Respiratory pathogens in infants and young children with acute respiratory illness: a prospective cohort study, China, 2023-2024.

Background: Infants are vulnerable to acute respiratory infections (ARIs), which result in pediatric morbidity and even fatalities. A surge of ARIs among infants and young children was reported in China in 2023, garnering global attention. We aimed to investigate the frequency and types of respiratory pathogens associated with the risk of acute respiratory illnesses in infants and young children during this period.

Discovery of novel microtubule destabilizing agents via virtual screening methods and antitumor evaluation.

Background And Objective: Agents targeting to Colchicine-site of tubulin have become a focus of attention in the development of new anti-cancer drugs due to their ability to overcome multi-drug resistant and anti-angiogenesis effects against tumor endothelium.

Methods: In this investigation, the machine learning methods and molecular docking approach were combined to identify promising destabilizing agents targeting for colchicine-site of tubulin.

Results: Among these screened agents, hit22 represented excellent anti-tumor activity, which exhibited anti-proliferative activity toward H1299 cell with IC value of 3.

Advance on Blast-Induced Traumatic Brain Injury.

Blast-induced traumatic brain injury (bTBI) is an injury to brain tissue caused by the blast shock wave of an explosive, which is the leading cause of death and disability among military personnel during wartime. By establishing animal models of bTBI that simulate different degrees and types of injuries, it is possible to clarify the neuropathological changes including molecular and cellular mechanisms. The aim of this review is to summarize the establishment of animal models of bTBI, the mechanism, diagnosis, treatment and brain-related diseases of bTBI, which will provide a basis for improving the understanding of bTBI.

NETs activate AIM2 to mediate synovial fibroblast pyroptosis and promote acute gouty arthritis development.

Background: Acute gouty arthritis is a metabolic disease characterized by hyperuricemia, with acute attacks involving neutrophil-released NETs activating immune responses through their major component, DNA, as danger-associated molecular patterns (DAMPs).

Objective: To investigate whether DNA from NETs activates the AIM2 inflammasome in synovial fibroblasts during acute gouty arthritis attacks, inducing pyroptosis and exacerbating inflammation.

Methods: The AIM2 gene knockdown mouse model of acute gouty arthritis was constructed, the joint pathological changes were observed by H&E staining, the synovium fibroblasts and neutrophils were sorted by flow cytometry, and the expressions of AIM2, Caspase-1 and GSDMD related proteins were detected by Western blot.

Identification of novel inhibitors targeting PI3Kα via ensemble-based virtual screening method, biological evaluation and molecular dynamics simulation.

PIK3CA gene encoding PI3K p110α is one of the most frequently mutated and overexpressed in majority of human cancers. Development of potent and selective novel inhibitors targeting PI3Kα was considered as the most promising approaches for cancer treatment. In this investigation, a virtual screening platform for PI3Kα inhibitors was established by employing machine learning methods, pharmacophore modeling, and molecular docking approaches.

Discovery of novel Akt1 inhibitors by an ensemble-based virtual screening method, molecular dynamics simulation, and in vitro biological activity testing.

Akt1, as an important member of the Akt family, plays a controlled role in cancer cell growth and survival. Inhibition of Akt1 activity can promote cancer cell apoptosis and inhibit tumor growth. Therefore, in this investigation, a multilayer virtual screening approach, including receptor-ligand interaction-based pharmacophore, 3D-QSAR, molecular docking, and deep learning methods, was utilized to construct a virtual screening platform for Akt1 inhibitors.

Seroepidemiology of pertussis in the east of China: Estimates of incidence of infection in adolescents and adults pre- and post-COVID-19.

Introduction: The dramatic decrease in the number of reported cases of pertussis during COVID-19 pandemic has been underestimated. The objective was to compare the estimated incidence rate of pertussis in populations pre- and post-COVID-19 pandemic by analyzing the anti-pertussis toxin (anti-PT) IgG and anti-filamentous hemagglutininant (anti-FHA) IgG antibodies in healthy Chinese population from 2018 to 2021.

Methods: All serum samples ( = 1,000) were collected from healthy population (aged ≥ 15 years) who attended an annual monitoring project of antibody levels in Jiangsu province in 2018-2021 were measured by ELISA.

Proteomic global proteins analysis in blast lung injury reveals the altered characteristics of crucial proteins in response to oxidative stress, oxidation-reduction process and lipid metabolic process.

Blast lung injury (BLI) is the most common fatal blast injury induced by overpressure wave in the events of terrorist attack, gas and underground explosion. Our previous work revealed the characteristics of inflammationrelated key proteins involved in BLI, including those regulating inflammatory response, leukocyte transendothelial migration, phagocytosis, and immune process. However, the molecular characteristics of oxidative-related proteins in BLI ar still lacking.

DDAH1 Promotes Lung Endothelial Barrier Repair by Decreasing Leukocyte Transendothelial Migration and Oxidative Stress in Explosion-Induced Lung Injury.

Explosion-induced injury is the most commonly encountered wound in modern warfare and incidents. The vascular inflammatory response and subsequent oxidative stress are considered the key causes of morbidity and mortality among those in blast lung injury. It has been reported dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays important roles in regulating vascular endothelial injury repair and angiogenesis, but its role in explosion-induced injury remains to be explained.

Tandem Mass Tag-Based Quantitative Proteomic Analysis Reveals Pathways Involved in Brain Injury Induced by Chest Exposure to Shock Waves.

Recurrent chest blast exposure can lead to brain inflammation, oxidative stress, and mental disorders in soldiers. However, the mechanism that underlies brain injury caused indirectly by chest blasts remains unclear. It is urgent to find additional reliable biomarkers to reveal the intimate details of the pathogenesis of this phenomenon.

Resveratrol ameliorates thoracic blast exposure-induced inflammation, endoplasmic reticulum stress and apoptosis in the brain through the Nrf2/Keap1 and NF-κB signaling pathway.

Blast injuries include the various types of internal and external trauma caused by the impact force of high-speed blast waves with multiple mechanisms involved. Thoracic blast exposure could induce neurotrauma as well, but effective therapies are lacking. Resveratrol is a polyphenol flavonoid secreted by plants and has been shown to provide cardiovascular protection and play anti-inflammatory, anti-oxidation and anti-cancer roles.

Solute carrier family 12 member 8 (SLC12A8) is a potential biomarker and related to tumor immune cell infiltration in bladder cancer.

The solute carrier family has been reported to play critical roles in the progression of several cancers; however, the relationship between solute carrier family 12 member 8 (SLC12A8) and bladder cancer (BC) has not been clearly confirmed. This study explores the prognostic value of SLC12A8 for BC and its correlation with immune cell infiltration. We found that the expression of SLC12A8 mRNA was significantly overexpressed in BC tissues compared with noncancerous tissues in multiple public databases, and the result was validated using real-time PCR and immunohistochemistry (IHC).

Proteomic Analysis Revealed the Characteristics of Key Proteins Involved in the Regulation of Inflammatory Response, Leukocyte Transendothelial Migration, Phagocytosis, and Immune Process during Early Lung Blast Injury.

Previous studies found that blast injury caused a significant increased expression of interleukin-1, IL-6, and tumor necrosis factor, a significant decrease in the expression of IL-10, an increase in Evans blue leakage, and a significant increase in inflammatory cell infiltration in the lungs. However, the molecular characteristics of lung injury at different time points after blast exposure have not yet been reported. Therefore, in this study, tandem mass spectrometry (TMT) quantitative proteomics and bioinformatics analysis were used for the first time to gain a deeper understanding of the molecular mechanism of lung blast injury at different time points.

Quantitative analysis of the global proteome in lung from mice with blast injury.

Aim Of The Study: The mechanism by which primary shock wave causes lung injury is unclear. The aim of this study is to find the changes of protein that can be helpful in understanding blast-induced lung injury.

Material And Methods: A quantitative analysis of their global proteome was conducted in lung from mice with blast injury using LC-MS/MS.

Novel Metabolomics Serum Biomarkers for Pancreatic Ductal Adenocarcinoma by the Comparison of Pre-, Postoperative and Normal Samples.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive human malignancies. The metabolomic approaches are developed to discover the novel biomarkers of PDAC. 550 preoperative, postoperative PDAC and normal controls (NCs) serums were employed to characterize metabolic alterations in training and validation sets by LC-MS.

Tanshinone IIA alleviates blast-induced inflammation, oxidative stress and apoptosis in mice partly by inhibiting the PI3K/Akt/FoxO1 signaling pathway.

Although Tanshinone IIA (Tan IIA) has been associated with inflammation, oxidative stress and apoptosis, the effects of Tan IIA on lung blast injury remain uncertain. In this study, we explored the effects of Tan IIA on lung blast injury, studied its possible molecular mechanisms. Fifty C57BL/6 mice were randomly divided into the control, blast, blast + Tan IIA, blast + LY294002 (a PI3K inhibitor), or blast + Tan IIA + LY294002 groups.

CD28 Deficiency Ameliorates Thoracic Blast Exposure-Induced Oxidative Stress and Apoptosis in the Brain through the PI3K/Nrf2/Keap1 Signaling Pathway.

Blast exposure is a worldwide public health concern, but most related research has been focused on direct injury. Thoracic blast exposure-induced neurotrauma is a type of indirect injuries where research is lacking. As CD28 stimulates T cell activation and survival and contributes to inflammation initiation, it may play a role in thoracic blast exposure-induced neurotrauma.

CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway.

Although CD28 is associated with the expression of inflammatory mediators, apoptosis-related protein, immunosuppression, and tumorigenesis, the effects of CD28 deficiency on blast exposure-induced lung injury have not been investigated. In this study, we have explored the effects of CD28 on blast exposure-induced lung injury and studied its potential molecular mechanisms. A mouse model of blast exposure-induced acute lung injury was established.

Metabolic profiling analysis upon acylcarnitines in tissues of hepatocellular carcinoma revealed the inhibited carnitine shuttle system caused by the downregulated carnitine palmitoyltransferase 2.

The carnitine shuttle system (CSS) plays a crucial role in the transportation of fatty acyls during fatty acid β-oxidation for energy supplementation, especially in cases of high energy demand, such as in cancer. In this study, to systematically characterize alterations of the CSS in hepatocellular carcinoma (HCC), acylcarnitine metabolic profiling was carried out on 80 pairs of HCC tissues and adjacent noncancerous tissues (ANTs) by using ultra-performance liquid chromatography coupled to mass spectrometry. Twenty-four acylcarnitines classified into five categories were identified and characterized between HCCs and ANTs.

Influence of chitosan oligosaccharide on the gelling and wound healing properties of injectable hydrogels based on carboxymethyl chitosan/alginate polyelectrolyte complexes.

In situ injectable hydrogels for wound healing based on carboxymethyl chitosan (CMCS) and alginate were developed in this work. The liquid mixture of CMCS and alginate solutions formed a gel by polyelectrolyte complexation after addition of d-glucono-δ-lactone (GDL), which slowly hydrolyzed and donated protons. When chitosan oligosaccharide (COS) was added into the mixture, a two-stage gelling process occurred.

Shock waves increase pulmonary vascular leakage, inflammation, oxidative stress, and apoptosis in a mouse model.

Severe lung damage is a major cause of death in blast victims, but the mechanisms of pulmonary blast injury are not well understood. Therefore, it is important to study the injury mechanism of pulmonary blast injury. A model of lung injury induced by blast exposure was established by using a simulation blast device.

Cold exposure induced oxidative stress and apoptosis in the myocardium by inhibiting the Nrf2-Keap1 signaling pathway.

Background: Exposure to cold weather is associated with infaust cardiovascular responses, including myocardial infarction and arrhythmias. However, the exact mechanisms of these adverse changes in the myocardium under cold stress are unknown. This study was designed to investigate the mechanisms of cardiac injury induced by cold stress in mice.

Chitosan oligosaccharide ameliorates acute lung injury induced by blast injury through the DDAH1/ADMA pathway.

Objective: To investigate the protective effect of chitosan oligosaccharide (COS) on acute lung injury (ALI) caused by blast injury, and explore possible molecular mechanisms.

Methods: A mouse model of blast injury-induced ALI was established using a self-made explosive device. Thirty mice were randomly assigned to control, ALI and ALI + COS groups.

Cold stress-induced brain injury regulates TRPV1 channels and the PI3K/AKT signaling pathway.

Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel that interacts with several intracellular proteins in vivo, including calmodulin and Phosphatidylinositol-3-Kinase/Protein Kinase B (PI3K/Akt). TRPV1 activation has been reported to exert neuroprotective effects. The aim of this study was to examine the impact of cold stress on the mouse brain and the underlying mechanisms of TRPV1 involvement.

[Purification and characterization of a novel alpha-galactosidase from penicillium sp. F63 CGMCC1669].

An a-galactosidase-producing fungus was screened out of 26 filamentous fungi isolated from soil by us. Phylogenetic analysis based on the alignment of 18S rDNA sequences, combined with the morphological identification, indicated that the strain F63 was a member of the genus Penicillium. The a-galactosidase from Penicillium sp.