In recent decades, the adverse effects of global warming on all living beings have been unanimously recognized across the world. A high environmental temperature that increases the respiration and rectal temperature of cattle is called heat stress (HS), and it can affect both male and female reproductive functions. For successful reproduction and fertilization, mature and healthy oocytes are crucial; however, HS reduces the developmental competence of oocytes, which compromises reproduction. HS disturbs the hormonal balance that plays a crucial role in successful reproduction, particularly in reducing the luteinizing hormone and progesterone levels, which leads to severe problems such as poor follicle development with a poor-quality oocyte and problems related to maturity, silent estrus, abnormal or weak embryo development, and pregnancy loss, resulting in a declining reproduction rate and losses for the cattle industry. Lactating cattle are particularly susceptible to HS and, hence, their reproduction rate is substantially reduced. Additionally, bulls are also affected by HS; during summer, semen quality and sperm motility decline, leading to compromised reproduction. In summer, the conception rate is reduced by 20–30% worldwide. Although various techniques, such as the provision of water sprinklers, shade, and air conditioning, are used during summer, these methods are insufficient to recover the normal reproduction rate and, therefore, special attention is needed to improve reproductive efficiency and minimize the detrimental effect of HS on cattle during summer. The application of advanced reproductive technologies such as the production of embryos in vitro, cryopreservation during the hot season, embryo transfer, and timed artificial insemination may minimize the detrimental effects of HS on livestock reproduction and recover the losses in the cattle industry.

Summary: The most important features of error correction tools for sequencing data are accuracy, memory efficiency and fast runtime. The previous version of BLESS was highly memory-efficient and accurate, but it was too slow to handle reads from large genomes. We have developed a new version of BLESS to improve runtime and accuracy while maintaining a small memory usage. The new version, called BLESS 2, has an error correction algorithm that is more accurate than BLESS, and the algorithm has been parallelized using hybrid MPI and OpenMP programming. BLESS 2 was compared with five top-performing tools, and it was found to be the fastest when it was executed on two computing nodes using MPI, with each node containing twelve cores. Also, BLESS 2 showed at least 11% higher gain while retaining the memory efficiency of the previous version for large genomes. Availability and implementation: Freely available at https://sourceforge.net/projects/bless-ec Contact:dchen@illinois.edu Supplementary information: Supplementary data are available at Bioinformatics online.

Leptin is a peptide hormone produced primarily in adipose tissues. Leptin is considered a biomarker associated with obesity and obesity-mediated diseases. Biosensor detection of leptin in the blood may play a critical role as an indicator of dynamic pathological changes. In this paper, we introduce an electrochemical biosensor that adopts o-Phenylenediamine (oPD) on screen-printed gold electrodes (SPGEs) for detecting the leptin from a mouse model of diet-induced obesity (DIO). A linear calibration curve for the leptin concentration was obtained in the ranges from 0.1 to 20 ng/mL with a lower detection limit of 0.033 ng/mL. The leptin concentration was quantified with HRP (horseradish peroxidase)-catalyzed oxidation of oPD by two voltammetry methods: cyclic voltammetry (CV) and square-wave voltammetry (SWV). The proposed sandwich enzyme-linked immunosorbent assay (ELISA)-based electrochemical biosensor for the leptin in mouse blood serum showed high stability, sensitivity, selectivity, and effectivity compared to the commercial Leptin ELISA measurement. Thus, we believe that this leptin biosensor can be a sensitive analytical tool to detect low-levels of biomarkers in clinics and point-of-care testing (POCT).

Understanding the levels of glucose (G) and lactate (L) in blood can help us regulate various chronic health conditions such as obesity. In this paper, we introduced an enzyme-based electrochemical biosensor adopting glucose oxidase and lactate oxidase on two working screen-printed carbon electrodes (SPCEs) to sequentially determine glucose and lactate concentrations in a single drop (~30 µL) of whole blood. We developed a diet-induced obesity (DIO) mouse model for 28 weeks and monitored the changes in blood glucose and lactate levels. A linear calibration curve for glucose and lactate concentrations in ranges from 0.5 to 35 mM and 0.5 to 25 mM was obtained with R-values of 0.99 and 0.97, respectively. A drastic increase in blood glucose and a small but significant increase in blood lactate were seen only in prolonged obese cases. The ratio of lactate concentration to glucose concentration (L/G) was calculated as the mouse’s gained weight. The results demonstrated that an L/G value of 0.59 could be used as a criterion to differentiate between normal and obesity conditions. With L/G and weight gain, we constructed a diagnostic plot that could categorize normal and obese health conditions into four different zones. The proposed dual electrode biosensor for glucose and lactate in mouse whole blood showed good stability, selectivity, sensitivity, and efficiency. Thus, we believe that this dual electrode biosensor and the diagnostic plot could be used as a sensitive analytical tool for diagnosing glucose and lactate biomarkers in clinics and for monitoring obesity.

Reactive oxygen species (ROS) are essential regulators of fertilization and early embryo development in mammals, including humans and various animal models, but they exert detrimental effects when produced in excess. In assisted reproductive technologies (ART), particularly in vitro fertilization (IVF), exposure to non-physiological conditions increases oxidative stress (OS), impairing gamete quality, embryo viability, and clinical outcomes. This review synthesizes experimental and clinical studies describing the endogenous and exogenous sources of ROS relevant to embryo development in IVF. Endogenous ROS arise from intrinsic metabolic pathways such as oxidative phosphorylation, NADPH oxidase, and xanthine oxidase. Exogenous sources include suboptimal laboratory conditions characterized by factors such as high oxygen tension, temperature shifts, pH instability, light exposure, media composition, osmolarity, and cryopreservation procedures. Elevated ROS disrupt oocyte fertilization, embryonic cleavage, compaction, blastocyst formation, and implantation by inducing DNA fragmentation, lipid peroxidation, mitochondrial dysfunction, and apoptosis. In addition, the review highlights how parental health factors establish the initial redox status of gametes, which influences subsequent embryo development in vitro. While antioxidant supplementation and optimized culture conditions can mitigate oxidative injury, the precise optimal redox environment remains a subject of ongoing research. This review emphasizes that future research should focus on defining specific redox thresholds and developing reliable, non-invasive indicators of embryo oxidative status to improve the success rates of ART.