出血性卒中与MTHFR C677T基因多态性的相关性研究

摘要 目的：探讨与分析出血性卒中与亚甲基四氢叶酸还原酶（MTHFR）C677T基因多态性的相关性。方法：2020年2月到2021年4月选择在本地区诊治的H型高血压患者220例作为研究对象,检测所有患者的MTHFR C677T基因多态性状况,检测血清同型半胱氨酸、叶酸、维生素B12含量。随访判定患者的出血性卒中状况并进行相关性分析。结果：随访调查1年,220例患者中出现出血性卒中20例（出血性卒中组）,占比9.1 %。出血性卒中组的血清同型半胱氨酸含量明显高于非出血性卒中组,血清维生素B12、叶酸明显低于非出血性卒中组（P<0.05）。两组的MTHFR C677T基因型分布均符合Hardy-Weinberg遗传平衡,出血性卒中组的TT基因型、等位基因T占比分别为70.0 %、80.0 %,都显著高于非出血性卒中组的24.0 %、35.0 %（P<0.05）。Spearman相关系数分析显示H型高血压患者的血清同型半胱氨酸、叶酸、维生素B12含量、TT基因型、等位基因T都与出血性卒中存在相关性（P<0.05）。多元回归分析显示血清同型半胱氨酸、叶酸、维生素B12含量、TT基因型、等位基因T都为导致H型高血压患者出血性卒中发生的重要因素（P<0.05）。结论：H型高血压在随访过程中容易发生出血性卒中,也伴随有血清同型半胱氨酸、维生素B12、叶酸含量异常,MTHFR C677T的T基因型、等位基因T与出血性卒中存在相关性,也是导致出血性卒中发生的重要危险因素。     

vWF与IL-6预测肾性高血压大鼠经历人工寒潮发生卒中的研究

目的:观察易卒中型肾血管性高血压大鼠(RHRSP)在经历人工寒潮中风前血液中vWF与IL-6含量变化从而预测中风的发生.方法:双肾双夹法制作RHRSP模型,经历人工寒潮并于寒潮前取血,酶联免疫吸附测定(ELISA)法检测vWF与IL-6含量.结果:脑梗塞组寒潮前vWF的表达明显高于非卒中组,脑梗死组和脑出血组寒潮前的IL-6含量明显高于非卒中组.结论:高血压患者血液中IL-6和vWF的含量可能预测经历寒潮时发生脑卒中的情况.     

进展性缺血性卒中预后的相关因素分析

目的:探究进展性缺血性卒中预后的相关危险因素。方法:选取进展性缺血性卒中患者98例,根据复发情况将患者分为复发组和无复发组,分析进展性缺血性卒中复发与二级预防的关系。无复发组的患者按根据随访的mRS评分高低分为:预后良好组(mRS 0~2分)和预后差组(mRS 3~5分),分析影响预后的相关因素。结果:98例进展性缺血性卒中患者六个月复发率为10.2%(10/98)。无复发组较复发组应用降压药、降糖药、抗血小板聚集药物、他汀类降脂药的患者比例较复发组高,两组比较差异均具有统计学意义(P0.05)。无复发组患者出院后一个月、三个月及六个月,单因素分析入院时白细胞计数、LDL、血糖与预后相关(P0.05)。多因素logistic回归分析LDL、血糖和白细胞计数是影响出院后一个月预后的危险因素;血糖和白细胞计数是影响出院后三个月预后的危险因素;LDL和血糖是影响出院后六个月预后的危险因素。结论:良好的二级预防依从性有利于降低进展性缺血性卒中的复发率。入院时白细胞计数、LDL、血糖是影响进展性缺血性卒中预后的相关因素。入院时白细胞计数、LDL及空腹血糖值较高的进展性缺血卒中患者,其预后往往较差。     

重症肺炎患者干扰素-r、IL-6 和TNF-alpha含量变化研究

目的：探究重症肺炎患者干扰素-r、白细胞介素-6 和肿瘤坏死因子-alpha含量变化及其临床意义。方法：选取我院收治并确诊 为肺炎的患者103 例,根据病情不同,将其分为重症肺炎组52 例及普通肺炎组51 例,同时选取同期参加健康体检人群50 例,为 对照组。比较三组成员不同时间段干扰素-r、白细胞介素-6 和肿瘤坏死因子-alpha含量,重症肺炎组患者存活与死亡组上述因子含 量情况。结果：入院6 h 后,与对照组比较,重症肺炎及普通肺炎组干扰素-r、白细胞介素-6 及肿瘤坏子因子-琢含量较高P＜ 0.05,与普通肺炎组比较,重症肺炎组重症肺炎组干扰素-r、白细胞介素-6 及肿瘤坏子因子-alpha含量较高P＜0.05;入院24 h后,与 对照组比较,重症肺炎组干扰素-r、白细胞介素-6 及肿瘤坏子因子-alpha含量较高P＜0.05,普通肺炎组与对照组比较无差异P＞ 0.05;重症肺炎死亡组患者干扰素-r、白细胞介素-6 及肿瘤坏子因子-alpha含量较高P＜0.05。结论：干扰素-r、白细胞介素-6 以及 肿瘤坏死因子-alpha参与患者的免疫调节,可间接提示患者的病程发展,可作为判断病情程度的有利依据。     

高血压病红／白细胞变形性的研究

本文观察了52例原发性高血压和24例正常人的红细胞、白细胞变形性,红细胞膜钙泵、钠泵活性,血粘度及血浆粘度,结果发现:原发性高血压组高、中切变率血粘度和钠泵活性显著高于正常组,红细胞变形性和钙泵活性显著高于正常组;红细胞变形性和钙泵活性显著低于正常组.白细胞变形性、低切变率血粘度及血浆粘度与正常组比较无显著差别.原发性高血压组红细胞变形性与年龄、平均动脉压、钙泵活性,高、中切变率血粘度相关.心痛定和川芎嗪治疗后,红细胞变形性显著改善,川芎嗪还能降低高切变率血粘度.结果提示:在高血压病中红细胞变形性降低、血粘度增高的分子水平机制主要是红细胞膜钙泵活性降低。基于微循环的改善,在扩大治疗例数后,心痛定和川芎嗪可能作为降压治疗的优选药与辅助药。     

硫酸镁联合硝苯地平治疗中重度妊娠高血压综合征患者的疗效观察

目的:探讨硫酸镁联合硝苯地平治疗中重度妊娠期高血压综合征的临床疗效。方法:选取2013年5月-2014年10月我院收治的中重度妊娠期高血压综合征患者70例,随机将患者分为研究组和对照组,每组35例。对照组患者应用硫酸镁治疗,研究组患者给予硫酸镁联合硝苯地平治疗,比较两组患者的临床疗效、血压变化、血液粘度、24 h尿蛋白含量以及血细胞压积情况。结果:研究组治疗总有效率显著优于对照组,差异具有统计学意义(P0.05);两组患者治疗后的血压水平显著低于治疗前,且研究组显著优于对照组,差异具有统计学意义(P0.05);两组患者治疗后的血液粘度、24 h尿蛋白含量及血细胞压积显著优于治疗前,且研究组优于对照组,差异具有统计学意义(P0.05)。结论:硫酸镁联合硝苯地平治疗中重度妊娠期高血压具有较好的临床疗效,能够显著改善患者的临床症状。     

血清胆红素水平与缺血性卒中的相关性研究

目的：脑卒中是威胁人类健康三大疾病之一,是我国成人致残的首要原因,其中80％是缺血性卒中。本文意在研究血清胆红素水平与缺血性卒中严重程度、发病机理以及颈动脉粥样硬化斑块的关系,以进一步为防治缺血性卒中的发生、发展提供新的途径。方法：选择缺血性脑卒中患者（观察组）150例和同期健康体检者（对照组）150例,分别测定两组的血清总胆红素水平（TBIL）、间接胆红素（DBIL）、直接胆红素（IBIL）,并对病例组进行TOAST分型、NIHSS评分及颈部血管超声检查。比较两组间血清胆红素,及观察组内不同分型组间血清胆红素的差异。结果：缺血性卒中患者TBIL、DBIL水平显著高于正常对照组,差异具有统计学意义（P〈0．05）。缺血性卒中患者按TOAST分型各亚型间血清TBIL、DBIL、IBIL水平差异无统计学意义（P〉0．05）。中重型脑梗死组与轻型脑梗死组比较,血清TBIL、DBIL、IBIL浓度均明显升高,差别具有统计学意义（P〈0．05）。缺血性卒中患者中有动脉粥样硬化斑块形成组血清TBIL、DBIL水平低于颈部动脉内膜光滑、完整者组,差别有统计学意义（P〉0．05）。结论：缺血性卒中患者血清胆红素升高,参与急性应激反应,可能作为衡量缺血性卒中严重程度的指标之一;高水平血清胆红素可能预防颈动脉粥样硬化斑块的形成,从而预防缺血性卒中的发生。     

原发性高血压合并冠心病患者血清CRP的变化

目的:探讨原发性高血压合并不同类型冠心病患者血清C-反应蛋白(CRP)的变化及其意义。方法:用全自动生化分析仪检测71例原发性高血压患者和28例健康对照组人群的血清CRP水平,所有研究对象均行选择性冠状动脉造影检查。将原发性高血压组病人根据冠脉造影检查分为单纯原发性高血压组(EH),原发性高血压合并稳定性心绞痛组(EH+SAP)、原发性高血压合并不稳定心绞痛组(EH+UAP)、原发性高血压合并心肌梗死组(EH+MI),比较各组患者血清CRP水平的差异。结果:①与对照组比较,EH组及EH合并CAD各组患者血清CRP均显著升高(P0.05);②与EH组比较,EH+UAP和EH+MI组血清CRP水平均显著升高(P0.01);③与EH+SAP组比较,EH+AMI组和EH+UAP组血清CRP水平均显著升高(P0.01)。结论:冠心病合并原发性高血压患者血CRP水平与冠状动脉病变程度与斑块稳定程度存在正相关性。     

进口预包装食品中钠、钾含量的现状分析

目的：了解市场上销售的进口高消费预包装食品钠、钾含量的现状。方法：通过对实体超市与网络超市中进口预包装食品的销量进行预调查,选取销量较高的8类预包装食品,每类食品采集至少5个品牌的样品,检测其钠、钾含量。结果：虾片、干脆面是本次调查钠含量最高的两类食品,钠钾比大于2.0;威化饼干钠含量较低,同时钾含量较高,钠钾比中位数为0.5;不同品牌同类预包装食品钠钾比值范围较广,最高值与最低值相差近25倍。结论：市场销售的预包装食品普遍都存在钠含量偏高钾含量偏低的状况,食品生产企业应探索减盐经验,进一步改善食品中钠钾比值。     

不同脑卒中风险中老年人群肠道菌群的差异

目的研究不同脑卒中风险中老年人群肠道菌群的差异,为后续研究提供参考。方法选取2017年2月至2019年2月来我院接受检查的中老年脑卒中风险者126例,根据不同卒中风险程度分为低危组(48例)、中危组(45例)、高危组(33例);同时进行认知功能筛查,选出轻度认知功能障碍患者35例为轻度障碍组,剩余91例认知功能正常者设为照组。采集所有受试者粪便并提取细菌DNA,分析肠道菌群构成情况;同时比较不同卒中风险者肠道短链脂肪酸水平并分析肠道菌群与认知功能的关系。结果低危组患者肠道菌群主要由瘤胃球菌科、柔嫩梭菌属、毛螺旋菌科、罗氏菌属及丁酸弧菌属构成。中危组患者肠道菌群主要由韦荣球菌科、埃希菌属及乳杆菌科构成。高危组患者肠道菌群主要由韦荣球菌科、肠杆菌科构成。低危组患者肠道瘤胃球菌科、毛螺旋菌科、普雷沃菌科丰富度显著高于中危组,肠杆菌科、韦荣球菌科、梭菌属及链球菌科丰富度显著低于中危组及高危组(均P0.05)。低危组患者肠道丁酸水平显著高于中危组和高危组(均P0.05)。轻度认知功能障碍患者肠道氨基酸球菌科、肠杆菌科、梭杆菌科丰富度显著高于对照组,而乳杆菌科、瘤胃菌科、毛螺菌科及普雷沃菌科丰富度显著低于对照组(均P0.05)。结论不同脑卒中风险及不同认知功能障碍中老年人肠道菌群存在显著差异。     

Sodium,potassium, and rate constants for sodium efflux in leucocytes from hypertensive Jamaicans.

Leucocyte sodium and potassium content and concentrations were measured along with ouabain-sensitive and ouabain-insensitive rate constants for sodium efflux in 14 controls and 20 black patients with essential hypertension. Leucocyte sodium content was significantly increased in the patients (mean 101.1 +/- 7.8 mmol/kg dry solids v 74.5 +/- 7.6 mmol/kg dry solids; p less than 0.05), whereas the rate constants for sodium efflux were not significantly reduced. There was no difference between the two groups in cell potassium values. The increase in leucocyte sodium content in the presence of normal rate constants for sodium efflux suggests an increase in membrane permeability to sodium, which might be important in the pathogenesis of essential hypertension.     

Calcium antagonists in hypertension: relation to abnormal sodium transport.

Leucocyte sodium efflux rate constants and intracellular electrolyte contents were estimated in 13 patients with untreated essential hypertension. There was no correlation between intracellular sodium or potassium content or efflux rate constant and blood pressure. The patients were then treated with oral nifedipine and blood pressure controlled. Sodium efflux rate constants and electrolyte contents were estimated one and three months after the start of treatment. There was a significant fall in blood pressure, but mean sodium efflux rate constant and intracellular sodium content were unchanged. There was no correlation between the fall in blood pressure, initial sodium efflux, or intracellular sodium content. These data do not support the hypothesis that the sodium pump and intracellular sodium content have a direct role in generating raised blood pressure, or that treatment of hypertension with calcium antagonists corrects a fundamental alteration of calcium-sodium exchange across the cell membrane.     

Dietary sodium and arterial blood pressure: evidence against genetic susceptibility.

Thirty five subjects with both parents in the top third of their age specific blood pressure distributions and 31 subjects with both parents in the bottom third of their blood pressure distributions restricted their intake of sodium for eight weeks while taking part in a double blind, randomised crossover trial of supplements of sodium and placebo. A comparison of two periods of four weeks at different intakes of sodium showed no differences in blood pressure in either the groups as a whole or the subgroups who complied best with the diet and tablets. In the compliant subgroups mean urinary sodium excretions were above 120 mmol(mEq) and below 50 mmol/day. The study provides evidence against the hypothesis that people with a family history of high blood pressure are more susceptible in their blood pressure response to dietary sodium.     

Genetic and epidemiological studies on electrolyte transport systems in hypertension

In recent years several different tests of cations in human cells have been studied to detect and to define possible roles in the development of essential hypertension. The goal of this report is to summarize what has been learned in genetic and epidemiological studies of human populations. The seven tests reviewed in greatest detail include sodium-lithium countertransport, intraerythrocytic sodium, sodium (or lithium)-potassium cotransport, lithium leak, sodium-potassium ATPase pump, sodium pump sites (ouabain binding), and circulating sodium pump inhibitor ('digoxin-like factor' in some studies). Countertransport, intraerythrocytic sodium and cotransport consistently show different values in hypertensives compared to normotensives and even in normotensives with a positive family history of hypertension when compared to controls without a positive family history. Thorough genetic studies have been carried out only for sodium-lithium countertransport and intraerythrocytic sodium. Both of these tests are highly heritable with a combination of both polygenic and major gene effects. Cotransport, leak, and pump sites also seem to be quite significantly heritable whereas the ATPase pump activity and the circulating pump inhibitor seem to be largely determined by nongenetic factors. Some of the most dramatic changes in these tests have been observed during pregnancy. Significant increases are seen in countertransport, cotransport, ouabain binding sites, and digoxin-like factor. Oral contraceptives also seem to affect at least cotransport. Plasma triglyceride level and body weight are some of the strongest correlates of countertransport, cotransport, and lithium leak. Cotransport increases with higher dietary sodium intake and decreases with the use of the diuretic medication. In the current developmental stage these tests have several significant limitations. In most population studies there is a considerable overlap of test values between persons with high and normal blood pressure. There are substantial variations in the methods used by different laboratories for the same tests. They are expensive, complex and usually must be done on fresh cells. There are conflicts between the results of several different reported studies that could be due to the way in which their subjects were selected, the effects of medications or other uncontrolled variables, or even due to the differences in laboratory methodologies.(ABSTRACT TRUNCATED AT 400 WORDS)     

Type 2 diabetes, impaired glucose tolerance, and hypertension in offspring of migrants and the structure of the population of origin

Data collected from Nisei men and women, offspring of immigrants to the United States from Japan, were examined for evidence of possible genetic heterogeneity in Japan with respect to type 2 diabetes or non-insulin-dependent diabetes mellitus (NIDDM), impaired glucose tolerance (IGT), and hypertension. The subjects were 391 men and women with a mean age of 62.0 (+/- 0.3) years. Patterns of disease expression in the Nisei with respect to the origins in Japan of their parents indicated that the genetic basis for NIDDM may be more frequent in northern Honshu than in southwestern Honshu, whereas that for IGT may be more frequent in southwestern Honshu. Further analyses indicate that the pattern for IGT is restricted to men. Hypertension appears more frequently in persons with parents from northern Honshu and less frequently in women but not in men from southwestern Honshu. For men an analysis of age and family history of diabetes by oral glucose diagnostic category revealed the presence of a group of younger men with IGT but, surprisingly, no family history of diabetes. Thus the data show an apparent lack of the consistency expected if diabetes and IGT simply represent stages of one disease entity. We suggest that IGT may represent a heterogeneous category including both an early or transitional stage of NIDDM and another condition found primarily in men in which less severe glucose tolerance appears and with which hypertension may be associated. Data on ancient settlement in Japan suggest a possible historical basis for the patterns found.     

Water, cations, and norepinephrine content of cardiovascular tissues of unilaterally nephrectomized dogs treated with deoxycorticosterone and NaCl.

Deoxycorticosterone pivalate (2.5 mg/kg) given intramuscularly on four occasions 10-15 days apart over a period of 45 days to unilaterally nephrectomized adult male mongrel dogs, receiving as drinking solution 0.9% NaCl in 5% dextrose, resulted in an average sustained rise in the mean arterial blood pressure of 30 mm Hg (1 mm Hg - 133 N/m2) in 60% of the animals. Hypertensive dogs had in their arterial tissues generally more sodium, potassium, magnesium, and calcium than the similarly treated but non-hypertensive dogs, but compared to the tissues of operated untreated or unoperated normotensive dogs, only sodium and calcium were significantly higher. The dogs who were similarly treated but did not develop hypertension had in their arterial tissues less sodium, potassium, and magnesium than operated untreated or unoperated normotensive dogs. Norepinephrine content in the branches of mesenteric arteries of all deoxycorticosterone- and NaCl-treated animals, irrespective of their blood pressure, was significantly lower, and in the myocardium significantly higher, than either the unoperated normotensive or operated but not further treated dogs. It is concluded, therefore, that in deoxycorticosterone + NaCl treatment the dogs which developed hypertension had more arterial sodium, potassium, magnesium, and calcium than those who were similarly treated but remained within the limits of normal blood pressure, and that there was no difference between hypertensive and non-hypertensive dogs in regard to their cardiovascular norepinephrine content.     

Estimating the magnitude of genetic factors by calculating the genetic relative risk of stroke in first-ever lacunar stroke patients

Background

Positive family history of stroke is an independent risk factor for lacunar stroke. However, the magnitude of familial aggregation of a certain disease is better evaluated by the genetic relative risk. This is calculated by dividing the prevalence of specific disease in family members of patients by the prevalence of this disease in the general population. In a cohort of lacunar stroke patients, who were subtyped clinically and radiologically, we determined the genetic relative risk of stroke.

Methods

By questionnaire and additional interview, we obtained a complete first-degree family history of stroke. The prevalence of stroke in first-degree relatives of these lacunar stroke patients was compared to the self-reported prevalence of stroke in a Dutch community based cohort of elderly volunteers. Secondly, the influence of proband characteristics and family composition on parental and sibling history of stroke were evaluated.

Principal Findings

We collected data of 1066 first-degree relatives of 195 lacunar stroke patients. Strokes occurred in 13.5% of first-degree relatives. The genetic relative risk was 2.94 (95%CI 2.45–3.53) for overall first-degree relatives, 4.52 (95%CI 3.61–5.65) for patients'' parents and 2.10 (95%CI 1.63–2.69) for patients'' siblings. Age of proband and proband status for hypertension influenced the chance of having a parent with a history of stroke whereas the likelihood of having a concordant sibling increased with sibship size.

Conclusions

We found an increased genetic relative risk of stroke in first-degree relatives of patients with lacunar stroke. Our data warrant further genomic research in this well-defined high risk population for stroke.     

Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects

Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.     

Subcellular compartmentation of elements in non-mycorrhizal and mycorrhizal roots of Pinus sylvestris: an X-ray microanalytical study. II. The distribution of calcium, potassium and sodium

The inter- and intracellular distribution of the elements calcium, potassium and sodium in non-mycorrhizal and mycorrhizal roots of Pinus sylvestris dependent on different external nutrient supply conditions was detected by energy-dispersive X-ray microanalysis after cryofixation, freeze-drying and pressure infiltration of the material. In non-mycorrhizal and mycorrhizal roots, calcium was mainly detectable in the apoplastic regions. The levels in vacuoles and cytoplasm were near the limits of detection by X-ray microanalysis. Incubation with high concentrations of potassium and sodium, or mycorrhizal infection with Suillus bovinus and Pisolithus tinctorius reduced the amounts of calcium detectable in the roots, especially in the apoplast of cortical cells. The studies revealed that: potassium is mainly localized in cytoplasm and cell walls; the cytoplasmic content is regulated over a wide range of external potassium concentrations; potassium levels in the inner parts of roots are higher than in the outer parts. Mycorrhizal infection with Suillus bovinus had no effect on the inter- and intracellular distribution of potassium in roots but, if the external supply was low, the potassium content in shoots was reduced. In non-mycorrhizal pine roots and those infected with Paxillus involutus an increase in the sodium content of all cell compartments was observed after treatment with high external concentrations of NaH₂PO₄. However, an increase in sodium content in mycorrhizas of S. bovinus was not detected. The X-ray microanalytical results are discussed in relation to the apoplastic movement of nutrients in non-mycorrhizal and mycorrhizal fine roots of pine and to the demand for these nutrients in different intracellular compartments.     

Velopharyngeal variations in relatives of cleft-affected individuals

Eighteen families each with two or more cleft lip and palate patients were studied by speech cephalometry for evidence of velopharyngeal inadequacy (VPI). With this total of 56 persons, three groups were recognized: 1) patients with cleft lip only (N = 7), 2) unaffected sibs of CL(P) probands and the unaffected parents with the positive clefting history on their side of the family (N = 33), and 3) unaffected parents with negative CL(P) history to their side of the family (N = 16). The latter served as controls. The velopharyngeal mechanism in function was evaluated by voicing the fricative/S/. The results showed no significant differences in the length of either the resting soft palate or pharyngeal depth among the three groups. Even though a significant (P less than 0.01) increase in soft palate length while voicing /S/ was found in group 2 relatives compared to group 3 controls, the failure to find differences in either resting palate length or pharyngeal depth coupled with a failure to demonstrate VPI in group 2 subjects by speech testing leaves the value of this observation uncertain.