生物学最新文献

Oxidative stress, characterized by an imbalance between excessive reactive oxygen species (ROS) production and impaired antioxidant defenses, is closely linked to the pathogenesis of various otorhinolaryngological disorders. Mitochondria, as the primary site of cellular energy production, play a crucial role in modulating oxidative stress. Mitochondrial dysfunction exacerbates ROS generation, leading to cellular damage and inflammatory responses. In otorhinolaryngological diseases, oxidative stress is strongly associated with conditions such as hearing loss, allergic rhinitis, and chronic sinusitis, where oxidative damage and tissue inflammation are key pathological features. Recent studies have highlighted the potential of antioxidant therapies to mitigate oxidative stress and restore homeostasis, offering promising avenues for alleviating symptoms in these diseases. However, despite the encouraging results from early-stage research, the clinical efficacy of antioxidant interventions remains to be fully established. This review provides an overview of the role of oxidative stress in otorhinolaryngological diseases and evaluates the therapeutic potential of antioxidant strategies.

Anaerobic fermentation (AF) processes are sensitive to temperature fluctuations, which can influence the microbial activity and overall metabolic performances. Anaerobic reactors can face unforeseen temperature control failures, leading to instabilities in the process. The present study investigated the effect of two short-term temperature perturbations (down to 20°C and 15°C) on AF of food wastes (FWs). While 20°C did not exhibit a negative impact on AF performance maintaining the bioconversion yields over 40%, the reactor subjected to 15°C presented an acidogenic limitation, which decreased the bioconversion yields (36.4 ± 1.8%). As a result, 2.2 ± 0.5 g/L of succinic acid was accumulated in the reactor, being identified as a temperature failure indicator. Once the conditions were reestablished (operation temperature of 25ºC), the metabolic redundancies identified in the reactors allowed the AFs recovery to initial fermentation yields. 20°C was further tested as operational temperature resulting in stable bioconversion yield similar to the Control Reactor (43.2 ± 0.3%). These results showed the feasibility of conducting AF under low temperatures, indicating the potential of this technology to increase the cost-effectiveness of AF at psychrophilic conditions.

Many factors involved in heparan sulfate (HS) biosynthesis and metabolism have been reported to play roles in viral infection. However, the detailed mechanisms are still not fully understood. In this study, we report that exostosin glycosyltransferase 1 (EXT1), the HS polymerase, is a critical regulatory factor for Zika virus (ZIKV) infection. Knocking out EXT1 dramatically restricts ZIKV infection, which is not due to the inhibition of virus entry resulting from HS deficiency, but mediated by the downregulation of autophagy. Induction of autophagy promotes ZIKV infection, and attenuated autophagy is found in distinct EXT1 knockout (EXT1-KO) cell lines. Induction of autophagy by rapamycin can relieve the ZIKV production defect in EXT1-KO cells. While over-expressing EXT1 results in the reduction of ZIKV production by targeting the viral envelope (E) protein and non-structural protein NS3 in a proteasome-dependent degradation manner. The different roles of EXT1 in ZIKV infection are further confirmed by the data that knocking down EXT1 at the early stage of ZIKV infection represses viral infection, whereas the increase of ZIKV infection is observed when knocking down EXT1 at the late stage of viral infection. This study discovers previously unrecognized intricate roles of EXT1 in ZIKV infection.

Viroids, small circular non-coding RNAs, act as infectious pathogens in higher plants, demonstrating high stability despite consisting solely of naked RNA. Their dependence of replication on host machinery poses the question of whether RNA modifications play a role in viroid biology. Here, we explore RNA modifications in the avocado sunblotch viroid (ASBVd) and the citrus exocortis viroid (CEVd), representative members of viroids replicating in chloroplasts and the nucleus, respectively, using LC - MS and Oxford Nanopore Technology (ONT) direct RNA sequencing. Although no modification was detected in ASBVd, CEVd contained approximately one m⁶A per RNA molecule. ONT sequencing predicted three m⁶A positions. Employing orthogonal SELECT method, we confirmed m⁶A in two positions A353 and A360, which are highly conserved among CEVd variants. These positions are located in the left terminal region of the CEVd rod-like structure where likely RNA Pol II and and TFIIIA-7ZF bind, thus suggesting potential biological role of methylation in viroid replication.

Mpox, is a zoonotic disease caused by the monkeypox virus and is primarily endemic to Africa. As countries gradually stop smallpox vaccination, resistance to the smallpox virus is declining, increasing the risk of infection with mpox and other viruses. On 14 August 2024, the World Health Organization announced that the spread of mpox constituted a public health emergency of international concern. Mpox's transmission routes and symptoms are complex and pose new challenges to global health. Several vaccines (such as ACAM2000, JYNNEOS, LC16m8, and genetically engineered vaccines) and antiviral drugs (such as tecovirimat, brincidofovir, cidofovir, and varicella immunoglobulin intravenous injection) have been developed and marketed to prevent and control this disease. This review aims to introduce the epidemic situation, epidemiological characteristics, physiological and pathological characteristics, and preventive measures for mpox in detail, to provide a scientific basis for the prevention and control of mpox viruses worldwide.

Uncontrolled immune responses resulting from overactivated cellular signaling pathways, leading to inflammation and tissue injury, are a major cause of death in pathogen-infected individuals. This phenomenon has been well studied in mammals but is less explored in invertebrates. Bacteria of the genus Vibrio are among the most harmful pathogens to humans and aquatic animals. In shrimp, Vibrio infection is generally characterized by the sudden onset of disease, with pathological signs of opaque and whitish muscle tissue. The current study shows that shrimp acutely infected with high dose of Vibrio parahaemolyticus develop inflammation-like pathological changes, leading to rapid death. Excessive activation of JAK-STAT signaling, rather than the Dorsal and Relish pathways, results in overactivation of shrimp immunity and is a major cause of inflammation induced by acute Vibrio infection. Weakening JAK-STAT signaling attenuates the inflammatory response and reduces mortality caused by acute Vibrio infection in shrimp, whereas enhancing JAK-STAT signaling can convert a normal infection into an acute one, accelerating shrimp death. Therefore, this study indicates that, similar to that in mammals, the pathogenesis of infectious diseases in invertebrates is complicated by inflammatory responses triggered by dysregulated immune signaling.

Sulfur metabolism is an essential aspect of fungal physiology and pathogenicity. Fungal sulfur metabolism comprises anabolic and catabolic routes that are not well conserved in mammals, therefore is considered a promising source of prospective novel antifungal targets. To gain insight into Aspergillus fumigatus sulfur-related metabolism during infection, we used a NanoString custom nCounter-TagSet and compared the expression of 68 key metabolic genes in different murine models of invasive pulmonary aspergillosis, at 3 time-points, and under a variety of in vitro conditions. We identified a set of 15 genes that were consistently expressed at higher levels in vivo than in vitro, suggesting that they may be particularly relevant for intrapulmonary growth and thus constitute promising drug targets. Indeed, the role of 5 of the 15 genes has previously been empirically validated, supporting the likelihood that the remaining candidates are relevant. In addition, the analysis of gene expression dynamics at early (16 h), mid (24 h), and late (72 h) time-points uncovered potential disease initiation and progression factors. We further characterized one of the identified genes, encoding the cytosolic serine hydroxymethyltransferase ShmB, and demonstrated that it is an essential gene of A. fumigatus, also required for virulence in a murine model of established pulmonary infection. We further showed that the structure of the ligand-binding pocket of the fungal enzyme differs significantly from its human counterpart, suggesting that specific inhibitors can be designed. Therefore, in vivo transcriptomics is a powerful tool for identifying genes crucial for fungal pathogenicity that may encode promising antifungal target candidates.

Peripheral nerve injury repair has always been a research concern of scientists. At the tissue level, axonal regeneration has become a research spotlight in peripheral nerve repair. Through transplantation of autologous nerve grafts or other emerging biomaterials functional recovery after facial nerve injury is not ideal in clinical scenarios. Great strides have been made to improve facial nerve repair at the micro-cellular level. Physical stimulation techniques can trigger Schwann cells (SCs) to migrate and differentiate into cells required for peripheral nerve repair. Classified by the sources of physical stimulations, SCs repair peripheral nerves through galvanotaxis, magnetotaxis and durotaxis. This article summarized the activation, directional migration and differentiation of SCs induced by physical stimulations, thus providing new ideas for the research of peripheral nerve repair.

This review summarizes key virulence factors associated with group B Streptococcus (GBS), a significant pathogen particularly affecting pregnant women, fetuses, and infants. Beginning with an introduction to the historical transition of GBS from a zoonotic pathogen to a prominent cause of human infections, particularly in the perinatal period, the review describes major disease manifestations caused by GBS, including sepsis, meningitis, chorioamnionitis, pneumonia, and others, linking each to specific virulence mechanisms. A detailed exploration of the genetic basis for GBS pathogenicity follows, emphasizing the roles of capsules in pathogenesis and immune evasion. The paper also examines the molecular structures and functions of key GBS surface proteins, such as pili, serine-rich repeat proteins, and fibrinogen-binding proteins, which facilitate colonization and disease. Additionally, the review discusses the significance of environmental sensing and response systems, like the two-component systems, in adapting GBS to different host environments. We conclude by addressing current efforts in vaccine development, underscoring the need for effective prevention strategies against this pervasive pathogen.

Two of the most important environmental factors that affect the sperm competitive ability in males are the availability of resources and the socio-sexual environment. Numerous studies have investigated the individual effects of these factors, but their combined effect on the evolution of sperm competitive ability remains untested. A crowded larval environment is unique because it simultaneously affects the fitness of the organism through both resource availability and the socio-sexual environment. In this study, we used a set of four laboratory populations of D. melanogaster, evolved under a crowded larval environment for more than 165 generations and their respective controls to investigate how the sperm competitive ability of the males is affected by a single generation of larval crowding versus evolution under a crowded larval environment for more than 165 generations. Our results show that larval crowding negatively affects the sperm defence ability of males evolved in a crowded larval environment, while it has no effect on the sperm defence ability of control males. Additionally, larval crowding negatively impacts the sperm offence ability in both control and evolved populations. Males from populations adapted to a crowded larval environment exhibit lower sperm offence ability at an older age compared to control populations.