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Abstract Background Vitamin D (VD) plays a critical role in regulating systemic inflammation, but its correlation with the systemic immune-inflammatory index (SII) remains unclear. This study aimed to explore the relationship between serum VD concentration, dietary VD intake, and SII using data from the National Health and Nutrition Examination Survey (NHANES). Methods Data from NHANES 2007–2018 and NHANES 2007–2020 were analyzed for serum VD levels and dietary VD intake, respectively. Restricted cubic splines (RCS) and logistic regression were used to assess associations between VD and SII. Mediation analysis was conducted to evaluate the role of SII in VD-related disease outcomes and mortality. Results Serum VD concentration exhibited a U-shaped correlation with SII (P-overall = 0.005; P-non-linear = 0.002). Severe VD deficiency significantly elevated SII levels compared to insufficiency or sufficiency groups. No association was observed between dietary VD intake and SII. Mediation analysis revealed that SII mediated the effects of VD on all-cause and cardiovascular disease-related mortality, but not on cancer, hypertension, or diabetes development. Conclusion A U-shaped relationship exists between serum VD and SII, with VD supplementation potentially reducing systemic inflammation and improving cardiovascular outcomes. Future studies should explore VD’s role in systemic inflammation and its clinical implications.

Abstract Background In recent years, conventional coagulation (CC) and thromboelastography (TEG) parameters have been reported to be closely related to the progression of pancreatic cancer (PC). However, the potential utility of these parameters in differentiating benign and malignant pancreatic diseases is still unclear. Objectives A retrospective study was conducted to evaluate the efficacy of coagulation parameters in differentiating pancreatic cancer/early stage pancreatic cancer (EPC, TNM stages I and II) from benign control conditions, and to further explore whether coagulation parameters could improve the differential value of CA199. Methods Receiver operating characteristic (ROC) curves and logistic regression analysis were used to identify the diagnostic value of each coagulation parameter or combination of parameters. Results Compared with benign pancreatic disease (BPD), patients with pancreatic malignant tumors had significant coagulation disorders, specifically manifested as abnormal increases or decreases in several CC and TEG parameters (such as activated partial thromboplastin time (APTT), fibrinogen (FIB), D-dimer (DD2), K time, R time, Angle, maximum amplitude (MA), coagulation index (CI), and Ly30). In the training group, ROC curve showed that FIB, DD2, Angle, MA, and CI had favorable efficacy at differentiating PC or EPC from BPD (for PC, AUC = 0.737, 0.654, 0.627, 0.602, 0.648; for EPC, AUC = 0.723, 0.635, 0.630, 0.614, 0.648). However, several combined diagnostic indicators based on FIB, DD2 and CI failed to outperform the individual coagulation indexes in diagnostic efficiency. Combinations of certain coagulation indexes with CA199 outperformed CA199 alone at identifying PC or EPC, especially FIB + CA199 (for PC, AUC = 0.904; for EPC, AUC = 0.905), FIB + DD2 + CA199 (for PC, AUC = 0.902; for EPC, AUC = 0.900), FIB + CI + CA199 (for PC, AUC = 0.906; for EPC, AUC = 0.906), and FIB + DD2 + CI + CA199 (for PC, AUC = 0.905; for EPC, AUC = 0.900). The results from a validation set also confirmed that these combinations have advantageous diagnostic value for PC and EPC. Conclusions A significant hypercoagulable state was common in PC. Some CC and TEG parameters are valuable in the differential diagnosis of benign and malignant pancreatic diseases. In addition, coagulation indexes combined with CA199 can further enhance the differential diagnosis efficacy of CA199 in PC and EPC.

Abstract Background In recent years, multiple coagulation and fibrinolysis (CF) indexes have been reported to be significantly related to the progression and prognosis of some cancers. Objective The purpose of this study was to comprehensively analyze the value of CF parameters in prognosis prediction of pancreatic cancer (PC). Methods The preoperative coagulation related data, clinicopathological information, and survival data of patients with pancreatic tumor were collected retrospectively. Mann Whitney U test, Kaplan-Meier analysis, and Cox proportional hazards regression model were applied to analyze the differences of coagulation indexes between benign and malignant tumors, as well as the roles of these indexes in PC prognosis prediction. Results Compared with benign tumors, the preoperative levels of some traditional coagulation and fibrinolysis (TCF) indexes (such as TT, Fibrinogen, APTT, and D-dimer) were abnormally increased or decreased in patients with pancreatic cancer, as well as Thromboelastography (TEG) parameters (such as R, K, α Angle, MA, and CI). Kaplan Meier survival analysis based on resectable PC patients showed that the overall survival (OS) of patients with elevated α angle, MA, CI, PT, D-dimer, or decreased PDW was markedly shorter than other patients; moreover, patients with lower CI or PT have longer disease-free survival. Further univariate and multivariate analysis revealed that PT, D-dimer, PDW, vascular invasion (VI), and tumor size (TS) were independent risk factors for poor prognosis of PC. According to the results of modeling group and validation group, the nomogram model based on independent risk factors could effectively predict the postoperative survival of PC patients. Conclusion Many abnormal CF parameters were remarkably correlated with PC prognosis, including α Angle, MA, CI, PT, D-dimer, and PDW. Furthermore, only PT, D-dimer, and PDW were independent prognostic indicators for poor prognosis of PC, and the prognosis prediction model based on these indicators was an effective tool to predict the postoperative survival of PC.

A urinary bladder stone in young adults is uncommon. Dislocation of an IUD to adjection organs is a rare condition. We present a case of a 28-year female with a chief complaint of right side pelvis discomfort, off and on with the urinary system. In this case, we performed cystoscopy assisted laser lithotripsy, hysteroscopy to localize and remove IUD, transurethral resectoscope for removing IUD residual, and resection sinus tract.This article's objective states that the multidisciplinary approach to removing dislocated IUD is safe and effective and raises awareness of forgotten contraceptive devices and their potential complications.

Objectives: Hyperinsulinemia is a risk factor for pancreatic cancer, but the function of insulin in carcinogenesis is unclear, so this study aimed to elucidate the carcinogenic effects of insulin and the synergistic effect with the KRAS mutation in the early stage of pancreatic cancer. Materials and methods: A pair of immortalized human pancreatic duct‐derived cells, hTERT‐HPNE E6/E7/st (HPNE) and its oncogenic KRASG12D variant, hTERT‐HPNE E6/E7/KRASG12D/st (HPNE‐mut‐KRAS), were used to investigate the effect of insulin. Cell proliferation, migration and invasion were assessed using Cell Counting Kit‐8 and transwell assays, respectively. The expression of E‐cadherin, N‐cadherin, vimentin and matrix metalloproteinases (MMP‐2, MMP‐7 and MMP‐9) was evaluated by Western blotting and/or qRT‐PCR. The gelatinase activity of MMP‐2 and MMP‐9 in conditioned media was detected using gelatin zymography. The phosphorylation status of AKT, GSK3β, p38, JNK and ERK1/2 MAPK was determined by Western blotting. Results: The migration and invasion ability of HPNE cells was increased after the introduction of the mutated KRAS gene, together with an increased expression of MMP‐2. These effects were further enhanced by the simultaneous administration of insulin. The use of MMP‐2 siRNA confirmed that MMP‐2 was involved in the regulation of cell invasion. Furthermore, there was a concentration‐ and time‐dependent increase in gelatinase activity after insulin treatment, which could be reversed by an insulin receptor tyrosine kinase inhibitor (HNMPA‐(AM)3). In addition, insulin markedly enhanced the phosphorylation of PI3K/AKT, p38, JNK and ERK1/2 MAPK pathways, with wortmannin or LY294002 (a PI3K‐specific inhibitor) and PD98059 (a MEK1‐specific inhibitor) significantly inhibiting the insulin‐induced increase in MMP‐2 gelatinolytic activity. Conclusions: Taken together, these results suggest that insulin induced migration and invasion in HPNE and HPNE‐mut‐KRAS through PI3K/AKT and ERK1/2 activation, with MMP‐2 gelatinolytic activity playing a vital role in this process. These findings may provide a new therapeutic target for preventing carcinogenesis and the evolution of pancreatic cancer with a background of hyperinsulinemia. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Thymidine kinase 1 (TK1) is one of the salvage enzymes engaged in the synthesis of DNA. Although a pro‐carcinogenetic role of TK1 has been reported in various types of cancers, its role in pancreatic ductal adenocarcinoma (PDAC) is still unknown. The study is aimed to elaborate the function of TK1 in PDAC and the potential mechanisms in the following study. Materials and methods: TK1 expression was analysed by immunohistochemistry, real‐time PCR and Western blot, and its relationship with clinicopathological characteristics of PDAC patients was further investigated. To verify the function of TK1 and potential mechanism, TK1 siRNA was used to transfect PDAC cells and performed a series of assays in cell and animal models. Results: The level of TK1 expression was higher in cancerous tissues compared with matched adjacent tissues. TK1 overexpression was associated with progression of PDAC and poor prognosis. Knockdown of TK1 could suppress cell proliferation via inducing S phase arrest mediated by upregulation of P21. Further mechanism investigation suggested that transcription factor E2F‐1 could directly regulate the TK1 and promote tumour proliferation. Conclusions: The results suggested that TK1 might be involved in the development and progression of PDAC by regulating cell proliferation and show that TK1 may work as a promising therapeutic target in patients with PDAC. [ABSTRACT FROM AUTHOR]

Cell proliferation ability was examined in the Blank, inhibitor-NC, PLL 3.7, miR-23a and inhibitor groups after (A) 24 h and (B) 48 h treatment. Effects of miR-23a on proliferation and metastasis ability of pancreatic cancer cells. [Extracted from the article]