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The 2019 novel coronavirus (2019-nCoV) causing an outbreak of pneumonia in Wuhan, Hubei province of China was isolated in January 2020. This study aims to investigate its epidemiologic history, and analyze the clinical characteristics, treatment regimens, and prognosis of patients infected with 2019-nCoV during this outbreak. Clinical data from 137 2019-nCoV-infected patients admitted to the respiratory departments of nine tertiary hospitals in Hubei province from December 30, 2019 to January 24, 2020 were retrospectively collected, including general status, clinical manifestations, laboratory test results, imaging characteristics, and treatment regimens. None of the 137 patients (61 males, 76 females, aged 20-83 years, median age 57 years) had a definite history of exposure to Huanan Seafood Wholesale Market. Major initial symptoms included fever (112/137, 81.8%), coughing (66/137, 48.2%), and muscle pain or fatigue (44/137, 32.1%), with other, less typical initial symptoms observed at low frequency, including heart palpitations, diarrhea, and headache. Nearly 80% of the patients had normal or decreased white blood cell counts, and 72.3% (99/137) had lymphocytopenia. Lung involvement was present in all cases, with most chest computed tomography scans showing lesions in multiple lung lobes, some of which were dense; ground-glass opacity co-existed with consolidation shadows or cord-like shadows. Given the lack of effective drugs, treatment focused on symptomatic and respiratory support. Immunoglobulin G was delivered to some critically ill patients according to their conditions. Systemic corticosteroid treatment did not show significant benefits. Notably, early respiratory support facilitated disease recovery and improved prognosis. The risk of death was primarily associated with age, underlying chronic diseases, and median interval from the appearance of initial symptoms to dyspnea. The majority of patients with 2019-nCoV pneumonia present with fever as the first symptom, and most of them still showed typical manifestations of viral pneumonia on chest imaging. Middle-aged and elderly patients with underlying comorbidities are susceptible to respiratory failure and may have a poorer prognosis.

As the burgeoning field of Artificial Intelligence (AI) continues to permeate the fabric of healthcare, particularly in the realms of patient surveillance and telemedicine, a transformative era beckons. This manuscript endeavors to unravel the intricacies of recent AI advancements and their profound implications for reconceptualizing the delivery of medical care. Through the introduction of innovative instruments such as virtual assistant chatbots, wearable monitoring devices, predictive analytic models, personalized treatment regimens, and automated appointment systems, AI is not only amplifying the quality of care but also empowering patients and fostering a more interactive dynamic between the patient and the healthcare provider. Yet, this progressive infiltration of AI into the healthcare sphere grapples with a plethora of challenges hitherto unseen. The exigent issues of data security and privacy, the specter of algorithmic bias, the requisite adaptability of regulatory frameworks, and the matter of patient acceptance and trust in AI solutions demand immediate and thoughtful resolution .The importance of establishing stringent and far-reaching policies, ensuring technological impartiality, and cultivating patient confidence is paramount to ensure that AI-driven enhancements in healthcare service provision remain both ethically sound and efficient. In conclusion, we advocate for an expansion of research efforts aimed at navigating the ethical complexities inherent to a technology-evolving landscape, catalyzing policy innovation, and devising AI applications that are not only clinically effective but also earn the trust of the patient populace. By melding expertise across disciplines, we stand at the threshold of an era wherein AI's role in healthcare is both ethically unimpeachable and conducive to elevating the global health quotient.

Oxidative stress is increasingly recognized as a central event contributing to the degeneration of dopaminergic neurons in the pathogenesis of Parkinson's disease (PD). Although reactive oxygen species (ROS) production is implicated as a causative factor in PD, the cellular and molecular mechanisms linking oxidative stress with dopaminergic neuron death are complex and not well characterized. The primary insults cause the greatest production of ROS, which contributes to oxidative damage by attacking all macromolecules, including lipids, proteins and nucleic acids, leading to defects in their physiological function. Consequently, the defects in these macromolecules result in mitochondrial dysfunction and neuroinflammation, which subsequently enhance the production of ROS and ultimately neuronal damage. The interaction between these various mechanisms forms a positive feedback loop that drives the progressive loss of dopaminergic neurons in PD, and oxidative stress-mediated neuron damage appears to serve a central role in the neurodegenerative process. Thus, understanding the cellular and molecular mechanisms by which oxidative stress contributes to the loss of dopaminergic neurons may provide a promising therapeutic approach in PD treatment.

Metallic nanostructures with nanometer gaps support hybrid plasmonic modes with an extremely small mode volume and strong local field intensity, which constitutes an attractive plasmonic platform for exploring novel light-matter interaction phenomena at the nanoscale. Particularly, the plasmonic nanocavity formed by a metal nanoparticle closely separated from a thin metal film has received intensive attention in the nanophotonics community, largely attributed to its ease of fabrication, tunable optical properties over a wide spectral range, and the ultrastrong confinement of light at the small gap region scaled down to sub-nanometer. In this article, we review the recent exciting progress in exploring the plasmonic properties of such metal particle-on-film nanocavities (MPoFNs), as well as their fascinating applications in the area of plasmon-enhanced imaging and spectroscopies. We focus our discussion on the experimental fabrication and optical characterization of MPoFNs and the theoretical interpretation of their hybridized plasmon modes, with particular interest on the nanocavity-enhanced photoluminescence and Raman spectroscopies, as well as photocatalysis and molecular nanochemistry.

Ischemic stroke (IS) is a common neurological disorder associated with high disability rates and mortality rates. At present, recombinant tissue plasminogen activator (r-tPA) is the only US(FDA)-approved drug for IS. However, due to the narrow therapeutic window and risk of intracerebral hemorrhage, r-tPA is currently used in less than 5% of stroke patients. Natural compounds have been widely used in the treatment of IS in China and have a wide range of therapeutic effects on IS by regulating multiple targets and signaling pathways. The keywords “ischemia stroke, traditional Chinese Medicine, Chinese herbal medicine, natural compounds” were used to search the relevant literature in PubMed and other databases over the past five years. The results showed that JAK/STAT, NF-κB, MAPK, Notch, Nrf2, and PI3K/Akt are the key pathways, and SIRT1, MMP9, TLR4, HIF-α are the key targets for the natural compounds from traditional Chinese medicine in treating IS. This study aims to update and summarize the signaling pathways and targets of natural compounds in the treatment of IS, and provide a base of information for the future development of effective treatments for IS.

Gasdermin E (GSDME) has an important role in inducing secondary necrosis/pyroptosis. Upon apoptotic stimulation, it can be cleaved by activated caspase-3 to generate its N-terminal fragment (GSDME-NT), which executes pyroptosis by perforating the plasma membrane. GSDME is expressed in many human lung cancers including A549 cells. Paclitaxel and cisplatin are two representative chemotherapeutic agents for lung cancers, which induce apoptosis via different action mechanisms. However, it remains unclear whether they can induce GSDME-mediated secondary necrosis/pyroptosis in lung A549 cancer cells. Here we showed that both paclitaxel and cisplatin evidently induced apoptosis in A549 cells as revealed by the activation of multiple apoptotic markers. Notably, some of the dying cells displayed characteristic morphology of secondary necrosis/pyroptosis, by blowing large bubbles from the cellular membrane accompanied by caspase-3 activation and GSDME-NT generation. But the ability of cisplatin to induce this phenomenon was much stronger than that of paclitaxel. Consistent with this, cisplatin triggered much higher activation of caspase-3 and generation of GSDME-NT than paclitaxel, suggesting that the levels of secondary necrosis/pyroptosis correlated with the levels of active caspase-3 and GSDME-NT. Supporting this, caspase-3 specific inhibitor (Ac-DEVD-CHO) suppressed cisplatin-induced GSDME-NT generation and concurrently reduced the secondary necrosis/pyroptosis. Besides, GSDME knockdown significantly inhibited cisplatin- but not paclitaxel-induced secondary necrosis/pyroptosis. These results indicated that cisplatin induced higher levels of secondary necrosis/pyroptosis in A549 cells than paclitaxel, suggesting that cisplatin may provide additional advantages in the treatment of lung cancers with high levels of GSDME expression.

Background Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor 21 (FGF21), a metabolic regulator secreted by the liver, in VILI development. Methods Serum FGF21 concentrations were determined in patients undergoing mechanical ventilation during general anesthesia and in a mouse VILI model. Lung injury was compared between FGF21-knockout (KO) mice and wild-type (WT) mice. Recombinant FGF21 was administrated in vivo and in vitro to determine its therapeutic effect. Results Serum FGF21 levels in patients and mice with VILI were significantly higher than in those without VILI. Additionally, the increment of serum FGF21 in anesthesia patients was positively correlated with the duration of ventilation. VILI was aggravated in FGF21-KO mice compared with WT mice. Conversely, the administration of FGF21 alleviated VILI in both mouse and cell models. FGF21 reduced Caspase-1 activity, suppressed the mRNA levels of Nlrp3 , Asc, Il-1β, Il-18, Hmgb1 and Nf-κb , and decreased the protein levels of NLRP3, ASC, IL-1β, IL-18, HMGB1 and the cleaved form of GSDMD. Conclusions Our findings reveal that endogenous FGF21 signaling is triggered in response to VILI, which protects against VILI by inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These results suggest that boosting endogenous FGF21 or the administration of recombinant FGF21 could be promising therapeutic strategies for the treatment of VILI during anesthesia or critical care.

Mare volcanics on the Moon are the key record of thermo-chemical evolution throughout most of lunar history 1 – 3 . Young mare basalts—mainly distributed in a region rich in potassium, rare-earth elements and phosphorus (KREEP) in Oceanus Procellarum, called the Procellarum KREEP Terrane (PKT) 4 —were thought to be formed from KREEP-rich sources at depth 5 – 7 . However, this hypothesis has not been tested with young basalts from the PKT. Here we present a petrological and geochemical study of the basalt clasts from the PKT returned by the Chang’e-5 mission 8 . These two-billion-year-old basalts are the youngest lunar samples reported so far 9 . Bulk rock compositions have moderate titanium and high iron contents  with KREEP-like rare-earth-element and high thorium concentrations. However, strontium–neodymium isotopes indicate that these basalts were derived from a non-KREEP mantle source. To produce the high abundances of rare-earth elements and thorium, low-degree partial melting and extensive fractional crystallization are required. Our results indicate that the KREEP association may not be a prerequisite for young mare volcanism. Absolving the need to invoke heat-producing elements in their source implies a more sustained cooling history of the lunar interior to generate the Moon’s youngest melts. Isotopic analysis of basalt clasts returned from the Moon by the Chang’e-5 mission indicates that the rocks were derived from a mantle source that lacked potassium, rare-earth elements and phosphorus.

For a long time, hydrogen sulfide (H S) has been considered as merely a toxic by product of cell metabolism, but nowadays is emerging as a novel gaseous signal molecule, which participates in seed germination, plant growth and development, as well as the acquisition of stress tolerance including cross-adaptation in plants. Cross-adaptation, widely existing in nature, is the phenomenon in which plants expose to a moderate stress can induce the resistance to other stresses. The mechanism of cross-adaptation is involved in a complex signal network consisting of many second messengers such as Ca , abscisic acid, hydrogen peroxide and nitric oxide, as well as their crosstalk. The cross-adaptation signaling is commonly triggered by moderate environmental stress or exogenous application of signal molecules or their donors, which in turn induces cross-adaptation by enhancing antioxidant system activity, accumulating osmolytes, synthesizing heat shock proteins, as well as maintaining ion and nutrient balance. In this review, based on the current knowledge on H S and cross-adaptation in plant biology, H S homeostasis in plant cells under normal growth conditions; H S signaling triggered by abiotic stress; and H S-induced cross-adaptation to heavy metal, salt, drought, cold, heat, and flooding stress were summarized, and concluded that H S might be a candidate signal molecule in plant cross-adaptation. In addition, future research direction also has been proposed.

It is well known that glutamate (Glu), a neurotransmitter in human body, is a protein amino acid. It plays a very important role in plant growth and development. Nowadays, Glu has been found to emerge as signaling role. Under normal conditions, Glu takes part in seed germination, root architecture, pollen germination, and pollen tube growth. Under stress conditions, Glu participates in wound response, pathogen resistance, response and adaptation to abiotic stress (such as salt, cold, heat, and drought), and local stimulation (abiotic or biotic stress)-triggered long distance signaling transduction. In this review, in the light of the current opinion on Glu signaling in plants, the following knowledge was updated and discussed. 1) Glu metabolism; 2) signaling role of Glu in plant growth, development, and response and adaptation to environmental stress; as well as 3) the underlying research directions in the future. The purpose of this review was to look forward to inspiring the rapid development of Glu signaling research in plant biology, particularly in the field of stress biology of plants.