary albumin was detected in 24 hours urine, and blood glucose was measured. The glomerular mesangial proliferation was observed by PAS staining in renal tissues. The foot processes in podocyte were observed by transmission electron microscopy. The expression of podocin in renal tissues was detected by immunofluorescence. The protein expressions of caspase-3, p-Bcl-2, p-JNKl/JNKl in renal cortex were detected by Western blot. Results Compared with saline group of db/db diabetic mice, urinary albumin in 24 hours urine, foot process fusion and mesangial width were all reduced after the treatment of Jinguishenqi decoction. Podocin fluorescence in glomerular increased, and the expression of caspase-3 in renal cortex decreased significantlyafter the treatment of Jinguishenqi decoction (P < 0. 05) . The phosphorylation of JNK1 and Bcl-2 was inhibitedsignificantly after the treatment of Jinguishenqi decoction (P < 0. 05). Conclusions Jinguishenqi decoction could alleviate apoptosis of podocyte, protect podocyte and delay the progression of diabetic nephropathy through JNK1/Bcl-2 signaling pathway.
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Aim: To investigate the effect of Jinguishenqi decoction on renal podocyte autophagy in db/db diabetic mice and its mechanism. Methods: Twenty 6-week old db/db diabetic mice were randomly divided into four groups, with five mice in each group: saline group, Jinguishenqi decoction low dose group, Jinguishenqi decoction high dose group, metformin positive control group, and 5 male db/m mice as normal control group. The animals were sacrificed at 18 weeks old, and urinary albumin and creatinine were detected in 24 hours' urine. Blood glucose and creatinine were measured. The glomerular extracellular matrix proliferation in renal tissues was observed by PAS staining. The expression of WT1 in renal tissues was detected by immunohistochemistry, and autophagy in podocyte was observed by transmission electron microscopy. The protein expressions of LC I/II, p62, p-mTOR/mTOR and p-AMPK/AMPK in renal tissues were detected by Western blot. Results Compared with saline group of db/db diabetic mice, urinary albumin, urinary albumin/creatinine in 24 hours urine, serum creatinine and glomerular mesangial width all decreased after the treatment of Jinguishenqi decoction. Autophagosome in podocyte and the number of WT1 positive cell increased (P < 0. 05), and the expression of LC3 II in renal cortex decreased significantly (P < 0. 05) after the treatment of Jinguishenqi decoction. The phosphorylation of AMPK increased significantly (P < 0. 05) and the phosphorylation of mTOR was inhibited (P < 0. 05) after the treatment of Jinguishenqi decoction. Conclusions: Jinguishenqi decoction could promote autophagy, protect podocyte and delay the progression of diabetic nephropathy through AMPK-mTOR pathway.
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Objective To investigate the effects of Panax Notoginseng saponins (PNS) on protein expression of Klotho in rats with renal ischemia reperfusion injury; To discuss its protective mechanism for model rats. Methods Experimental rats were randomly divided into sham-operation group, model group, positive medicine group, PNS high-, medium- and low-dosage groups. Each administration group was given relevant medicine for gavage, once a day. Renal ischemia reperfusion injury model was established. Rats were sacrificed by taking blood from abdominal aorta after 4 hours of modeling. Serum levels of blood urea nitrogen (BUN), creatinine (SCr), malondialdehyde (MDA) content in kidney tissue, superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-Px) activity were measured. HE staining was used to observe the morphological changes of renal tissue. The protein expressions of Klotho and NF-κB p65 were measured by immunohistochemical method. Results Compared with the sham-operation group, the levels of BUN and SCr in the model group increased significantly (P<0.05); protein expression of Klotho in renal tissue decreased and the protein expression of NF-κB p65 increased (P<0.05). Compared with the model group, the expression of Klotho increased but protein expression of NF-κB p65 decreased in each administration group (P<0.05); Compared with the positive medicine group, the expression of Klotho in PNS high-dosage group increased but protein expression of NF-κB p65 decreased (P<0.05). The protein expression of NF-κB p65 was negatively related to protein expression of Klotho (r=-0.895, P<0.05). Conclusion PNS can inhibit oxidative stress and anti-inflammatory effects through upregulating protein expression of Klotho, and reduce the protein expression of NF-κB p65, and thus exerts renal protective effects.
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Objective: To understand the distribution and treatment of malaria patients, and the characteristics of sampled hospitals in thephase of eradication of malaria,and provide support for medical resources allocation in the later stages of malaria eradication phase. On this basis, this study aims at promoting the realization of the ultimate goal of total eradication of malaria in China by 2020. Methods : A multi-stage stratified cluster sampling method was used. A total number of 102 hospitals in Zhejiang, Jiangsu, Anhui, Henan, Sichuan and Yunnan Provinces were selected to collect original information on in-patient and out-patient of malaria in terms of medical records and treatment costs during the periodfrom January 1st 2014 toDecember 31th2016. In order to conduct accurate statistical analysis, Excel 2016, SPSS 20. 0 and other Software were used. Results: The survey results collected a total number of 1633 malaria patients, and these patients showed a W-shaped distribution during the months of treatment. Most of malaria patients from Henan and Sichuan Provinceswere diagnosed as having been affected by falciparum and vivax malaria, and their number sharply increased. This is paper also revealed the ratios of malaria patientsin terms of their choice of health services,namely from tertiary hospitals, municipal medical institutions and provincial medical institutions; those were77.10%,52.05% and 23.58%,respectively. Conclusions : A new period of peak incidence of malariais detected from 2014 to 2016. With hospitals' line of malaria defending ability shrinking,it was found that malaria treatment capacitiesare relatively concentrated in the high level hospitals,which plays a greater role when it comes to the prevention and control of malaria. It is recommended that regional malaria treatment lines should be built,and severe malaria treatment knowledge trainingsshould be prepared and attended in mass in orderto improve malaria treatment capacities.
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Objective To investigate the expression of USP22 in cervical cancer cells,and the effects of USP22 on cell proliferation and chemosensitivity to cisplatin in cervical cancer cells. Methods Quantitative real-time polymerase chain reaction(qRT-PCR)was conducted to detect the expression of USP22 mRNA in cervical cancer cells.Cell count kit-8,flow cytometry,and tumorigenesis were performed to detect the effects of USP22 on the proliferation,apoptosis,cycle cycle,and chemosensitivity of cervical cancer cells to cisplatin in vitro and in vivo. Results USP22 was upregulated in cervical cancer cells compared to human immortalized epidermal cells. Cell proliferation was inhibited,cell apoptosis was promoted,cell cycle was arrested in G1 stage and chemosensi-tivity to cisplatin was enhanced in cervical cancer cells transfected with USP22-siRNAs.Furthermore,tumorigene-sis assays proved tumor growth was inhibited and chemosensitivity to cisplatin was enhanced when USP22 was silenced in HeLa cells. Conclusion USP22 expression is upregulated in cervical cancer cells,and USP22 could promote cell proliferation and inhibit chemosensitivity to cisplatin in cervical cancer cells.
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Objective: To explore the expression of SLAMF6 on CD8(+) T cells in patients with severe aplastic anemia (SAA) and its correlation with disease immune status. Methods: By flow cytometry (FCM), SLAMF6 expression level in peripheral blood CD8(+) T cells was detected in 21 patients with SAA and 15 normal controls respectively from February 2017 to April 2018. The correlation between SLAMF6 expression level and hematopoietic functions, including HGB, PLT, the neutrophil granulocyte and reticulocyte absolute value in peripheral blood, hyperplasia degree (percentage of granulocytes, erythrocytes, lymphocytes and megakaryocytes in bone marrow) and perforin, granzyme B, IFN-γ expression level in CD8(+) T cells were evaluated. To further confirm the effect of SLAMF6 on CD8(+) T cells, anti-SLAMF6 Ab was used to block SLAMF6 pathway (IgG as control), and FCM was used to detect the perforin, granzyme B, and IFN-γ production of CD8(+) T cells. Results: The expression of SLAMF6 on CD8(+) T cells in untreated SAA patients[(56.29±12.97)%]was significantly lower than that of normal controls[(80.96±7.36)%](t=-7.672, P<0.001). The expression of SLAMF6 on CD8(+) T cells in SAA patients were positively correlated with the HGB, PLT, the neutrophil granulocyte and reticulocyte absolute value in peripheral blood, percentage of granulocytes, erythrocytes in bone marrow (all P<0.05), but they were negatively correlated with the percentage of lymphocytes in bone marrow, and the expression of perforin, granzyme B, and IFN-γ of CD8(+) T cells (all P<0.05). After blocking SLAMF6 pathway by anti-SLAMF6 Ab, the expression levels of perforin, granzyme B and IFN-γ in SAA patients were significantly higher than those in the untreated group, and the differences were statistically significant (all P<0.05). Conclusions: SLAMF6 is significantly down-regulated on CD8(+) T cells in SAA patients, which may act as a negative immunoregulatory molecule participating in the mechanism of SAA by affecting the functional molecules secretion on CD8(+) T cells.
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Humanos , Anemia Aplásica , Médula Ósea , Linfocitos T CD8-positivos , Citometría de Flujo , Perforina , Familia de Moléculas Señalizadoras de la Activación LinfocitariaRESUMEN
<p><b>OBJECTIVE</b>To analyze the subtype and functional biomarker expression changes of natural kill cells(NK) in peripheral blood of patients with myelodysplastic syndrome(MDS) and normal people, so as to evaluate the relationships between these changes and hematopoietic functions and to explore the role of NK cells in the pathogenesis of MDS.</p><p><b>METHODS</b>The quantity of NK cells and the expression of biomarkers(NKp30,NKp46,NKG2A) on NK cells were detected by flow cytometry in 35 MDS patients from 2015 to 2016 in our hospital and 34 normal controls. The correlation between these changes and hematopoietic functions, including the percentages of neutrophil(ANC), hemoglobin in peripheral blood and the hematopoietic function in bone marrow(CD34%) were evaluated.</p><p><b>RESULTS</b>The percentage and quantity of NK cells and CD56NK cells in MDS patients were significantly lower than those in normal controls(P<0.05); the percentage of CD56NK cells was higher than that in controls. The percentage of CD56NK cells in NK cells of MDS patients was significantly lower than that of controls; the percentage of CD56NK cells in NK cells of MDS patients was significantly higher than that of controls. The expression of NKp30 and NKp46 of MDS patients was significantly lower than that of controls. In MDS group, the percentage of NK cells and CD56NK cells of peripheral blood lymphocytes in high risk MDS group was significantly lower than that in low risk MDS group. The percentage of NK and CD56NK cells negatively correlated with that of CD34% in bone marrow, but positively correlated with ANC and Hb. The CD34% in bone marrow negatively correlated with expression of NKp46, but positively correlated with expression of NKG2A.</p><p><b>CONCLUSION</b>The decrease of NK number and function may cause the immune surveillance and lead to disease progression.</p>
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To study the inhibitory effect of Rhaponticum uniflorum on apoptosis induced by H2O2 in HepG2 cells. Human HepG2 cells injury models were established by H2O2, then cell survival rate was assayed by MTT method; levels of LDH, ALT, and AST were detected by chemical colorimetric method;SOD activity was detected by xanthine oxidase method; GSH content was detected by dithio-bis-nitrobenzoic acid(DTNB); MDA level was detected by thiobarbituric acid (TBA) method;and the relative activities of Caspase-3, 8 and 9 were measured by Colorimetry. The expression levels of Cleaved Caspase-3(Casp-3), cytochrome(Cyto c), NF-κB, ERK, JNK, p38 MAPK, as well as the phospharylated proteins were determined with Western blotting method. The results showed that R. unifloru had no significant effect on cell viabilities of HepG2 cells at the concentrations of 25-400 mg•L⁻¹. However, H2O2decreased the cell viabilities, increased the cellular oxidative stress, and up-regulated the protein expressions of Casp-3, cytoplasmic Cyto c, p-JNK and nuclear NF-κB. As compared with the model group,R. unifloru could increase the cell viability, reduce LDH, ALT and AST leakage, reduce the MDA formation, increase the SOD and GSH levels,reduce the relative activities of Caspase-3, 8 and 9, down-regulated the protein expressions of Casp-3 and cytoplasmic Cyto c, and down-regulate the p-JNK and nuclear NF-κB levels.The results indicated that R. unifloru had the inhibitory effect on apoptosis induced by H2O2in HepG2 cells, and the mechanism maybe associated with inhibiting JNK activation and NF-κB nuclear translocation.
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<p><b>OBJECTIVE</b>To explore the relationship between polymorphisms of interleukin-17A (IL-17A) gene promoter (-197G/A and -692C/T) and the susceptibility to childhood asthma, to further identify the candidate genes for asthma, and to provide a basis for early prevention of asthma in high-risk children.</p><p><b>METHODS</b>Sixty-five outpatients or inpatients with childhood asthma between August 2013 and August 2015 were assigned to asthma group. Seventy healthy children within the same period were assigned to control group. Using peripheral venous blood from the two groups, PCR with sequence-specific primers was carried out to determine single nucleotide polymorphisms at positions -197G/A and -692C/T in IL-17A gene promoter. A statistical analysis was used to evaluate differences in genotype and allele frequencies between the two groups.</p><p><b>RESULTS</b>Compared with the control group, the asthma group had significantly higher frequencies of TT genotype (29% vs 16%; P=0.012) and T allele (52% vs 42%; P=0.039) at position -692C/T of IL-17A gene. Children with T allele had 1.413-fold higher risk of childhood asthma than those with C allele (OR=1.413, 95%CI: 1.015-1.917). There were no significant differences in genotype and allele frequencies at position -197G/A in IL-17A gene between the two groups (p>0.05).</p><p><b>CONCLUSIONS</b>Polymorphisms at position -692C/T in IL-17A gene promoter is associated with the susceptibility to childhood asthma. Children with -692T allele are more susceptible to childhood asthma. There is no significant relationship between polymorphisms at position -197G/A in IL-17A gene promoter and the susceptibility to childhood asthma.</p>
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Femenino , Humanos , Masculino , Asma , Genética , Predisposición Genética a la Enfermedad , Genotipo , Interleucina-17 , Genética , Polimorfismo de Nucleótido SimpleRESUMEN
This study aims to investigate the genetic characteristics of BZLF1 gene and its promoter Zp of the epidemic strains in children with primary Epstein-Barr virus (EBV)-associated diseases. Total DNA was extracted from the peripheral blood of 134 children with EBV-associated infectious mononucleosis (EBV-IM) and 32 children with EBV-associated hemophagocytic lymphohistiocytosis (EBV-HLH) who were admitted to Beijing Children's Hospital from 2006 to 2011. The EBNA3C, BZLF1, and Zp genes were amplified by PCR assay. Typing of EBV was performed according to the size of the amplification product of EBNA3C gene; the amplification products of BZLF1 and Zp genes were subjected to direct sequencing, and sequence analysis was performed using BioEdit 7. 0. 9. The results were as follows: (1) EBV-1 was present in 140 samples (97.2%, 140/144) and EBV-II in 4 samples (2.8%, 4/144). (2) Three BZLF1 genotypes and their 12 subtypes (including 6 newly found subtypes) were detected in this study; there were no significant differences in the frequencies of BZLF1-A and BZLF1-B between the children with EBV-IM and EBV-HLH (P = 0.083); BZLF1-A1 was the dominant genotype in children with EBV-associated diseases; t BZLF1-A mostly had three 29-bp repeats in the first intron of BZLF1 gene, and BZLF1-B mostly had 30-bp repeats (P = 0.000), with the number of repeats varying from 1 to 13. (3) Four Zp genotypes were detected in this study, including Zp-P, Zp-V3, Zp-V4, and Zp-V1; there were no significant differences in the frequencies of these Zp genotypes between children with EBV-IM and EBV-HLH (P = 0.272, 0.252, 1.0, and 1.0, respectively). (4) The linkage analysis of BZLF1 gene and its promoter Zp showed that BZLF1-A1 was highly associated with Zp-V3 (P = 0.000), while BZLF1-B4 with Zp-P (P = 0.000); EBV-I + BZLF1 A1 was highly associated with Zp-V3 (P = 0.000), while EBV-I+BZLF1-B4 with Zp-P (P = 0.000). The conclusions are as follows: (1) BZLF1-A1 is the dominant genotype in children with EBV-associated diseases; there are mostly 29-bp repeats in the first intron of BZLF1 gene for BZLF1-A genotype and 30-bp repeats for BZLF1-B genotype. (2) Zp-P and Zp-V3 are dominant Zp genotypes of EBV in children, which shared similar detection rates. (3) BZLF1-A1 is highly associated with Zp-V3, while BZLF1-B4 with Zp-P; EBV-I+BZLF1-A1 is highly associated with Zp-V3, while EBV-I+BZLF1-B4 with Zp-P.
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Niño , Preescolar , Femenino , Humanos , Lactante , Recién Nacido , Masculino , China , Epidemiología , Infecciones por Virus de Epstein-Barr , Epidemiología , Virología , Genotipo , Herpesvirus Humano 4 , Genética , Fisiología , Intrones , Genética , Regiones Promotoras Genéticas , Genética , Secuencias Repetitivas de Ácidos Nucleicos , Genética , Transactivadores , GenéticaRESUMEN
This study was purposed to investigate the role of regulatory T cells (Treg) in the immune unbalance for patients with acquired severe aplastic anemia (SAA). The flow cytometry was used to detect the quantity of CD4(+) CD25(+) CD127(dim) Tregs, T cell subset (CD4(+)/CD8(+) ratio), dendritic cell(DC) subset(mDC/pDC ratio) in 44 SAA patients(25 untreated patients and 19 recovery patients) and 23 normal controls. The correlation between Tregs and T cell subset, DC subset and hemogram were analyzed. The results showed that the percentage of CD4(+) CD25(+) CD127(dim) Tregs in peripheral blood lymphocyte(PBL) of untreated patients was (0.83 ± 0.44) %, which was obviously lower than that in recovery patients (2.91 ± 1.24)% and normal controls (2.18 ± 0.55)% (P < 0.05), but the difference was not statistically significant between latter two groups. The ratio of CD4(+)/CD8(+) was (0.5 ± 0.3) in untreated patients, which was obviously lower than that in recovery patients (1.2 ± 0.4) and normal controls (1.11 ± 0.24) (P < 0.05). The ratio of mDC/pDC was (3.08 ± 0.72) in untreated patients, which was significantly higher than that in recovery patients(1.61 ± 0.49) and normal controls (1.39 ± 0.36) (P < 0.05). The percentage of CD4(+) CD25(+)CD127(dim) Tregs in PBL positively correlated with CD4(+)/CD8(+) ratio (r = 0.695, P < 0.01), and that negatively correlated with mDC/pDC ratio (r = -0.796, P < 0.01). There were significant positive correlations between CD4(+)CD25(+)CD127(dim) Tregs/PBL and WBC, Ret% (r = 0.761, 0.749 respectively, P < 0.01). It is concluded that the decrease of CD4(+)CD25(+)CD127(dim) Tregs quantity in SAA may be one of mechanisms underlying bone marrow failure resulting from the deterioration of immune tolerance and hyperfunction of T-cells.
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Adolescente , Adulto , Niño , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven , Anemia Aplásica , Sangre , Estudios de Casos y Controles , Citometría de Flujo , Recuento de Linfocitos , Linfocitos T Reguladores , Biología Celular , MetabolismoRESUMEN
From February 2013, a novel avian influenza A H7N9 virus causing human infection with fatal outcomes has been identified in eastern China. This avian influenza A H7N9 virus is a triple reassortant of viruses that are avian-origin only and it is low pathogenic in poultry. Several characteristic amino acid mutations in HA and PB2 polymerase subunit (including G186V, Q226L and E627K substitution) have been found through sequence analysis, and these mutations probably facilitate binding to human-type receptors and efficient replication in mammals. Other mutations in NA, M2 and NS genes were also found. Although sustained human-to-human transmission has not been conclusively established, limited human-to-human transmission of the H7N9 virus remains possible. Intensified surveillance for the H7N9 virus in humans and animals is needed to answer questions about the viral origin, spread and potential threat.