Objective To summarize the clinical features of infectious mononucleosis(IM)in aduIt patients.Methods Thirty cases of adult patients with IM were analyzed retrospectively being inDatient in Huashan Hospital from 2002 to 2007.Results Of these 30 patients with IM,male was slightly more than female with average age of 31.8 years old.Liver function of 77 percent patients were abnormal,while 70%splenomegaly,33%skin rash,20%EB virus-IgM positive and 10%hepatomegaly.Two cases were diagnosed with chronic active EB virus infection(CAEBV).Treatment strategies of IM were antiviral and symptomatically therapy.Conclusions IM diagnosis is difficult due to the variety of clinical features.CAEBV is rare in adult patients.The clinical prognosis of IM is good if treated properly.

Objective To analyze the clinical presentation and the effects on both mothers and fetuses with HELLP syndrome induced hyregtensive disorder complicating pregrancy and to investigate the effective methods for diagnosis and treatment. Methods 15 cases of HELLP syndroms were retrospectively analyzed on material and perinatal outcomes. Results In 15case of women with HELLP syndrome, all of them presented antepartum HELLP. Mean gestational age at delivery was 34 weeks. Severe maternal complications included placental abruption,DIC ,postpartum hemorrhage,fetal distress, et al. All of them underwent cesaresn section and required transfusions with blood or blood products. 1 case of perinatal death was related to placental abruption. Conclusion HELLP syndrome is a severe obstetric complication. Better prognosis may be achiveved by early diagnosis, synthetic therapy and optimal termination of pregnancy.

[Abstract ] CHD1L is a newly identified oncogene located at Chr 1q21,its oncogenic role in tumorigenesis is through unleashed cell proliferation, G1/S transition, inhibition of apoptosis and Chromatin instability .It is an independent biomarker that can affect tumour′s process, prognosis and survival rate.The underlying mechanisms of CHD1L activation may disrupt the cell death program via binding the apoptotic protein Nur77 or exterting relevant function by mediate CHD 1L′s target genes (ARHGEF9, TCTP, SPOCK1, and NTKL) .This paper mainly introduces its oncogenic role and research progress of related molecular mechanism .

AIM: To investigate the expression of stem cell factor (SCF) in tryptase -positive mast cells ( MCs) in different types of human periapical diseases for determining the role of SCF and MCs in the pathogenesis of peria-pical diseases.METHODS: A total 50 cases of specimens were involved in this study, including healthy control (n=20), periapical cyst (n=15) and periapical granuloma (n=15).The tissue material was fixed in 10%formalin for at least 48 h, stained with hematoxylin and eosin for the observation of histopathology, stained with immunohistochemistry for identifying MCs and MCs degranulation, and stained with double immunofluorescence for identification of tryptase-SCF double positive MCs.RESULTS:Compared with healthy control, significantly higher densities of both total and degranu-lated MCs in human periapical lesions were observed.The densities of both total and degranulated MCs in the periapical cyst were significantly higher than that in the periapical granuloma.The density of tryptase-SCF double positive MCs in the periapical lesions was significantly higher than that in the healthy controls.The density oftryptase-SCF double positive MCs in the periapical cyst was significantly higher than that in periapical granuloma.No significant difference in the density of MCs between immunohistochemistry staining and double immunofluorescence staining was observed.CONCLUSION:The tryptase-SCF double positive MCs play an active role in the pathogenesis of the periapical inflammatory lesions, particularly in the formation of fibrous tissue in periapical cyst.The potential role of the tryptase-SCF double positive MCs relates with the initiation, development, and persistence of the periapical inflammatory process.

OBJECTIVE:To develop a capillary electrophoresis method for determing the enantiomer of ceftriaxone Na.METHODS:A chiral resolving agent,?-cyclodextrin,was employed as chiral additive for ceftriaxone Na enantiomeric separation by capillary electrophoresis.In different electrophoresis polarity mode,the effect of pH of background electrolyte and the concentration of ?-cyclodextrin were investigated.RESULTS:The optimal conditions for enantiomeric separation were as follows:separation voltage:28kV,buffer solution:NaH2 PO4 50mmol/L,?-CD 0.04mmol/L,Tirs 3.0mmol/L,pH7.15.CONC_LUSION:The method is simple,sensitive,rapid and accurate,and can be used for the quality control of ceftriaxone Na enantiomers.There was significant difference in contents of enantiomers of ceftriaxone Na between products of two factories.We suggest that a quality control method for ceftriaxone Na enantiomer should be established,which will provide scientific basis for quality control of drug and clinical choice of effective antibioties.

Objective To investigate the effect of resveratrol on high glucose-induced oxidative stress and cardiomyo-cyte hypertrophy and possible mechanism .Methods H9C2 cardiomyocytes were divided into normal glucose group , high glucose group , resveratrol group and resveratrol +DAPT group respectively .The cell surface was measured by rhodamine-labeled phalloidin .Reactive oxygen species generation was measured using DCFH-DA.The contents of SOD and MDA were evaluated by colorimetry .The mRNA and protein levels of Notch 1, Hes1, ANP and BNP were evaluated by RT-qPCR and western blot .Results High glucose exposure significantly increased cell surface area ( P<0.01) and enhanced ROS and MDA generation ( P <0.01 ) with concomitant decrease of SOD activity ( P <0.01).It also decreased the mRNA and protein expressions of Notch 1 and Hes1(P<0.05), and increased the ex-pression levels of ANP and BNP ( P<0.05 ) .Resveratrol treatment inhibited cell surface expanding ( P<0.01 ) and decreased ROS and MDA generation (P<0.01) with concomitant enhance SOD activity (P<0.01), as well as in-creased the expression level of Notch 1 and Hes1 ( P<0.05 ) , and decreased the expression of ANP and BNP ( P<0.05).Conclusions Resveratrol may inhibit high glucose induced H9C2 cardiomyocytes hypertrophy by improving oxidative stress and activating Notch 1/Hes1 signaling pathway .

OBJECTIVE:To develop a method to control the quality of Guanxinshu tablets by HPLC.METHODS:Using HPLC as the determination method,the separation was performed on C 18 column(150mm?4.6mm,5?m)with a mobile phase of MeOH∶0.1%H 3 PO 4 (1∶2).The detective wavelength was320nm.RESULTS:The calibration curve was linear(r=0.9994)within the range of1.2～48?g/ml for ferulic acid and the average recovery was101.00%,RSD=4.56%(n=6).CONCLUSI_ ON:The method is simple and quick and it is suitable for the quality control of Guanxinshu tablets.

AIM:To investigate the expression of aryl hydrocarbon receptor (AhR) in atrial tissues of the patients with rheumatic heart disease (RHD), and the effects of AhR on rheumatic atrial fibrosis.METHODS:Right atrial specimens obtained from the patients with RHD requiring valve replacement surgery were divided into chronic atrial fibrillation (RHD+cAF, n=11) group and sinus rhythm (RHD+sinus rhythm, n=25) group.The patients with congenital heart disease (CHD) and sinus rhythm (CHD+sinus rhythm, n=12) who underwent heart surgery served as controls.The collagen volume fraction in the atrial specimens was examined by Masson`s trichrome staining.The protein expression and distribution of AhR, AhR nuclear translocator (ARNT) and CYP1A1 were detected by the methods of immunohistochemistry and Western blot.The mRNA expression of AhR, ARNT and CYP1A1 was detected by real-time fluorescence quantitative PCR.RESULTS:Compared with CHD+sinus rhythm group, the collagen content and the expression of AhR, ARNT and CYP1A1 were significantly increased in RHD+sinus rhythm group and RHD+cAF group.Compared with RHD+sinus rhythm group, the collagen content and the expression of AhR, ARNT and CYP1A1 were significantly increased in RHD+cAF group (P<0.05).CONCLUSION:The expression of AhR is correlated with the degree of fibrosis.The expression of AhR/ARNT/CYP1A1 is increased in atrial tissues of patients with RHD, suggesting that AhR/ARNT/CYP1A1 should be involved in atrial fibrosis of the patient with RHD.

AIM:To investigate the changes of aryl hydrocarbon receptor (AhR) in the process of cardiomyo-cyte hypertrophy induced by high glucose , and to explore its potential mechanisms .METHODS: The rat cardiomyocytes (H9c2 cells) were divided into normal glucose group , high glucose group, DMSO group and resveratrol (an AhR antago-nist) group.The content and distribution of AhR were observed with immunofluorescence staining .The myocardial cells were stained with rhodamine-labeled phalloidin to visualize cytoskeleton , and the cell surface area were determined after im-aging by fluorescence microscopy .The generation of reactive oxygen species ( ROS) in the cardiomyocytes was measured u-sing a fluorescent probe DCFH-DA.The mRNA expression of AhR , CYP1A1, atrial natriuretic peptide ( ANP) and brain natriuretic peptide ( BNP) were evaluated by real-time quantitative PCR ( RT-qPCR).The protein levels of AhR, CYP1A1, ANP and BNP were assessed by Western blot .RESULTS:AhR was constitutively presented in the cytosol un-der normal-glucose condition and was translocated to the nuclei under high-glucose condition .High glucose induced cardiac hypertrophy , and increased ROS generation .Significant reductions in the cell size and ROS generation were observed after treated with resveratrol.The expression of AhR, CYP1A1, ANP and BNP at mRNA and protein levels in high glucose group was increased as compared with normal glucose group and resveratrol group , and the above-mentioned indexes signifi-cantly decreased in resveratrol group as compared with DMSO group .CONCLUSION: High glucose-induced cardiac hy-pertrophy increases AhR expression , which may be involved in the maintenance of glucose homeostasis in the cardiomyo-cytes.AhR translocation to the nucleus induced by high glucose results in the increases in CYP 1A1 expression and ROS generation, which may be an important mechanism of high glucose-induced cardiomyocyte hypertrophy .

Objective:To investigate the effect of transforming growth factor (TGF- β) signal in muscle fiber itself during inflammation/immunity response on intramuscular inflammation. Methods:Sixteen wild C57BL/6 mice (wild group) and sixteen mice with skeletal muscle-specific deficiency of T βRⅡ (knock-out group) between 4-8 weeks of age were selected for this study. Acute muscle injury in mice was induced by injection of myotoxin cardiotoxin (CTX) into gastrocnemius. The differences in intramuscular inflammation were compared between the wild and knock-out groups on 0, 4, 7 and 10 d after CTX injection by observing exudation of mononuclear phagocytes, macrophages, M1 type macrophages, CD4 +T cells and helpers T cells (Th1, 2&17). Two newborn C57BL/6 wild mice and 2 SM TGF- βr2-/- knock-out mice were selected to culture primary myoblasts in vitro which were divided into 2 groups: an interferon group subjected to interferon simulation and a control group subjected to addition of an equal amount of solvent. The differences in expression of IL-6, IL-10, MCP-1, MIP-1α, H-2K b, H2-Ea, Toll-like receptor (TLR)3 and TLR7 were compared between the interferon and control groups, as well as between the wild and knock-out groups. Results:On 4&7 d after CTX injection, the ratios of mononuclear/macrophage (75.73%±3.62%, 45.27%± 2.32%), macrophages (38.67%±2.76%, 24.87%±2.19%), M1 macrophages (43.21%±0.11%, 30.43%±2.19%), CD4 +T cells (20.13%±1.62%, 5.67%±0.32%) in the muscle tissue from the knock-out mice were significantly higher than those from the wild mice (58.52%±2.43%, 29.21%±2.45%; 20.63%±2.32%, 16.23%±1.25%; 24.98%±0.35%, 14.23%±1.69%; 10.70%±0.43%, 2.50%±0.45%), with a majority of Th1&Th17 ( P<0.05). In vitro results showed that the levels of IL-6, MCP-1, MIP-1α, H-2K b, H2-Ea and TLR3 were significantly upregulated in the interferon group compared with the control group and that such upregulation in the nock-out mice was more significant than in the wild mice ( P<0.05). Conclusions:Endogenous TGF- β signal activation plays a role in the functional recovery after muscle trauma, because it is involved in the regulation of immune behavior of muscle fibers, thus affecting intramuscular inflammation and muscle regeneration.