A new role for PGRP-S (Tag7) in immune defense: lymphocyte migration is induced by a chemoattractant complex of Tag7 with Mts1

PGRP-S (Tag7) is an innate immunity protein involved in the antimicrobial defense systems, both in insects and in mammals. We have previously shown that Tag7 specifically interacts with several proteins, including Hsp70 and the calcium binding protein S100A4 (Mts1), providing a number of novel cellular functions. Here we show that Tag7–Mts1 complex causes chemotactic migration of lymphocytes, with NK cells being a preferred target. Cells of either innate immunity (neutrophils and monocytes) or acquired immunity (CD4⁺ and CD8⁺ lymphocytes) can produce this complex, which confirms the close connection between components of the 2 branches of immune response.     

吐鲁番市胃食管反流病发生相关危险因素分析（附280例报道）

目的：探讨280例胃食管反流病（GERD）的分布特点及危险因素。方法：对临床诊断和胃镜确诊的280例GERD患者进行临床和风险因子相关性分析。结果：不论汉族还是维族,男性患者比例均明显高于女性;汉族患者高发年龄段早于维族患者（z=-2．939,P=0．003,）;汉族和维族患者占反流性食管炎和Barrett食管比例分别为42．4％、81_3％及56．5％、18．8％,其中汉族患者Barrett食管比例较高（X2=14．358,P=0．000）;肥胖、习惯性便秘、重体力活动者、饮食习惯不良在维族患者中的比例较高（P〈0．001）。结论：GERD与性别、年龄密切相关,男性多于女性,汉族患者发病年龄高峰旱于维族患者;汉族患者Barrett食管发生比例高于维族患者;肥胖、习惯性便秘、重体力活动、饮食习惯不良可能是GERD尤其是维族人群GERD的危险因素。     

湖南省双季稻生产系统碳效率

提高农作物生产系统的碳效率是实现低碳农业的重要途径之一.本文采用2004—2012年农作物产量、农田作物生产系统农资投入等统计数据,利用生命周期法和投入产出法,对湖南省双季稻生产系统碳排放、碳吸收和碳效率特征及其动态进行估算.结果表明:湖南省2004—2012年双季稻生产系统年均碳排放总量为656.4×107kg CE,其中化肥和农药生产运输碳排放占农资投入碳排放总量的大部分,分别约占70.0%和15.9%,碳排放总量年际间持续降低,年均降低率为2.4%,碳排放强度则表现为增长趋势;湖南双季稻生产系统2004—2012年年均碳吸收总量为1547.0×107kg C,也呈现逐年降低的趋势,年降低率为1.2%,单位面积稻田碳吸收强度则表现为增长趋势;碳生产效率呈现缓慢增加的趋势,碳经济效率随着年份递进增加幅度较大,年均增长率为9.9%,碳生态效率则表现为稳定且较低,保持在2.4kg C·kg-1CE左右.表明湖南近几年双季稻生产系统碳综合效率提高缓慢,降低肥料和农药的投入量,提高利用效率是提高双季稻生产系统碳效率的关键.     

Genome-wide association studies identified novel loci for non-high-density lipoprotein cholesterol and its postprandial lipemic response

Non-high-density lipoprotein cholesterol(NHDL) is an independent and superior predictor of CVD risk as compared to low-density lipoprotein alone. It represents a spectrum of atherogenic lipid fractions with possibly a distinct genomic signature. We performed genome-wide association studies (GWAS) to identify loci influencing baseline NHDL and its postprandial lipemic (PPL) response. We carried out GWAS in 4,241 participants of European descent. Our discovery cohort included 928 subjects from the Genetics of Lipid-Lowering Drugs and Diet Network Study. Our replication cohorts included 3,313 subjects from the Heredity and Phenotype Intervention Heart Study and Family Heart Study. A linear mixed model using the kinship matrix was used for association tests. The best association signal was found in a tri-genic region at RHOQ-PIGF-CRIPT for baseline NHDL (lead SNP rs6544903, discovery p = 7e?7, MAF = 2 %; validation p = 6e?4 at 0.1 kb upstream neighboring SNP rs3768725, and 5e?4 at 0.7 kb downstream neighboring SNP rs6733143, MAF = 10 %). The lead and neighboring SNPs were not perfect surrogate proxies to each other (D′ = 1, r ² = 0.003) but they seemed to be partially dependent (likelihood ration test p = 0.04). Other suggestive loci (discovery p < 1e?6) included LOC100419812 and LOC100288337 for baseline NHDL, and LOC100420502 and CDH13 for NHDL PPL response that were not replicated (p > 0.01). The current and first GWAS of NHDL yielded an interesting common variant in RHOQ-PIGF-CRIPT influencing baseline NHDL levels. Another common variant in CDH13 for NHDL response to dietary high-fat intake challenge was also suggested. Further validations for both loci from large independent studies, especially interventional studies, are warranted.     

无症状吸烟者的肺功能改变情况分析

目的:探讨烟龄≥15年,日吸烟量≥15支的无症状男性吸烟者的肺功能改变情况。方法:选择男性无症状吸烟者190人及非吸烟者180人,进行肺功能测定,并比较两组人群的肺功能改变情况。结果:吸烟组与非吸烟组比较,肺活量(VC)、用力肺活量(FVC)、第1秒用力呼气容积(FEV1)、Tiffeneau 1秒率(FEV1/VC)结果改变不明显,而Gaensler 1秒率(FEV1/FVC)、最大分钟通气量(MVV)、用力呼气50%肺活量的呼气流量(FEF50%)、用力呼气75%肺活量的呼气流量(FEF75%)、呼出25%～75%肺活量时的平均流量(FEF25%～75%)、肺一氧化碳弥散量(DLCO)结果均有显著降低,有统计学意义。结论:通过对无症状吸烟人群肺功能测定结果进行分析。发现有些吸烟者虽无临床症状,但已经出现了小气道及肺弥散功能的损伤,提醒吸烟者应早期戒烟,关爱自身健康,净化生存环境,提高生活质量。     

Relationships between platelet and plasma monoamine oxidase,plasma dopamine-B-hydroxylase,and urinary 3-methoxy-4-hydroxy phenylglycol

The activity of dopamine-B-hydroxylase in blood has recently been demonstrated to be under genetic control and to correlate closely with urinary catecholamine excretion. The results of the present study did not demonstrate any relationship between a major catecholamine metabolite in urine, 3-methoxy-4-hydroxy phenylglycol, and dopamine-B-hydroxylase activity in plasma, monoamine oxidase activity in platelets, or monoamine oxidase activity in plasma. Differences in the origin of urinary catecholamines and urinary 3-methoxy-4-hydroxy phenyglycol may be responsible for these divergent results.     

Association of TLR4 polymorphisms with symptomatic respiratory syncytial virus infection in high-risk infants and young children

Respiratory syncytial virus (RSV) is a leading cause of infant mortality worldwide. Although anti-RSV Ab prophylaxis has greatly reduced infant mortality in the United States, there is currently no vaccine or effective antiviral therapy. RSV fusion (F) protein activates cells through TLR4. Two single nucleotide polymorphisms (SNPs) encoding Asp299Gly and Thr399Ile substitutions in the TLR4 ectodomain were previously associated with TLR4 hyporesponsiveness and increased susceptibility to bacterial infection. Prevalence of these SNPs was analyzed in a case series of 105 DNA samples extracted from archived nasal lavage samples from high-risk infants/young children with confirmed RSV disease who participated in two seminal clinical trials for anti-RSV prophylaxis. Frequencies of TLR4 SNPs in the case series were compared with those of literature controls, healthy adults, infants, and young children who presented with symptoms of respiratory infections (but not preselected for high risk for RSV). Both SNPs were highly associated with symptomatic RSV disease in this largely premature population (p < 0.0001), with 89.5% and 87.6% of cases being heterozygous for Asp299Gly and Thr399Ile polymorphisms versus published control frequencies of 10.5% and 6.5%, respectively. The other two control groups had similarly low frequencies. Our data suggest that heterozygosity of these two extracellular TLR4 polymorphisms is highly associated with symptomatic RSV disease in high-risk infants and support a dual role for TLR4 SNPs in prematurity and increased susceptibility to RSV not revealed by analysis of either alone.     

棉叶中棉酚的快速提取与测定方法研究

棉酚(G)及其相关物甲氧基半棉酚(DHG)、半棉酚酮(HGQ)、半棉酚(HG)、杀实夜蛾素(H1-4)等是棉花中重要的抗虫性萜烯类次生物质.利用高效液相色谱法(HPLC)对棉酚及其相关物进行了分离,测定了棉叶中的棉酚含量,讨论了不同的提取方法和测定条件对结果的影响,给出了一套简便、快速的分析测试方法,同时与紫外-可见分光光度法(苯胺法)的结果进行了对比,认为对于棉花的抗虫性的研究来说,HPLC是比较适宜的方法.     

Genetic Modulation of Lipid Profiles following Lifestyle Modification or Metformin Treatment: The Diabetes Prevention Program

Weight-loss interventions generally improve lipid profiles and reduce cardiovascular disease risk, but effects are variable and may depend on genetic factors. We performed a genetic association analysis of data from 2,993 participants in the Diabetes Prevention Program to test the hypotheses that a genetic risk score (GRS) based on deleterious alleles at 32 lipid-associated single-nucleotide polymorphisms modifies the effects of lifestyle and/or metformin interventions on lipid levels and nuclear magnetic resonance (NMR) lipoprotein subfraction size and number. Twenty-three loci previously associated with fasting LDL-C, HDL-C, or triglycerides replicated (P = 0.04–1×10⁻¹⁷). Except for total HDL particles (r = −0.03, P = 0.26), all components of the lipid profile correlated with the GRS (partial |r| = 0.07–0.17, P = 5×10⁻⁵–1×10⁻¹⁹). The GRS was associated with higher baseline-adjusted 1-year LDL cholesterol levels (β = +0.87, SEE±0.22 mg/dl/allele, P = 8×10⁻⁵, P _interaction = 0.02) in the lifestyle intervention group, but not in the placebo (β = +0.20, SEE±0.22 mg/dl/allele, P = 0.35) or metformin (β = −0.03, SEE±0.22 mg/dl/allele, P = 0.90; P _interaction = 0.64) groups. Similarly, a higher GRS predicted a greater number of baseline-adjusted small LDL particles at 1 year in the lifestyle intervention arm (β = +0.30, SEE±0.012 ln nmol/L/allele, P = 0.01, P _interaction = 0.01) but not in the placebo (β = −0.002, SEE±0.008 ln nmol/L/allele, P = 0.74) or metformin (β = +0.013, SEE±0.008 nmol/L/allele, P = 0.12; P _interaction = 0.24) groups. Our findings suggest that a high genetic burden confers an adverse lipid profile and predicts attenuated response in LDL-C levels and small LDL particle number to dietary and physical activity interventions aimed at weight loss.