2004～2010年日照市部分居民户碘盐监测分析

[目的]了解居民户食用盐的碘含量情况,以便采取针对性的防控措施,为持续性消除碘缺乏病工作提供参考依据。[方法]对2004～2010年日照市居民户食用盐监测资料进行分析。[结果]2004～2010年累计检测7 760份居民户食用盐,合格碘盐7 362份,不合格碘266份,非碘盐132份,碘盐覆盖率为98.30%,碘盐合格率为96.51%,合格碘盐食用率为94.87%,非碘盐率为1.70%,盐碘中位数为29.30mg/kg。2004～2010年,碘盐合格率分别为95.11%、96.65%、92.58%、96.70%、97.30%、98.60%、98.20%,合格碘盐食用率分别为94.56%、95.27%、91.34%、92.60%、95.60%、97.60%、96.90%。东港区、岚山区、莒县、五莲县,碘盐合格率分别为95.59%、95.15%、96.95%、98.11%,合格碘盐食用率分别为93.50%、91.65%、96.03%、97.82%。[结论]日照市碘盐质量稳定,居民合格碘盐食用率符合国家消除碘缺乏病的标准。     

艾滋病毒感染者和艾滋病患者死亡危险因素的研究进展

艾滋病已在全球广泛流行,由于艾滋病患者的临床表现多样,病情进展快,死亡率高,如何降低HIV感染者和艾滋病患者的死亡率已成为当前艾滋病防治的重要任务.HIV感染者和艾滋病患者的死亡与多种因素有关,既涉及宿主本身的因素,又涉及病毒方面的因素,还有治疗及其他社会心理因素等.此文主要对国内外在HIV感染者和艾滋病患者死亡危险因素的相关研究作一综述.     

The nerve-heart connection in the pro-oxidant response to Mg-deficiency

Magnesium is a micronutrient essential for the normal functioning of the cardiovascular system, and Mg deficiency (MgD) is frequently associated in the clinical setting with chronic pathologies such as CHF, diabetes, hypertension, and other pathologies. Animal models of MgD have demonstrated a systemic pro-inflammatory/pro-oxidant state, involving multiple tissues/organs including neuronal, hematopoietic, cardiovascular, and gastrointestinal systems; during later stages of MgD, a cardiomyopathy develops which may result from a cascade of inflammatory events. In rodent models of dietary MgD, a significant rise in circulating levels of proinflammatory neuropeptides such as substance P (SP) and calcitonin gene-related peptide among others, was observed within days (1–7) of initiating the Mg-restricted diet, and implicated a neurogenic trigger for the subsequent inflammatory events; this early “neurogenic inflammation” phase may be mediated in part, by the Mg-gated N-methyl-D-aspartate (NMDA) receptor/channel complex. Deregulation of the NMDA receptor may trigger the abrupt release of neuronal SP from the sensory-motor C-fibers to promote the subsequent pro-inflammatory changes: elevations in circulating inflammatory cells, inflammatory cytokines, histamine, and PGE₂ levels, as well as formation of nitric oxide, reactive oxygen species, lipid peroxidation products, and depletion of key endogenous antioxidants. Concurrent elevations of tissue CD14, a high affinity receptor for lipopolyssacharide, suggest that intestinal permeability may be compromised leading to endotoxemia. If exposure to these early (1–3 weeks MgD) inflammatory/pro-oxidant events becomes prolonged, this might lead to impaired cardiac function, and when co-existing with other pathologies, may enhance the risk of developing chronic heart failure.     

Visceral Manifestation of Cat Scratch Disease in Children. A Consequence of Altered Immunological State?

Summary A 12-year-old girl with a 2-month history of fever and abdominal pain was admitted to our hospital. Ultrasound and CT scans of the abdomen showed multiple hypoechoic lesions of liver and spleen. Screening for zoonosis revealed high positive titers to Bartonella henselae. T-cell deficiency was demonstrated and remained almost unchanged during a follow-up of 11 months. A review of the literature shows that disseminated visceral affection is a rare presentation of cat scratch disease (CSD) in childhood and adolescence. Further immunological investigations are needed in more patients with CSD to confirm whether an altered imunological state may be responsible for the atypical visceral manifestation of CSD. Received: May 18, 1999 · Revision accepted: January 19, 2000     

Recombinant factor VIIa prophylaxis in a patient with severe congenital factor VII deficiency

Use of recombinant factor VIIa (rFVIIa, NovoSeven in patients with congenital FVII deficiency has been reported for the prophylactic management of surgical bleeding and for the treatment of acute bleeding episodes. Because of its short half-life, the use of rFVIIa on a regular prophylactic regimen has not been routinely adopted. In this report, we describe our successful experience with rFVIIa prophylaxis in preventing recurrent target joint bleeding in a severely FVII-deficient adolescent.     

GlARDlA INFECTION CAUSES VITAMIN B12 DEFICIENCY

Abstract A patient presented with hematological evidence of vitamin B12 deficiency. The Schilling test performed suggested intestinal malabsorption and further investigation revealed heavy infestation with Giardia lamblia. Specific treatment of the giardiasis with tinidazole resulted in correction of the abnormalities in vitamin B12 absorption. These findings, together with the absence of other causes of vitamin B12 deficiency, suggest that giardiasis should be considered as a cause of vitamin B12 deficiency.     

A novel two base pair deletion in the factor V gene associated with severe factor V deficiency

We studied a family in which the proband, a 13-year-old boy, had unmeasurable plasma levels of coagulation factor V antigen and activity. Clinical symptoms were severe, with several episodes of haemorrhages in the mucosal tracts (gastrointestinal, nose and urinary) and recurrent haemarthroses that caused permanent arthropathy. Sequence analysis of the factor V gene demonstrated the presence of a novel 2 base pair (bp) homozygous deletion in exon 13 at positions 2833-2834. This mutation, present in the heterozygous state in the asymptomatic mother and absent in the healthy brother, introduced a frameshift and a premature stop at codon 900. This would predict the synthesis of a truncated factor V molecule, lacking part of the B domain and the complete light chain. Because of the existence of a surveillance mechanism that selectively recognizes and degrades mRNA molecules carrying premature termination codons, we analysed the relative abundance of mutant vs. wild-type mRNA molecules in the platelets of the heterozygous proband's mother. The mutant mRNA was significantly reduced in amount (mutant/wild-type ratio 0.35). This is the first reported mutation in the factor V gene causing severe factor V deficiency, the effect of which was quantitatively analysed at mRNA level.     

Red cell glucose-6-phosphate dehydrogenase status and pyruvate kinase activity in a Nigerian population

Glucose-6-phosphate dehydrogenase A- (G6PD A-) deficiency is a common enzymopathy in Africa that sporadically leads to manifest haemolytic anaemia. It is not exactly known how far the haematological status of individuals with either homozygous or heterozygous G6PD A- deficiency differs from that of individuals with normal G6PD activity. In a field study in Nigeria, we determined G6PD gene variants, the corresponding G6PD and pyruvate kinase (PK) activities, and basic haematological parameters in clinically healthy individuals, who were, in part, asymptomatically infected by malaria parasites. Red blood cell counts and haemoglobin levels were lower in G6PD A- deficient than in G6PD normal subjects. PK activities were higher in G6PD deficients, indicating a younger red cell population in these individuals. These findings suggest that G6PD A- deficiency is accompanied by chronic subclinical haemolysis. As a consequence, the reduced life span of red cells leads to an impaired diagnosis of G6PD heterozygosity when applying routine biochemical methods.     

Does milk have a cataractogenic effect?

We undertook a prospective study to test Simoons' hypothesis that in certain susceptible races milk exerts a cataractogenic effect. Overall milk intake in low lactase deficiency areas did not correlate with cataract occurrence. Subgrouping of cataract patients revealed that greater milk intake did show positive correlation with cortical cataracts. Cortical cataracts were also markedly more common in females. Analysis of data from three different regions showed greater milk intake in cortical cataract patients only. Our data indicate the importance of specifying cataract type in cataract studies and highlight the problem this approach brings forth. We noted no different trends in subjects from northwest and southeast India, although the number of subjects from the southeast was considerably less. Patients with early cortical cataracts may be advised to restrict milk intake.Part of this material was presented at second cataract epidemiology meeting at Bonn in March 1988. A brief report has been accepted for publication in the proceedings of the meeting to be published inDevelopment of Ophthalmology, Vol. 17, 1988.     

Gene mutations and three-dimensional structural analysis in 13 families with severe factor X deficiency

Factor X (FX) deficiency is a rare autosomal recessive disorder. The phenotype and genotype of 15 Iranian patients with FX deficiency from 13 unrelated families with a high frequency of consanguinity were analysed. Five different assays identified four patients from three families with a discrepancy between low-FX coagulant activity (FX:C) and higher-FX antigen (FX:Ag) (a type II deficiency). The remaining 11 patients had parallel reductions of FX:C and FX:Ag (a type I deficiency). Nine different homozygous candidate mutations were identified, of which eight were novel. The four type II cases were associated with an Arg(-1)Thr missense mutation in the prepropeptide: Arg(-1) is highly conserved in all vitamin K-dependent proteins. Four type I mutations (Gly78Asp, Cys81Tyr, Gly94Arg and Asp95Glu) were localized to the EGF-1 and EGF-2 domains, for which molecular views showed that the protein folding would be disrupted. The type I mutation Gly222Asp was localized in the catalytic domain of FX, and is sufficiently close to the Asp-His-Ser catalytic triad to disrupt its correct protein folding. The two type I splice site mutations were IVS1+3, A-->T and IVS2-3, T-->G. These novel homozygous FX mutations were consistent with their phenotypes and agree with experimental data from knockout mice, indicating that FX is an essential protein for survival.