Amino acid analysis of bone from a possible case of prehistoric iron deficiency anemia from the American southwest

It is possible that dietary conditions can result in the production of abnormal bone protein. For example, a heavily maize-dependent diet could be deficient in one or more essential amino acids necessary to normal human biochemistry and consequently necessary for normal bone protein synthesis. Amino acid analysis of bone tissues, thus, could provide a useful diagnostic tool in paleopathology. To test this potential we have compared the amino acid analyses of bone samples from a prehistoric Southwest Indian child exhibiting porotic hyperostosis with samples taken from (1) two children's skeletons lacking bone lesions but from the same area and time, (2) a modern child who died from accidental causes, and (3) adult human compact bone. Analytical results of the nonpathological prehistoric specimens were virtually identical to that of the modern infant, indicating remarkable preservation of bone protein. The pathological bone sample differed from the three control specimens by having as much as 25% less of those amino acids containing hydroxyl group and acidic side chains. We interpret the amino acid profile for the diseased child as indicating the presence of a greater proportion of helical protein (or less noncollagenous protein) as well as a lowered degree of hydroxylation of proline and lysine. One explanation for our data is that protein biosynthesis is altered in the child exhibiting porotic hyperostosis, and either some proteins important in the early phases of mineralization are not produced in sufficient quantity, or some necessary enzyme cofactors (e.g., dietary ferrous ions) are missing. We conclude that our data are compatible with, but do not prove, the hypothesis that the porotic hyperostosis exhibited by the Southwest Indian child is the result of iron deficiency anemia.     

Porotic hyperostosis: new evidence to support the anemia theory

The etiology of skull lesions known as porotic hyperostosis has long been a matter for speculation. The most widely accepted theory at present suggests that an anemia, either acquired or genetic, is responsible for lesion development. However, acceptance of this theory is not universal and the nature of the relationship between orbital and vault lesions remains a controversial issue. This paper provides a much broader field of supportive evidence on which to base the anemia theory. This involves a synthesis of information from the clinical and anthropological literature as well as new data from two skeletal collections: Poundbury Camp, a Romano-British series, and the Hodgson collection, a 19th century East Asian series. A comparison is made between clinical and anthropological data at the macroscopic, microscopic, radiographic, and demographic levels of analysis. This approach reveals the similarities in expression between clinically diagnosed anemias and porotic hyperostosis.     

中国十个地理品系卤虫同工酶的研究

本文采用聚丙烯酰胺凝胶垂直板电泳法,对中国十个不同地理品系卤虫的十种同工酶进行了研究。分析了编码七种多态酶的19个座位、42个等位基因,用Nei(1972、1975)的方法计算各地理品系卤虫的遗传相似系数、遗传距离和平均杂合度并进行聚类分析。实验和分析结果证明十个不同地理品系的卤虫可分为A.parthenogenetica和有性品系A.sp.两大姊妹种;十种同工酶中三种酶为单态酶,七种为多态酶;雌雄个体无电泳差异。     

FANCD2, FANCJ and BRCA2 cooperate to promote replication fork recovery independently of the Fanconi Anemia core complex

Fanconi Anemia (FA) is an inherited multi-gene cancer predisposition syndrome that is characterized on the cellular level by a hypersensitivity to DNA interstrand crosslinks (ICLs). To repair these lesions, the FA pathway proteins are thought to act in a linear hierarchy: Following ICL detection, an upstream FA core complex monoubiquitinates the central FA pathway members FANCD2 and FANCI, followed by their recruitment to chromatin. Chromatin-bound monoubiquitinated FANCD2 and FANCI subsequently coordinate DNA repair factors including the downstream FA pathway members FANCJ and FANCD1/BRCA2 to repair the DNA ICL. Importantly, we recently showed that FANCD2 has additional independent roles: it binds chromatin and acts in concert with the BLM helicase complex to promote the restart of aphidicolin (APH)-stalled replication forks, while suppressing the firing of new replication origins. Here, we show that FANCD2 fulfills these roles independently of the FA core complex-mediated monoubiquitination step. Following APH treatment, nonubiquitinated FANCD2 accumulates on chromatin, recruits the BLM complex, and promotes robust replication fork recovery regardless of the absence or presence of a functional FA core complex. In contrast, the downstream FA pathway members FANCJ and BRCA2 share FANCD2's role in replication fork restart and the suppression of new origin firing. Our results support a non-linear FA pathway model at stalled replication forks, where the nonubiquitinated FANCD2 isoform – in concert with FANCJ and BRCA2 – fulfills a specific function in promoting efficient replication fork recovery independently of the FA core complex.     

The effect of reticulocyte hemoglobin content on the diagnosis of iron deficiency anemia: A meta-analysis study

BackgroundIron deficiency anemia (IDA) is the most common type of anemia worldwide and has many adverse effects on life quality. This meta-analysis study aims to show that reticulocyte hemoglobin content (CHr) is more effective than routinely used parameters in the diagnosis of IDA.MethodsComprehensive and systematic research was done using international databases including PubMed, Web of Science, Cochrane Library, Science Direct, and Google Scholar, which contain all articles published on IDA until December 29, 2020. Seventeen articles were included in the meta-analysis.ResultsThe analyses found the Cohen''s deffect size (Standardized Mean Difference) values of the parameters. Accordingly, CHr is 2.84 (95% CI 2.36 to 3.31), mean corpus volume (MCV) is 2.46 (95% CI 1.97 to 2.95), ferritin is 2.37 (95% CI 1.63 to 3.11), and transferrin saturation (TSAT) is 3.76 (95% CI 2.14 to 5.38). To diagnose IDA, the sensitivity value of the CHr concentration was found as 83.5% (95% CI 76.1 to 89.8), specificity value to be 91.8% (95% CI 85.5 to 96.4), and mean cut-off value as 28.2 pg.ConclusionsThe results of our study reveal the findings that CHr is a better biomarker than MCV and ferritin used in determining IDA, and its efficacy is lower than TSAT. It is very important to use it routinely for the pre-diagnosis of IDA, which is very important for public health. The groups in the study are heterogeneous but contain bias. Therefore, meta-analyses of studies with less heterogeneity of CHr are needed.     

Ethylene is a positive regulator for GA<Subscript>3</Subscript>-induced male sex in<Emphasis Type="Italic"> Anemia phyllitidis</Emphasis> gametophytes

Effects of the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) on the development and expression of male sex were tested using the model of the three-zonal structure of 12-day-old (15-celled) Anemia phyllitidis gametophyte. ACC at 10 M concentration enhanced the number of antheridia induced by gibberellic acid. Cytomorphological measurements showed that this effect was limited to only the antheridial region of gametophytes and depended on transverse expansion of antheridial mother cells. Time-course cytophotometrical measurements showed that this promotive effect of ACC was preceded by reorganization of nuclear chromatin and induction of DNA synthesis in nuclei in the antheridial region cells of fern gametophytes.Abbreviations ACC: 1-Aminocyclopropane-1-carboxylic acid. - CPA: Cell profile area. - GA: Gibberellin. - GA₃: Gibberellic acid. - NPA: Nuclear profile area. - TE: Tris-EDTA buffer.Communicated by D. Bartels     

妊娠贫血对产科结局的影响

目的:了解妊娠中、晚期贫血的发生率及其对产科结局的影响。方法:对951例孕妇产前及产后血红蛋白(Hb)检测结果与产科结局的关系进行回顾性分析。Hb<100g/L的孕妇为贫血组,Hb≥100g/L的孕妇为正常对照组,分别对孕中期及孕晚期贫血与产科结局进行对照分析。结果:孕中期贫血导致孕晚期贫血、产后贫血、早产、过期妊娠、胎盘功能欠佳发生率增加(P<0.05)。孕晚期贫血导致产后贫血、早产、低体重儿的出生、胎盘早剥发生率增加(P<0.05),孕晚期贫血可增加妊高征、死胎、胎膜早破的发生率(P>0.05)。双胎妊娠增加妊娠贫血的发生率。结论:妊娠中、晚期贫血对产科结局有不良影响,应加强妊娠期贫血的防治,从妊娠中期常规补铁,降低妊娠期贫血的发生率,保障母婴健康。     

Conserved features of germination and polarized cell growth: a few insights from a pollen-fern spore comparison

BACKGROUND: The germination of both pollen and fern spores results in the emergence of a cell-pollen tube from pollen, rhizoid from spore-that grows in a polar fashion, primarily at its apical end. In both of these tip-growing cells, the delivery of secretory vesicles to the growing end is guided in part by a calcium gradient, with calcium entering at the tip where it is most highly concentrated. The similarities between the two systems extend beyond tip-focused calcium gradients to encompass signalling pathways and elements including calmodulin, nitric oxide, annexins and Rop-GTPases. SCOPE AND AIMS: This review is limited to those pathways and elements that function similarly in fern and pollen systems based on currently available evidence. The aim is to illustrate the common mechanisms by which tip growth occurs, facilitate further investigations into this area, and examine the implications for the evolutionarily conserved control of tip growth. CONCLUSIONS: The interplay of calcium, nitric oxide and other effectors in both pollen and fern spores suggests certain signalling pathways became important regulators of germination and growth early in the evolution of land plants. Both large- and small-scale comparative genomic methods have shown to be promising in their ability to find new and relevant comparisons for further research. Cross-species comparisons may serve to speed up this process by highlighting both basic pathways and system-specific deviations.     

Severe malarial anemia: innate immunity and pathogenesis

Greater than 80% of malaria-related mortality occurs in sub-Saharan Africa due to infections with Plasmodium falciparum. The majority of P. falciparum-related mortality occurs in immune-naïve infants and young children, accounting for 18% of all deaths before five years of age. Clinical manifestations of severe falciparum malaria vary according to transmission intensity and typically present as one or more life-threatening complications, including: hyperparasitemia; hypoglycemia; cerebral malaria; severe malarial anemia (SMA); and respiratory distress. In holoendemic transmission areas, SMA is the primary clinical manifestation of severe childhood malaria, with cerebral malaria occurring only in rare cases. Mortality rates from SMA can exceed 30% in pediatric populations residing in holoendemic transmission areas. Since the vast majority of the morbidity and mortality occurs in immune-naïve African children less than five years of age, with SMA as the primary manifestation of severe disease, this review will focus primarily on the innate immune mechanisms that govern malaria pathogenesis in this group of individuals. The pathophysiological processes that contribute to SMA involve direct and indirect destruction of parasitized and non-parasitized red blood cells (RBCs), inefficient and/or suppression of erythropoiesis, and dyserythropoiesis. While all of these causal etiologies may contribute to reduced hemoglobin (Hb) concentrations in malaria-infected individuals, data from our laboratory and others suggest that SMA in immune-naïve children is characterized by a reduced erythropoietic response. One important cause of impaired erythroid responses in children with SMA is dysregulation in the innate immune response. Phagocytosis of malarial pigment hemozoin (Hz) by monocytes, macrophages, and neutrophils is a central factor for promoting dysregulation in innate inflammatory mediators. As such, the role of P. falciparum-derived Hz (PfHz) in mediating suppression of erythropoiesis through its ability to cause dysregulation in pro- and anti-inflammatory cytokines, growth factors, chemokines, and effector molecules is discussed in detail. An improved understanding of the etiological basis of suppression of erythropoietic responses in children with SMA may offer the much needed therapeutic alternatives for control of this global disease burden.