Using structural equation modelling to understand the contributors to anaemia among young Burkinabe children

Anaemia is a persistent problem among young Burkinabe children, yet population‐specific information on its determinants is scant. We used baseline data from an evaluation of Helen Keller International's Enhanced Homestead Food Production Program (n=1210 children) to quantify household‐, mother‐, and child‐level factors associated with anaemia in Burkinabe children aged 6‐12 months. We used structural equation modelling to assess a theoretical model, which tested four categories of factors: (a) household food security and dietary diversity, (b) household sanitation and hygiene (latrine and poultry access and bednet ownership), (c) maternal factors (anaemia, stress, cleanliness, and health, hygiene and feeding knowledge and practices), and (d) child nutrition and health (iron deficiency (ID), retinol binding protein (RBP), malaria, and inflammation). The model also included household socio‐economic status, size, and polygamy; maternal age and education; and child age and sex. Results showed that ID, malaria, and inflammation were the primary direct determinants of anaemia, contributing 15%, 10%, and 10%, respectively. Maternal knowledge directly explained improved child feeding practices and household bednet ownership. Household dietary diversity directly explained 18% of child feeding practices. Additionally, RBP, child age and sex, and maternal anaemia directly predicted child haemoglobin. Our findings suggest that program effectiveness could be increased by addressing the multiple, context‐specific contributors of child anaemia. For young Burkinabe children, anaemia control programs that include interventions to reduce ID, malaria, and inflammation should be tested. Other potential intervention entry points suggested by our model include improving maternal knowledge of optimal health, hygiene, and nutrition practices and household dietary diversity.     

Changes in iodine status among US adults, 2001–2012

Urinary iodine concentrations (UICs) in the US have been reported to be stable since 1988–1994, although those in selected subgroups remained low. We aimed to investigate iodine status among adults (≥20 years) by two different criteria of assessing iodine deficiency in population. Utilizing National Health and Nutrition Examination Surveys 2001–2012, we conducted linear logistic regressions adjusting for covariates. The prevalence of <50?μg/L UIC was higher in women than in men; increased from 11.6% (2001–2004) to 13.2% (2009–2012) at the national level and in young adults, non-Hispanic blacks (NHBs) and non-users of iodine-containing supplements (all, p?<0.05); the adjusted odds ratios (95%CI) in young adults (1.54 [1.11–2.15], p =?0.0007) and NHBs (1.70 [1.15–2.52], p =?0.0078). Median UICs confirm women and NHBs being in borderline iodine status. Recognizing the critical consequence of iodine deficiency particularly in women and NHBs, regular monitoring of iodine status is important for public health in the US.     

通心络胶囊联合阿托伐他汀及氯吡格雷治疗冠心病心绞痛临床研究

目的:观察通心络胶囊联合阿托伐他汀、氯吡格雷治疗冠心病心绞痛的临床疗效。方法:选取84例冠心病心绞痛患者,按随机数字表法分为观察组与对照组,对照组40例给予阿托伐他汀联合氯吡格雷治疗,观察组44例在对照组基础上给予通心络胶囊治疗,3个月后比较2组临床疗效。结果:观察组总有效率(93.18%)显著高于对照组(70.00%),差异有统计学意义(P<0.05)。治疗前,2组心绞痛的持续时间、心绞痛发作次数、心功能指标、血管内皮功能指标比较,差异无统计学意义(P>0.05)。治疗后,2组心绞痛持续时间、心绞痛发作次数较治疗前明显降低,观察组心绞痛持续时间、心绞痛发作次数显著低于对照组(P<0.05);2组心功能指标包括心输出量(CO)、心博出量(SV)、心脏指数(CI)及射血分数(EF)均较治疗前明显上升,且观察组各项心功能指标明显高于对照组(P<0.05);2组内皮功能指标内皮素(ET)、血栓素B2(TXB2)水平较治疗前明显降低,一氧化氮(NO)水平较治疗前明显上升(P<0.05),观察组ET、TXB2水平明显低于对照组,NO水平明显高于对照组(P<0.05)。结论:对冠心病心绞痛患者给予通心络胶囊联合阿托伐他汀、氯吡格雷治疗疗效显著,可有效降低心绞痛持续时间和发作次数,改善患者心功能和内皮功能,值得临床推广应用。     

微小RNA在皮肤鳞状细胞癌中的研究进展

皮肤鳞状细胞癌(cSCC)是角质形成细胞来源的恶性肿瘤之一。转录组是特定条件下细胞内全部转录产物的总和,包括编码mRNA和非编码RNA。研究发现,与正常细胞相比,鳞癌细胞在基因转录水平和模式上存在很大差异,具有不同转录表达谱。微小RNA(miRNA)可通过抑制转录产物的翻译,从而调控靶基因的表达,影响cSCC细胞的增殖、分化和凋亡等病理过程。越来越多的研究表明,miRNAs作为cSCC诊断、预测预后和治疗靶点的生物标志物,在临床上具有广阔的应用前景。本文通过回顾分析cSCC的miRNA表达谱,主要对其中经实验证实表达上调和下调的miRNAs在cSCC中的研究进展作一综述。     

CYP17基因新的突变导致两姐妹17α羟化酶/17,20裂链酶联合缺乏

目的分析一家庭中患17α羟化酶／17，20裂链酶联合缺乏症的两姐妹及其父母的CYP17基因序列。方法外周血中提取基因组DNA。设计引物行PCR反应并对PCR产物进行序列测定。结果两姐妹均表现为典型的17α羟化酶／17，20裂链酶联合缺乏，其CYP17基因均为985缺失TAC插入AA的纯合子突变，而其父母是杂合子突变。结论985缺失TAC插入AA杂合子仅是一遗传标志，并不能引起疾病，但这种纯合子突变或在此基础上再发生另一突变可导致疾病的发生。     

Leber’s hereditary optic neuropathy and vitamin B12 deficiency

Background Leber’s hereditary optic neuropathy (LHON) is a maternally inherited optic neuropathy caused by mutations in mitochondrial DNA (mtDNA). It is also believed that several epigenetic factors have an influence on the development of LHON.Methods A case series was observed.Results Three patients who developed bilateral optic neuropathy are presented. All patients had a primary LHON mutation in their mtDNA, but also a subnormal vitamin B12 serum level at the time of presentation.Conclusions The clinical picture of optic neuropathy associated with vitamin B12 deficiency shows similarity to that of LHON. Both involve the nerve fibres of the papillomacular bundle. The present case reports suggest that optic neuropathy in patients carrying a primary LHON mtDNA mutation may be precipitated by vitamin B12 deficiency. Therefore, known carriers should take care to have an adequate dietary intake of vitamin B12 and malabsorption syndromes like those occurring in familial pernicious anaemia or after gastric surgery should be excluded.     

国产rhGH的免疫原性及其对临床疗效的影响

目的　通过测定生长激素缺乏症 (GHD)患儿用国产重组人生长激素 (recom bined hum angrowth horm one,rh GH)治疗时血清生长激素抗体 (GH- Ab)水平及其结合特性 ,探讨 rh GH的免疫原性及其对疗效的影响。方法　对 6 1例 (男 49例 ,女 12例 ) GHD患儿用国产 rh GH治疗 ,每晚睡前皮下注射 rh GH 0 .1IU /kg共6个月 ;用放射免疫法测定治疗期间患儿血清 GH- Ab水平和滴度 ,并计算抗体结合容量、亲和常数 (Ka)。结果　48%患儿 (2 9/6 1)用药后 3个月血清 GH - Ab呈阳性至试验结束时仍未消失 ,其中 2 0例抗体为弱阳性 (结合率 <10 % ) ,9例呈强阳性 (结合率 >15 % ) ;5 2 %患儿 (32 /6 1)治疗期间抗体为阴性 ;血清 GH- Ab的结合容量、Ka及滴度均为低水平 ,分别为 (0 .1～ 4.8) pmol/L、(1.7× 10 7～ 6 .5× 10 8) L /mol和 1∶ 4～ 1∶ 8。GH- Ab阳性患儿治疗后的身高、身高增长速率及身高落后于正常 SD值的变化与同期阴性者比较无统计学差异 (P>0 .0 5 )。结论　本试验所用国产 rh GH对 GHD患儿身高增长具有确切的促进作用 ,其免疫原性所导致产生的 GH - Ab未对患儿体格线性增长产生负性影响     

Transient low level of IgG3 induced by sepsis

Staphylococcus aureus sepsis developed in a 14 year old girl. Immunological evaluation revealed low level of IgG3, although total IgG level was normal. The level of IgG3 increased gradually along with the recovery from sepsis. Immunoglobulin replacement therapy might have been useful in this patient, even though the total immunoglobulin level was within normal limits.     

D1 Dopamine receptor-mediated substance P depletion in the striatonigral neurons of rats subjected to neonatal dopaminergic denervation: implications for self-injurious behavior

The present study examined the influences of dopamine (DA) receptor stimulation on enkephalin (Met5-enkephalin; ME) and tachykinin (substance P; SP) systems of basal ganglia of Sprague-Dawley rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA). It has been proposed that the neonatal 6-OHDA-lesioned rat could serve as a model for the DA deficiency and self-injurious behavior (SIB) observed in the childhood neurological disorder. Lesch-Nyhan syndrome. In agreement with earlier work, the present study found that the neonatal 6-OHDA treatment at 3 days of age, reduced DA and caused an increase in ME and a decrease in SP content in the striatum and substantia nigra, when tested as adults. Administration of the DA precursor, L-dihydroxyphenylalanine (L-DOPA), to lesioned animals, induced SIB; increased DA and DOPAC levels; produced a greater decrease (-64%) in SP levels in the striatum and substantia nigra than was observed with lesion alone (-28%). The L-DOPA-induced decrease in SP levels and the SIB observed in the lesioned animals were blocked by pretreatment with the D1 receptor antagonist, SCH-23390. Moreover, administration of the D1 receptor agonist, SKF-38393, but not the D2 agonist, LY-171555, to lesioned animals mimicked the L-DOPA responses in all respects, except that the agonists did not alter DA or DOPAC levels. None of the DA agonists or antagonists treatments affected lesion-induced increase in ME levels in the striatum. These results indicate for the first time, that SIB precipitated by DA agonists in neonatal dopaminergic denervated animals, is associated with a marked and selective decrease in SP in the striatonigral SP neurons. This process has two components: (a) a retarded development of the SP system due to neonatal dopaminergic denervation: and (b) a depletion of the remaining SP, presumably by enhanced release due to D1 DA receptor-mediated activation of striatonigral SP neurons.     

A HIGH FREQUENCY OF INHERITED DEFICIENCY OF COMPLEMENT COMPONENT C4 IN DARWIN ABORIGINES

Abstract A high frequency of serum complement component C4A deficiency may explain the higher prevalence and greater severity of systemic lupus erythematosus reported in Australian Aborigines. Inherited deficiencies of serum complement components C4A, C4B, and C2 were examined in two Australian Aboriginal populations from Darwin and Alice Springs and compared with the prevalence of complement deficiencies in white Australian blood donors. The frequency of C4A deficiency alleles was 29% in Darwin Aborigines compared with 12% in Alice Springs and 17% in Canberra blood donors. Partial C4B deficiency was also higher in Darwin Aborigines than in the other populations. Inherited deficiency of serum complement component C2 was not observed.