Association of Combined Healthy Lifestyle Factors With Incident Dementia in Participants With and Without Multimorbidity: A Large Population-Based Prospective Cohort Study.

BACKGROUND: The effect of a healthy lifestyle on dementia associated with multimorbidity is not well understood. Our objective is to examine whether the adoption of a healthy lifestyle could potentially reduce the elevated risk of dementia in individuals with and without multimorbidity. METHODS: We utilized data from the UK Biobank cohort. A comprehensive healthy lifestyle score, ranging from 0 to 6, was generated. Cox proportional hazards models were used to examine the associations between multimorbidity, the healthy lifestyle score, and the incidence risk of dementia. RESULTS: Over a median follow-up period of 12.5 years, 5 852 all-cause dementia were recorded. Multimorbidity including cardiovascular, metabolic, neuropsychiatric, and inflammation-related diseases was associated with a higher risk of subsequent dementia. Each additional chronic disease was associated with a hazard ratio (HR) of 1.38 (95% CI: 1.33, 1.44). Compared to individuals without multimorbidity and a healthy lifestyle score of 5-6, patients with multimorbidity and a lifestyle score of 0-1 had a significantly higher risk of dementia (HR: 3.13; 95% CI: 2.64, 3.72), but the risk was markedly attenuated among those with multimorbidity and a lifestyle score of 5-6. Among patients with 3 or more diseases, the HR for dementia was 0.53 (95%CI: 0.42, 0.68) when comparing a lifestyle score of 5-6 to 0-1. And we observed more pronounced association between them among people younger than 60 years old. CONCLUSIONS: Adherence to a combination of healthy lifestyle factors, especially at a young age, was associated with a significantly lower risk of dementia among participants with multimorbidity.

Exosomal miR-1910-3p promotes proliferation, metastasis, and autophagy of breast cancer cells by targeting MTMR3 and activating the NF-κB signaling pathway.

Exosomes are key mediators of intercellular communication and play a role in the pathogenesis and progression of cancer. Exosomes in circulating body fluids serve as molecular markers for cancer diagnosis. This study aimed to investigate the role of exosomal microRNA (miR)-1910-3p in breast cancer and determine its clinical diagnostic value. MiR-1910-3p promoted proliferation and migration of breast cancer cells in vitro and in vivo. In vitro, exosomes enriched in miR-1910-3p transferred miR-1910-3p to mammary epithelial cells and breast cancer cells, promoting proliferation and migration, inhibiting apoptosis, and inducing autophagy. In vivo, exosomes enriched in miR-1910-3p promoted the proliferation and migration of breast cancer cells. MiR-1910-3p downregulated myotubularin-related protein 3, activated the NF-κB and wnt/ß-catenin signaling pathway, and promoted breast cancer progression. Serum miR-1910-3p in exosomes was an effective diagnostic marker that improved the sensitivity of breast cancer diagnosis when used in combination with the traditional tumor marker CA153. In conclusion, breast cancer cell-derived exosomes promoted the growth, metastasis, and autophagy of breast cancer cells by transferring miR-1910-3p. MiR-1910-3p in serum exosomes may serve as a novel molecular marker for breast cancer diagnosis.

Natural History of Seroma Following the Immediate Latissimus Dorsi Flap Method of Breast Reconstruction / 中华医学杂志(英文版)

<p><b>Background</b>The latissimus dorsi (LD) flap procedure remains a popular and useful breast reconstruction tool in China and Western countries, and donor site seroma formation is the main complication. This study was conducted in Chinese patients to determine whether stable cases of seromas would resolve without treatment.</p><p><b>Methods</b>A.</p><p><b></b>retrospective review of 45 consecutive cases of immediate breast reconstruction with LD flap from April 2012 to February 2017 was conducted. The scope of the seroma was demarcated with a marker pen, and cases that remained stable over time (i.e. the size of the seroma did not increase) were observed without treatment. The measured outcomes included the incidence of seromas, the volume and duration of postoperative wound drainage, and other demographic characteristics.</p><p><b>Results</b>Twenty-four patients (53.3%) developed a seroma at the donor site. Of these, 21 patients (87.5%) did not require treatment, and the seroma resolved over time. The mean duration of a sustained seroma was 6.8 ± 1.4 weeks (range: 4-9 weeks).</p><p><b>Conclusions</b>This study observed the scope and progression of the seromas and found that seromas at the LD donor sites resolved over time without treatment.</p>

Nicorandil improves cognitive dysfunction in mice with streptozotocin-induced diabetes / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the protective effects of potassium channel opener nicorandil against cognitive dysfunction in mice with streptozotocin (STZ)-induced diabetes.</p><p><b>METHODS</b>C57BL/6J mouse models of type 1 diabetes mellitus (T1DM) were established by intraperitoneal injection of STZ and received daily treatment with intragastric administration of nicorandil or saline (model group) for 4 consecutive weeks, with normal C57BL/6J mice serving as control. Fasting blood glucose level was recorded every week and Morris water maze was used to evaluate the cognitive behavior of the mice in the 4th week. At the end of the experiment, the mice were sacrificed to observe the ultrastructural changes in the hippocampus and pancreas under transmission electron microscopy; the contents of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) in the hippocampus and SOD activity and MDA level in the brain tissue were determined.</p><p><b>RESULTS</b>Compared with the control group, the model group showed significantly increased fasting blood glucose (P<0.001), significantly prolonged escape latency (P<0.05) and increased swimming distance (P<0.01) with ultrastructural damage of pancreatic β cells and in the hippocampus; GIP and GLP-1 contents in the hippocampus (P<0.01) and SOD activity in the brain were significantly decreased (P<0.05) and MDA content was significantly increased in the model group (P<0.05). Compared with the model group, nicorandil treatment did not cause significant changes in fasting blood glucose, but significantly reduced the swimming distance (P<0.05); nicorandil did not improve the ultrastructural changes in pancreatic β cells but obviously improved the ultrastructures of hippocampal neurons and synapses. Nicorandil also significantly increased the contents of GIP and GLP-1 in the hippocampus (P<0.05), enhanced SOD activity (P<0.05) and decreased MDA level (P<0.01) in the brain tissue.</p><p><b>CONCLUSION</b>Nicorandil improves cognitive dysfunction in mice with STZ-induced diabetes by increasing GIP and GLP-1 contents in the hippocampus and promoting antioxidation to relieve hippocampal injury.</p>

Driver Genes Mutation and Survival Analysis in 200 Patients with Pulmonary Adenocarcinoma Brain Metastasis / 昆明医科大学学报

Objective To investigate the relationship between the driver genes mutation and the survival in patients with pulmonary adenocarcinoma brain metastasis. Methods We enrolled 200 patients with pulmonary adenocarcinoma brain metastasis confirmed histologically from Jan 2013 to Dec 2015, and tested EGFR, KRAS, ALK, Her-2 gene mutation, analyzed the relationship between EGFR gene mutation and clinicopathological data and prognosis of the patients.Results The mutation rates of EGFR, KRAS, ALK and Her-2 gene mutation were 48.5％, 5.5％, 6.5％, 3.5％, respectively. Compared with EGFR gene mutation patients, the sex, age, BMI, differentiation were significant different (P＜0.05), however, the smoking was not significant different (P＞0.05). Patients with EGFR gene mutation who received targeted therapy survived longer than who did not receive targeted therapy, (28.0 ±4.5) months vs (11.2 ±1.4) months. By Log Rank (Mantel-Cox), the median survival time between the two groups was statistically significant (P＜0.05).Conclusions The mutation rate of EGFR gene mutation was high in patients with pulmonary adenocarcinoma brain metastasis, and the patients will survivel longer by targeted therapy.

Toll-like receptor 2 promotes invasion by SGC-7901 human gastric carcinoma cells and is associated with gastric carcinoma metastasis.

Toll-like receptors (TLRs) play a key role in cancer metastasis. The biological role of TLR2 in invasion and metastasis in gastric carcinoma cells and gastric carcinoma is not clear; therefore, we aimed to investigate the biological role of TLR2 in invasion by SGC-7901 human gastric carcinoma cells and to determine whether TLR2 is associated with gastric carcinoma metastasis. RT-PCR, real-time PCR, flow cytometry, and western blotting showed that TLR2 activation significantly increased TLR2 expression at the mRNA and protein levels and notably promoted the transcription of genes related to angiogenesis and invasion, such as VEGF-C and MMP-9. The invasive capacity of SGC-7901 cells was strikingly advanced by TLR2 stimulation on Transwell invasion assay. IL-6 in the supernatants of cultured SGC-7901 cells was increased under the condition of TLR2 stimulation and reduced after TLR2 blockade by ELISA. Combined with clinicopathological parameters, the expression of TLR2 protein examined by immunohistochemical analysis was higher in gastric carcinoma tissues than in adjacent non-cancerous tissues (p<0.001). There was a significant relationship between TLR2 expression and lymph node metastasis (p<0.01), distant metastasis (p<0.01). There was no significant correlation between gastric carcinoma and age (p>0.05), sex (p>0.05), or degree of differentiation (p>0.05). These findings indicate that TLR2 may participate in the progression and metastasis of human gastric carcinoma and provide a new therapeutic target against metastasis of gastric carcinoma.