The influence mechanism analysis of family doctor team effectiveness: a mixed-method approach.

Background: Team-based delivery of family doctor services is associated with improved patient experiences, better health outcomes, and more efficient healthcare utilization. Team effectiveness is related to the team's output, and family doctor team effectiveness (FDTE) directly impacts the quality and efficiency of contracted family doctor services. We aimed to explore the path and mechanisms influencing FDTE, propose strategies for improvement, and enhance both team effectiveness and service quality.

The formation mechanism of primary health care team effectiveness : a qualitative comparative analysis research.

Background: Team-based care is an essential part of primary health care (PHC), and its team service delivery process is a systematic one involving multiple and complex influences. Research on the formation mechanism can help improve the effectiveness of primary health care teams (PHCTs).

Methods: First, based on the Donabedian model, we explored the theoretical framework of a PHC team's effectiveness formation mechanism.

Low dose Emodin induces tumor senescence for boosting breast cancer chemotherapy via silencing NRARP.

Purpose: The resistance to 5-FU often limits its clinical effectiveness on breast cancer treatment. Combination therapy thus is employed to overcome this treatment resistance. We here report a potent antitumor effect of Emodin at low dose on chemotherapy sensitivity of MCF-7 breast cancer cells.

Emodin induces apoptosis of human breast cancer cells by modulating the expression of apoptosis-related genes.

The aim of this study was to investigate the effects of emodin on the proliferation of human breast cancer cells Bcap-37 and ZR-75-30. Cell viability following emodin treatment was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of emodin on apoptosis were determined by flow cytometry using Annexin V-fluorescein isothiocyanate and propidium iodide staining.

Predictive value of phosphorylated mammalian target of rapamycin for disease-free survival in breast cancer patients receiving neoadjuvant chemotherapy.

The mammalian target of rapamycin (mTOR)/eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) pathway plays a critical role in cell growth, survival and angiogenesis, and has been demonstrated to correlate with human epidermal growth factor receptor 2 (HER2) status. Neoadjuvant chemotherapy (NAC), also known as preoperative therapy, is now well established in the treatment of inoperable locally advanced and inflammatory breast cancer. study has shown that mTOR inhibitors, together with cytotoxic agents, exhibit tumor cell killing activity.

The combined effect of survivin-targeted shRNA and emodin on the proliferation and invasion of ovarian cancer cells.

Survivin has been shown to be highly expressed in ovarian cancers, but not normal ovarian tissue, which makes it an attractive target for ovarian cancer treatment. Emodin is a traditional Chinese medicine that has been found to inhibit proliferation and induce apoptosis in ovarian cancer cells. Thus, in our study, we combined survivin-targeted shRNA (sur-shRNA) with emodin and tested the effects of this combination on ovarian cancer cells to identify more effective therapeutics against ovarian cancer.

Conditionally replicating adenovirus SG500-expressed mutant Dm-dNK gene for breast cancer therapy.

The purpose of this analysis was to investigate the enzyme activity and specificity of using adenovirus-mediated Drosophila melanogaster deoxyribonucleoside kinase (Dm-dNK) mutants in combination with gemcitabine. Compared with herpes simplex type 1 thymidine kinase (HSV-TK) and other known dNKs, this Dm-dNK enzyme has a broader substrate specificity and a higher catalytic rate. We created the Dm-dNK mutants (dNKmu) by site-directed mutagenesis at the sites of 244E, 245S, 251S and 252R, with the last 10 amino acids in the amino acid sequence randomly mutated.

Adenovirus-mediated Drosophila melanogaster deoxyribonucleoside kinase mutants combined with gemcitabine harbor a safe cancer treatment profile.

The purpose of this analysis was to investigate the enzyme activity and specificity of adenovirus-mediated Drosophila melanogaster deoxyribonucleoside kinase (Dm-dNK) mutants in combination with gemcitabine. Compared to herpes simplex type 1 thymidine kinases (HSV-TK) and other known dNKs, this Dm-dNK enzyme has a broader substrate specificity and a higher catalytic rate. We created the Dm-dNK mutants (dNKmut) by site-directed mutagenesis at the sites of 244E, 245S, 251S, and 252R, with the last 10 amino acids in the amino acid sequence randomly alternated.

Retrovirus-mediated Drosophila melanogaster multisubstrate deoxyribonucleoside kinase gene therapy of gastric cancer cells in vitro and in vivo.

Aim: The cytotoxicity of the Drosophila melanogaster multisubstrate deoxyribonucleoside kinase (Dm-dNK)/nucleoside analog system to human gastric carci-noma cells was evaluated in vitro and in vivo for the development of novel gene therapy for gastric cancer.

Methods: MGC-803 and BGC-823 cells were infected with retroviral vectors containing the Dm-dNK gene expressing Dm-dNK in its active form. [(3)H]-labeled substrates were used for enzyme activity assays and cytotoxicities were evaluated in vitro by MTT assay and annexin-V-FITC labeled FACS methods.

Effects of MK-801, taurine and dextromethorphan on neurotoxicity caused by manganese in rats.

The effects of manganese on the activities of GS, PAG, SDH and Na(+)-K(+)-ATPase were investigated and the impact of MK-801, Tau and DM on manganese-induced neurotoxicity were observed in rats. Seventy Wistar rats were divided into seven groups, 10 animals for each group. The first group was the control group, the second to fourth groups were 8, 40 and 200 micromol/kg MnCl(2) groups, the fifth to seventh groups were 0.