辽西地区农村汉族青少年体型发育规律的Heath-Carter体型法分析

目的:分析辽西地区农村汉族青少年的体型发育规律和特点,为体质人类学补充必要的数据。对象:按整群分层抽样法,抽取2001-07/2003-09辽西地区锦州、盘锦、葫芦岛、义县和绥中的农村13所中小学7～19岁经学校正常体质检查证明身体健康的汉族学生为调查对象,按性别分两大组,每大组按年龄分12小组,7～18岁每岁为1个年龄组,18～19岁为1个年龄组,每小组44～82人,共分24组,搜集完整资料1280名(男666名,女614名)。采用Heath-Carter体型法,每项指标测量2次,取平均值,10项指标由专人负责,测试数据按年龄和性别在微机中建立数据库,依次计算出各年龄组的内因子、中因子和外因子,体型图上的X,Y坐标值,身高/体质量1/3,样本中平均体型点到所有体型点空间距离的均数,三维空间中两个体型点间的差异,体脂百分比和各类体型分布频数。结果:参加调查1280名,均进入结果分析。①7～17岁青少年身高、体质量随年龄的增加而增长。平均身高、体质量男生大于女生。身高/体质量1/3指数除7、8、10、12和13岁外,各年龄组男生>女生,平均值男生>女生。体脂含量除8岁外,其他年龄组女生>男生,平均值女生>男生。②男生的体型均值3.6-2.5-3.7,属外胚层-内胚层均衡体型,女生平均体型值为4.3-2.2-3.3,属于偏外胚层的内胚层体型。体型频数的变化提示辽西农村汉族男生体型分布在内胚层和外胚层的体型较多,女生分布较集中,主要在内胚层体型。③内因子男生在3.0～4.0,女生在3.5～5.2,各年龄组女生>男生;中因子男生在1.6～3.9,女生在0.8～3.4,除7、11和17岁女生>男生外,其他年龄组男生>女生或男女相等,平均值男生>女生。外因子男生在3.0～5.0,女生在3.0～4.1,7、8、10、12、13岁女生>男生,11、14、15、16、17、18岁男生>女生。因此,女生的内因子占优势,皮下脂肪更发达,体态丰满,男生中因子占优势,骨骼粗壮,肌肉发达,随着年龄的增长,男生的身体相对瘦高程度增长,身材修长。④男女各年龄组间体型比较,7,8,9,10,11,12,13,14,15,16,17,18～19岁三维空间中两个体型点间的差异值分别为0.45,0.67,1.03,0.56,0.76,0.30,0.93,2.60,1.86,1.37,1.21,1.47,8～11岁年龄组男女间体型差异有显著性(t=2.66,2.75,2.95,3.58,P<0.05)。⑤与城市青少年相比,农村青少年身高低5～6cm(男女分别为u=6.24,5.90,P<0.01),体质量低3～6kg(男女分别为u=6.93,4.60,P<0.01)。结论:辽西地区农村男生较女生骨骼粗壮,肌肉发达,女生的皮下脂肪更发达,体态丰满,随着年龄的增长,男生的身体相对瘦高,身材修长。与城市青少年相比,农村青少年仍矮瘦,与国外资料和国内少数民族相比,辽西地区农村汉族青少年骨骼肌肉欠发达,身材修长。     

Loss of myeloid differentiation antigens precedes blastic transformation in chronic myelogenous leukemia

In order to determine whether antigenic patterns alter with disease progression and are thereby suggestive of impending blast crisis in chronic myelogenous leukemia, 50 bone marrow biopsy specimens from 32 patients were examined retrospectively using indirect immunoperoxidase labeling with three monoclonal antibodies that detect myeloid antigens. Monoclonal antibodies PMN13F6, PMN7C3, and PMN8C7 detect human neutrophil antigens that first appear at the myeloblast, promyelocyte, and metamyelocyte stages of differentiation, respectively, and persist throughout later differentiation. Percentages of antigen-positive bone marrow cells during the chronic phase were compared with percentages of antigen-positive cells at blast transformation, and time from bone marrow biopsy until blast crisis was correlated with the percentage of bone marrow cells expressing these antigens. Bone marrow biopsy samples from patients in the chronic phase who continue to remain clinically stable 4 to 106 months after biopsy expressed PMN13F6 antigen on 82% +/- 9% (mean +/- SD) of cells, PMN7C3 antigen on 62% +/- 14% of cells, and PMN8C7 on 68% +/- 14% of cells. Bone marrow biopsy specimens obtained from patients 1 or more years prior to blast transformation expressed PMN13F6 antigen on 81% +/- 12%, PMN7C3 antigen on 71% +/- 16%, and PMN8C7 on 64% +/- 16% of cells. Bone marrow biopsy samples obtained between 2 months and 1 year prior to blast crisis expressed PMN13F6 antigen on 68% +/- 15%, PMN7C3 on 51% +/- 17%, and PMN8C7 antigen on 46% +/- 18% of cells. Bone marrow biopsy specimens taken at the time of blast transformation expressed PMN13F6 antigen on 20% +/- 25%, PMN7C3 antigen on 19% +/- 25%, and PMN8C7 antigen on 13% +/- 25% of cells. The difference between the mean of antigen-positive cells from bone marrow biopsy samples obtained at the time of blast crisis was significant compared with the mean of positive cells from biopsy specimens obtained at all other phases of the disease (P less than .001 for all three antibodies). There was a positive correlation between loss of myeloid antigens and disease progression as determined by simple regression of log time and correlation analysis (PMN13F6, r = .6533, P less than .005; PMN7C8, r = .6304, P less than .005; PMN8C7, r = .5215, P less than .05). There was a negative correlation between percentage of immature cells and time to blastic crisis (r = -.6206, P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)     

hs-CRP is a potential predictor of no-reflow in patients with AMI after emergency PCI

The paper aims to determine whether the inflammation,a powerful risk factor that has been demonstrated for the development of coronary artery disease,plays a role in no-reflow phenomenon in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI).Methods We prospectively analyzed 656 patients with AMI after primary PCI.Based on post-PCI angiography data,patients were divided into two groups:the no-reflow group (TIMI=2,n =60) and the reflow group (TIMI=3,n =596).Results Our results showed that the inflammatory factors including leukocyte count (×109/L) (10.90±4.04 vs.9.12±2.98 P =0.002),hs-CRP (5.04±0.71 vs.4.70±0.75 P =0.001) and other factor platelet count (×109/L) (210.96±33.42 vs.196.41±46.06 P =0.033) in no-reflow group are significantly higher than those in reflow group,major adverse cardiac events happened in the patients with no-reflow are higher than in reflow patients no matter in hospital or at the end of follow-up.We also found the left ventricular ejection fraction (LVEF) dramatically decreased (58.65±9.34 vs.51.29±11.38,P＜0.001) and left ventricular end-diastolic dimension (LVEDD) significantly increased (49.94±6.75 mm vs.54.66±6.68mm,P＜0.001) in no-reflow patients at the end of follow-up.Conclusions Our results suggest that inflammation factors function in no-reflow phenomenon,and no-reflow is a serious complication after primary PCI which predicts poor left ventricular systolic functional recovery and mortality in patients with AMI.(J Geriatr Cardiol 2008;5:217-222)     

Wasp sting anaphylaxis

Profuse hemostatic defects were demonstrable 14 hr after wasp sting anaphylaxis. The patient's plasma contained an agent or agents that interfered with the action of thrombin, impeding the release of fibrinopeptide A from fibrinogen and the hydrolysis of the synthetic amide H-D-prolyl-L-phenylalanyl-L-arginine p-nitroanilide. This inhibitor could not be equated with known plasma inhibitors of thrombin nor with heparin. Additionally, the titers of nearly all other known clotting factors were reduced as compared to levels obtained after the patient's recovery. Of particular interest were profound reductions in the titers of proaccelerin (factor V) and high molecular weight kininogen. A normal titer of Hageman factor (factor XII) argued against participation of contact-activated mechanisms in the induction of the multiple abnormalities observed. Attempts to demonstrate the release of procoagulant or anticoagulant substances from the patient's convalescent blood, plasma, serum, or leukocytes upon challenge with wasp venom were unsuccessful. The observations reported confirm and extend information concerning hemostatic abnormalities in anaphylaxis, and point out the need to examine further this puzzling association.     

Synergistic growth inhibitory and differentiating effects of trimidox and tiazofurin in human promyelocytic leukemia HL-60 cells

Increased ribonucleotide reductase (RR) activity has been linked with malignant transformation and tumor cell growth. Therefore, this enzyme is considered to be an excellent target for cancer chemotherapy. We have examined the effects of a newly patented RR inhibitor, trimidox (3,4,5-trihydroxybenzohydroxamidoxime). Trimidox inhibited the growth of human promyelocytic leukemia HL-60 cells with an IC50 of 35 mumol/L. Incubation of HL-60 cells with 50 mumol/L trimidox for 24 hours decreased deoxyguanosine triphosphate (dGTP) and deoxycytidine triphosphate (dCTP) pools to 24% and 39% of control values, respectively. Incubation of HL-60 cells with 20 to 80 mumol/L trimidox even up to a period of 4 days did not alter the distribution of cells in different phases of cell cycle. Sequential incubation of HL-60 cells with trimidox (25 mumol/L) for 24 hours and then with 10 mumol/L tiazofurin (an inhibitor of inosine monophosphate dehydrogenase) for 4 days produced synergistic growth inhibitory activity, and the cell number decreased to 16% of untreated controls. When differentiation- linked cell surface marker expressions were determined in cells treated with trimidox and tiazofurin, a significantly increased fluorescence intensity was observed for the CD 11b (2.9-fold). CD 33 (1.9-fold), and HLA-D cell surface antigens. Expression of the transferrin receptor (CD71) increased 7.3-fold in cells treated with both agents, compared with untreated controls. Our results suggest that trimidox in combination with tiazofurin might be useful in the treatment of leukemia.     

A bicistronic retrovirus vector containing a picornavirus internal ribosome entry site allows for correction of X-linked CGD by selection for MDR1 expression

Chronic granulomatous disease (CGD) is an inherited hematologic disorder involving failure of phagocytic cell oxidase to produce superoxide (O2-.), resulting in recurrent infections. The success of retrovirus gene therapy for hematopoietic diseases will be limited both by the efficiency of ex vivo transduction of target cells and by the ability of corrected cells to replace uncorrected cells in vivo. Using MFG-based retrovirus vectors containing oxidase genes, we have previously demonstrated in vitro correction of CGD, but transduction rates were low. In the present study we explore a strategy for providing a selective growth advantage to transduced cells, while retaining the single promoter feature of MFG responsible for high virus titer and enhanced protein production. We constructed a bicistronic retrovirus producing a single mRNA encoding both the therapeutic gene for the X-linked form of CGD (X-CGD), gp91phox, and the selectable human multidrug resistance gene, MDR1 linked together by the encephalomyocarditis virus internal ribosome entry site (IRES). As a control we constructed a bicistronic vector with the polio virus IRES element and using the bacterial neomycin resistance gene (neor) as the selective element. In Epstein-Barr virus transformed B (EBV-B) cells from an X-CGD patient, a tissue culture model of CGD, we show correction of the CGD defect and complete normalization of the cell population using either of these vectors and appropriate selection (vincristine for MDR1 and G418 for neor). Using a chemiluminescence assay of O2-. production, populations of cells transduced with either vector demonstrated initial correction levels of from less than 0.1% up to 2.7% of normal EBV-B cell oxidase activity. With either construct, cell growth under appropriate selection enriched the population of transduced cells, resulting in correction of X-CGD EBV-B cells to a level of O2-. production equalling or exceeding that of normal EBV-B cells. These studies show that a therapeutic gene can be linked to a resistance gene by an IRES element, allowing for selective enrichment of cells expressing the therapeutic gene. Furthermore, the use of MDR1 as a selective element in our studies validates an important approach to gene therapy that could allow in vivo selection and is generalizable to a number of therapeutic settings.     

以磷酸肌醇3激酶通路为靶点的抗肿瘤药物

磷酸肌醇3激酶(PI3K)通路是一个关键的信号转导系统,它可将癌基因和多种受体与许多细胞功能联系在一起,还是肿瘤中最常被激活的通路。靶向PI3K同工酶和通路中包括AKT和mTOR在内的其他主要节点的抑制剂已进入临床试验阶段,但存在一定问题。本文重点阐述人们在理解PI3K通路方面取得的进展,并讨论研发靶向这条通路的抗肿瘤药物的机遇与面临的挑战。     

Chronic morphine use does not induce peripheral tolerance in a rat model of inflammatory pain

Although opioids are highly effective analgesics, they are also known to induce cellular adaptations resulting in tolerance. Experimental studies are often performed in the absence of painful tissue injury, which precludes extrapolation to the clinical situation. Here we show that rats with chronic morphine treatment do not develop signs of tolerance at peripheral mu-opioid receptors (micro-receptors) in the presence of painful CFA-induced paw inflammation. In sensory neurons of these animals, internalization of mu-receptors was significantly increased and G protein coupling of mu-receptors as well as inhibition of cAMP accumulation were preserved. Opioid receptor trafficking and signaling were reduced, and tolerance was restored when endogenous opioid peptides in inflamed tissue were removed by antibodies or by depleting opioid-producing granulocytes, monocytes, and lymphocytes with cyclophosphamide (CTX). Our data indicate that the continuous availability of endogenous opioids in inflamed tissue increases recycling and preserves signaling of mu-receptors in sensory neurons, thereby counteracting the development of peripheral opioid tolerance. These findings infer that the use of peripherally acting opioids for the prolonged treatment of inflammatory pain associated with diseases such as chronic arthritis, inflammatory neuropathy, or cancer, is not necessarily accompanied by opioid tolerance.