The Impact of Standardized Training Resident on Pain Management in Patients with Advanced Lung Cancer.

This study aimed to investigate the effects of Standardized Training Resident on pharmacological interventions for pain management in patients with advanced lung cancer. A total of 84 patients with advanced lung cancer and associated pain were enrolled in the study from December 2019 to August 2023 and were divided into two groups based on their attending physician: a group managed by physician-ST Training Physicians (joint group) (n = 42) and physician-only group (usual group) (n = 42). The Brief Pain Inventory (BPI), oral morphine equivalent, and length of hospital stay.

T63 inhibits osteoclast differentiation through regulating MAPKs and Akt signaling pathways.

Inhibition of excessive osteoclast differentiation and activity is a valid approach for the treatment of osteoporosis. T63 is a small-molecule compound identified from a high throughput screening based on RUNX2 transcriptional activity, and has been reported to stimulate osteoblast formation. However, whether the compound has any effect on osteoclast differentiation remains unknown.

Small molecule T63 suppresses osteoporosis by modulating osteoblast differentiation via BMP and WNT signaling pathways.

Osteoporosis results from the imbalance between bone resorption and bone formation, and restoring the normal balance of bone remodeling is highly desirable for identification of better treatment. In this study, using a cell-based high-throughput screening model representing Runt-related transcription factor 2 (RUNX2) transcriptional activity, we identified a novel small-molecular-weight compound, T63, as an efficient up-regulator of osteogenesis. T63 increased the alkaline phosphatase (ALPL) activity and mineralization as well as gene expression of Alpl and other osteogenic marker genes in mouse osteoblasts and mesenchymal stem cell-like cells.

Methods to detect NF-κB acetylation and methylation.

Posttranslational modifications of NF-κB, including acetylation and methylation, have emerged as an important regulatory mechanism for determining the duration and strength of NF-κB nuclear activity as well as its transcriptional output. Within the seven NF-κB family proteins, the RelA subunit of NF-κB is the most studied for its regulation by lysine acetylation and methylation. Acetylation or methylation at different lysine residues modulates distinct functions of NF-κB, including DNA-binding and transcription activity, protein stability, and its interaction with NF-κB modulators.

Synthesis and biological evaluation of geldanamycin analogs against human cancer cells.

Purpose: To find novel potential and less toxic benquinone anamycin heat shock protein 90 (Hsp90) inhibitors as anticancer agents, a limited series of 17-substituted or 17,19-disubstituted 17-demethoxygeldanamycin analogs were synthesized and tested for anti-proliferation activity against human cancer cells. Liver toxicity was also tested in vivo.

Methods: Five 17-alkylamino-17-demethoxygeldanamycins and two 17-alkylamino-19-methylthio-17-demethoxygeldanamycins were synthesized from geldanamycin (GA) and 19-methylthiogeldanamycin (19-S(methyl)-GA), respectively.

Association between infection of hepatitis B virus and onset risk of B-cell non-Hodgkin's lymphoma: a systematic review and a meta-analysis.

Whether an association between hepatitis B virus (HBV) infection and B-cell non-Hodgkin's lymphoma (B-NHL) risk exists is an open question. In order to provide quantification of the issue, we carried out a meta-analysis of the published data. We identified 4 case-control and 2 nested case-control studies, including a total of 5,396 B-NHL cases.

Salidroside stimulates osteoblast differentiation through BMP signaling pathway.

Salidroside (SAL) is one of main active components of Rhodiola rosea L. and possesses diverse pharmacological effects. However, the direct role of SAL in bone metabolism remains elusive.

Helicobacter pylori activates NF-κB by inducing Ubc13-mediated ubiquitination of lysine 158 of TAK1.

The Helicobacter pylori virulence factor CagA targets a variety of host proteins to alter different cellular responses, including the induction of pro-inflammatory cytokines. We have previously shown that CagA-facilitated lysine 63-linked ubiquitination of TAK1 is essential for the H. pylori-induced NF-κB activation and the expression of proinflammatory cytokines.