Association of serum 25-hydroxyvitamin D3 levels with carotid artery intima-media thickness and carotid atherosclerotic plaques in smokers.

OBJECTIVE: This study explores the association of serum 25-hydroxyvitamin D3 (25(OH)D3) levels with carotid artery intima-media thickness (CIMT), and the presence of carotid atherosclerotic plaques in individuals with a history of smoking. METHODS: A total of 469 patients suspected of having carotid atherosclerosis, aged 52 to 73 years with an average age of 65.26 ±â€¯4.37 years, were recruited from the author's hospital from January 2023 to October 2023. All patients had a smoking history of nearly 5 years. Based on their serum 25(OH)D3 levels, they were divided into two groups: the normal group (serum level 30-50 ng/mL, n = 300) and the deficiency group (<30 ng/mL, n = 169). General details of the two patient groups were collected. Carotid artery ultrasound was employed to assess pulse wave velocity (PWV), carotid artery compliance coefficient (CC), and CIMT. Blood chemistry analysis measured serum lipid metabolism indicators including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HD-LC). The relationship between CIMT and each variable was analyzed through Pearson correlation, and logistic regression was used to identify risk factors influencing carotid artery plaque development. RESULTS: General patient information between the two groups showed no significant differences (P > 0.05). Patients in the 25(OH)D3 deficiency group exhibited elevated left and right PWV and CC compared to the 25(OH)D3 normal group (P < 0.05). The deficiency group exhibited larger CIMT and plaque area compared to the normal group (P < 0.05). Additionally, the deficiency group demonstrated higher levels of TC, LDL-C, and HD-LC compared to the normal group (P < 0.05). A moderate positive correlation was found between TC, LDL-C, and CIMT (P < 0.05), while a strong positive correlation existed between 25(OH)D3 and CIMT (P < 0.05). In smokers, the formation of carotid artery plaque was associated with factors such as patient age, CIMT, serum LDL-C, and 25(OH)D3 levels (P < 0.05). As age, CIMT, LDL-C levels increased, and 25(OH)D3 levels decreased, the risk of carotid plaques in smokers increased (P < 0.05). CONCLUSIONS: Smokers with lower 25(OH)D3 levels exhibit higher CIMT and more prominent carotid atherosclerotic plaques, indicating increased arterial stiffness and elevated cardiovascular risk. These findings demonstrate crucial implications that insufficient levels of vitamin D may potentially contribute to a higher risk of atherosclerosis among smokers.

Research progress in effects of MAGE-A family on gastric cancer. / MAGE-Aå®¶æ—åœ¨èƒƒç™Œä¸­ä½œç”¨çš„ç ”ç©¶è¿›å±•.

Gastric cancer (GC) is one of the most common malignant tumors worldwide, and most of the patients are diagnosed at the advanced stage. Most of the treating options are comprehensive treatment, in which immunotherapy plays more and more important role. Melanoma antigen-associated gene-A (MAGE-A) family is a kind of cancer testis antigens. Except in germ cells of testis and trophoblast cells of placenta, MAGE-A family is highly expressed in cancerous tissues and participates in a variety of biological processes, such as cancer cell proliferation, differentiation and metastasis. In addition, cancer testis antigen also possesses good immunogenicity, which can induce humoral and cellular immune responses, is a good target for immunotherapy, and has good application value in the diagnosis, treatment and prognosis of GC. A variety of targeted therapeutic drugs based on MAGE-A are in phase I or II clinical trials, it has good safety and potential clinical application value. With the continuous progress of clinical trials and basic research on MAGE-A targets in GC, it is expected to provide a theoretical basis for clinical transformation and immunotherapy of MAGE-A in the future.

Influence of Management of Intensive Weight, Blood Pressure, and Lipids on Disease Severity in Patients with Carotid Atherosclerosis.

Context: Cardiovascular diseases (CVDs caused by atherosclerosis, such as coronary heart disease and stroke, have become major causes of death and disability worldwide. Atherosclerosis is the primary pathological factor causing CVDs. Managing weight, blood pressure, and lipids is one of the tenets of chronic-disease management, including atherosclerosis. Objective: The study intended to investigate the effects of managing weight, blood pressure, and lipids on disease severity in patients with carotid atherosclerosis. Design: The research team designed a randomized, controlled trial. Setting: The study took place in the pediatric department at the First Hospital of Hebei Medical University in Shijiazhuang, Hebei Province, China. Participants: Participants were 380 patients with carotid atherosclerosis who entered the hospital between March 2018 and June 2020. Intervention: Participants were randomly assigned, using the random-number-table method, to an intervention or a control group, with 190 participants in each group. Both groups received anti-atherosclerotic treatments, and the intervention group also took part in a program for combined management of weight, blood pressure, and blood lipids. Outcome Measures: All measurements occurred at baseline and postintervention. Using a questionnaire, the study measured the changes in the two groups related to alcohol consumption, smoking, high-fat diet, high-salt diet, and lack of exercise. A physical examination provided participants' weights, blood pressures, and lipid levels, and the Self-Care Ability Assessment Scale (ESCA) provided the changes in their self-management ability. A carotid-artery examination measured parameters related to carotid atherosclerosis, including intima-media thickness (IMT), Crouse scores, plaque-class scores, and plaque-grade scores. Results: At baseline, no statistically significant differences existed between the groups. Postintervention, the intervention group had significantly greater decreases than the control group for alcohol consumption, smoking, high-fat diet, high-salt diet, lack of exercise, weight, blood pressure, lipid levels, intima-media thickness (IMT) scores, Crouse scores, and plaque-grade scores. Postintervention, the intervention group had significantly greater increases than the control group for self-responsibility, health knowledge, self-concept, and self-care-skills scores. Conclusions: A program for management of body weight, blood pressure, and blood lipids can effectively control the severity of carotid atherosclerosis, can prevent the disease's progression, and can be promoted as a clinical application.

Study on Inflammatory Factors in Aneurysmal Perimembranous Ventricular Septal Defect in Congenital Heart Disease.

To detect the expression of inflammatory factors such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), transforming growth factor (TGF-ß), and tumor necrosis factor (TNF-α) in the tumor tissue of ventricular septal defect (VSD) in congenital heart disease and to explore the role of inflammatory response in the formation of aneurysmal perimembranous VSD(APVSD). Children with APVSD of congenital heart disease treated by surgery were selected and divided into true aneurysmal perimembranous group (TAP group) and pseudoaneurysmal perimembranous group (PAP group) according to echocardiography and surgical findings. There were 15 children in the TAP group and 31 in the PAP group. The aneurysmal perimembranous tissue of the two groups of children was collected during the operation. IL-1ß, IL-6, TGF-ß, and TNF-α were positively expressed in the aneurysmal perimembranous tissue of the two groups, and the expression levels of all inflammatory factors in the PAP group were higher than those in the TAP group, and the difference was statistically significant (P < 0.05). The expression levels of IL-1ß, IL-6, TGF-ß, and TNF-α in the aneurysmal perimembranous tissue of the two groups were negatively correlated with the width of the APVSD breach. IL-1ß, IL-6, TGF-ß, and TNF-α may be involved in the occurrence and development of APVSD through inflammatory mechanism.

KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis.

The study is aimed at exploring the potential biological process and molecular mechanism of KIF22 involved in the development and progression of pancreatic cancer. First, we used the GEPIA database and tissue qRT-PCR to examine the expression of KIF22 mRNA in pancreatic cancer. Meanwhile, immunohistochemistry revealed the presence of KIF22 in 71 pancreatic cancer tissues versus 30 paracarcinoma tissues. Then, we also explored the relationship between KIF22 expression level and clinical prognosis. Furthermore, in pancreatic cancer cells, we silenced KIF22 by transfecting KIF22 SiRNA, and we investigated the effect of KIF22 on the proliferation of pancreatic cancer cells with MTT and colony formation assays. Finally, we used Gene Set Enrichment Analysis (GSEA) to look at the effect of KIF22 on the cell cycle regulation of pancreatic cancer cells, and we used Western blot to look at the relationship between KIF22 and the phosphorylated MEK1/2, ERK1/2 (p-MEK1/2, p-ERK1/2), and the cyclin-dependent kinase inhibitor (P21). In this study, we found that KIF22 was highly expressed in pancreatic cancer tissues, and patients with high expression of KIF22 demonstrated significantly worse clinical prognosis outcomes (P < 0.05). When the KIF22 gene was silenced in pancreatic cancer cells (PANC-1 and MIA PaCa-2), the cells' ability to proliferate was significantly reduced. Furthermore, GSEA confirmed that KIF22 is involved in cell cycle regulation in pancreatic cancer patients (FDR = 0.00158, P < 0.0001). Besides, the level of KIF22 expression was positively correlated with Ki67 (r = 0.8043, P < 0.0001), and KIF22 can promote the transmutation of G1/S. The expression of p-MEK1/2 and p-ERK1/2 was significantly downregulated, while P21 expression was significantly upregulated (P < 0.05). According to our findings, KIF22 is highly expressed in pancreatic cancer and demonstrates a poor clinical prognosis. It regulates the cell cycle via the MEK/ERK/P21 signaling axis and promotes the development of pancreatic cancer.

Laparoscopic hepatectomy produces better outcomes for hepatolithiasis than open hepatectomy: An updated systematic review and meta-analysis.

BACKGROUND: The present meta-analysis focused on comparing the efficacy and safety of laparoscopic hepatectomy (LH) versus open hepatectomy (OH) for hepatolithiasis. In detail, short-term outcomes including operative time, intraoperative blood loss, intraoperative blood transfusion, postoperative time to oral intake, length of hospital stay, overall postoperative complication rate, initial residual stone, and stone recurrence were analyzed systematically. METHODS: PubMed, Embase, Web of Science and Cochrane Library were comprehensively searched for eligible studies up to Jun. 30. 2017. Bibliographic citation management software (EndNoteX7) was applied to literature management. Quality assessment was carried out according to the modification of the Newcastle-Ottawa Scale (NOS). The data were analyzed by Stata SE12.0 (StataCorp, College Station, TX). Sensitivity analysis was conducted by deleting single study step by step. Odds ratio (OR) were calculated for dichotomous data, and standard mean difference (SMD) with 95% confidence intervals (CI) was calculated continuous data. RESULTS: A total of 17 eligible studies with 1351 patients were identified after a thorough literature search. The pooled results of the present meta-analysis showed that laparoscopic approach was related to significantly less intraoperative estimated blood loss in patients with hepatolithiasis (SMD: -0.52; 95% CI: -0.93 to -0.1; I2 = 91%; P < 0.0001); lower overall postoperative complication rate (OR: 0.52; 95% CI: 0.39 to 0.70; I2 = 0%; P < 0.0001) and intraoperative transfusion rate (OR = 0.25; 95% CI: 0.12 to 0.53; P < 0.0001; I2 = 30.1%; P = 0.239); shorter time to oral intake (SMD: -1.66; 95% CI: -2.41 to -0.92; I2 = 91%; P < 0.0001), and shorter stay in hospital (SMD: -0.89; 95% CI: -1.19 to -0.59; I2 = 83%; P < 0.00001). However, no significant differences was detected between LH and OH in terms of operative time (SMD: 0.22; 95% CI: -0.21 to 0.65; I2 = 92%; P = 0.31), initial residual stones (OR: 0.79; 95% CI: 0.50 to 1.25; I2 = 0%; P = 0.31), and stone recurrence (OR: 0.67; 95% CI: 0.35 to 1.27; I2 = 0%; P = 0.22). In addition, our stratified analysis according to types of LH indicated that the laparoscopic approach still produced more favorable outcomes whatever patients underwent left lateral sectionectomy (LLS) or left hemihepatectomy (LHH). CONCLUSION: The laparoscopic hepatectomy is a better alternative to open approach in patients with hepatolithiasis, providing less overall complication rate, shorter postoperative stay of hospital stay, less blood loss, and shorter time to oral intake. However, high-quality randomized controlled trials (RCTs) are badly needed to provide higher-level evidence due to unavoidable bias from non-randomized trials.

Bisdemethoxycurcumin attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.

Bisdemethoxycurcumin (BDMC) is a demethoxy derivative of curcumin. In this study, a human gastric adenocarcinoma xenograft model was generated in vivo using nude mice and BDMC was observed to suppress the growth and activity of tumors, in addition to improving the physical and mental capacity of the mice. An increased number of apoptotic cells, decreased ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein and increased caspase-3 expression was also observed following treatment with BDMC, indicating that BDMC may promote apoptosis in tumors via mitochondrial modulation. The growth of SGC 7901 gastric cancer cells was inhibited and arrested at G1 phase. Specific indicators of mitochondrial dysfunction, a reduction in adenosine triphosphate generation, the inner mitochondrial membrane potential, augmentation of reactive oxygen species production and cytochrome c were also detected in the mitochondria following treatment with BDMC. These results indicate that BDMC attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.