Objective To explore the influencing factors of daunorubicin (DNR) induced apoptosis in Jurkat cells of acute lymphoblastic leukemia. Methods Jurkat cells were treated with different concentrations of DNR(0, 0.05, 0.1, 0.5 and 1 μg/mL)or pretreated with N-acetylcysteine (NAC). Cell proliferation was detected by MTT assay, cell apoptosis was observed by Hoechst/PI, reactive oxygen species (ROS) level and apoptosis were determined by flow cytometry, and the expression of survivin, bax, bcl-2 and bcl-xl mRNA was examined by RT-PCR. Results DNR siguificantly inhibited the proliferation of Jurkat cells. After treatment with 0, 0.05, 0.1, 0.5, 1 μg/mL DNR and pretreated with NAC for 24 h, ROS levels were (7.98±0.55)%, (8.88±0.86)%, (9.46±0.98)%, (17.48±2.98)%, (24.46±2.43)% and (11.59±1.29)%, respectively, and cell apoptosis rates were (11.41±1.44)%, (34.96±3.32)%, (45.58± 3.12)%, (84.19±2.65)%, (87.93±1.74)% and (80.47±0.63)%, respectively. After pretreatment with NAC, the levels of ROS were siguifieantly inhibited (P < 0.01). There was no significant difference in apoptosis rates between treatment with 0.5μg/mL DNR and pretreatment with NAC(P>0.05). The expression of bax mRNA was down regulated and the expression of survivin, bcl-2 and bcl-xl was up regulated (P < 0.05). Conclusion DNR can induce apoptosis of Jurkat cells. ROS may participate in the DNR induced Jurkat cell apoptosis, and apoptosis-related gene bax, bcl-2, bcl-xl and survivin may interact with ROS in the regulation of DNR induced Jurkat cell apoptosis.

Objective: To analyze the death among children under 5 years of age in Huzhou City, Zhejiang Province from 2012 and 2021, so as to provide insights into reduction of mortality among children. Methods: The mortality surveillance data among children under 5 years of age in Huzhou City from 2012 to 2021 were collected from Children Death Report Cards and Surveillance Report among Children under 5 Years of Age, including gender, place of residence, date of death and death diagnosis. The trends in mortality and cause of death were analyzed among children under 5 years of age in Huzhou City from 2012 to 2021. Results: A total of 1 262 deaths occurred among children under 5 years of age in Huzhou City from 2012 to 2021, with mean annual mortality of 4.39‰, and the mortality appeared a tendency towards a decline (χ2trend=132.695, P<0.001). A total of 899 infants died, with mean annual mortality of 3.13‰, and 363 children at ages of 1 to <5 years died, with mean annual mortality of 1.26‰. The mortality appeared a tendency towards a decline among both infants (χ2trend=117.778, P<0.001) and children at ages of 1 to <5 years (χ2trend=19.201, P<0.001). A total of 724 local children died, with mean annual mortality of 3.33‰, and there were 538 deaths among floating children, with mean annual mortality of 7.65‰. The mortality appeared a tendency towards a decline among both local (χ2trend=43.728, P<0.001) and floating children (χ2trend=94.038, P<0.001). The five most common causes of death included preterm birth or low birth weight (207 deaths, 16.40%), drowning (155 deaths, 12.28%), accidental asphyxia (138 deaths, 10.94%), other congenital abnormalities (126 deaths, 9.98%), and congenital heart diseases (113 deaths, 8.95%). Conclusions The mortality appeared a tendency towards a decline among children under 5 years of age in Huzhou City from 2012 to 2021, and preterm birth or low birth weight was the predominant cause of death.

Aged ; Aged, 80 and over ; Atrial Fibrillation ; blood ; Biomarkers ; blood ; Female ; Humans ; Male ; Middle Aged ; Natriuretic Peptide, Brain ; blood

American Medical Association ; Congresses as Topic ; Hematology ; United States

Objective To explore the association between Xeroderma pigmentosum complementation C group (XPC) Lys939Gln (A/C) gene polymorphism and the susceptibility of gastric cancer.Methods By searching PubMed,Cochrane Library,Elsevier,Springer-Verlag,China National Knowledge Infrastructure,Chinese Biomedical Literature Data,VIP Database and Wanfang Database,all eligible case-control studies published up to September 2015 were selected and the quality of each article was valuated by two reviewers independently according to the inclusion and exclusion criteria.Meta-analysis was performed by using STATA 12.0 software.Odds ratio (OR) and 95％ confidence interval (CI) were calculated.The text was estimated for the subgroup analysis,sensitivity analysis and publication bias test.Results A total of 7 case-control studies were included,including 2 336 cases with gastric cancer and 3 502 controls.The Meta-analysis showed that compared with the allele A,the allele C increased the risk of gastric cancer (OR =1.09,95％ CI:1.01-1.18,Z =2.12,P =0.034);compared to the genotype AA,the homozygous model (CC) and dominant model (CC + AC) also increased the risk of gastric cancer (CC vs.AA:OR =1.19,95％ CI:1.00-1.42,Z =2.00,P=0.046;CC+ACvs.AA:OR=1.12,95％CI:1.00-1.25,Z=2.03,P=0.042).The Meta-analysis showed the statistical significance between XPC Lys939Gln (A/C) gene polymorphism and the gastric cancer risk in subgroup of Asian people (C vs.A:OR =1.10,95％ CI:1.01-1.20,Z =2.28,P =0.023;CC vs.AA:OR=l.21,95％CI:1.01-1.46,Z=2.02,P=0.043;CC +AC vs.AA:OR =1.13,95％ CI:1.01-1.27,Z =2.11,P =0.035) and the source of community in the control group (C vs.A:OR =1.11,95％ CI:1.01-1.21,Z=2.25,P =0.024;CC vs.AA:OR =1.23,95％ CI:1.02-1.50,Z =2.12,P =0.034).Conclusion XPC Lys939G1n (A/C) gene polymorphism may be associated with the susceptibility of gastric cancer,and genotype CC,CC + AC and allele C can increase the risk of gastric cancer.

Peking University Health Science Center has various characteristics of educational manage-ment practice such as clear three level management, diversified management training and strict quality control, and at the same time there exist many deficiencies, such as lack of the implementation of management regulations and the requirements caused by multi-level management and management quality having ups and downs be-cause of human factors and etc.. By introducing life cycle management into national continuing medical educa-tion project management, we make management run through the whole life cycle of national continuing medical education project, namely five aspects of management from reporting and publishing, planning and publicity, holding and supervision, graduation and certificates, as well as summary and feedback, which plays an impor-tant role in standardizing the national continuing medical education project and improving the quality of the project.

Objective To quantitatively examine the relationship between xeroderma pigmentosum complementation C group (XPC)rs2228000 (C /T)polymorphism and the susceptibility of breast cancer. Methods The relevant case-control studies published up to December 2015 which investigated XPC rs2228000 (C /T)polymorphism and breast cancer risk were identified by searching PubMed,Cochrane Library,Chinese Biomedical Literature Data,Wanfang Database,China National Knowledge Infrastructure and VIP Database. Meta-analysis was conducted using STATA 12.0 software and odds ratio (OR)with its 95%CI were estimated. Results A total of 8 researches involving 9 case-control studies (3 850 breast cancer cases and 5 047 healthy controls) were included.The Meta-analysis showed that there was statistical association between XPC rs2228000(C /T)variance and breast cancer risk in the homozygous model (TT vs.CC:OR =1.28,95%CI:1.08-1.52,Z =2.80,P =0.005)and recessive model (TT vs.TC +CC:OR =1.23,95%CI:1.05-1.43, Z =2.64,P =0.008),but not in the allele model,heterozygote model and dominant model.In the subgroup of ethnicity and genotyping methods,the different significant correlation was existed between them under Asian and PCR-RFLP in genetic models (T vs.C:OR =1.21,95%CI:1.05-1.40,Z =2.63,P =0.009;TT vs. CC:OR =1.55,95%CI:1.13-2.13,Z =2.70,P =0.007;TT +TC vs.CC:OR =1.26,95%CI:1.02-1.55,Z =2.19,P =0.028;TT vs.TC +CC:OR =1.39,95%CI:1.04-1.87,Z =2.23,P =0.026).We also found significant association between them in subgroup of population-based controls in the homozygous model (TT vs.CC:OR =1.27,95%CI:1.02-1.57,Z =2.16,P =0.031).Conclusion XPC rs2228000 (C /T)polymorphism may be associated with the susceptibility of breast cancer,especially in Asian,and gene-type TT may increase the risk of breast cancer.

To investigate whether glutamate and voltage-gated calcium channels-independent calcium influx exists during acute anoxic neuronal damage and its possible relationship to neuronal protective function of NGF. In in vitro model of acute anoxia, hippocampal cultures from newborn rats were exposed to 3 mmol/L KCN. Changes of intracellular Ca(2+) concentration ([Ca(2+)](i)) were monitored by con-focal imaging and cell viability was assayed by PI and cFDA staining. The results showed that after treatment with primary hippocampal cultures with 3 mmol/L KCN for 15 min, [Ca(2+)](i) was significantly increased 6.27-fold compared to pre-anoxia level and 73.3% of the cells died. When combination of 20 mumol/L MK-801 (glutamate receptor antagonist), 40 mumol/L CNQX (AMPA receptor antagonist) and 5 mumol/L nimodipine (voltage-gated calcium channel antagonist) (hereafter denoted as MCN) were administrated to hippocampal cultures, levels of [Ca(2+)](i) and cell death rate induced by KCN were partially reduced by 35.9% and 47.5% respectively. However, Gd(3+) (10 mumol/L) almost completely blocked KCN-mediated [Ca(2+)](i) elevation by 81.9% and reduced neuronal death by 88.8% in the presence of MCN. It is noteworthy that NGF, used in combination with MCN, inhibited KCN-induced [Ca(2+)](i) increase by 77.4% and reduced cell death by 87.1%. Only PLC inhibitor U73122 (10 mumol/L) abolished NGF effects. It is concluded that Gd(3+)-sensitive calcium influx, which is NMDA (glutamate receptor) and voltage-gated calcium channels-independent, is responsible for acute anoxic neuronal death. NGF can inhibit Gd(3+)-sensitive calcium influx and reduce anoxic neuronal death through activating PLC pathway.

Objective To develop and charaterize a series of Poloxamer-and Carbopol-based in situ gel for ophthalmic use as to enhance the ability of drug to retain in eyes and delay drug release.Methods The gel was prepared using Poloxamer 407/188 and Carbopol 974P as gelling agent and viscosity enhancer,respectively.Rheological characteristics were evaluated and behaviour of drug release in vitro was investigated by modified Franz diffusion cells.Results The rheological study indicated that the gel was physically entangled polymer solutions at 20 ℃ and then converted into a network structure with secondary bonds at 35 ℃.The gel released the drug molecules slowly in 4 h.The best fit model was Higuchi matrix model(r=0.992 3).Formulations consisting of Poloxamer 188 and Carbopol 974P were proved to be able to decrease the drug release speed efficiently.The impact on elastic modulus G" of the gel caused by those two were different.Conclusion An in situ gel with suitable sol-gel transition temperature and satisfactory release pattern could be achieved by adjusting the ratio of Poloxamer 407 to Poloxamer 188.The developed formulations have the ability to prolong the ocular residence time,which suggests it may be a new durg delivery system with bright future.

Peroxisome proliferator-activated receptors (PPARs) are nuclear transcriptional factors closely related to glucose and lipid metabolism, insulin sensitivity. Activation of PPARs targets treated type 2 diabetes, obesity, hypertension and other metabolic diseases by insulin resistance. Recently, a variety of active ingredients of traditional Chinese medicines (TCMs) have been proved to activate PPARs targets for improving insulin resistance, which has attracted widespread attention at home and abroad. In this paper, we reviewed the pathological mechanisms between insulin resistance and PPARs, and summarized the active ingredients of TCMs improved insulin resistance based on PPARs targets. This paper may provide some theoretical guidance for the development of new drugs and TCMs.
Animals ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Insulin Resistance ; Metabolic Diseases ; drug therapy ; genetics ; metabolism ; Peroxisome Proliferator-Activated Receptors ; antagonists & inhibitors ; genetics ; metabolism