出生体重对学龄前期儿童生长发育影响分析

【目的】分析出生体重对儿童在其婴儿至学龄前期体格发育的影响及其血红蛋白（hemoglobin，Hb）水平改变。【方法】3～6岁儿童268名，孕周〉36周，性别不限。记录人体测量指标：出生体重及6个月、1岁、3～6岁时身高、体重。问卷调查其早期喂养特点包括完全母乳喂养时间、辅食添加起始月份、母亲育龄、家庭经济状况等内容。血液检查测定外周Hb值。按出生体重和性别分成四组，A组（男）和C组（女）出生体重2000～2999g；B组（男）和D组（女）出生体重3000～3999g。【结果】婴儿期B组和D组体重均分别明显高于A组和C组（=P〈0．05）；学龄前期B组和D组身高均分别明显高于A组和C组（P〈0．05）。B组和D组儿童身长、体重均数值位于1995年中国城区儿童身高体重百分位数表P45～P85之间，A组和C组则位于P3～P30之间。出生体重较轻婴儿0～6个月中体重增速快于出生体重较重组（P〈0．05）。出生体重较高的女童（D组）Hb水平轻度降低（110〈Hb〈120g／L）发生率明显高于其他各组（P〈0．05）。【结论】在早期喂养和家庭经济状况相当的情况下．出生体重影响婴儿至学龄前期体格增长。出生体重较轻者易发生长迟缓，追赶生长多发生在O～6个月中。出生体重较高者体格增长较理想，然而在学龄前期较易发生Hb轻度下降，考虑应作为铁营养重点关注人群。     

糖化血红蛋白测定在妊娠糖尿病诊断中的临床意义

目的:探讨糖化血红蛋白在妊娠糖尿病诊断中的临床意义。方法:对正常妊娠组60例、糖耐量异常组60例及糖尿病组56例等血清进行FPG、口腹50g葡萄糖筛选实验和HbAIc的测定。结果:HbA lc的阳性率在正常妊娠组、糖耐量异常组和GDM组中分别为3.33%、25%和80.4%,GDM组与正常妊娠组和糖耐量异常组相比均有显著性差异(P<0.05),空腹血糖阳性率在三组中分别为8.33%、10%和37.5%,糖筛查实验阳性率在三组中分别为20%、20%和83.9%,妊娠糖尿病的并发症随HbAIc的增高而增多。结论:HbAIc在妊娠糖尿病诊断和监测中具有重要意义。     

多项血糖指标对急性冠脉综合征患者30天心力衰竭的预测价值

目的：研究急性冠脉综合征（ACS）患者糖化血红蛋白（HbA1c）、入院血糖（AG）及第二日清晨空腹血糖（FG）值对发病30天时发生心力衰竭（HF）的预测价值。方法：测定102例ACS患者的HbA1c、AG及FG值。根据发病30天时有无HF分为两组，观察上述指标与HF的关系。结果：102例ACS患者的HbA1c（P=0．046）和FG（P=0．044）与30天的HF预后相关，且HbA1c（P=0．017）为ACS30天HF预后的独立危险因子。结论：高血糖能预测ACS近期HF发生。HbA1c是ACS短期HF预后的独立危险因子。     

补脾肾活血法防治糖尿病肾病机理探讨

目的观察补脾肾活血方对糖尿病大鼠肾脏病变的影响,以探讨其防治糖尿病肾病的机制.方法用链脲佐菌素(STZ)制备糖尿病大鼠模型,12周后,测定肾功能指标、糖化血红蛋白(GHb)、血清和肾皮质糖基化终产物(AGEs)水平,并对大鼠肾脏进行光镜和电镜观察.结果补脾肾活血中药治疗后肾功能指标、血糖、糖化血红蛋白、血清和肾皮质AGEs都显著低于糖尿病组(P＜0.01 或 P＜0.05),且肾脏病理改变得以改善.结论补脾肾活血中药能够通过降低血糖、减少尿蛋白和抑制蛋白非酶糖化防治糖尿病肾病的发生.     

Fe3+及血红蛋白铁对眼源性蜡样芽胞杆菌生长能力的影响

目的 探讨Fe³⁺及血红蛋白铁对眼源性蜡样芽胞杆菌生长能力的影响。方法 实验研究。收集2011年6月至2017年2月温州医科大学附属眼视光医院外伤性蜡样芽胞杆菌性眼内炎患者26例并分离出蜡样芽胞杆菌26株。根据患者治疗后有无光感将菌株分为有光感（LP）组和无光感（NLP）组,以蜡样芽胞杆菌模式菌株ATCC14579作为对照组,检测不同菌株在缺铁环境、不同Fe³⁺浓度环境、富含Hb环境中生长的光密度（OD）值。采用独立样本t检验对数据进行统计分析。结果 26株眼部来源的蜡样芽胞杆菌在缺铁环境中生长的OD值小于模式菌株ATCC14579（t=54.098,P<0.001）。在一定范围内（0~500 μmol/L）增加Fe³⁺浓度,菌株生长的OD值随之逐渐增加,当Fe³⁺浓度高于1 000 μmol/L时,细菌生长的OD值开始下降。在Fe³⁺或血红蛋白铁为主要铁资源的环境中,NLP组菌株生长的OD值均高于LP组（t=2.618,P=0.015;t=2.202,P=0.037）。结论 眼源性蜡样芽胞杆菌的生长对Fe³⁺具有较强的依赖性;在Fe³⁺或血红蛋白铁为主的铁资源环境中生长较快的菌株感染患者,其临床预后较差。     

Higher executive abilities following a blood transfusion in children and young adults with sickle cell disease

Individuals with sickle cell disease (SCD) experience cognitive deficits; however, it remains unclear whether medical treatments for SCD improve cognition. Given that executive abilities are typically impaired in individuals with SCD, they were the focus of the current study. Our primary hypothesis was that executive abilities would be higher acutely soon after a blood transfusion in children and young adults with SCD. We used tests from the NIH Toolbox to assess executive abilities in 27 participants with SCD receiving chronic transfusion in comparison to 34 participants with SCD receiving hydroxyurea (HU) and 41 non‐SCD demographically matched controls, all of whom were tested at two time points. Participants in the transfusion group completed cognitive testing within 3 days after a transfusion (soon after transfusion) and then within 3 days before their next transfusion (long after transfusion) over an interval of 3‐7 weeks. We found that executive abilities were significantly poorer for the transfusion and HU groups than for the control group. In support of our primary hypothesis, executive abilities for the transfusion group were significantly better soon after a transfusion compared to long after a transfusion, χ²(1) = 17.8, P < .0001. Our results demonstrate that executive abilities were higher acutely following a blood transfusion. These findings have implications for daily functioning, medical decision making, and academic achievement in children and young adults with SCD.     

Hb Manukau [β67(E11)Val → Gly; HBB: c.203T>G]: The Role of Genetic Testing in the Diagnosis of Idiopathic Hemolytic Anemia

The increasing availability of DNA sequencing of globin genes has improved our ability to detect conditions that were presumed to be extremely rare. These conditions may remain undiagnosed due to unfamiliarity with clinical presentation, relative unavailability of advanced diagnostic alternatives, or may defy detection by being electrophoretically silent or extreme instability rendering their presence to be below detection level. Genetic studies were pursued in a mother and daughter with severe hemolytic anemia as initial testing failed to be diagnostic. DNA sequence analysis of the β-globin gene identified Hb Manukau [β67(E11)Val?→?Gly; HBB: c.203T?>?G], an extremely unstable hemoglobin (Hb) variant. This is the second family described with this condition (first in the western hemisphere). An astute clinician may benefit from being persistent and pursuing additional testing including molecular genetic characterization where clinical suspicion remains high.     

Investigation on the interaction of the toxicant,gentian violet,with bovine hemoglobin

Gentian violet (GV) is a well-known triarylmethane dye that is used in aquacultural, industrial and medicinal fields. But concerns in growing number have been paid to its potential health problems to human beings and its hazardous effects to environment. Herein, the toxic interaction of GV with bovine hemoglobin (BHb) was investigated by a series of spectroscopic methods and molecular modeling method. The fluorescence emission profile exhibited a remarkable quenching upon addition of GV to the buffered aqueous solution of BHb and the analysis of results revealed the dominant role of static quenching mechanism in GV–BHb interaction. The negative ΔH and positive ΔS values demonstrated that the electrostatic interactions mainly stabilized this toxicantprotein complex. Synchronous fluorescence, UV–Vis absorption and CD spectroscopic studies proved that the conformational change of BHb was induced by GV’s combination. Molecular modeling studies exhibited the binding mode of GV–BHb complex and the detailed information of related driving forces. During the ¹H nuclear magnetic resonance spectra (¹H NMR) study, the chemical shift perturbation and spin–lattice relaxation times of different protons were further used to investigate the interaction of GV with BHb and the results indicated that GV bound orientationally to BHb.     

Fetal Hemoglobin in the Maternal Circulation – Contribution of Fetal Red Blood Cells

The major hemoglobin (Hb) during fetal life is fetal Hb (Hb F). It is mostly replaced by adult Hbs before birth and during the first year of life. In adults, where Hb F comprises <2.0% of the total Hb, it is not homogenously distributed among the red blood cells (RBCs) but is concentrated in a few RBCs, termed F-cells. Interestingly, for reasons that are unclear, Hb F increases in the maternal circulation during pregnancy. This increased Hb F could have two potential origins that are not mutually exclusive: A) maternal origin, due to inducing environment of Hb F in the maternal erythroid precursors; B) fetal origin, due to fetal cells crossing the placenta and entering the maternal circulation. The question we present herein is whether the observed increased Hb F in the maternal circulation during pregnancy is, at least partially, derived from the fetal origin. Peripheral blood was obtained from normal neonates (1–3 days old), adult men and pregnant and non pregnant women. The RBCs were stained for Hb F and carbonic anhydrase (CA) using a fetal cell count kit and analyzed by flow cytometry. Fetal and adult F-cells were distinguished by their expression of Hb F and CA. Fetal F-cells were Hb F⁺⁺/CA^?, while adult F-cells were Hb F⁺/CA⁺. Comparing pregnant and non pregnant women samples (n?=?10), we found six samples of pregnant women with 0.2–1.7% fetal cells, but none in the non pregnant group. These results support the possibility that at least part of the increase in Hb F during pregnancy is due to fetal cells entering the maternal circulation.