According to the age of onset, childhood acne can be divided into neonatal acne, infantile acne, preschool acne, and prepubertal acne. Neonatal acne and infantile acne can serve as predictive factors for severe adolescent acne, preschool acne may be related to underlying endocrine diseases, and prepubertal acne is a sign of pubertal maturation. The treatment of childhood acne is similar to that of adolescent acne, and adverse effects of drugs and their impact on the growth and development of children should be considered.

Drug addiction is a chronic relapsing brain disease that is characterized by compulsive drug use and persistence of drug craving. Drug abuse can lead to changes in the neuron structure and function of plasticity,alterations in molecules and cells,and ultimately to individual abnormal behavior. Current studies have found that epigenetic changes leading to the sustainability of gene expression is an important mechanism of drug addiction. In this review,we will systematically summarize the latest advances in epigenetic mechanisms of drug addiction. This review is expected to provide robust evidence that repeated exposure to drugs of abuse induces changes within the brain′s reward regions in three major modes of epigenetic regulation-histone modifications such as acetylation and methylation , DNA methylation,and non-coding RNAs. It promises a new perspective from which to gain insights into the genetic and epigenetic mechanisms of drug addiction and a new area for epigenetic research on clinical drug addiction treatment.

Objective To study the effects of lidocaine on inflammatory mediators and myocardial enzymes in patients undergoing off-pump coronary artery bypass grafting (OPCAB).Methods Twenty patients underging OPCAB were randomly divided into 2 groups of L and C with 10 cases each. After anesthesia induction, group L was given a bolus of lidocaine 2 mg/kg, which was followed by an infusion of lidocaine 2 mg·kg~(-1)·h~(-1) till the end of operation. Group C was given normal saline instead of lidocaine as the control. Blood samples were taken for the measurements of TNF-a, IL-8, SOD, MDA, cTnⅠ, CK-MB and MYO. The hemodynamics, early postoperative clinical informations and ICU and hospital stay were recorded. Results The increases of TNF-α and IL-8 were significiently less in group L than those in group C(P<0.01 or P<0.05). MDA at 24 h after operation was higher in group C than that in group L(P<0.05). The increases of CK-MB and cTnⅠ at 24 h and 48 h after operation were significiently less in group L than those in group C(P<0. 01 or P <0. 05). The ICU and hospital stays were shorter in group L than those in group C(P<0. 05). Conclusion Continuous infusion of lidocaine during OPCAB can decrease the inflammatory mediators and myocardial enzymes and protect the myocardium.

ObjectiveTo observe the curative effect of alprostadil combined with cilostazol in treatment of patients with lower limb atherosclerosis.MethodsSixty-two patients with lower limb atherosclerosis were divided into cilostazol group (cilostazol 100 mg,2 times a day,oral) and therapeutic alliance group (cilostazol 100 mg,2 times a day,oral; alprostadil 10 μ g dissolved in 100 ml intravenous infusion of 0.9％ sodium chloride,once a day) by random number table with 31 cases each.The changes of ankle-brachial index (ABI),distance of 6-minute walk test(6-MWT) and the dorsal blood flow were compared before and after treatment.Results | After treatment,the distance of 6-MWT,ABI and the level of dorsal blood flow were significantly improved in two groups (P ＜ 0.05 or ＜ 0.01 ).Distance of 6-MWT and the level of dorsal blood flow in therapeutic alliance group was significantly higher than that in cilostazol group after treatment [(425.4±138.5) m vs.(379.5±124.6) m,(0.77±0.18) ml/ (s·cm2) vs.(0.66±0.14) ml/( s· cm2)] ( P＜0.05 ).The total effective rate in the treatment of cold feel in therapeutic alliance group was significantly higher than that in cilostazol group [ 87.5％(21/24) vs.61.9％( 13/21 ) ](P＜ 0.05).Conclusion Alprostadil combined with cilostazol is safe and effective in treating lower limb atherosclerosis.

Drug addiction is a chronic relapsing brain disease. Repeated drug exposure can cause neuroadaptations in major brain circuitries,leading to compulsive drug consumption behav-ior and relapse after abstinence.Many studies have found that intercellular signaling cascades mediated central nervous system remodeling in the rewarding circuitry and addiction associated neuroplasticity of learning and memory are important molecular mechanism of drug addiction.Studies show that extracellular sig-nal-regulated kinase (ERK)is associated with drug-mediated psychomotor activity,rewarding properties and relapse of drug seeking behaviors.Therefore,this article has reviewed the role of ERK signaling pathway in drug addiction.Research on the role of ERK signaling pathway in drug addiction will provide im-portant theoretical foundation for in-depth understanding of the molecular mechanism of drug addiction and shine a light on new molecular targets and treatment strategies for drug addiction.

Objective To observe the clinical efficacy and the economic effectiveness of different therapeutic schemes for Chronic hepatitis UB.Methods Patients with Chronic Hepatitis B were treated by using different drugs:Interferon ?1b(group A),Lamivudine(group B),Interferon ?1b combination with Lamivudine(group C),Interferon ?1b combination with thymotentin(group D),Interferon ?1b combination with thymosin alphal(group E).Evaluation was carried out with pharmacoeconomic cost-effectiveness.Results At the end of therapy,the clearance rate of serum HbeAg was lowest in group B(10 94%),the other groups were more than 50%.The clearance rate of serum HBV-DNA was higher in group B and C than in the other groups,it was 85 94%,87 93% respectively.Normalizing ALT values was higher in group C,group D and group E than in group A and group B.The costs of several therapeutic schemes were RMB 8156 7(group A),6935(group B),15091 7(group C),26033 4(group D) and 89978 4(group E) yuans,respectively.Conclusions According to the evaluation with pharmacoeconomic cost-effectiveness analysis,the therapeutic scheme of Interferon ?1b,Lamivudine and Interferon ?1b combination with Lamivudine is best one for treating chronic hepatitsi B,in this groups,Interferon ?1b combination with Lamivudine was better than the other two groups.

Magnetic nanoparticle application in the biological sciences and medicine get rapid development over the past decades.In the current cancer therapy,hyperthermia has become a new treatment method after surgical therapy,radiotherapy,chemotherapy and biological therapy.With the advent of magnetic nanoparticles,magnetic targeting hyperthermia has provided a new method for tumor hyperthermia,and has a broad development prospects.

Objective To investigate effects of Tanshinone Ⅱ A (Tan Ⅱ) on proliferation and apoptosis of myeloblastic leukemia cell lines.Methods NB4,K562 and THP-1 cells were incubated with TanⅡA for 24,48 and 72 hours.Ddaunorubicin was used as a positive control.Cell proliferation was monitored by MTT assay.Cell apoptosis and cell cycle were determined by Annexin Ⅴ-FITC/PI flow cytometry.Expression of Caspase-3 was quantified by spectrophotometry.Results After incubation with various leukemia cells for 24,48 and 72 hours,Tan Ⅱ inhibited proliferation of NB4 cells with IC50 of 24.11,9.60 and 7.28 μmol/L,inhibited K562 cells with IC50 of 31.75,11.88 and 6.81 μmol/L and inhibited THP-1 cells with IC50 of 111.10,32.82 and 11.82,respectively.After treatment with Tan Ⅱ for 48 hours,cell apoptosis,the number of G1 phase cells and the expression of Caspase-3 in all three leukemia cell lines were increased significantly comparing with the blank control group (P ＜ 0.05).Conclusions Tan Ⅱ A has proliferation inhibitory effect on myeloblastic leukemia cell lines by the order of effect NB4＞K562＞THP-1.Tan ⅡA displays anti-leukemia activity possibly through arresting leukemia cells in G1 phase and inducing apoptosis by increasing Caspase-3 expression.

Objective Our previous study showed that the expression of C 3aR was increased in renal tubular epithelial cells (RTEC).However, the role of C3aR in diabetic nephropathy remains unknown, and so does the exact physiological and pathological signifi-cance of C3aR in relevant renal tissues.In the present study, we investigated the physiological and pathological significance of C3aR in RTECs using a lentivirus expression vector and anRTEC strain overexpressing C3aR. Methods Based on the sequence of C3aR mRNA, the human C3aR gene was synthesized and cloned into the multi-clonal site of the lentivirus expression vector pLenti6.3-MCS-IRES2-EGFP to construct a C3aR expression vector pLenti6.3-C3aR-IRES2-EGFP.After identification by sequencing, the recombinant lentivirus expressing C3aR was packaged by cotransfecting293T cellswith the recombinant lentivirusexpression vector and packaged plasmid .Then,the recombinant lentivirus was used to infect the human RTECline HK 2.After screening in the medium with blasticidin, blasticidinr-esistant cell clones were obtained, followed by identification ofthe human RTECline stably overexpressing C 3aR by real-time PCR and immunochemical staining. Results TheC3aR expression vector pLenti6.3-C3aR-IRES2-EGFP was successfully constructed and the sequence was proved to be correct. C3aR expression recombinant lentivirus was successfully packaged with a titer of 5×108/mL.Blasticidin-resistant HK2 cell clones were ob-tained and the expression of HK2-C3aR mRNA was significantly higherin the HK2-C3aR cells than in the non-transfected HK2 cells (2.33± 0.45 sv 1.00±0.09, P<0.05). Conclusion We successfully constructed a C3aR expression lentivirus vector pLenti6.3-C3aR-IRES 2-EGFP and a C3aR overexpression renal tubular epithelial cell strain HK2-C3aR, which is very contributive to further studies of the roles of C3aR in renal tubular epithelial cells and other types of cells.

AIM: This study was designed to investigate the apoptotic effect of doxycycline in THP-1 cells.METHODS: After differentiated by PMA, THP-1 cells were treated with doxycycline at different concentrations ranging from zero to 80 mg/L. The morphological changes of THP-1 cells were observed under light microscope. MTT assay were used to examine the effects of doxycycline on proliferation of THP-1 cells. Apoptotic THP-1 cells were measured by Annexin-V flow cytometry analysis and TdT-mediated dUTP nick end labeling assay.RESULTS: Treated with a certain concentration of doxycycline, differentiated THP-1 cells contracted and turn round, a number of cells were dead. MTT assay and positive Annexin V-FITC on cell membrane and TUNEL assay showed that doxycycline induced apoptosis in THP-1 cells in a dose-dependent manner.CONCLUSION: Doxycycline induces apoptosis in THP-1 cells in a dose-dependent manner.