Functional analysis of the musculo‐skeletal system of the gill apparatus in Heptranchias perlo (Chondrichthyes: Hexanchidae)

Musculo‐skeletal morphology is an indispensable source for understanding functional adaptations. Analysis of morphology of the branchial apparatus of Hexanchiform sharks can provide insight into aspects of their respiration that are difficult to observe directly. In this study, I compare the structure of the musculo‐skeletal system of the gill apparatus of Heptranchias perlo and Squalus acanthias in respect to their adaptation for one of two respiratory mechanisms known in sharks, namely, the active two‐pump (oropharyngeal and parabranchial) ventilation and the ram‐jet ventilation. In both species, the oropharyngeal pump possesses two sets of muscles, one for compression and the other for expansion. The parabranchial pump only has constrictors. Expansion of this pump occurs only due to passive elastic recoil of the extrabranchial cartilages. In Squalus acanthias the parabranchial chambers are large and equipped by powerful superficial constrictors. These muscles and the outer walls of the parabranchial chambers are much reduced in Heptranchias perlo , and thus it likely cannot use this pump. However, this reduction allows for vertical elongation of outer gill slits which, along with greater number of gill pouches, likely decreases branchial resistance and, at the same time, increases the gill surface area, and can be regarded as an adaptation for ram ventilation at lower speeds.     

Reactive Oxygen Species: Potential Regulatory Molecules in Response to Hypomagnetic Field Exposure

Organisms, including humans, could be exposed to hypomagnetic fields (HMFs, intensity <5 μT), e.g. in some artificially shielded magnetic environments and during deep-space flights. Previous studies have demonstrated that HMF exposure could have negative effects on the central nervous system and embryonic development in many animals. However, the underlying mechanisms remain unknown. Studies have revealed that HMFs affect cellular reactive oxygen species (ROS) levels and thereby alter physiological and biological processes in organisms. ROS, the major component of highly active free radicals, which are ubiquitous in biological systems, were hypothesized to be the candidate signaling molecules that regulate diverse physiological processes in response to changes in magnetic fields. Here, we summarize the recent advances in the study of HMF-induced negative effects on the central nervous system and early embryonic development in animals, focusing on cellular ROS and their role in response to HMFs. Furthermore, we discuss the potential mechanism through which HMFs regulate ROS levels in cells. © 2020 Bioelectromagnetics Society     

Investigation on the effect of alkyl chain linked mono-thioureas as Jack bean urease inhibitors,SAR, pharmacokinetics ADMET parameters and molecular docking studies

The increasing resistance of pathogens to common antibiotics, as well as the need to control urease activity to improve the yield of soil nitrogen fertilization in agricultural applications, has stimulated the development of novel classes of molecules that target urease as an enzyme. In this context, the newly developed compounds on the basis of 1-heptanoyl-3-arylthiourea family were evaluated for Jack bean urease enzyme inhibition activity to validate their role as potent inhibitors of this enzyme. 1-Heptanoyl-3-arylthioureas were obtained in excellent yield and characterized through spectral and elemental analysis. All the compounds displayed remarkable potency against urease inhibition as compared to thiourea standard. It was found that novel compounds fulfill the criteria of drug-likeness by obeying Lipinski’s rule of five. Particularly compound 4a and 4c can serve as lead molecules in 4D (drug designing discovery and development). Kinetic mechanism and molecular docking studies also carried out to delineate the mode of inhibition and binding affinity of the molecules.     

Liquid chromatographic separation of chiral diarylcarbinols

The direct HPLC separation of three chiral carbinols of general formula Mesityl-CH(OH)-Aryl has been achieved using Pirkle (R)-DNBPG ionic or covalent columns and, for Aryl = o-tolyl, on a Chiralpak OP(+) phase. It is apparent that steric hindrance and hydrogen bonding play important roles in chiral recognition. Two compounds structurally very similar but lacking the hydroxyl group were not resolved in their enantiomeric pairs. © 1992 Wiley-Liss, Inc.     

A Double‐Edged Sword: Complement Component 3 in Toxoplasma gondii Infection

Sprague Dawley rats and Kunming (KM) mice are artificially infected with type II Toxoplasma gondii strain Prugniaud (Pru) to generate toxoplasmosis, which is a fatal disease mediated by T. gondii invasion of the central nervous system (CNS) by unknown mechanisms. The aim is to explore the mechanism of differential susceptibility of mice and rats to T. gondii infection. Therefore, a strategy of isobaric tags for relative and absolute quantitation (iTRAQ) is established to identify differentially expressed proteins (DEPs) in the rats’ and the mice's brains compared to the healthy groups. In KM mice, which is susceptible to T. gondii infection, complement component 3 (C3) is upregulated and the tight junction (TJ) pathway shows a disorder. It is presumed that T. gondii‐stimulated C3 disrupts the TJ of the blood–brain barrier in the CNS. This effect allows more T. gondii passing to the brain through the intercellular space.     

Death domain of p75 neurotrophin receptor: a structural perspective on an intracellular signalling hub

The death domain (DD) is a globular protein motif with a signature feature of an all‐helical Greek‐key motif. It is a primary mediator of a variety of biological activities, including apoptosis, cell survival and cytoskeletal changes, which are related to many neurodegenerative diseases, neurotrauma, and cancers. DDs exist in a wide range of signalling proteins including p75 neurotrophin receptor (p75^NTR), a member of the tumour necrosis factor receptor superfamily. The specific signalling mediated by p75^NTR in a given cell depends on the type of ligand engaging the extracellular domain and the recruitment of cytosolic interactors to the intracellular domain, especially the DD, of the receptor. In solution, the p75^NTR‐DDs mainly form a symmetric non‐covalent homodimer. In response to extracellular signals, conformational changes in the p75^NTR extracellular domain (ECD) propagate to the p75^NTR‐DD through the disulfide‐bonded transmembrane domain (TMD) and destabilize the p75^NTR‐DD homodimer, leading to protomer separation and exposure of binding sites on the DD surface. In this review, we focus on recent advances in the study of the structural mechanism of p75^NTR‐DD signalling through recruitment of diverse intracellular interactors for the regulation and control of diverse functional outputs.     

Toward a Reversible Calcium‐Sulfur Battery with a Lithium‐Ion Mediation Approach

Calcium represents a promising anode for the development of high‐energy‐density, low‐cost batteries. However, a lack of suitable electrolytes has restricted the development of rechargeable batteries with a Ca anode. Furthermore, to achieve a high energy density system, sulfur would be an ideal cathode to couple with the Ca anode. Unfortunately, a reversible calcium‐sulfur (Ca‐S) battery has not yet been reported. Herein, a basic study of a reversible nonaqueous room‐temperature Ca‐S battery is presented. The reversibility of the Ca‐S chemistry and high utilization of the sulfur cathode are enabled by employing a Li⁺‐ion‐mediated calcium‐based electrolyte. Mechanistic insights pursued by spectroscopic, electrochemical, microscopic, and theoretical simulation (density functional theory) investigations imply that the Li⁺‐ions in the Ca‐electrolyte stimulate the reactivation of polysulfide/sulfide species. The coordination of lithium to sulfur reduces the formation of sturdy Ca‐S ionic bonds, thus boosting the reversibility of the Ca‐S chemistry. In addition, the presence of Li⁺‐ions facilitates the ionic charge transfer both in the electrolyte and across the solid electrolyte interphase layer, consequently reducing the interfacial and bulk impedance of Ca‐S batteries. As a result, both the utilization of active sulfur in the cathode and the discharge voltage of Ca‐S batteries are significantly improved.     

Pb‐Reduced CsPb0.9Zn0.1I2Br Thin Films for Efficient Perovskite Solar Cells

Fabrication of efficient Pb reduced inorganic CsPbI₂Br perovskite solar cells (PSC) are an important part of environment‐friendly perovskite technology. In this work, 10% Pb reduction in CsPb_0.9Zn_0.1I₂Br promotes the efficiency of PSCs to 13.6% (AM1.5, 1sun), much higher than the 11.8% of the pure CsPbI₂Br solar cell. Zn²⁺ has stronger interaction with the anions to manipulate crystal growth, resulting in size‐enlarged crystallite with enhanced growth orientation. Moreover, the grain boundaries (GBs) are passivated by the Cs‐Zn‐I/Br compound. The high quality CsPb_0.9Zn_0.1I₂Br greatly diminishes the GB trap states and facilitates the charge transport. Furthermore, the Zn4s‐I5p states slightly reduce the energy bandgap, accounting for the wider solar spectrum absorption. Both the crystalline morphology and energy state change benefit the device performance. This work highlights a nontoxic and stable Pb reduction method to achieve efficient inorganic PSCs.     

纳他霉素对芒果采后胶孢炭疽菌的抑菌效果及机理

以纳他霉素为抑菌剂, 实验测定了离体条件下不同浓度纳他霉素对胶孢炭疽菌(Colletotrichum gloeosporioides)的孢子萌发及菌丝生长的抑制效果, 以及活体损伤接种炭疽病菌后, 纳他霉素对芒果(Mangifera indica)果实炭疽病的防治效果。通过测定纳他霉素处理后胶孢炭疽菌的细胞膜相对渗透率、可溶性蛋白含量、细胞膜完整性、孢子内活性氧水平和线粒体分布情况, 初步探明其抑菌机理。结果表明, 3 mg∙L ^-1纳他霉素可显著抑制胶孢炭疽菌孢子萌发、芽管伸长和菌落生长, 80 mg∙L ^-1纳他霉素可有效抑制芒果贮存过程中果实炭疽病斑的扩展。纳他霉素处理后胶孢炭疽菌细胞膜相对渗透率和可溶性蛋白含量增加; 2 mg∙L ^-1纳他霉素处理8小时, 处理组胶孢炭疽菌孢子细胞膜损伤染色率为33.6%, 对照组染色率为13.9%; 处理组胞内活性氧产生染色率达46.9%, 比对照组高39.7%; 同时观察到纳他霉素使胞内线粒体分布不均且荧光信号微弱。以上结果表明, 纳他霉素可以破坏胶孢炭疽病菌细胞膜, 诱导活性氧大量积累, 并降低线粒体活性, 从而干扰菌体正常生理活性, 使其代谢活动受影响, 从而达到抑菌目的。     

心肌纤维化的信号转导机制及新型抑制剂的研究进展

心肌纤维化(myocardial fibrosis, MF)是心肌重构发生的重要病理过程,能够引起心脏衰竭甚至死亡。心肌组织中成纤维细胞异常增殖并转化为肌成纤维细胞以及心肌细胞外基质代谢紊乱导致沉积是心肌纤维化形成的主要病理基础。心肌纤维化发生的分子机制较复杂,已发现多种信号通路参与了心肌纤维化的发生。该文主要对参与调控心肌纤维化的信号转导机制进行了综述,并对新型信号抑制剂的研究进展进行了小结。