甲状腺激素与糖尿病患者的血脂、血糖代谢的临床相关性分析

目的 探究糖尿病患者甲状腺激素与血脂、血糖的相关关系及临床意义.方法 选择2015年6月至2016年8月入住本院治疗的280例甲状腺功能正常的糖尿病患者为研究对象,分别按照患者体内TSH和HbA1C水平高低进行分组,测定并分析患者TSH、FT3、FT4、血脂、HbA1C、FPG等指标变化情况.结果 不同性别患者组间比较,女性患者的TSH值明显高于男性患者(P<0.05),而FT3和FT4值明显低于男性患者(P均<0.05).按HbAlc水平分为3组,随着HbA1c的升高,HbA1C≤8%组、8%11%组3组患者TSH值分别为2.0±1.0、1.7±1.2L、1.3±1.1mIU/L和FT3值分别为4.7±0.7、4.5±0.6、4.4±0.6 pmol/L,TSH和FT3均逐渐降低,差异具有统计学意义(P均<0.05),并且TSH和FT3均与HbA1c呈负相关(r=-0.133、-0.132,P=0.025、0.001).按TSH水平分为3组,随着患者TSH水平的升高,0.3mIU/L≤TSH≤1.7mIU/L组,1.7mIU/L相似文献   

小而密低密度脂蛋白及常见血脂指标与冠心病的相关性研究

目的 探讨血清小而密低密度脂蛋白(small dense low-density lipoprotein, sd-LDL)水平与血清胆固醇(cholesterol,CHO)、甘油三酯(triglyceride, TG)、低密度脂蛋白(low density lipoprotein,LDL)指标与冠心病(coronary heart disease, CHD)的发生发展及各指标之间的相互关系.方法 选取CHD患者87例作为病例组,其中男48例,女39例.纳入109例健康体检者作为对照组,男52例,女57例.采用全自动日立7600仪器,日本积水相关检测试剂测定各组血清CHO、TG、LDL水平,血清sd-LDL水平采用九强小而密低密度脂蛋白测定试剂于雅培C16000仪器上进行测定.采用SPSS 22.0软件进行相关数据分析.结果 病例组血清CHO水平、LDL水平及sd-LDL水平高于正常对照组,差异具有统计学意义(P<0.01).女性病例组TG水平高于对照组,男性及总体病例组与对照组TG水平差异无统计学意义.年龄和sd-LDL水平为冠心病相关的独立危险因素.冠心病患者血清sd-LDL与CHO、TG及LDL水平均呈显著正相关,血清LDL与CHO呈显著正相关(P<0.01).结论 血清sd-LDL是独立的冠心病危险因素,血脂常规项目联合sd-LDL对于冠心病的早期预测可能具有更好的提示和诊断作用.     

自身抗体与血浆炎症因子联合检测对肝硬化合并肝功能衰竭的诊断价值

目的 探讨和分析自身抗体、血浆炎症指标联合检测在肝硬化合并肝功能衰竭患者中的诊断价值.方法 选取2014年10月至2016年8月我院收治的62例肝硬化合并肝功能衰竭患者作为试验组,并选取同一时段于我院治疗的42例慢性肝炎患者作为疾病对照组,以及42例健康体检志愿者作为健康对照组.分别采用电化学发光法(ECLIA)检测3组的血清PCT水平,采用免疫散射比浊法(INA)检测血清CRP水平,以及酶联免疫标记法(ELISA)检测其血清AMA-M2和抗-gp210水平.结果 试验组血清PCT、CRP表达水平与疾病对照组和健康对照组相比,差异具有统计学意义(P<0.05);而对疾病对照组和健康对照组的血清PCT、CRP表达水平比较发现,同样呈现显著性差异(P<0.05);试验组血清AMA-M2、抗-gp210、PCT及CRP检测的阳性率均明显高于两对照组,差异有统计学意义(P<0.05);血清AMA-M2、抗-gp210、PCT及CRP检测的灵敏度分别为82.3%、71.0%、74.1%和58.1%,特异性分别为91.7%、80.9%、76.2%和67.9%,准确度分别为76.7%、79.5%、78.8%和72.6%,而四者联合检测的灵敏度、特异度及准确度分别为43.5%、96.9%和92.7%,与各指标单独检测相比,灵敏度下降、特异度和准确度提升,差异有统计学意义(P<0.05).此外AMA、抗-gp210和PCT或CRP三者联合检测同样会显著降低灵敏度,提升特异性,但准确度变化不大.结论 AMA-M2、抗-gp210、PCT及CRP单独检测在肝硬化合并肝功能衰竭的诊断中具有一定的价值,但也存在着误诊及漏诊的情况,而自身抗体与血浆炎症指标的联合检测可有效提高检测特异度及准确度,增加疾病的检测率,值得临床推广运用.     

基因重组干扰素治疗急性乙型肝炎疗效观察

目的　以基因重组干扰素治疗急性乙型肝炎病人,观察其减少急性乙肝转慢率的效果。方法　用基因重组α干扰素（３００ 万Ｕ,肌内注射,隔日１ 次,１２ 周为一个疗程） 治疗１９ 名急性乙肝病人,对治疗后未产生抗ＨＢｓ 者,加用乙肝疫苗（３０ μｇ,肌内注射,每周注射１ 次,连用３ 周）;对照组为病情相似的１５ 例病人,服用一般保肝药物。结果　治疗组１８ 例（９５－０％ ,１８１９）ＨＢｓＡｇ 阴转,但均未产生抗ＨＢｓ,再用乙肝疫苗后,１７ 例（９４－０％ ,１７１９） 产生抗ＨＢｓ。２４～２４０ 周随访期间,１８ 例ＨＢｓＡｇ 阴转者无复发;１ 例ＨＢｓＡｇ 未阴转者,至随访结束时仍为阳性。对照组８ 例（５３－０ ％ ,８１５）ＨＢｓＡｇ 阴转,同时,８７－５ ％（７８）的病例产生抗ＨＢｓ,另７ 例ＨＢｓＡｇ 未阴转者,在２４ ～２４０ 周的随访期间,仅１ 例ＨＢｓＡｇ阴转,余６ 例ＨＢｓＡｇ 持续阳性。结论　对于急性乙型肝炎发病８ 周后ＨＢｓＡｇ 仍未阴转者,采用干扰素合用乙肝疫苗,对防止转慢及ＨＢｓＡｇ 阴转后抗ＨＢｓ 的产生可能有一定作用     

Affinity of hemoglobin for oxygen and prooxidant-antioxidant equilibrium after administration of lipopolysaccharide during correction of the L-arginine—NO pathway

Effects of correction of the L-arginine—NO pathway on the fever reaction, oxygen transport function of the blood, and prooxidant-antioxidant equilibrium in rats injected intramuscularly with lipopolysaccharide were studied. pH, Pco₂, Po₂, and the index of hemoglobin oxygen affinity (p50) were measured in mixed venous blood. Levels of Schiff bases, α-tocopherol, and catalase activity were determined in erythrocytes and in the liver, kidneys, and heart. NO synthase inhibitor attenuated the fever reaction and decreased p50 to 28.89±0.83 mm Hg (in rats administered with lipopolysaccharide, p50 was 34.21±1.63 mm Hg). The increase in the content of Schiff bases and the exhaustion of the antioxidant system in erythrocytes and tissues were less pronounced in rats injected with the NO synthase inhibitor than in animals receiving lipopolysaccharide only. Various parameters of the prooxidant-antioxidant equilibrium correlated with p50. Thus, hemoglobin oxygen affinity and NO are important factors involved in the maintenance of the prooxidant-antioxidant equilibrium in the body. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 6, pp. 616–619, June, 1999     

高血压病患者血浆神经肽Y的释放特点及其与血脂代谢的关系

应用放射免疫法测定５０例不同期高血压病患者血浆神经肽Ｙ（ＮＰＹ）释放变化特点并比较其与吸烟、血脂代谢之间的关系。结果发现：高血压病患者血浆ＮＰＹ含量为１４０．３±７３．８ｐｇ／ｍｌ,与对照组比较（７１．１±２１．８ｐｇ／ｍｌ）有显著性差异（Ｐ＜０．０１）;Ⅲ期高血压病患者血浆ＮＰＹ含量明显高于Ⅰ、Ⅱ期高血压病患者（Ｐ＜０．０１）;既往有吸烟史或血糖（ＢＧ）、血甘油三酯（ＴＧ）异常的高血压病患者血浆ＮＰＹ含量较无吸烟史及ＢＧ、ＴＧ正常者明显增高（Ｐ＜０．０１）。提示：高血压病患者血浆ＮＰＹ水平明显升高,而它的升高与吸烟、血甘油三酯及血糖增高有一定关系,它们的共同作用进一步使动脉血管弹性减退,导致微循环障碍,参予了高血压病、冠心病的发病机制与病理生理过程。     

血浆与血小板中NPY、NT在慢性肾功能衰竭患者血液透析中的变化及意义

采用RIA法检测40例慢性肾功能衰竭(CRF)患者血液透析(以下简称血透)过程中,血浆和血小板中神经肽Y(NPY)、神经降压素(NT)的含量变化及其临床意义。并以30例健康人作为对照。结果显示,①CRF患者血透前血浆NPY、NT含量分别为432.34±52.27ng/L、138.44±80.35ng/L;血透后分别为324.52±48.16ng/L、211.6±124.69ng/L。②CRF患者血透前血小板中NPY、NT含量分别为34.86±18.82ng/L、41.12±24.12ng/L;血透后分别为66.97±21.81ng/L、14.89±12.56ng/L。结果表明,CRF患者存在NPY及NT分泌异常。NPY与NT作为体内重要的神经递质,参与了肾脏病及其并发高血压的病理生理过程。     

Physical activity modulates the effect of a lipoprotein lipase mutation (D9N) on plasma lipids and lipoproteins

We investigated interactions between a mutation (D9N) in the lipoprotein lipase (LPL) gene and physical activity, as well as other lifestyle factors, on lipid traits in a population-based sample of Dutch men and women (n = 379). We used questionnaire information to classify physical activity, alcohol consumption, and smoking habits, while overweight was defined as a body mass index (BMI) > 25 kg/m2. Non-fasting blood samples were used for the determination of lipid traits and the D9N genotype. Fifteen subjects (4%) carried the mutation. They presented with higher levels of total cholesterol, apolipoprotein (apo) B and triglycerides compared to non-carriers. While no interactions with overweight, alcohol consumption, and smoking were found, a strong interaction between the D9N mutation and physical activity became apparent. Physically inactive D9N carriers (n = 5) had considerably higher total cholesterol (+2 mmol/l, p < or = 0.0001) and apo B levels (+63 mg/dl, p < or = 0.0001) compared to non-carriers of this mutation, whereas their high-density lipoprotein (HDL)-cholesterol concentrations were lower (-0.22 mmol/l, p < 0.05). This was not the case for physically active D9N carriers (n = 10). In conclusion, a common variant of the LPL gene (D9N) adversely affects plasma lipid and lipoprotein profiles. However, the unfavorable consequences may be counteracted by physical activity.     

Fetal RhD genotyping: A more efficient use of anti-D immunoglobulin

The most important application of blood group genotyping by molecular genetics is the prediction of fetal RhD phenotype in pregnant women with anti-D, in order to assess the risk of haemolytic disease of the fetus and newborn. This diagnostic test performed on cell-free fetal DNA in the maternal plasma, is now a routine procedure in some countries. High-throughput modifications of this form of fetal D-typing would be valuable for testing fetuses of all D-negative pregnant women to avoid unnecessary antenatal treatment with anti-D immunoglobulin in the 40% of D-negative pregnant women with a D-negative fetus. The results of trials in Bristol and Amsterdam suggest that such routine testing is feasible and accurate.     

Structural and functional analysis of the apoptosis-associated tyrosine kinase (AATYK) family

Apoptosis-associated tyrosine kinase (AATYK) is a protein kinase that is predominantly expressed in the nervous system and is involved in apoptosis and neurite growth of cerebellar granule cells. In this study, we cloned three new members of the mouse AATYK family, AATYK1B, AATYK2 and AATYK3. AATYK1B is a splicing variant of the previously reported AATYK1 (referred to as AATYK1A hereafter). In comparison with AATYK1A, these three AATYK members were characterized by having an extra N-terminal region that consists of a signal peptide-like sequence and a predicted transmembrane (TM) region, which is followed by a kinase domain and a long C-terminal domain. Both TM-containing AATYK isoforms (AATYK(+)TM: AATYK1B, 2, and 3) and TM-lacking isoform (AATYK(-)TM: AATYK1A) were recovered in membrane fractions, suggesting that AATYK(+)TM and AATYK(-)TM are transmembrane- and peripheral-membrane protein kinases, respectively. AATYK1A was recovered in the soluble fraction when the cells were treated with 2-bromo palmitate, suggesting that AATYK1A associates with membrane via palmitoylation. The kinase domain was highly conserved among all AATYK members and was shown to be catalytically active. Three AATYK family members were predominantly expressed in adult mouse brains with almost similar expression profiles: widespread distribution over the various brain regions, especially in the cerebellum and hippocampus, and up-regulated expression during development of the cerebellum. In cultured cerebellar granule cells, AATYK1 was abundantly localized in both soma and axons, AATYK2 distribution was restricted to soma, and AATYK3 was punctately present over the cells. AATYK1 was concentrated in the central domain of growth cones of dorsal root ganglion neurons. Our results indicate that AATYK family members are brain-dominant and membrane-associated kinases with slightly different distribution patterns in the developing and adult mouse brain, which may be involved in fine regulation of neuronal functions including neurite extension and apoptosis.