Daily zinc supplementation effect on zinc deficiency in rats during prolonged restriction of motor activity

The objective of this investigation was to evaluate the effect of 47 mg zinc supplementation on deficiency of zinc in rats during 98 d of restriction of motor activity (hypokinesia), which appeared by higher plasma zinc concentration. One Hundred 13-week-old Sprague-Dawley male rats weighing 360–390 g were used to perform the studies: They were equally divided into four groups: 1. Unsupplemented control animals (UCA); 2. Unsupplemented hypokinetic animals (UHA); 3. Supplemented control animals (SCA); and 4. Supplemented hypokinetic animals (SHA). For the simulation of the effect of hypokinesia (HK), the UHA and SHA were kept in small individual cages made of wood, which restricted their movements in all directions without hindering food and water intake. The SCA and SHA received daily with their food an additional amount of zinc. Before and during the experimental period of 98 d, plasma, urinary and fecal zinc, balance of zinc, food intake, and body weight were determined at different intervals. In the SHA and UHA, the concentration of zinc in plasma, and the elimination of zinc in urine and feces increased significantly when compared with the SCA and UCA, whereas the balance of zinc was negative. The body weight and food intake decreased significantly in the SHA and UHA when compared with the SCA and UCA. The increased plasma concentration of zinc in both the SHA and UHA groups was in contrast to the observed hypozincnemia during prolonged immobilization as during prolonged hospitalization. This reaction suggests that there may be some other mechanisms that are affecting the process of control and regulation of zinc metabolism during prolonged HK. It was concluded that exposure to prolonged restriction of motor activity of rats induces significant increases in plasma concentration, fecal and urinary elimination of zinc in the presence of negative zinc balance and regardless the daily intake of large amounts of zinc with their food, leading to zinc deficiency.     

Interaction of flooding with carbon metabolism of forest trees

Waterlogging and flooding cause oxygen deprivation in the root system of trees. Since oxygen is essentially for mitochondrial respiration, this process cannot be maintained under anoxic conditions and must be replaced by other pathways. For the roots it is therefore a matter of survival to switch from respiration to alcoholic fermentation. Due to the low efficiency of this process to yield energy equivalents (ATP), energy and carbon metabolism of trees are usually strongly affected by oxygen deprivation, even if a rapid switch from respiration to fermentation is achieved. The roots can compensate for the low energy yield of fermentation either (1) by decreasing the demand for energy by a reduction of energy-dependent processes such as root growth and/or nutrient uptake, or (2) by consuming more carbohydrates per unit time in order to generate sufficient energy equivalents. In the leaves of trees, flooding and waterlogging cause a decline in the rates of photosynthesis and transpiration, as well as in stomatal conductance. It is assumed that, due to reduced phloem transport, soluble sugars and starch accumulate in the leaves of flooded trees, thereby negatively affecting the sugar supply of the roots. Thus, root growth and survival is negatively affected by both changes in root internal carbon metabolism and impaired carbon allocation to the roots by phloem transport. In addition, accumulation of toxic products of fermentation in the roots, such as acetaldehyde, can further impair root metabolism. A main feature of tolerance against flooding and waterlogging of trees seems to be the steady supply of carbohydrates to the roots in order to maintain alcoholic fermentation; in addition, roots of tolerant trees seem to avoid accumulation of fermentation-derived ethanol and acetaldehyde. From studies with flooding tolerant and non-tolerant tree species, it is hypothesized that (1) the transport of ethanol produced in the roots under hypoxic conditions into the leaves via the transpiration stream, (2) its conversion into acetyl-CoA in the leaves, and (3) its use in the plant's general metabolism, are mechanisms of flooding tolerance of trees.     

EFFECTS OF SELENIUM DEFICIENCY ON THE MORPHOLOGY AND ULTRASTRUCTURE OF THE COASTAL MARINE DIATOM THALASSIOSIRA PSEUDONANA (BACILLARIOPHYCEAE)1,2

The effects of selenium deficiency on the siliceous and nonsiliceous components of the planktonic marine diatom Thalassiosira pseudonana (Hust.) Hasle and Heimdal (clone 3H) are examined using light and electron microscopy. Selenium deficiency induces elongation along the pervalvar axis initially as a result of chain formation caused by the failure of sibling cells to separate and subsequently by cell elongation via the production of hyaline girdle bands. In Se-deficient cultures cell elongation involves the blockage of both mitotic and cytokinetic components of cell division. Selenium deficiency results in ultrastructural alterations in the reticular membrane system and in mitochondrial and chloroplast membranes. Various types of inclusions are seen in vacuolar areas and the accumulation of lipid reserves is evident in Se-deficient cells. These results provide indirect evidence for a metabolic Se requirement in this algal species.     

Application of diagnostic methods and molecular diagnosis of hemoglobin disorders in Khuzestan province of Iran

BACKGROUND:

The hemoglobinopathies refer to a diverse group of inherited disorders characterized by a reduced synthesis of one or more globin chains (thalassemias) or the synthesis of structurally abnormal hemoglobin (Hb). The thalassemias often coexist with a variety of structural Hb variants giving rise to complex genotypes and an extremely wide spectrum of clinical and hematological phenotypes. Hematological and biochemical investigations and family studies provide essential clues to the different interactions and are fundamental to DNA diagnostics of the Hb disorders. Although DNA diagnostics have made a major impact on our understanding and detection of the hemoglobinopathies, DNA mutation testing should never be considered a shortcut or the test of first choice in the workup of a hemoglobinopathy.

MATERIALS AND METHODS:

A careful three-tier approach involving: (1) Full blood count (2) Special hematological tests, followed by (3) DNA mutation analysis, provides the most effective way in which to detect primary gene mutations as well as gene-gene interactions that can influence the overall phenotype. With the exception of a few rare deletions and rearrangements, the molecular lesions causing hemoglobinopathies are all identifiable by PCR-based techniques. Furthermore, each at-risk ethnic group has its own combination of common Hb variants and thalassemia mutations. In Iran, there are many different forms of α and β thalassemia. Increasingly, different Hb variants are being detected and their effects per se or in combination with the thalassemias, provide additional diagnostic challenges.

RESULTS:

We did step-by-step diagnosis workup in 800 patients with hemoglobinopathies who referred to Research center of Thalassemia and Hemoglobinopathies in Shafa Hospital of Ahwaz Joundishapour University of medical sciences, respectively. We detected 173 patients as iron deficiency anemia (IDA) and 627 individuals as thalassemic patients by use of different indices. We have successfully detected 75% (472/627) of the β-thalassemia mutations by using amplification refractory mutation system (ARMS) technique and 19% (130/627) of the β-thalassemia mutations by using Gap-PCR technique and 6% (25/627) as Hb variants by Hb electrophoresis technique. We did prenatal diagnosis (PND) for 176 couples which had background of thalassemia in first pregnancy. Result of PND diagnosis in the first trimester was 35% (62/176) affected fetus with β-thalassemia major and sickle cell disease that led to termination of the pregnancy.

CONCLUSION:

Almost all hemoglobinopathies can be detected with the current PCR-based assays with the exception of a few rare deletions. However, the molecular diagnostic service is still under development to try and meet the demands of the population it serves. In the short term, the current generation of instruments such as the capillary electrophoresis systems, has greatly simplified DNA sequence analysis.     

Studies on DNA binding to metal complexes of Sal<Subscript>2</Subscript>trien

The complexes [Fe(Sal2trien)]NO3 and Cu(Sal2trien) have been synthesized and their interaction with calf thymus DNA has been investigated for the first time using UV spectra, fluorescence spectra, thermal denaturation, and viscosity measurements. The experimental results show conformably that the mode of binding of the complex [Fe(Sal2trien)]NO3 to DNA is nonclassical electrostatic action, but the mode of binding of the complex Cu(Sal2trien) to DNA is classical intercalation.     

Plasticity of epidermal adult stem cells derived from adult goat ear skin

Here we report the isolation and characterization of pluripotent stem cells from adult goat skin. We found that these primary cells have the properties of embryonic stem cells (ESC), including the expression of appropriate immunological markers and the capability of forming embryoid bodies. The subcultured cells also show the characteristics of stem cells, such as the expression of CK19, beta(1-)integrin, P63, and formation of holo-clones in culture. Therefore, we termed these cells epidermal adult stem cells (EpiASC), although their origin was not identified. We have shown that clones of individual EpiASC proliferate and differentiate in culture to produce neurons, cardiomyocytes, osteoblasts, and occytes. Further, we cultivated EpiASC on bioengineered dermis and denuded human amniotic membrane (HAM), to reconstruct artificial skin and corneal epithelium. We successfully transplanted those artificial tissues in goats with acute full-thickness skin defect (AFTSD) and limbal stem cell deficiency (LSCD), respectively. Our results showed that indeed EpiASC reconstructed the skin (hair was observed in restored areas), and repaired the damaged cornea of goats with total LSCD. These data confirm that EpiASC can differentiate into different functional cell types in vivo or in vitro. Due to their high degree of inherent plasticity, and to their easy accessibility for collection from the skin, EpiASC are excellent candidate sources for diverse cell therapies.     

中国极小种群野生植物保护理论与实践研究进展

极小种群野生植物大都分布范围狭窄、个体数量稀少且自然更新困难, 面临随时灭绝的风险, 迫切需要拯救性保护。极小种群野生植物这一概念自提出以来受到了保护生物学领域的广泛关注, 已成为当前中国生物多样性保护的一个热点方向。我国于2010年正式启动实施极小种群野生植物拯救保护工程, 并开展了大量的保护研究和实践。以“extremely small population*”和“plant”为检索词在Web of Science进行了主题检索, 以“极小种群”和“植物”为检索词在中国知网进行了主题检索, 对获取的的学术期刊论文、学位论文和会议论文进行了梳理。本文从极小种群野生植物种群、群落及生境调查与监测、适应性、遗传多样性、繁殖生物学、濒危机制、动态模型6个方面对近年来极小种群野生植物的理论研究工作进行了较为系统的综述。在此基础上, 从就地保护、迁地保护与种质资源保存、野外回归、人工繁育、标准化体系5个方面回顾了极小种群野生植物保护实践及取得的进展。基于极小种群野生植物保护理论与实践研究现状, 我们建议在极小种群野生植物未来保护工作中不断调整和完善保护名录, 加强种群结构的观测和预测、小种群形成和恢复机制的针对性研究以及特定物种的长期系统性研究, 同时促进这一概念在国际上的推广。希望本文能为国家生物多样性保护和生态文明建设提供参考。     

‘Candidatus ferrigenium straubiae’ sp. nov., ‘Candidatus ferrigenium bremense’ sp. nov., ‘Candidatus ferrigenium altingense’ sp. nov., are autotrophic Fe(II)-oxidizing bacteria of the family Gallionellaceae

Iron(II) [Fe(II)] oxidation coupled to denitrification is recognized as an environmentally important process in many ecosystems. However, the Fe(II)-oxidizing bacteria (FeOB) dominating autotrophic nitrate-reducing Fe(II)-oxidizing enrichment cultures, affiliated with the family Gallionellaceae, remain poorly taxonomically defined due to lack of representative isolates. We describe the taxonomic classification of three novel FeOB based on metagenome-assembled genomes (MAGs) acquired from the autotrophic nitrate-reducing enrichment cultures KS, BP and AG. Phylogenetic analysis of nearly full-length 16S rRNA gene sequences demonstrated that these three FeOB were most closely affiliated to the genera Ferrigenium, Sideroxydans and Gallionella, with up to 96.5%, 95.4% and 96.2% 16S rRNA gene sequence identities to representative isolates of these genera, respectively. In addition, average amino acid identities (AAI) of the genomes compared to the most closely related genera revealed highest AAI with Ferrigenium kumadai An22 (76.35–76.74%), suggesting that the three FeOB are members of this genus. Phylogenetic analysis of conserved functional genes further supported that these FeOB represent three novel species of the genus Ferrigenium. Moreover, the three novel FeOB likely have characteristic features, performing partial denitrification coupled to Fe(II) oxidation and carbon fixation. Scanning electron microscopy of the enrichment cultures showed slightly curved rod-shaped cells, ranging from 0.2-0.7 μm in width and 0.5–2.3 μm in length. Based on the phylogenetic, genomic and physiological characteristics, we propose that these FeOB represent three novel species, ‘Candidatus Ferrigenium straubiae’ sp. nov., ‘Candidatus Ferrigenium bremense’ sp. nov. and ‘Candidatus Ferrigenium altingense’ sp. nov. that might have unique metabolic features among the genus Ferrigenium.     

Integrins in periodontal disease

Cell surface integrin receptors mediate cell adhesion, migration and cellular signaling in all nucleated cells. They are activated by binding to extracellular ligands or by intracellular proteins, such as kindlins that engage with their cytoplasmic tails. Cells in the periodontal tissues express several integrins with overlapping ligand-binding capabilities. A distinct phenotype in the periodontium has only been described for knockouts or mutations of three integrin subunits, α11, β6 and β2. Integrin α11β1 appears to have some regulatory function in the periodontal ligament of continuously erupting incisors in mice. Integrin αvβ6 is expressed in the junctional epithelium (JE) of the gingiva. Animals deficient in this receptor develop classical signs of periodontal disease, including inflammation, apical migration of the JE and bone loss, suggesting that it plays a role in the regulation of periodontal inflmmation, likely through activation of transforming growth factor-β1. Lack of integrin activation in the JE is also associated with periodontitis. Patients with kindlin-1 mutations have severe early-onset periodontal disease. Finally, patients with mutations in the leukocyte-specific β2 integrin subunit have severe periodontal problems due to lack of transiting neutrophils in the periodontal tissues.