Retinal endothelial cell apoptosis

Retinal endothelial cell (REC) apoptosis occurs in response to a number of stressors, including high glucose, oxidative stress, hypoxia. Because these stressors are common factors in a number of ocular diseases, it is critical to understand the cellular mechanisms by which apoptosis occurs in REC. This review discusses the various models of REC used in ophthalmological research. The mechanisms responsible for REC apoptosis are discussed, as well as potential therapeutics currently under development to prevent REC apoptosis. The primary goal of this review is provide the reader with a background knowledge of the current state of research ongoing in REC apoptosis and potential avenues for future testing.     

Climate impact of diverting residual biomass to cement production

Co-firing residual lignocellulosic biomass with fossil fuels is often used to reduce greenhouse gas (GHG) emissions, especially in processes like cement production where fuel costs are critical and residual biomass can be obtained at a low cost. Since plants remove CO₂ from the atmosphere, CO₂ emissions from biomass combustion are often assumed to have zero global warming potential (${\mathrm{GWP}}_{{\mathrm{bCO}}_2}$= 0) and do not contribute to climate forcing. However, diverting residual biomass to energy use has recently been shown to increase the atmospheric CO₂ load when compared to business-as-usual (BAU) practices, resulting in ${\mathrm{GWP}}_{{\mathrm{bCO}}_2}$ values between 0 and 1. A detailed process model for a natural gas-fired cement plant producing 4200 megagrams of clinker per day was used to calculate the material and energy flows, as well as the lifecycle emissions associated with cement production without and with diverted biomass (supplying 50% of precalciner energy demand) from forestry and landfill sources. Biomass co-firing reduced natural gas demand in the precalciner of the cement plant by 39% relative to the reference scenario (100% natural gas), but the total demands for thermal, electrical, and diesel (transportation) energy increased by at least 14%. Assuming ${\mathrm{GWP}}_{{\mathrm{bCO}}_2}$ values of zero for biomass combustion, cement's lifecycle GHG intensity changed from the reference (natural gas only) plant by −40, −23, and − 89 kg CO₂/Mg clinker for diverted biomass from slash burning, forest floor and landfill biomass, respectively. However, using the calculated ${\mathrm{GWP}}_{{\mathrm{bCO}}_2}$ values for diverted biomass from these same fuel sources, the lifecycle GHG intensities changes were −37, +20 and +28 kg CO₂/Mg clinker, respectively. The switch from decreasing to increasing cement plant GHG emissions (i.e., forest floor or landfill feedstocks scenarios) highlights the importance of calculating and using the ${\mathrm{GWP}}_{{\mathrm{bCO}}_2}$ factor when quantifying lifecycle GHG impacts associated with diverting residual biomass to bioenergy use.     

Rice with SUB1 QTL possesses greater initial leaf gas film thickness leading to delayed perception of submergence stress

Background and AimsSubmergence tolerance in rice is primarily attributed to the action of the SUB1 gene, but other associated traits such as leaf gas film (LGF) thickness, leaf hydrophobicity, porosity and leaf density have been known to aid submergence tolerance in rice. However, association of these traits with SUB1 quantitative trait locus (QTL) has not been demonstrated. In this study, we aim to investigate (1) whether the presence of the SUB1 QTL in the genetic background has any influence on the thickness of the LGF and (ii) whether its removal has any impact on stress perception and submergence tolerance in Sub1 and non-Sub1 rice.MethodsWe examined 12 genotypes (including both Sub1 and non-Sub1 types) for different leaf traits such as initial LGF thickness, leaf hydrophobicity, tissue porosity and leaf density in order to work out the relatioship of these traits to the SUB1 QTL in rice. Furthermore, we investigated the changes in the gene expression profile and different metabolic processes in selected genotypes in the presence and absence of their LGF to study its impact on stress perception and adaptation.Key ResultsThe initial thickness of the LGF and hydrophobicity seemed to have a highly positive correlation with the presence of the SUB1 QTL in the genetic background of rice; however, other leaf traits such as porosity and density seemed to be independent of it. Artificial removal of the LGF resulted in partial loss of tolerance, showing increased ethylene production and early induction of anoxia-related genes (SUB1A-1, ACS5, Ramy3D and ADH1) which manifested symptoms such as increased stem elongation, faster chlorophyll and starch breakdown, and partial loss of quiescence in SUB1-containing rice genotypes. Stripping of the LGF resulted in early and enhanced induction of SUB1A-1, indicating a quicker perception of stress.ConclusionsThe presence of SUB1 in the genetic background positively influences surface hydrophobicity and the concomitant LGF thickness of rice. Furthermore, LGF helps in terms of providing better ethylene dissipation and reduced in planta accumulation, owing to the slowing down of ethylene-induced leaf senescence under submergence stress.     

Expression,Purification, and Biophysical Characterization of Klebsiella Pneumoniae Nicotinate Nucleotide Adenylyltransferase

The Protein Journal - Patients in health-care settings develop nosocomial infections due to prolonged hospital stay. The Gram negative Klebsiella pneumoniae (K. pneumoniae), is a bacterial pathogen...     

Paternal contributors in recurrent pregnancy loss: Cues from comparative proteome profiling of seminal extracellular vesicles

Recent evidence entail paternal factors as plausible contributors in spontaneous recurrent pregnancy loss (RPL). Seminal extracellular vesicles secreted from cells of male reproductive tract carry regulatory proteins and RNAs. They are proposed to regulate sperm maturation and function while their fusion to endometrial stromal cells helps in decidualization. Nevertheless, the mechanism(s) involved in these processes are poorly understood. This study aims at elucidating the molecular basis of paternal contribution by comparative proteomics (label‐free LC‐MS/MS) of isolated seminal extracellular vesicles from fertile men and partners of patients with RPL (n = 21 per group). Bioinformatics analysis revealed the identified differentially expressed proteins to be involved in DNA replication, recombination and repair, gene expression, cellular assembly and organization, cell death, and survival. Major disease pathways affected were identified as developmental, hereditary, and immunological disorders. Of the three identified hub genes regulating the above disease pathways, two (HNRNPC and HNRNPU) are overexpressed while RUVBL1 is underexpressed along with over expression of HIST1H1C, DDX1, surmising defective chromatin packaging, and histone removal in spermatozoa resulting in improper expression in paternal genes thereby leading to abnormal embryo development. Besides, alteration in GSTP1 expression points oxidative predominance in RPL group. Differential expression of C3, C4a/C4b, CFB, and GDF 15 may be involved in altered maternal immune response to paternal antigens resulting in impaired decidualization.     

The pathophysiology of traumatic brain injury at a glance

Traumatic brain injury (TBI) is defined as an impact, penetration or rapid movement of the brain within the skull that results in altered mental state. TBI occurs more than any other disease, including breast cancer, AIDS, Parkinson’s disease and multiple sclerosis, and affects all age groups and both genders. In the US and Europe, the magnitude of this epidemic has drawn national attention owing to the publicity received by injured athletes and military personnel. This increased public awareness has uncovered a number of unanswered questions concerning TBI, and we are increasingly aware of the lack of treatment options for a crisis that affects millions. Although each case of TBI is unique and affected individuals display different degrees of injury, different regional patterns of injury and different recovery profiles, this review and accompanying poster aim to illustrate some of the common underlying neurochemical and metabolic responses to TBI. Recognition of these recurrent features could allow elucidation of potential therapeutic targets for early intervention.