Background The nutritional status of COVID‐19 patients is unknown. This study evaluates the clinical and nutritional characteristics of severe and critically ill patients infected with SARS‐CoV‐2, and investigates the relationship between nutritional risk and clinical outcomes. Methods A retrospective, observational study was conducted at West Campus of Union Hospital in Wuhan. Patients confirmed with SARS‐CoV‐2 infection by a nucleic acid‐positive test and identified as severe or critically ill, were enrolled in this study. Clinical data and outcomes information was collected and nutritional risk was assessed by using Nutritional Risk Screening 2002 (NRS). Results Totally, 413 patients were enrolled in this study, including 346 severe patients and 67 critically ill patients. Most patients, especially critically ill patients, had significant changes in nutrition‐related parameters and inflammatory markers. As for nutritional risk, the critically ill patients had significantly higher proportion of high NRS scores ( P <0.001), which were correlated with inflammatory and nutrition‐related markers. Among 342 patients with NRS score ≥3, only 84 (25%) received nutritional support. The critically ill patients and the patients with higher NRS score had a higher risk of mortality and longer stay in hospital. In logistic regression models, one unit increased in NRS score was associated with the risk of mortality increased by 1.23 times (adjusted OR = 2.23, 95% CI : 1.10, 4.51, P = 0.026). Conclusions Most severe and critically ill patients infected with SARS‐CoV‐2 are at nutritional risk. The patients with higher nutrition risk have worse outcome, and require nutritional therapy. This article is protected by copyright. All rights reserved

Type 3 adenylyl cyclase (Adcy3) is localized to the cilia of olfactory sensory neurons (OSNs) and is an essential component of the olfactory cyclic adenosine monophosphate (cAMP) signaling pathway. Although the role of this enzyme in odor detection and axonal projection in OSNs was previously characterized, researchers will still have to determine its function in the maturation of postnatal OSNs and olfactory cilium ultrastructure. Previous studies on newborns showed that the anatomic structure of the main olfactory epithelium (MOE) of Adcy3 knockout mice (Adcy3-/-) is indistinguishable from that of their wild-type littermates (Adcy3+/+), whereas the architecture and associated composition of MOE are relatively underdeveloped at this early age. The full effects of sensory deprivation on OSNs may not also be exhibited in such age. In the present study, following a comparison of postnatal OSNs in seven-, 30-, and 90-day-old Adcy3-/- mice and wild-type controls (Adcy3+/+), we observed that the absence of Adcy3 leads to cumulative defects in the maturation of OSNs. Upon aging, Adcy3-/- OSNs exhibited increase in immature cells and reduction in mature cells along with elevated apoptosis levels. The density and ultrastructure of Adcy3-/- cilia were also disrupted in mice upon aging. Collectively, our results reveal an indispensable role of Adcy3 in postnatal maturation of OSNs and maintenance of olfactory cilium ultrastructure in mice through adulthood.

Wearable flexible electronic strain sensor devices have developed rapidly in recent years due to their potential capacity to detect human motion in various situations. However, it still remains still a big challenge to fabricate strain sensors with high sensitivity over a wide workable strain range. In order to meet this challenge, a new type of strain sensor based on elastomer/carbon nanotube composite fiber is reported in this work. Elastomer fibers are initially prepared via the electrospinning of styrene ethylene butene styrene block copolymer (SEBS). The resultant SEBS fibers are then functionalized by sequentially coating with dopamine (DA) coating and carboxyl group (‐COOH) grafted multi‐walled carbon nanotubes (MWCNTs) under vacuum filtration and ultrasonication. Scanning electron microscopy (SEM) and thermogravimetric analysis reveals that a large amount of MWCNTs is firmly bonded onto the SEBS fibers and evenly distributed. SEBS@PDA/MWCNTs composite fibers based strain sensors exhibit excellent performance, including a high gauge factor of 3717 and large workable strain range up to 530%. Furthermore, the developed sensors demonstrate excellent washing fastness and superior sensitivity in monitoring both small strains (e.g., pulse beats and vocal cord vibrations) and large strains (e.g., finger, elbow, and knee bending).

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspase-3. Prolonged Hcy treatment also upregulated glucose-regulated protein 78 (GRP78), activated protein kinase RNA-like ER kinase (PERK), and induced the expression of C/EBP homologous protein (CHOP) and the phosphorylation of NF-κb. The inhibition of NOX4 decreased the production of ROS and alleviated the Hcy-induced HUVEC apoptosis and ER stress. Blocking the PERK pathway partly alleviated Hcy-induced HUVEC apoptosis and the activation of NF-κb. Taken together, our results suggest that Hcy-induced mitochondrial dysfunction crucially modulated apoptosis and contributed to the activation of ER stress in HUVEC. The excessive activation of the PERK pathway partly contributed to Hcy-induced HUVEC apoptosis and the phosphorylation of NF-κb.