[Application of drug delivery microspheres in cancer therapy].

Microspheres are a novel drug delivery system, which provides a new approach for cancer therapy. Anti-cancer agents loaded in microspheres can be released in a controlled and sustained pattern, thereby enhancing the therapeutic efficacy and reducing the side effects and toxicity. The preparation methods for drug delivery microspheres include solvent evaporation, phase separation, spray drying, and microfluidic technology, each of these have advantages and limitations.

Enhancing the antibacterial efficacy of vancomycin analogues: targeting metallo-β-lactamases and cell wall biosynthesis.

Vancomycin is a crucial last-resort antibiotic for tackling Gram-positive bacterial infections. However, its potency fails against the more difficult-to-treat Gram-negative bacteria (GNB). Vancomycin derivatives have shown promise as broad-spectrum antibacterials, but are still underexplored.

Combining deep learning and crowd-sourcing images to predict housing quality in rural China.

Housing quality is essential to human well-being, security and health. Monitoring the housing quality is crucial for unveiling the socioeconomic development status and providing political proposals. However, depicting the nationwide housing quality in large-scale and fine detail is exceedingly rare in remote rural areas owing to the high cost of canonical survey methods.

Mobility restrictions and their implications on the rental housing market during the COVID-19 pandemic in China's large cities.

The COVID-19 pandemic has caused significant mobility restrictions and generated profound impacts on global socio-economic development. Mobility restrictions can generate significant impacts on the demand and supply sides of the rental housing market. By taking 77 large Chinese cities as cases, this research establishes a stepwise mediation effect test to evaluate the impacts of the pandemic on the rental housing market during Q1 2020.

In Vivo Visualization of γ-Glutamyl Transpeptidase Activity with an Activatable Self-Immobilizing Near-Infrared Probe.

γ-Glutamyl transpeptidase (GGT), a type of cell membrane-bound enzyme, is closely involved in a wide range of physiological and pathological processes, and a large number of fluorogenic probes have been developed to detect the activity of GGT. However, the use of these imaging reagents to visualize GGT activity in vivo is largely limited because of rapid diffusion and clearance of activated fluorophores. Herein, by merging quinone methide and a fluorogenic enzyme substrate, we report an activatable self-immobilizing near-infrared probe for the in vitro and in vivo imaging of GGT activity.

Downregulation of DEC1 by RNA interference attenuates ischemia/reperfusion-induced myocardial inflammation by inhibiting the TLR4/NF-κB signaling pathway.

Inflammation has been implicated in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury (MIRI). Previous studies have confirmed that deleted in esophageal cancer 1 (DEC1) is an important transcription factor in inflammation. However, the role of DEC1 in MIRI remains unclear.

A minor structure modification serendipitously leads to a highly carbapenemase-specific fluorogenic probe.

Reported herein is a fluorogenic probe for the detection of carbapenemase activity. This reagent features carbapenem as an enzyme recognition motif and a carbon-carbon double bond between carbapenem and the fluorophore, exhibiting high specificity to all carbapenemases, including metallo carbapenemases and serine carbapenemases, over other β-lactamases.

TRAF5 protects against myocardial ischemia reperfusion injury via AKT signaling.

During the processes of myocardial ischemia reperfusion (I/R) injury, inflammation and apoptosis play an important role. I/R and its induced acute myocardial infarction (AMI) with high morbidity and mortality, and there is no effective treatment for it so far. TRAF5 has been shown to regulate inflammation and apoptosis in atherosclerosis, steatosis and melanoma cells, but its function in myocardial I/R injury is still unclear.

The inverted U-shaped effect of urban hotspots spatial compactness on urban economic growth.

The compact city, as a sustainable concept, is intended to augment the efficiency of urban function. However, previous studies have concentrated more on morphology than on structure. The present study focuses on urban structural elements, i.

TRAF1 Exacerbates Myocardial Ischemia Reperfusion Injury via ASK1-JNK/p38 Signaling.

Background After acute myocardial infarction, the recovery of ischemic myocardial blood flow may cause myocardial reperfusion injury, which reduces the efficacy of myocardial reperfusion. Ways to reduce and prevent myocardial ischemia/reperfusion (I/R) injury are of great clinical significance in the treatment of patients with acute myocardial infarction. TRAF1 (tumor necrosis factor receptor-associated factor 1) is an important adapter protein that is implicated in molecular events regulating immunity, inflammation, and cell death.

Highly selective and wash-free visualization of resistant bacteria with a relebactam-derived fluorogenic probe.

Reported herein is a relebactam-derived fluorogenic reagent for covalent labeling of serine β-lactamases (SBLs), which are the major causes of bacterial resistance to β-lactam antibiotics. This highly selective imaging reagent generates over 300-fold stronger near-infrared fluorescence signals upon covalently bonding to SBLs, allowing wash-free visualization of live antimicrobial-resistant bacteria.

A carbapenem-based fluorescence assay for the screening of metallo-β-lactamase inhibitors.

Reported herein is a fluorescence assay for the rapid screening of metallo-β-lactamase (MBL) inhibitors. This assay employs a fluorogenic carbapenem CPC-1 as substrate and is compatible with all MBLs, including B1, B2 and B3 subclass MBLs. The efficiency of this assay was demonstrated by the rapid inhibition screening of a number of molecules against B2 MBL CphA and 2,3-dimercaprol was identified as a potent CphA inhibitor.

Inhibition of autophagy via activation of PI3K/Akt/mTOR pathway contributes to the protection of hesperidin against myocardial ischemia/reperfusion injury.

Hesperidin has been reported to attenuate myocardial ischemia/reperfusion (I/R) injury; however, its effect on autophagy during myocardial I/R and the underlying mechanism remains unknown. The present study aimed to investigate whether hesperidin inhibited I/R‑induced excessive myocardial autophagy through activating the phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway. Male adult rats were pretreated with hesperidin for a total of 3 days prior to ischemia in the absence or presence of LY294002, a PI3K inhibitor, and then subjected to ischemia for 30 min followed by reperfusion for 4 h.

Downregulation of microRNA-17-5p improves cardiac function after myocardial infarction via attenuation of apoptosis in endothelial cells.

MicroRNA-17-5p (miR-17-5p) was indicated to suppress the formation of blood vessels, which is associated with cardiac function after myocardial infarction. In this study, the relationship between miR-17-5p and cardiac function was researched. Human umbilical vein endothelial cells were infected with adenoviruses.

The HMGB1‑IL‑17A axis contributes to hypoxia/reoxygenation injury via regulation of cardiomyocyte apoptosis and autophagy.

Both the high‑mobility group box 1 protein (HMGB1) and interleukin (IL)‑17A serve important roles in myocardial ischemia and reperfusion injury. The purpose of the present study was to evaluate whether HMGB1 could induce IL‑17A secretion and lead to cardiomyocyte hypoxia/reoxygenation (H/R) injury. Neonatal rat cardiomyocytes were treated with HMGB1‑neutralizing antibody, IL‑17A‑neutralizing antibody, recombinant HMGB1 (rHMGB1) and recombinant IL‑17A (rIL‑17A), respectively.

Promoting effects of IL‑23 on myocardial ischemia and reperfusion are associated with increased expression of IL‑17A and upregulation of the JAK2‑STAT3 signaling pathway.

Interleukin (IL)‑23, as a novel pro‑inflammatory cytokine, is important in several inflammatory diseases, including myocardial ischemia and reperfusion (I/R) injury, however, the underlying mechanism remains to be elucidated. The present study was designed to investigate the specific role of IL‑23 in myocardial I/R injury, and whether the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2‑STAT3) signaling pathway, one of the important downstream signaling pathways of IL‑23, and the IL‑17A downstream pro‑inflammatory cytokine, were involved. Anesthetized rats underwent different treatments with adenovirus (Ad) vectors (Ad‑GFP, Ad‑IL‑23, Anti‑IL‑23 or Ad‑IL‑23+AG490) and were then subjected to ischemia for 30 min prior to 4 h reperfusion.

Short-Term Hesperidin Pretreatment Attenuates Rat Myocardial Ischemia/Reperfusion Injury by Inhibiting High Mobility Group Box 1 Protein Expression via the PI3K/Akt Pathway.

Background/aims: Hesperidin pretreatment has been shown to protect against myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism is poorly understood. This study aimed to investigate the cardioprotective effects of a 3-day hesperidin pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the PI3K/Akt pathway.

Methods: In a fixed-dose study, hematoxylin and eosin staining and myocardial enzyme measurements were used to determine the optimal dose of hesperidin that elicited the best cardioprotective effects against I/R injury.

Low-level environmental arsenic exposure correlates with unexplained male infertility risk.

Humans are exposed to arsenic via drinking water, dietary intake and inhaled particulates. Endemic chronic arsenic exposure related reproductive toxicity is well documented, but the effect of low-level general environmental arsenic exposure on unexplained male infertility (UMI) remains unclear. In this case-control study, we aimed to investigate the relationship between non-geogenic environmental arsenic exposure and UMI risk.

IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions.

Background/aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress.

Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group.

Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A.

Interleukin (IL)-17A has an important role in myocardial ischemia/reperfusion (I/R) injury, and vagal stimulation (VS) has been demonstrated to exert cardioprotective effects. The present study aimed to investigate the effects of VS on a rat model of myocardial I/R injury, and detected an association between VS and IL-17A. Anesthetized rats underwent VS (2 msec; 10 Hz) or were treated with anti-IL-17A neutralized monoclonal antibodies (mAbs) (200 µg; iv), and subjected to ischemia for 30 min prior to 4 h reperfusion.

Effects of high-mobility group box 1 on the expression of Beclin-1 and LC3 proteins following hypoxia and reoxygenation injury in rat cardiomyocytes.

The mechanisms underlying autophagy during myocardial ischemia and reperfusion remain unclear. The present study investigated the relationship between high-mobility group box 1 protein (HMGB1) and autophagy in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes. Neonatal rat cardiomyocytes were treated with recombinant HMGB1 (200 ng/L) or ammonium glycyrrhizinate (100 μM) at appropriate concentrations.

Beta-1-adrenergic receptors mediate Nrf2-HO-1-HMGB1 axis regulation to attenuate hypoxia/reoxygenation-induced cardiomyocytes injury in vitro.

Unlabelled: BACKGROUD/AIMS: The aim of the study was to evaluate the effects of beta1-adrenergic receptors (β1-ARs) -mediated nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 (HO-1)-high mobility group box 1 protein (HMGB1) axis regulation in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes.

Methods: The neonatal cultured cardiomyocytes were concentration-dependently pretreated by dobutamine (DOB), a selective β1-adrenergic receptor agonist, in the absence and/or presence of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), SB203580 (a p38mitogen-activated-protein kinase (p38MAPK) inhibitor), Nrf2siRNA and HO-1siRNA, respectively, and then treated by H/R. The effects and mechanisms by which H/R-induced cardiomyocytes injury were evaluated.

Exposure to arsenic via drinking water induces 5-hydroxymethylcytosine alteration in rat.

Arsenic exposure has been implicated to alter DNA methylation process in vitro and in vivo, but it remains obscure whether it disrupts DNA demethylation process, which is pivotal for epigenetic regulation. The objective of this descriptive study was to investigate the relationship between arsenic exposure and 5-methylcytosine (5mC), 5-hydroxymethylcytosine (5hmC) alterations in various organs. In this study, we exposed male Sprague-Dawley rats to sodium arsenite (0.

Urinary metabolomics revealed arsenic internal dose-related metabolic alterations: a proof-of-concept study in a Chinese male cohort.

Urinary biomonitoring provides the most accurate arsenic exposure assessment; however, to improve the risk assessment, arsenic-related metabolic biomarkers are required to understand the internal processes that may be perturbed, which may, in turn, link the exposure to a specific health outcome. This study aimed to investigate arsenic-related urinary metabolome changes and identify dose-dependent metabolic biomarkers as a proof-of-concept of the information that could be obtained by combining metabolomics and targeted analyses. Urinary arsenic species such as inorganic arsenic, methylarsonic acid, dimethylarsinic acid and arsenobetaine were quantified using high performance liquid chromatography (HPLC)-inductively coupled plasma-mass spectrometry in a Chinese adult male cohort.