At present, there is a lack of research on the correlation between cumFPG and digestive malignancies, and previous cohort studies have not considered the competitive risk between death and digestive malignancies, which may overestimate the impact of related risk factors. To explore the correlation between cumFPG and malignant tumors of the digestive system. In this study, 53,747 participants who had undergone 3 consecutive physical examinations since 2006 were collected. Finally, a total of 53,747 participants were included in this study. According to the grouping method of previous studies, cumFPG was divided into 4 groups according to the quartile. Cox regression model and competitive risk model were used to assess the risk of new digestive system malignancy. In sensitivity analyses, participants with cancer within 5 years of follow-up were excluded to eliminate the possibility of reverse causation. Subjects taking hypoglycemic drugs were excluded to eliminate the effect of the drug on blood glucose. Restricted cubic splineregresion (RCS) was then used to calculate the relationship between cumFPG and GI cancers. The mean age of participants was 49.02 ± 11.78 years. During a mean follow-up of 10.58 years, 817 new Gastrointestinal cases were identified, and the Cox proportional hazards model suggested that the risk of incidence in the Q2 to Q4 group increased sequentially compared with the lowest Q1 group, even after excluding the diagnosis of digestive malignancy within 5 years, the participants taking hypoglycemic drugs, and the death competition risk model analysis. In site-specific analysis, we observed that this risk was more pronounced in colorectal cancer, liver cancer, and pancreatic cancer, while gastric cancer, small bowel cancer, and bile duct cancer all had a similar trend to the main model but were not statistically significant, while esophageal cancer was U-shaped but not statistically significant. RCS results showed that cumFPG was associated with a similar risk of digestive system tumors, showing an inverted “√” type relationship. High levels of cumFPG are an independent factor in malignancy of the digestive system. cumFPG can provide a new idea for the prevention of Gastrointestinal cancers.
To determine the dynamic change in serum levels of activin A (ACTA) and C-reaction protein (CRP) in patients with brain injury, and to investigate its significance.A prospective study was conducted. A total of 57 adult patients with brain injury occurring within 24 hours admitted to intensive care unit (ICU) of the First Affiliated Hospital of Zhengzhou University from August 2012 to June 2013 were enrolled. The patients were allocated into three groups according to their Glasgow coma scale (GCS) as follows: minor brain injury (GCS 13-15, n=17), moderate brain injury (GCS 9-12, n=18), heavy brain injury (GCS 3-8, n=22). The clinical and related laboratory data (reflecting the function of liver, kidney, lung, blood coagulability etc.) were recorded after ICU admission. At the same time, venous samples were collected on the day 1, 2, 3, 5, 7 after ICU admission for determination of ACTA with enzyme linked immunosorbent assay (ELISA) and CRP with fluorescence immunoassay technology. The correlation between ACTA and CRP was analyzed by linear correlation. The receiver operating characteristic (ROC) curve was plotted to analyze the accuracy of ACTA and CRP as a prognostic indicator in brain injury. Fifteen healthy persons were enrolled as the control group.The serum levels of ACTA and CRP in patients with minor, moderate and heavy brain injury were significantly higher than those in healthy control group [ACTA (μg/L): 23.96±3.55, 42.06±5.67, 52.32±4.46 vs. 13.66±2.45, all P<0.01; CRP (mg/L): 14.12±2.45, 23.05±2.85, 30.93±2.35 vs. 3.42±2.25, all P<0.01]. As the patients' condition worsening, levels of ACTA and CRP tended to elevate (all P<0.01). Levels of ACTA and CRP in minor, moderate and heavy brain injury groups were increased after ICU admission. On day 3, levels of serum ACTA and CRP reached the peak values [ACTA (μg/L):30.62±2.54, 51.35±2.55, 60.52±2.55; CRP (mg/L): 18.62±2.64, 30.35±2.25, 37.52±2.55], and then they lowered gradually. In minor and moderate brain injury groups, the levels of ACTA and CRP were slowly descending, and on day 7, they maintained at a lower level [ACTA (μg/L): 13.68±2.54, 37.74±2.55; CRP (mg/L): 6.68±2.44, 19.74±2.55]. On the contrary, the levels of ACTA and CRP in heavy brain injury group persistently maintained at a high level on day 7 [ACTA: (42.32±2.54) μg/L, CRP: (33.32±2.56) mg/L]. There were significant differences in ACTA and CRP among different degrees of brain injury groups (all P<0.01). There was a positive correlation between ACTA and CRP (r=0.958, P=0.007). ROC curve analysis showed that the sensitivity for brain injury prediction was 93.3% for ACTA with specificity 95.0%, area under ROC curve(AUC) 0.843, and the sensitivity for CRP was 89.1% with specificity 68.2%, AUC 0.723.Serum levels of ACTA and CRP in patients with brain injury are strongly correlated with the severity of the injury. Furthermore, ACTA is more sensitive than CRP in detecting early brain injury. Therefore, ACTA is a specific factor for detecting brain injury.
The relationship between serum Mg and blood cell counts in Chinese adult diabetes or central obesity was assessed by investigating 8163 subjects with China Health and Nutrition Survey (mean age 59⋅6 years, 54⋅9 % men). Participants were classified according to blood Mg (below 0⋅65 mmol/l, or 0⋅66-0⋅94 mmol/l or above 0⋅95 mmol/l), type 2 diabetes (yes/no) and central obesity (yes/no). Leucocytes, erythrocytes, platelets (PLT), Hb and glycated Hb (HbA1c) were determined using standardised methods and conditions. HbAc1, leucocytes and PLT were significantly higher among subjects with central obesity than without central obesity (P < 0⋅05). A significant increase for Hb, erythrocytes, PLT, but not leucocytes, across progressive Mg groups was observed in subjects without diabetes (P < 0⋅05). Hb, erythrocytes and HbAc1 were significantly higher among subjects with higher Mg than in subjects with lower Mg with diabetes (P < 0⋅05). Central obesity disturbed the positive association between PLT count and serum Mg. Type 2 diabetes caused metabolism disorder in serum Mg, blood sugar and blood cell count. Hb, erythrocytes and PLT, but not leucocytes, are positively correlated with serum Mg, but this association is somehow disturbed by type 2 diabetes or central obesity.
Abstract Background Cholesterol gallstones are a disease with increasing incidence due to improvements in living standards. This study aims to investigate the impact of highly expressed THY1 in the gallbladder on disease progression during gallstone formation. Methods We conducted multi-omics analyses, including transcriptomics, proteomics, and single-cell sequencing, to examine changes in the gallbladder during gallstone formation. We used a gallstone mouse model induced by a lithogenic diet and a THY1 knockdown gallstone mouse model via sh-RNA to assess the role of THY1 in gallstone formation. HE staining and qRT-PCR were performed to measure inflammation levels in THY1 knockdown mice during gallstone formation. Western Blot, immunohistochemistry, and immunofluorescence were used to detect the expression of FN and COL I to determine the role of THY1 in ECM synthesis during gallstone progression. Kits were used to measure bile acids, phospholipids, cholesterol, and triglycerides, and the cholesterol saturation index (CSI) was calculated. Results THY1 expression was significantly elevated in gallbladder fibroblasts during gallstone formation. Knockdown of THY1 alleviated gallstone formation induced by a lithogenic diet in mice. In THY1 knockdown mice, cholesterol levels in gallbladder bile were significantly reduced, bile acid concentration increased, and the CSI index decreased. Additionally, the expression of inflammatory cytokines in the gallbladders of THY1 knockdown mice was reduced, leading to decreased gallbladder inflammation. ECM synthesis in the gallbladders of THY1 knockdown mice was also alleviated. Conclusion This study reveals that high expression of THY1 in gallbladder fibroblasts promotes the progression of gallstones by increasing inflammation levels and ECM synthesis.
Breast adenoid cystic carcinoma is an extremely rare tumor that is incompletely understood, accounting for less than <0.1% of all breast cancers, with an average diameter of 3 cm, and it is extremely rare to see a large, non-metastatic breast adenoid cystic carcinoma with a diameter of about 30 cm. Since this disease is extremely rare, there are few reports in the literature and limited data on clinical diagnosis and treatment. We present a case of a 71-year-old woman with a large, non-metastatic adenoid cystic carcinoma of the left breast and share our opinion on the diagnosis and treatment of this case.
Several studies have confirmed the important role of endometrial cancer (EC) in the development and progression of breast cancer (BC), and this study will explore the causal relationship between EC and BC by 2-sample Mendelian randomization analysis. Pooled data from published genome-wide association studies were used to assess the association between EC and BC risk in women using 5 methods, namely, inverse variance weighting (IVW), MR-Egger, weighted median (WME), simple multimaximetry (SM) and weighted multimaximetry (WM) with the EC-associated genetic loci as the instrumental variables (IV) and sensitivity analyses were used to assess the robustness of the results. The statistical results showed a causal association between EC and BC (IVW: OR = 1.07, 95% CI = 1.01-1.32, P = .02; MR-Egger: OR = 1.21, 95% CI = 0.71-1.51, P = .11; weighted median: OR = 1.05, 95% CI = 0.97-1.31, P = .19; simple plurality method: OR = 0.98, 95% CI = 0.81-1.15, P = .78; weighted plurality method: OR = 0.98, 95% CI = 0.81-1.14, P = .75), and the results of the sensitivity analyses showed that there was no significant heterogeneity or multiplicity, and the results were stable. EC is associated with an increased risk of developing BC. The results of this MR analysis can be used as a guideline for screening for BC in women with EC and to help raise awareness of screening for early detection and treatment.
The Lymphoid specific tyrosine phosphatase (Lyp) has elicited tremendous research interest due to the high risk of its missense mutation R620W in a wide spectrum of autoimmune diseases. While initially characterized as a gain-of-function mutant, R620W was thought to lead to autoimmune diseases through loss-of-function in T cell signaling by a recent study. Here we investigate the biochemical characters and T cell signaling functions of two uncharacterized Lyp variants S201F and R266W, together with a previously characterized Lyp variant R263Q, which had reduced risk in several autoimmune diseases, including systemic lupus erythematosus (SLE), ulcerative colitis (UC) and rheumatoid arthritis (RA). Our kinetic and functional studies of R263Q polymorphism basically reproduced previous findings that it was a loss-of-function mutant. The other variant S201F reduced Lyp phosphatase activity moderately and decreased Lyp function in T cell slightly, while R266W severely impaired phosphatase activity and was a loss-of-function variant in T cell signaling. A combined kinetic and structure analysis suggests that the R266W variant may decrease its phosphatase activity through perturbing either the Q-loop or the WPD loop of Lyp. As both R266W and R263Q significantly change their phosphatase activity and T cell functions, future work could be considered to evaluate these mutants in a broader spectrum of autoimmune diseases.
This study is aimed at exploring the relationship between serum ferritin and blood lipids and the influence of diabetes and different hs-CRP levels. A total of 8163 subjects were analyzed. Participators were classified according to serum ferritin, diabetes, and two hs-CRP levels. Blood lipids were determined using standardized methods and conditions. Except for HDL-C, there was a significant increase in blood lipids in the progressive ferritin group with normal hs-CRP levels (
Rationale: Small bowel adenocarcinoma (SBA) is an extremely rare tumor that is not fully understood, SBA accounts for less than 5% of gastrointestinal cancers, Krukenberg tumors account for a lower proportion of all ovarian tumors, close to 2%. Stomach is the most common primary site of Krukenberg tumor. The phenomenon of bilateral ovarian Kukenberg tumor caused by implantation and metastasis of small bowel cancer is extremely rare, with few literature reports and limited clinical diagnosis and treatment data. We present a case of a 55-year-old woman with bilateral Kukenberg’s tumor caused by small bowel cancer implantation and share our views on the diagnosis and treatment of this case. Patient concerns: A 55-year-old woman presented with vaginal bleeding and persistent lower abdominal pain after fatigue 10 days ago. Pelvic ultrasound at a local hospital revealed 2 solid masses in her pelvis, and she came to our hospital for further diagnosis and treatment. The results of colonofiberscope examination and histopathological examination confirmed intramucosal adenocarcinoma in the small intestine. Diagnoses: The results of colonofiberscope examination and histopathological examination confirmed intramucosal adenocarcinoma in the small intestine. Contrast-enhanced computed tomography showed multiple cystic space-occupying lesions in the pelvic cavity, and the possibility of ovarian tumor was considered. Interventions: Radical treatment of right half colon cancer and pelvic mass resection were performed under general anesthesia. Combined with intraoperative and postoperative pathological examination, the diagnosis was mucinous adenocarcinoma of the small intestine stage IV (pT4N1M1). Bilateral ovarian metastasis, metastatic cancer (3/19): lymph nodes around the small intestine (3/12), lymph nodes around the colon (0/7). Outcomes: He is currently receiving chemotherapy, the chemotherapy regimen is XELOX regimen. The specific drugs were oxaliplatin and capecitabine. Lessons: SBA is often difficult to diagnose due to few specific symptoms and is usually detected at stage IV. Bilateral ovarian Kukenberg tumor caused by small bowel cancer implantation metastases is extremely rare, and clinicians must be vigilant for women with fewer specific symptoms of gastrointestinal discomfort and conduct further diagnostic studies to avoid delayed diagnosis and treatment.
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