Activity

The overall 1-year and 3-year freedom from recurrent MR rates were 94.3% and 65.3%, respectively, and a significant difference was found between the SA group and the non-SA group (93.8% and 93.8%

. 95.5% and 44.2%, P=0.035). In a subgroup analysis, this significant difference was only found in the small LA group (≤60 mm).

Our results suggest that MV repair for AFMR is safe and effective. It improves heart failure symptoms and results in reverse-remodeling of both the LA and LV. Concomitant SA might benefit patients in terms of recurrent MR, especially in the small LA group (≤60 mm).

Our results suggest that MV repair for AFMR is safe and effective. It improves heart failure symptoms and results in reverse-remodeling of both the LA and LV. Concomitant SA might benefit patients in terms of recurrent MR, especially in the small LA group (≤60 mm).

The removal of permanent internal fixation devices by secondary surgery could be avoided if these devices were made of degradable magnesium and magnesium alloys. Before such implants can be used clinically, however, the biological effect of magnesium exposure on surrounding bone must be evaluated. Previous studies have focused on bone formation; few have examined the effects of magnesium on the bone quality that affect many biomechanical properties.

Using bone quality parameters, we analyzed

changes in bone properties and biomechanics after exposure to locally high levels of magnesium.

Local bone mineralization was significantly disrupted following exposure to a porous rod of pure magnesium. Normal crystal formation and crystallinity were inhibited and the mineral-to-matrix ratio decreased. These results were consistent with those of

experiments, in which high levels of magnesium inhibited mineral deposition by mesenchymal stem cells (MSCs) but increased alkaline phosphatase (ALP) expression. The same mineralization inhibition was observed around magnesium implants via micro-computerized tomography (micro-CT) and von Kossa staining. Such reduced bone quality around degrading magnesium rods could negatively impact bone biomechanics.

This study showed that exposure to the local high magnesium levels that arise from rapidly degrading magnesium devices may significantly disrupt bone mineralization and negatively impact bone biomechanics.

This study showed that exposure to the local high magnesium levels that arise from rapidly degrading magnesium devices may significantly disrupt bone mineralization and negatively impact bone biomechanics.

Cigarette smoke (CS)-induced build-up of oxidative stress is the leading cause of chronic obstructive pulmonary disease (COPD). Monoamine oxidases (MAOs) are novel sources of reactive oxygen species (ROS) due to the production of hydrogen peroxide (H

O

). However, it remains unclear whether MAO signaling is involved in CS-induced oxidative stress

. This study aimed at investigating the impact of selegiline, a selective MAO-B inhibitor, on CS-induced lung oxidative stress and inflammation

and its underlying mechanism.

Sprague Dawley rats were randomly divided into four groups saline plus sham air (Saline/air), saline plus cigarette smoke (Saline/CS), selegiline plus sham air (Slg/air) and selegiline plus cigarette smoke (Slg/CS). Rats from Saline/air and Saline/CS groups were intraperitoneally injected with saline (2 mL/kg body weight) while rats from Slg/air and Slg/CS groups were injected with selegiline (2 mg/kg body weight) about 30 min prior to exposure daily. The Saline/air and Slg/air groups o effect. Selegiline attenuated CS-induced elevation of pro-inflammatory mediators (CINC-1, MCP-1 and IL-6) and restored CS-induced reduction of anti-inflammatory mediator IL-10 in BAL, which was driven through MAPK and NF-κB.

Inhibition of MAO-B may provide a promising therapeutic strategy for CS-mediated oxidative stress and inflammation in acute CS-exposed rat lungs.

Inhibition of MAO-B may provide a promising therapeutic strategy for CS-mediated oxidative stress and inflammation in acute CS-exposed rat lungs.

Hereditary factors contributed to breast cancer susceptibility. Low

mutation prevalence was demonstrated in previous

mutation screening in Chinese breast cancer patients. Multiple-gene sequencing may assist in discovering detrimental germline mutation in.

negative breast cancers.

A total of 384 Chinese subjects with any two of high-risk factors were recruited and screened by next-generation sequencing (NGS) for 30 cancer susceptible genes. Variants with a truncating, initiation codon or splice donor/acceptor effect, or with pathogenicity demonstrated in published literature were classified into pathogenic/likely-pathogenic mutations.

In total, we acquired 39 (10.2%) patients with pathogenic/likely-pathogenic germline mutations, including one carrying two distinct mutations. Major mutant non-

genes were

(n=11, 2.9%),

(n=7, 1.8%),

(n=6, 1.6%) and

(n=5, 1.3%). Other mutant genes included

(n=3, 0.8%),

(n=2, 0.5%),

(n=1, 0.3%),

(n=1, 0.3%),

(n=1, 0.3%),

(n=1, 0.3%),

(n=1, 0.3%) and

(n=1, 0.3%). this website A splicing germline mutation,

c.934-2A>G, was a hotspot (9/384, 2.3%) in Chinese breast cancer.

Among

-negative breast cancer patients with high hereditary risk in China, 10.2% carried mutations in cancer associated susceptibility genes.

and

had relatively high mutation rates (2.9% and 1.8%). Multigene testing contributes to understand genetic background of

-negative breast cancer patients with high hereditary risk.

Among BRCA-negative breast cancer patients with high hereditary risk in China, 10.2% carried mutations in cancer associated susceptibility genes. MUTYH and PTCH1 had relatively high mutation rates (2.9% and 1.8%). Multigene testing contributes to understand genetic background of BRCA-negative breast cancer patients with high hereditary risk.

Glucocorticoids, such as dexamethasone, are widely used for prevent vomiting and allergic reactions associated with cancer immunotherapy and chemotherapy. Although such use is reported to reduce the immunotherapy’s efficacy, nevertheless, how dexamethasone associates with specific immune cells, particularly inside the tumor microenvironment, still remains unclear.

We integrate multi-omics data, including transcriptome, mutation, copy number variation (CNV), and methylation, to explore the dexamethasone responsive genes.

We surprisingly found that dexamethasone responsive genes are transcriptionally down-regulated in general, where heterozygous deletion underlie such dysregulation. We further perform the pathway analysis and demonstrate that such dysregulation associates with cancer hallmarks such as epithelial-to-mesenchymal transformation (EMT) activation. Next, by performing the drug sensitivity analysis, we generate a list of drugs whose efficacy potentially associates with dexamethasone response, including Methotrexate and Navitoclax.