Journal of Biosciences最新文献

Climate change is a significant global issue characterized by rising temperatures, altered weather patterns, and increased frequency of extreme weather events. It can have immediate and serious implications for global health, both directly and indirectly. The latest reports suggest that several climatic factors can alter health parameters, many of which could directly impact ocular health. This review discusses how aspects of climate changes that include increased frequencies of severe weather events, such as floods, heatwaves, extreme temperatures, rising carbon dioxide, and rising sea levels, may influence ocular health. Similarly, air and water pollution, food scarcity, disruption of healthcare delivery systems and medical supply chains, as well as an increase in zoonoses and food-, water-, and vector-borne diseases can affect multiple organs, including the eyes. Reports suggest that the repercussions of climate change and its consequences can have a more substantial effect on a specific subset of people, including elderly, low-income, physically disabled, and malnourished populations. This review aims to provide a perspective on the relationship between climate change and its impact on human ocular health, including epidemiological shifts in the occurrence of ocular problems. This review also discusses how climatic shifts cause ocular problems and emphasizes their effects on specific population groups.

Bemisia tabaci (Gennadius), one of the most destructive insect pests worldwide, damages plants and transmits numerous harmful virus species, including begomoviruses. One novel control approach that has been suggested is silencing the vacuolar H⁺-ATPase (V-ATPase), a vital enzyme found in the endomembranes and plasma membranes responsible for pH homeostasis. Engineered V-ATPase dsRNA can be delivered to B. tabaci through feeding (via transgenic plants as well as root and foliar delivery of naked or formulated dsRNA) and non-feeding (spraying dsRNAs and recombinant entomopathogens) methods. This review considers the potential use of V-ATPase RNAi in combination with cultural/mechanical practices, biorational insecticides/ natural compounds, natural enemies, and biotechnological control strategies. These approaches are promising for integrated whitefly management (IWM) programs, and can potentially reduce excessive use of chemical pesticides and the likelihood of pesticide resistance. Despite their specificity and high efficiency, emerging resistance and the effects on non-target organisms remain concerns. Also, RNAi of different subunits could lead to various outcomes, and V-ATPase silencing may show dissimilar effects against various whitefly biotypes. Here, some challenges have been addressed with various solutions, e.g., appropriate formulations for protecting, carrying, and spreading dsRNAs, along with the use of strong promoters to optimize the effective dosage of the administered dsRNA molecules.

Numerous scientific studies have established that the BCG vaccination reduces susceptibility to bacterial and viral infections, particularly those causing respiratory tract ailments. This effect is partly attributed to the crossreactivity of BCG antigens, which reinforces immunity and presents an important avenue for therapeutic interventions against bladder cancer, Buruli ulcer, and leprosy. Remarkably, individuals residing in tuberculosis (TB)-endemic regions who have received BCG vaccinations exhibit a significant reduction in the incidence of monkeypox virus (MPV) infections. This observation could be attributed to shared T-cell and B-cell epitopes between mycobacteria and MPV, raising the possibility of eliciting cross-reactive immune responses. Such cross-reactivity could account for the enhanced protection conferred by the BCG vaccination against MPV infections. To explore this possibility, we employed advanced immunoinformatics tools. Our analysis successfully identified common CD4 T-cell, CD8 T-cell, and B-cell epitopes shared between MPV and mycobacteria. Notably, the T-cell epitopes demonstrated high immunogenicity and substantial affinity, with promiscuous binding to multiple human leukocyte antigen (HLA) class I and class II alleles, indicating the potential for these epitopes to trigger robust immune responses. Indeed, the predicted outcomes encompassed the induction of Th1-cell and Th2-cell responses via the predicted epitopes. These findings carry profound implications. They imply that prior exposure to cross-reactive mycobacterial antigens during recent pandemics could have contributed to increased levels of protection against MPV infections in TB-endemic regions, in contrast to areas non-endemic for TB. The identified T-cell and B-cell epitopes may thus serve as promising candidates for developing vaccines to combat MPV and mitigate its spread.

Hippeastrum species and their hybrids, valued for their vibrant flowers and ease of cultivation, are significant in the ornamental industry. This study employed de novo transcriptome analysis to investigate the molecular basis of floral color and fragrance in Hippeastrum brasilianum, Hippeastrum papilio, and their F1 hybrid. A high-quality transcriptome was assembled from 637,934,284 paired-end reads, resulting in 557,833 highconfidence transcripts. BUSCO analysis confirmed the completeness of the assembly, with 94.5% of eukaryotic, 88.1% of monocot, and 90.7% of land plant genes identified as complete. Differential gene expression analysis revealed that the genes involved in monoterpene, diterpenoid, and sesquiterpenoid biosynthesis were upregulated in H. brasilianum, contributing to its distinct fragrance profile, while their downregulation in H. papilio and their hybrid suggests a loss of scent, consistent with previous fragrance analyses in Hippeastrum species. The upregulation of flavonoid and phenylpropanoid biosynthesis genes in H. papilio and their hybrid enhanced anthocyanin production, leading to vibrant pigmentation, whereas H. brasilianum showed reduced expression, aligning with its white flowers. Gene Ontology (GO) and EuKaryotic Orthologous Groups (KOG) classifications highlighted the prominence of metabolic and cellular processes, supporting their roles in floral trait development. These findings provide a molecular framework for understanding floral trait variation in Hippeastrum, offering insights for breeding programs aimed at enhancing ornamental qualities.

The present study aims to investigate the differences between cork oak acorns from natural and semi-natural stands in terms of morphology, insect attack rate, and acorn chemical composition. Moreover, it examines the metabolic responses induced by insect attacks. The results show that acorns from the semi-natural stand in our study are larger than those from the natural stand. In addition, the insect attack rate was higher in the natural stand (8.25%) than in the semi-natural stand (6.25%). Furthermore, acorns in the semi-natural stand exhibit high total flavonoid content (TFC), whereas those in the natural stand are rich in total phenolic content (TPC). In terms of biochemical changes in acorns, the study revealed a remarkably significant difference in TPC, TFC, and antioxidant activity subsequent to infestation by Cydia and Curculio insects. Cydia-infested acorns from the natural stand had higher TPC levels, with a value of 93.96±0.39 mg GAE/g, showing a 17.7% increase over healthy acorns. Acorns from the semi-natural stand attacked by Curculio show the highest TFC with a value of 0.288±0.004 mg EQ/g, showing a 121.5% increase over healthy acorns. Moreover, both DPPH and FRAP methods revealed that antioxidant activity of the acorns from the semi-natural stand attacked by Curculio was more effective. This research is crucial for providing a solid foundation for the selection of high-quality cork oak germplasm resources and exploring the potential valorization of insect-affected acorns in the realms of food and agriculture.

We computationally predicted all phosphorylation sites in the sequence of the human laminin γ1-chain (LAMC1), and computationally identified, for the first time, all kinases for experimentally observed phosphorylated residues of the LAMC1 and all missense deleterious LAMC1 mutations found in different cancer types that interfere with LAMC1 phosphorylation. Also, we mapped the above data to all the biologically functional interaction sequences of the LAMC1. Five kinases (CKII, GPCRK1, PKA, PKC, and CKI) are most enriched for LAMC1 phosphorylation, and the significance of ecto-kinases in this process was emphasized. PKA and PKC targeted more residues inside and close to functional interaction sequences compared with other kinases and in the functional interaction sequence RPESFAIYKRTR. Most phosphorylation-interfering mutations were found in cutaneous melanoma and uterine endometrioid carcinoma. The mutation R255H interfered with the experimentally observed phosphorylation of LAMC1 inside the functional interaction sequence TDIRVTLNRLNTF, while the mutations S181Y and S213Y interfered with the experimentally observed phosphorylation of LAMC1 outside the functional interaction sequences. Mutations R359C,H, R589H, R657C,H, R663I,G, and T1207 interfered with the predicted phosphorylation inside or close to the functional interaction sequences, whereas other mutations interfered outside. PKA- and PKC-predicted phosphorylation was mostly interfered with by mutations inside functional interaction sequences. Phosphorylation-interfering mutations and functional interaction sequences were suggested to promote specific cancer types or cancer progression in general.

Atherosclerosis is a common cardiovascular disease in which the arteries are thickened due to buildup of plaque. This study aims to identify programmed cell death (PCD)-related biomarkers and explore the crucial regulatory mechanisms of atherosclerosis. Gene expression profiles of atherosclerosis and control groups from GSE20129 and GSE23746 were obtained. Necroptosis was elevated in atherosclerosis. Weighted gene co-expression network analysis (WGCNA) was conducted in GSE23746 and GSE56045 to identify PCD-related modules and to perform enrichment analysis. Two necroptosis-related genes (IRF9 and STAT1) were identified and considered as biomarkers. Enrichment analysis showed that these gene modules were mainly related to immune response regulation. In addition, single-cell RNA sequencing data from GSE159677 were obtained and the characteristic cell types of atherosclerosis were identified. A total of 11 immune cell types were identified through UMAP dimension reduction. Most immune cells were mainly enriched in plaque samples, and STAT1 and IRF9 were primarily expressed in T-cells and macrophages. Moreover, the roles of IRF9 and STAT1 were assessed and found to be significantly upregulated in atherosclerosis, which was associated with increased risk of atherosclerosis. This study provides a molecular feature of atherosclerosis, offering an important basis for further research on its pathological mechanisms and the search for new therapeutic targets.

One of the integral part of the network analysis is finding groups of nodes that exhibit similar properties. Community detection techniques are a popular choice to find such groups or communities within a network and it relies on graph-based methods to achieve this goal. Finding communities in biological networks such as gene co-expression networks are particularly important to find groups of genes where we can focus on further downstream analysis and find valuable insights regarding concerned diseases. Here, we present an effective community detection method called community detection using centrality-based approach (CDCA), designed using the graph centrality approach. The method has been tested using four benchmark bulk RNA-seq datasets for schizophrenia and bipolar disorder, and the performance has been proved superior in comparison to several other counterparts. The quality of communities are determined using intrinsic graph properties such as modularity and homogeneity. The biological significance of resultant communities is decided using the pathway enrichment analysis.

Circadian clocks, biochemical oscillators that are regulated by environmental time cues including the day/night cycle, have a central function in the majority of biological processes. The disruption of the circadian clock can alter breast biology negatively and may promote the development of breast tumors. The expression status of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) were used to classify breast cancer into different molecular subtypes such as triple-negative breast cancer (TNBC). Receptor status-dependent expression of circadian clock genes have been previously studied in breast cancer using relatively small sample sizes in a particular population. Here, using TCGA-BRCA data (n=1119), we found that the expressions of CRY1, PER1, PER2, PER3, BMAL1, CLOCK, RORA, RORB, RORC, NR1D1, NR1D2, and FBXL3 were higher in ER+ breast cancer cells compared with those of ER− status. Similarly, we showed that transcript levels of CRY2, PER1, PER2, PER3, BMAL1, RORA, RORB, RORC, NR1D1, NR1D2, and FBXL3 were higher in PR+ breast cancer cells than in PR− breast cancer cells. We report that the expressions of CRY2, PER1, BMAL1, and RORA were lower, and the expression of NR1D1 was higher, in HER2+ breast cancer cells compared with HER2− breast cancer cells. Moreover, we studied these receptor status-dependent changes in the expressions of circadian clock genes also based on the race and age of breast cancer patients. Lastly, we found that the expressions of CRY2, PER1, PER2, PER3, and CLOCK were higher in non-TNBC than in TNBC, which has the worst prognosis among subtypes. We note that our findings are not always parallel to the observations reported in previous studies with smaller sample sizes performed in different populations and organisms. Our study suggests that receptor status in breast cancer (thus, subtype of breast cancer) might be more important than previously shown in terms of its influence on the expression of circadian clock genes and on the disruption of the circadian clock, and that ER or PR might be important regulators of breast cancer chronobiology that should be taken into account in personalized chronotherapies.