Effects of thyroid hormone withdrawal on natriuretic peptides during radioactive iodine therapy in female patients with differentiated thyroid cancer

Objective: We aimed to investigate the effects of thyroid hormone withdrawal on N-terminal prohormone forms of atrial natriuretic peptide (NT-proANP) and brain natriuretic peptide (NT-proBNP) during radioiodine therapy in female patients with differentiated thyroid cancer (DTC).

Methods: Serum concentrations of thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), NT-proANP and NT-proBNP were measured in 51 female patients with DTC (48.7?±?4.2 years) at three time-points: day of radioiodine therapy (t1 – under acute hypothyroidism), 5 days after radioiodine (t2 – under acute hypothyroidism) and 3 months after radioiodine (t3 – under TSH suppression). Thirty healthy euthyroid women served as controls (42.8?±?5.6 years).

Results: At t1/t2/t3, median NT-proANP was 5.2/1.7/487?pmol/L vs. 297.7?pmol/L in control group (p?p?p?r?=?0.38, p?=?0.005), NT-proANP/NT-proBNP ratios (r?=?0.47, p?=?0.001), heart rate (r?=?0.39, p?=?0.005), and negatively with mean arterial blood pressure (r?=??0.58, p?Conclusions: Our results indicate that NT-proANP reflects more accurately direct thyroid hormone effects than NT-proBNP. Thyroid hormone-dependent hemodynamic effects seem to be overlapped on the direct stimulatory effect of thyroid hormones on NT-proANP secretion by cardiac myocytes.     

Fish oil prevents colon cancer by modulation of structure and function of mitochondria

Cancer cells are more susceptible to metabolic perturbations due to impaired electron transport chain (ETC) that promote uncontrolled proliferation. Mitochondria play a pivotal role in bioenergetics and apoptosis, hence are considered as a promising target in tumor cell eradication. Therefore, the present study is designed to elucidate chemopreventive action of fish oil (FO) in combination with corn oil (CO) on mitochondria in colorectal cancer (CRC). Male Wistar rats were divided into groups depending on dietary regimen—Control group, FO + CO(1:1) and FO + CO(2.5:1). These groups were further subdivided depending on whether these received a weekly intraperitoneal injection of ethylenediamine tetra-acetic acid (EDTA) or N,N-dimethylhydrazine dihydrochloride (DMH) for a period of 4 weeks. The animals sacrificed 48 h and 16 weeks after EDTA/DMH treatment constituted initiation and post-initiation phase respectively. The structural and functional alterations in mitochondria were evaluated using transmission electron microscopy (TEM) and by assaying electron transport chain (ETC) enzymes. Mitochondrial lipid composition and cholesterol levels were also assessed. DMH treatment led to mitochondrial degeneration, disrupted cristae and a significant decrease in ETC complexes suggestive of metabolic reprogramming. Moreover, an increase in cholesterol and cardiolipin (CL) levels in post-initiation phase led to evasion of apoptosis. FO in both the ratios resulted in stabilization and increase in number of mitochondria, however, FO + CO(2.5:1) + DMH group also exhibited mitophagy and crystolysis alongwith altered dynamics in ETC which facilitated apoptosis. It also decreased cholesterol and CL levels to increase apoptosis. Fish oil targets mitochondria in a dose dependent manner that augments apoptosis and hence attenuates carcinogenesis.     

2型糖尿病并发冠心病患者血清游离脂肪酸及超敏CRP水平的分析

目的探讨血清游离脂肪酸(FFA)及超敏C反应蛋白(hs-CRP)水平与2型糖尿病(T2DM)并发冠心病(CHD)的相关性。方法选取该院2011年1月至2014年12月收治的80例CHD并发T2DM(CHD+T2DM)的患者及同期收治的单纯T2DM患者80例。测定两组患者血清葡萄糖(FPG)、三酰甘油(TG)、总胆固醇(TC)、hs-CRP和FFA水平。根据患者的血管狭窄程度将CHD+T2DM患者分为单支病变(SVD)和多支病变(MVD)组,比较不同严重程度的患者上述5项指标水平的差异,并且采用Logistic回归分析其与CHD的相关性。结果 T2DM+CHD组患者FPG、TC、TG、hs-CRP和FFA水平高于T2DM组(P0.01);MVD组FPG、TC、TG、hs-CRP和FFA水平高于SVD组(P0.01);Logistic分析表明,hs-CRP和FFA为T2DM+CHD的相关因素(P0.05)。结论 FFA和hs-CRP水平与T2DM患者并发CHD相关,临床治疗需要重点关注。     

Spontaneous hemolytic activity of rat alveolar lining material

During assays of the complement hemolytic activity in lavage fluids (LF) from humans and various laboratory animals (hamsters, rabbits, rats, guinea pigs), we have observed that rat bronchoalveolar lavages had a spontaneous, complement-independent, hemolytic activity to sheep red blood cells (SRBC). Rat lavage fluids were able to lyse sheep and autologous red blood cells at 2°C as well as at 37°C. Together with these observations, the inverse relationship that existed between the LF hemolytic activity and the calcium concentration in the incubation medium suggested that lysis could be due to the presence of large amounts of lysophospholipids in rat lavage fluid. However, thin layer chromatography did not reveal any abnormal amount in lysoderivative, whereas the free fatty acid (FFA) content was very high. Pure palmitic acid, at a concentration similar to that observed in LF from rat, was able to lyse SRBC (8.5μg lyzed 50% of 10⁸ SRBC); its lytic activity decreased when Ca⁺⁺ or bovine serum albumin was added to the incubation mixture. FFA through their detergent effect, appear to account for the hemolytic activity of the rat alveolar lining material.     

Cardiovascular Therapeutic Aspects of Soluble Epoxide Hydrolase Inhibitors

Soluble epoxide hydrolase (sEH) is an enzyme responsible for the conversion of lipid epoxides to diols by the addition of water. Biological actions on the cardiovascular system that are attributed to epoxides include vasodilation, antiinflammatory actions and vascular smooth muscle cell antimigratory actions. Conversion of arachidonic acid epoxides to diols by sEH diminishes the beneficial cardiovascular properties of these epoxyeicosano‐ids. Cardiovascular diseases in animal models and humans have been associated with decreased epoxygenase activity or increased sEH activity and these changes are responsible for the progression of the disease state. More recently, sEH gene polymorphisms in the human population have been associated with increased risk for cardiovascular diseases. Thus the biological actions of epoxyeicosanoids and the sEH enzyme are ideal therapeutic targets for cardiovascular diseases. The rapid development of 1,3‐disubstituted urea based sEH inhibitors over the past five years has resulted in a number of studies demonstrating cardiovascular protection. sEH inhibitors have antihypertensive and antiinflammatory actions and have been demonstrated to decrease cerebral ischemic and renal injury in rat models of hypertension. These findings of beneficial actions in animal models of disease position the sEH enzyme as a promising therapeutic target for cardiovascular diseases.     

Afferent arteriolar dilation to 11, 12-EET analogs involves PP2A activity and Ca2+-activated K+ Channels

The epoxygenase metabolite, 11, 12-epoxyeicosatrienoic acid (11, 12-EET), has renal vascular actions. 11, 12-EET analogs have been developed to determine the structure activity relationship for 11, 12-EET and as a tool to investigate signaling mechanisms responsible for afferent arteriolar dilation. We hypothesized that 11, 12-EET mediated afferent arteriolar dilation involves increased phosphoprotein phosphatase 2A (PP2A) and large-conductance calcium activated K+ (KCa) channels. We evaluated the chemically and/or metabolically table 11, 12-EET analogs: 11, 12-EET-N-methylsulfonimide (11, 12-EET-SI), 11-nonyloxy-undec-8(Z)-enoic acid (11, 12-ether-EET-8-ZE), and 11, 12-trans-oxidoeicosa-8(Z)-eonoic acid (11, 12-tetra-EET-8-ZE). Afferent arteriolar responses were assessed. Activation of KCa channels by 11, 12-EET analogs were established by single cell channel recordings in renal myocytes. Assessment of renal vascular responses revealed that 11, 12-EET analogs increased afferent arteriolar diameter. Vasodilator responses to 11, 12-EET analogs were abolished by K+ channel or PP2A inhibition. 11, 12-EET analogs activated renal myocyte large-conductance KCa channels. 11, 12-EET analogs increased cAMP by 2-fold and PP2A activity increased 3-8 fold in renal myocytes. PP2A inhibition did not significantly affect the 11, 12-EET analog mediated increase in cAMP and PP2A increased renal myocyte KCa channel activity to a much greater extent than PKA. These data support the concept that 11, 12-EET utilizes PP2A dependent pathways to activate large-conductance KCa channels and dilate the afferent arteriole.     

38例甲型H1N1流感病毒核糖核酸阴转影响因素分析

目的分析甲型H1N1流感患者病毒核糖核酸（RNA）阴转的规律和特点。方法对北京地坛医院收治的38例甲型H1N1流感确诊患者的RNA转归情况、可能影响RNA转归的相关因素进行统计分析。结果甲型H1N1流感患者病毒RNA一般在病程的第6天发生阴转,热程越长、流感样症状持续时间越长,RNA阴转的时间越长。早期应用磷酸奥司他韦抗病毒治疗可促进RNA阴转、缩短热程和促使症状恢复,但性别、年龄不影响RNA的阴转。结论体温和抗病毒治疗是影响甲型H1N1流感患者病毒RNA阴转的主要因素,热程、流感样症状持续时间也有一定影响,但仍有必要继续观察和探索。     

广东省布鲁氏菌菌株脂肪酸成分分析

目的探讨脂肪酸成分分析方法对广东布鲁氏菌菌株进行分型的可能性,获得广东布鲁氏菌脂肪酸成分的本底资料。方法选择历年从广东不同地区分离到的29株布鲁氏菌进行了菌体脂肪酸成分分析,利用MIDI公司Sherlock系统的软件进行聚类分析。结果广东布鲁氏菌的主要脂肪酸成分为19：0cycloω8c酸、16：0酸、18：0酸,其中牛种菌的19：0cycloω8c酸含量最高,羊种次之,猪种最低,其中羊种和猪种布鲁氏菌19：0cycloω08c酸、18：0酸含量差异有统计学意义,1965年和近3年的羊种布鲁氏菌株19：0cycloω8c酸、18：0酸含量差异有统计学意义。结论菌株的脂肪酸成分稳定,但各种间脂肪酸含量存在差异,一定的欧氏距离时,可以在种的水平上区分布鲁氏菌的3个种。     

2009年广东省甲型流行性感冒暴发流行期间首株甲型H1N1流行性感冒病毒血凝素基因分析

目的 检测和分析2009年广东省甲型流行性感冒(流感)暴发流行期间首株甲型H1N1流感病毒血凝素(HA)基因.方法 对2009年广东省首例确诊的甲型H1N1流感患者的咽拭子进行病毒分离,取细胞培养上清液提取病毒核酸,采用HA基因的特异性引物进行RT-PCR,PCR产物进行克隆、测序和同源性分析.结果 获得2009年广东省首株甲型H1N1流感病毒的HA基因,大小为1710 bp,命名为A/GuangzhouSB/01/2009(H1N1)HA,GenBank登录号为GQ268003.与疫情发源地近期报告的277株甲型H1N1流感病毒的HA基因比对,同源性为99.0%～99.8%;其中与美国报告的病毒株的同源性高达99.8%,与患者发病前曾到美国旅游的流行病学史一致.与25株中国季节性甲型H1N1流感病毒的HA基因比对,同源性为72.3%～85.6%.结论 2009年广东省甲型流感暴发流行期间首株甲型H1N1流感病毒与目前流行的甲型H1N1流感病毒同源性高,与中国季节性甲型H1N1流感病毒同源性较低.