Emerging Topics in Life Sciences最新文献

Bacteria employ diverse mechanisms to manage toxic copper in their environments, and these evolutionary strategies can be divided into two main categories: accumulation and rationalization of metabolic pathways. The strategies employed depend on the bacteria's lifestyle and environmental context, optimizing the metabolic cost-benefit ratio. Environmental and opportunistically pathogenic bacteria often possess an extensive range of copper regulation systems in order to respond to variations in copper concentrations and environmental conditions, investing in diversity and/or redundancy as a safeguard against uncertainty. In contrast, obligate symbiotic bacteria, such as Neisseria gonorrhoeae and Bordetella pertussis, tend to have specialized and more parsimonious copper regulation systems designed to function in the relatively stable host environment. These evolutionary strategies maintain copper homeostasis even in challenging conditions like encounters within phagocytic cells. These examples highlight the adaptability of bacterial copper management systems, tailored to their specific lifestyles and environmental requirements, in the context of an evolutionary the trade-off between benefits and energy costs.

Through homeostatic processes, bacterial cells maintain intracytoplasmic metal ions at concentrations which enable the 'correct' metal to be inserted into an enzyme, thereby ensuring function. However, fluctuations in intracytoplasmic metal ion concentrations mean that under different conditions certain enzymes may contain different metals at their active site. This perspective describes examples of such cases and suggests that metalloproteome plasticity may contribute to the dynamic adaptation of pathogens to stresses in the host environment.

It is well-known that antibiotics target energy-consuming processes and a significant body of research now supports the conclusion that the metabolic state of bacteria can have a profound impact upon the efficacy of antibiotics. Several articles implicate bacterial energetics and the respiratory inhibitor nitric oxide (NO) in this process, although pinpointing the precise mechanism for how NO can diminish the potency of a range of antibiotics through modulating bacterial energy metabolism has proved challenging. Herein, we introduce the role of NO during infection, consider known links between NO and antibiotic efficacy, and discuss potential mechanisms via which NO present at the site of infection could mediate these effects through controlling bacterial energetics. This perspective article highlights an important relationship between NO and antibiotic action that has largely been overlooked and outlines future considerations for the development of new drugs and therapies that target bacterial energy metabolism.

Neisseria gonorrhoeae, the causative agent of the sexually transmitted infection gonorrhea, is a human-adapted pathogen that does not productively infect other organisms. The ongoing relationship between N. gonorrhoeae and the human host is facilitated by the exchange of nutrient resources that allow for N. gonorrhoeae growth in the human genital tract. What N. gonorrhoeae 'eats' and the pathways used to consume these nutrients have been a topic of investigation over the last 50 years. More recent investigations are uncovering the impact of N. gonorrhoeae metabolism on infection and inflammatory responses, the environmental influences driving N. gonorrhoeae metabolism, and the metabolic adaptations enabling antimicrobial resistance. This mini-review is an introduction to the field of N. gonorrhoeae central carbon metabolism in the context of pathogenesis. It summarizes the foundational work used to characterize N. gonorrhoeae central metabolic pathways and the effects of these pathways on disease outcomes, and highlights some of the most recent advances and themes under current investigation. This review ends with a brief description of the current outlook and technologies under development to increase understanding of how the pathogenic potential of N. gonorrhoeae is enabled by metabolic adaptation.

Short-chain fatty acids are known modulators of host-microbe interactions and can affect human health, inflammation, and outcomes of microbial infections. Acetate is the most abundant but least well-studied of these modulators, with most studies focusing on propionate and butyrate, which are considered to be more potent. In this mini-review, we summarize current knowledge of acetate as an important anti-inflammatory modulator of interactions between hosts and microorganisms. This includes a summary of the pathways by which acetate is metabolized by bacteria and human cells, the functions of acetate in bacterial cells, and the impact that microbially derived acetate has on human immune function.

Metal ions such as zinc and copper play important roles in host-microbe interactions and their availability can drastically affect the survival of pathogenic bacteria in a host niche. Mechanisms of metal homeostasis protect bacteria from starvation, or intoxication, defined as when metals are limiting, or in excess, respectively. In this mini-review, we summarise current knowledge on the mechanisms of resistance to metal stress in bacteria, focussing specifically on the homeostasis of cellular copper and zinc. This includes a summary of the factors that subvert metal stress in bacteria, which are independent of metal efflux systems, and commentary on the role of small molecules and metabolic systems as important mediators of metal resistance.

This review centres around the recent evidence in examining the intersection of sleep and cardiovascular disease (CVD). Sleep in this review will be further subdivided to consider both sleep quantity and quality along and will also consider some of the more common sleep disorders, such as insomnia and obstructive sleep apnoea, in the context of CVD. Sleep disorders have been further explored in several specific populations which are both at risk of sleep disorders and CVD. Secondly, the review will present some of the risk factors for CVD that are affected by sleep and sleep disorders which include hypertension, diabetes, and obesity. It will also examine the potential underlying mechanisms including inflammation, appetite control, endocrine, and genetic processes that are affected by sleep and sleep disorders leading to increased risk of CVD development. In addition, we will consider the observed bi-directional relationships between sleep and cardiovascular risk factors. For example, obesity, a risk factor for CVD can be affected by sleep, but in turn can increase the risk of certain sleep disorder development which disrupts sleep, leading to further risk of obesity development and increased CVD risk. Finally, the review will explore emerging evidence around lifestyle interventions that have included a sleep component and how it impacts the management of CVD risk factor. The need for increased awareness of the health effects of poor sleep and sleep disorders will be discussed alongside the need for policy intervention to improve sleep to facilitate better health and well-being.

Depression is associated with general sleep disturbance and abnormalities in sleep physiology. For example, compared with control subjects, depressed patients exhibit lower sleep efficiency, longer rapid eye movement (REM) sleep duration, and diminished slow-wave activity during non-REM sleep. A separate literature indicates that depression is also associated with many distinguishing memory characteristics, including emotional memory bias, overgeneral autobiographical memory, and impaired memory suppression. The sleep and memory features that hallmark depression may both contribute to the onset and maintenance of the disorder. Despite our rapidly growing understanding of the intimate relationship between sleep and memory, our comprehension of how sleep and memory interact in the aetiology of depression remains poor. In this narrative review, we consider how the sleep signatures of depression could contribute to the accompanying memory characteristics.

This review systematically assesses the impact of sleep on memory and cognition in healthy individuals across different life stages. It specifically examines how sleep affects memory processes in children, adults, and older adults. The methodology involved a comprehensive literature search, starting with 46 known papers. Keywords and Mesh terms related to sleep and memory consolidation were derived using the Word Frequency Analysis tool in SR Accelerator and Mesh on Demand. A detailed search on PubMed yielded a large set of records. Classifier training on 4854 decisions, these were narrowed down to 1437 papers for full-text screening, culminating in 19 systematic reviews and meta-analyses. Sleep enhances memory consolidation, especially for complex declarative information. While the role of sleep in procedural memory consolidation in children remains less robust compared to declarative memory, findings suggest potential but inconsistent benefits. Sleep improves prospective memory consolidation and aids in complex associative memory tasks. Memory reactivation during sleep, specifically slow-wave sleep, and spindles are implicated in memory consolidation. Meta-analytic evidence suggests that while sleep benefits both emotional and neutral memory consolidation, there is no strong preferential effect of sleep on emotional memory in comparison to neutral memory. In older adults, there is a noticeable reduction in sleep-dependent memory consolidation, particularly for declarative memory, likely linked to a decline in slow-wave sleep. This suggests a decrease in the benefits of sleep for memory consolidation with aging. Overall, the review underscores the importance of sleep in memory processes across all ages, highlighting variations in its impact on different types of memory and across age groups. It points to future research directions for enhancing understanding and practical applications in clinical and educational settings.

Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) is a common disorder characterised by repetitive episodes of the complete or partial collapse of the pharyngeal airway during sleep. This results in cessation (apnoea) or reduction (hypopnoea) of airflow, leading to oxygen desaturation and sleep fragmentation. An individual's disposition to develop OSAHS depends on the collapsibility of a segment of the upper airway. The degree of collapsibility can be quantified by the balance between occluding or extraluminal pressures of the surrounding tissues. Patients can experience snoring, unrefreshing sleep, witnessed apnoeas, waking with a choking sensation and excessive daytime sleepiness. OSAHS has a broad range of consequences, including cardiovascular, metabolic, and neurocognitive sequelae. Treatment options include lifestyle measures, in particular weight loss, and strategies to maintain upper airway patency overnight, including continuous positive airway pressure, mandibular advancement devices and positional modifiers.