Correlation Between Blood Cadmium Levels and Platelet Characteristics, As Well As Their Impact on Susceptibility to Coronary Heart Disease: Findings from NHANES 2005-2018 Data.

Investigating the correlation between blood cadmium levels, platelet characteristics, and susceptibility to coronary heart disease (CHD). Utilized NHANES 2005-2018 data with covariates such as age, sex, race, marital status, and socio-economic status. Blood cadmium served as the independent variable, while platelet count (PC) and mean platelet volume (MPV) were dependent variables. The average age of the participants was 68.77 ± 11.03 years, and 67.4% of them were male. The mean values for WBC, MPV, PC, and blood cadmium were 7.53 ± 3.36 × 103 cells/µL, 11.33 ± 0.27fL, 57.61 ± 5.34 × 103 cells/µL, and 2.58 ± 0.61 µg/L, respectively. Adjusting for other variables revealed increased MPV and PC with rising blood cadmium levels in cardiac patients, indicating a higher risk of CHD in those with elevated blood cadmium. The average age of the participants was 68.77 ± 11.03 years, and 67.4% of them were male. The mean values for WBC, MPV, PC, and blood cadmium were 7.53 ± 3.36 × 103 cells/µL, 11.33 ± 0.27fL, 57.61 ± 5.34 × 103 cells/µL, and 2.58 ± 0.61 µg/L, respectively. Adjusting for other variables revealed increased MPV and PC with rising blood cadmium levels in cardiac patients, indicating a higher risk of CHD in those with elevated blood cadmium. This study enhances understanding of how cadmium impacts platelet characteristics, contributing to increased CHD risk, providing insights for primary prevention strategies.

Sigmoido-rectal intussusception anastomosis in the Altemeier procedure for complete rectal prolapse: preliminary results of a new technique.

Purpose: Our research introduces an innovative surgical approach, combining the Altemeier Procedure with Sigmoido-rectal Intussusception Anastomosis, effectively reducing recurrence, minimizing complications, and improving postoperative anal function in rectal prolapse patients. Materials and methods: This retrospective study, conducted at tertiary referral hospitals including Shandong University of Traditional Chinese Medicine's Affiliated Hospital, Linyi People's Hospital, and Pingyi People's Hospital, examined data from patients undergoing conventional Altemeier surgery or Altemeier combined with Sigmoido-rectal Intussusception Anastomosis. Analyzing hospitalization and follow-up data from January 2009 to December 2022, the study focused on prolapse recurrence, complications, and anal function as primary outcome indicators across these three study centers. Results: In the study, both groups had an average follow-up of (12.5 ± 2.41) months, and only two traditional group patients experienced mortality. Recurrence rates significantly differed, with 26.47% in the traditional group and 1.54% in the modified group (P < 0.001). The modified group showed no perioperative anastomotic dehiscence, contrasting with a 13.24% occurrence in the conventional group (P = 0.003). Primary complications in the modified group included anastomotic hemorrhage, with rates of 17.65% and 6.15% in the traditional and modified groups, respectively (P = 0.077). At 12 months postoperatively, both groups improved in anal manometry parameters and the Wexner anal incontinence score. Resting pressure was significantly lower in the traditional group (32.50 ± 1.76 mmHg) than the modified group (33.24 ± 2.06 mmHg) (P = 0.027), while the extrusion pressure was higher in the modified group (64.78 ± 1.55 mmHg) than the traditional group (62.85 ± 2.30 mmHg) (P < 0.001). The Wexner anal incontinence score was significantly lower in the modified group (2.69 ± 1.65) than the traditional group (3.69 ± 1.58, P = 0.001). Conclusion: This retrospective study affirms that adding Sigmoido-rectal Intussusception Anastomosis to the Altemeier procedure reduces recurrence and complications. While both approaches enhance postoperative anal function in complete rectal prolapse patients, the combined method, particularly with Sigmoido-rectal Intussusception Anastomosis, proves more effective.

Erratum: [Corrigendum] Effects of histone deacetylase inhibitors on ATP­binding cassette transporters in lung cancer A549 and colorectal cancer HCT116 cells.

[This corrects the article DOI: 10.3892/ol.2019.10319.].

Correlation between systemic inflammatory response index and thyroid function: 2009-2012 NHANES results.

Aims: This study investigates the relationship between the Systemic Inflammatory Response Index (SIRI) and thyroid function. Methods: Utilizing data from the National Health and Nutrition Examination Survey (NHANES) 2009-2012, we excluded participants lacking SIRI or thyroid function data, those under 20 years, and pregnant individuals. SIRI was determined using blood samples. We conducted weighted multivariate regression and subgroup analyses to discern the independent relationship between SIRI and thyroid function. Results: The study included 1,641 subjects, with an average age of 47.26±16.77 years, including 48.65% males and 51.35% females. The population was divided into three SIRI-based groups (Q1-Q3). Q3, compared to Q1, exhibited higher age-at-onset, greater male prevalence, and increased levels of FT3, FT4, TT4, leukocytes, and triglycerides. This group also showed a higher incidence of diabetes, hypertension, and smoking. Notably, Q1 had lower LDL and HDL levels. SIRI maintained a positive association with FT4 (ß = 0.01, 95% CI = 0.00-0.03, P for trend = 0.0071), TT4 (ß = 0.20, 95% CI = 0.10, 0.31, P for trend=0.0001), and TPOAb (ß = 8.0, 95% CI = 1.77-14.30, P for trend = 0.0120), indicating that each quartile increase in SIRI corresponded to a 0.01 ng/dL increase in FT4, a 0.2 g/dL increase in TT4, and an 8.03 IU/mL rise in TPOAb. The subgroup analysis suggested the SIRI-thyroid function correlation was influenced by hypertension. Conclusion: Inflammation may impact the development and progression of thyroid function disorders. Proactive anti-inflammatory treatment might mitigate thyroid abnormalities.

Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling.

Despite the advancement in the diagnosis and therapeutic strategies for colorectal cancer, the outcomes of patients with colorectal cancer remain unsatisfactory. Alisol A is a natural constituent of Alismatis rhizoma (zexie) and has demonstrated anti-cancer properties; however, the function of Alisol A in colorectal cancer is still unknown. In the present study, the effect of Alisol A on colorectal cancer progression was investigated. MTT and colony formation assays showed that treatment with Alisol A repressed colorectal cancer cell proliferation in a dose-dependent manner. Similarly, western blot analysis demonstrated that Alisol A upregulated E-cadherin protein expression levels, but downregulated N-cadherin and Vimentin protein expression levels in colorectal cancer cells. In addition, the number of cells in G0/G1 phase was enhanced, while that of S phase was reduced in Alisol A-treated colorectal cancer cells. Apoptosis and pyroptosis of colorectal cancer cells were stimulated following treatment with Alisol A. Alisol A suppressed the migration ability of colorectal cancer cells in a dose-dependent manner. Moreover, Alisol A increased the chemotherapeutic sensitivity of colorectal cancer cells to cisplatin. Mechanically, western blot analysis confirmed that Alisol A repressed the phosphorylation levels of PI3K, Akt and mTOR in colorectal cancer cells. The Akt activator, SC79 reversed the effect of Alisol A on colorectal cancer cell proliferation and apoptosis. In conclusion, Alisol A induced an inhibitory effect on colorectal cancer progression by inactivating PI3K/Akt signaling.

ISLR affects colon cancer progression by regulating the epithelial-mesenchymal transition signaling pathway.

This study aims to determine the mechanism of ISLR on the progression of colon cancer. TCGA database was used to analyze ISLR expression in colon cancer tumor tissues. QRT-PCR and western blotting were used to detect ISLR expression in colon cancer cells. CCK-8, colony formation, EDU, wound healing and transwell assays were used to measure cell viability, proliferation, migration and invasion of colon cancer cells, respectively. The signaling pathway enrichment analysis of ISLR was analyzed on the basis of the KEGG database. The protein expression of genes related to signaling pathway was measured by western blotting. Results of TCGA analysis, qRT-PC and western blotting showed that ISLR was upregulated in colon cancer tumor tissues and cells. High level of ISLR was related to low overall survival of patients with colon cancer. ISLR silence significantly inhibited cell viability, proliferation, migration and invasion of colon cancer cells. ISLR overexpression markedly enhanced the cell viability, proliferation, migration and invasion of colon cancer cells. KEGG database analyzed showed that ISLR can activate the EMT signaling pathway. Inhibition of the EMT signaling pathway can suppress the growth, migration, and invasion of colon cancer cells and eliminate the promoted effect of ISLR overexpression on colon cancer progression. ISLR promotes the progression of colon cancer by activating the EMT signaling pathway.

Silencing of Long Noncoding RNA LINC00346 Inhibits the Tumorigenesis of Colorectal Cancer Through Targeting MicroRNA-148b.

PURPOSE: This study was aimed to explore the regulatory effect of long noncoding RNA LINC00346 (LINC00346) on colorectal cancer (CRC) and the potential molecular mechanisms. METHODS: The expression of LINC00346 and microRNA-148b (miR-148b) in CRC tissues and cells was detected by qRT-PCR. LINC00346 was overexpressed and silenced in HT29 and HCT116 cells by the transfection of pcDNA-LINC00346 and si-LINC00346, respectively. The cell proliferation, migration, invasion, and apoptosis were analyzed by cell counting kit-8 (CCK-8), wound-healing, transwell, and flow cytometry assay, respectively. The targeting relationship between LINC00346 and miR-148b was predicted by TargetScan and determined by dual-luciferase reporter assay. A tumor xenograft model was established in mice to evaluate the tumor growth in vivo. RESULTS: The expression of LINC00346 was up-regulated in CRC tissues and cells. The expression of LINC00346 was positively associated with the TNM stage, lymphoma metastasis and histological grade. Overexpression of LINC00346 promoted the proliferation, migration and invasion and inhibited the apoptosis of HT29 and HCT116 cells. MiR-148b was a target of LINC00346. Silencing of miR-148b reversed the anti-tumor effect of si-LINC00346 on CRC cells. Furthermore, silencing of LINC00346 inhibited the tumor growth in mice through up-regulating miR-148b. CONCLUSION: Silencing of LINC00346 inhibited the proliferation, migration and invasion, and promoted the apoptosis of CRC cells through targeting miR-148b.

CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis.

Accumulating evidences indicate that 3'UTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that acvr1b gene 3'UTR (acv3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of acv3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that acv3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in acv3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of acv3UTR. The positive correlation of acv3UTR and YAP1 expression, and the negative correlation of acv3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to acv3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of acv3UTR transcription in GC tumorigenesis, and indicates a correlation between 3'UTR trans-regulatory effect and GC development.

Effects of histone deacetylase inhibitors on ATP-binding cassette transporters in lung cancer A549 and colorectal cancer HCT116 cells.

Histone deacetylase (HDAC) inhibitors and DNA alkylators are effective components used in combination chemotherapy. In the present study, the effects of HDAC inhibitors on the expression of ATP-binding cassette (ABC) transporters were investigated. It was observed that HDAC inhibitors induced the expression of multidrug-resistant ABC transporters differently in lung cancer A549 cells than in colorectal cancer HCT116 cells. In these two cell lines, the HDAC inhibitors suberoylanilide hydroxamic acid (SAHA) and trichostatin A (TSA) significantly increased ABCB1 expression at the mRNA and protein levels, whereas they had no evident effect on ABCG2 protein expression. SAHA and TSA decreased ABCG2 mRNA expression in A549 cells and had no evident effect on ABCG2 mRNA expression in HCT116 cells. Notably, SAHA and TSA increased the mRNA expression levels of ABCC5, ABCC6, ABCC10, ABCC11 and ABCC12, as well as the protein expression levels of ABCC2, ABCC10 and ABCC12. By contrast, these inhibitors decreased the mRNA expression levels of ABCC1, ABCC2, ABCC3 and ABCC4, as well as the expression of ABCC1 and ABCC3 proteins. Furthermore, SAHA and TSA were found to downregulate HDAC3 and HDAC4, but not HDAC1 and HDAC2. Taken together, the results suggested that HDAC inhibitors work synergistically with DNA alkylators, in part, due to the inhibitory effect of these inhibitors on ABCC1 expression, which translocates these alkylators from inside to outside of cancer cells. These results further suggested the possibility of antagonism when HDAC inhibitors are combined with anthracyclines and other ABCB1 drug ligands in chemotherapy.

High Expression of Angiogenic Factor with G-Patch and FHA Domain1 (AGGF1) Predicts Poor Prognosis in Gastric Cancer.

BACKGROUND Angiogenic factor with G-patch and FHA domain1 (AGGF1 or VG5Q) is a newly identified human angiogenic factor. The aim of this study was to explore AGGF1 expression level in gastric cancer and detect its correlation with the prognosis. MATERIAL AND METHODS Immunohistochemistry was performed to detect AGGF1 level in gastric cancer and its adjacent noncancerous samples of 198 cases, and the relationships among the expression levels of AGGF1, vascular endothelial growth factor (VEGF), and prognosis were analyzed. RESULTS Expression of AGGF1 in gastric cancer samples was significantly higher than that in adjacent noncancerous samples (P<0.001). The overall survival rate (OS) of patients with high AGGF1 expression was significantly lower than that of patients with low AGGF1 expression (P=0.000). The Cox model analysis demonstrated that expression of AGGF1 was an independent biomarker for prediction of patients' survival in gastric cancer. CONCLUSIONS High expression of AGGF1 predicts poor prognosis in gastric cancer patients. AGGF1 can be used as an independent factor to predict postoperative survival of patients with gastric cancer.