Kaohsiung Journal of Medical Sciences最新文献

The present study aimed to investigate the factors associated with the level of rumination about the war among people living in Poland and Ukraine. This cross-sectional study recruited internet users from advertisements on social media. Levels of rumination, Depression, Anxiety and Stress Scale (DASS), Impact of Event Scale-Revised (IES-R), time spent on news of the war, and related demographic variables were collected. The reliability and construct validity of rumination were estimated. Potential factors associated with the level of rumination were identified using univariate linear regression analysis, and further entered into a stepwise multivariate linear regression model to identify independent factors. Due to the non-normality of distribution, multivariate linear regression with 5000 bootstrap samples was used to verify the results. A total of 1438 participants were included in the analysis, of whom 1053 lived in Poland and 385 lived in Ukraine. The questionnaires on rumination were verified to have satisfactory reliability and validity. After analysis with stepwise and bootstrap regression, older age, female gender, higher DASS and IES-R scores, and longer time spent on news of the war were significantly associated with higher levels of rumination for both people living in Poland and Ukraine. Lower self-rated health status, history of chronic medical illness and coronavirus disease 2019 infection were also positively associated with rumination for people living in Poland. We identified several factors associated with the level of rumination about the Russo-Ukrainian War. Further investigations are warranted to understand how rumination affects individuals' lives during crises such as war.

Plasma miRNAs can characterize several diseases, including acute ischemic stroke (AIS), which is noninvasive and currently affordable in most laboratories worldwide. We aimed to demonstrate plasma miR-140-3p, miR-130a-3p, and miR-320b as diagnostic biomarkers in AIS.GSE110993 and GSE86291 datasets were analyzed to obtain plasma differentially expressed miRNAs between AIS and healthy control subjects (HCs). We further applied RT-qPCR for the validation in 85 AIS patients and 85 HCs. Receiver operating characteristic (ROC) curve were conducted to evaluate their diagnostic utility in AIS. Correlation was analyzed between DEmiRNAs and clinical and laboratory parameters, as well as inflammatory markers. The plasma levels of miR-140-3p, miR-130a-3p, and miR-320b were found to be consistently altered in both GSE110993 and GSE86291 datasets. In comparison to HCs, AIS patients at admission exhibited lower levels of miR-140-3p and miR-320b and higher level of miR-130a-3p in their plasma. The ROC analysis revealed that plasma miR-140-3p, miR-130a-3p, and miR-320b had area under the curve values of 0.790, 0.831, and 0.907, respectively. When combined, these miRNAs showed superior discriminatory power with a sensitivity of 91.76% and specificity of 95.29%. Plasma miR-140-3p and miR-320b negatively correlated glucose levels and inflammatory markers (IL-6, MMP-2, MMP-9, and VEGF) in AIS patients. Conversely, plasma miR-130a-3p levels were positively associated with glucose levels and these markers. Plasma miR-140-3p, miR-130a-3p, and miR-320b levels varied significantly among AIS patients with different NIHSS scores. Plasma miR-140-3p, miR-130a-3p, and miR-320b had high diagnostic value in AIS patients, which were correlated with inflammation and severity in stroke.

This study was to explore the regulatory effect of long non-coding RNA LINC01559 on Docetaxel resistance in breast carcinoma (BCa) and its underlying mechanism. In the present study, we found that LINC01559 expression was elevated and LINC01559 overexpression facilitated docetaxel resistance in BCa cells. Moreover, it was revealed that the upregulation of LINC01559 in BCa cells was induced by FTO-mediated demethylation in an m6A-YTHDF2-dependent manner. Additionally, Dual-luciferase reporter assay confirmed the binding ability between LINC01559 and miR-1343-3p, and Pearson correlation analysis showed a negative correlation between them. Particularly, miR-1343-3p inhibition partly abolished the suppression on docetaxel resistance in BCa cells caused by LINC01559 knockdown. To sum up, FTO-mediated epigenetic upregulation of LINC01559 promoted cell resistance to Docetaxel in BCa by negatively regulating miR-1343-3p.

The interleukin-23 (IL-23)/IL-17 immune axis has been linked to the pathology of psoriasis, but how this axis contributes to skin inflammation in this disease remains unclear. We measured inflammatory cytokines associated with the IL-23/IL-17 immune axis in the serum of patients with psoriasis using enzyme-linked immunosorbent assays. Psoriasis was induced in male C57BL/6J mice using imiquimod (IMQ) cream, and animals received intraperitoneal injections of recombinant mouse anti-IL-23A or anti-IL-17A antibodies for 7 days. The potential effects of the IL-23/IL-17 immune axis on skin inflammation were assessed based on pathology scoring, hematoxylin-eosin staining of skin samples, and quantitation of inflammatory cytokines. Western blotting was used to evaluate levels of the following factors in skin: ACT1, TRAF6, TAK1, NF-κB, and pNF-κB. The serum of psoriasis patients showed elevated levels of several cytokines involved in the IL-23/IL-17 immune axis: IL-2, IL-4, IL-8, IL-12, IL-17, IL-22, IL-23, and interferon-γ. Levels of IL-23p19 and IL-17 were increased in serum and skin of IMQ-treated mice, while ACT1, TRAF6, TAK1, NF-κB, and pNF-κB were upregulated in the skin. A large proportion of NF-κB p65 localized in nucleus of involucrin⁺ cells in the epidermis and in F4/80⁺ cells of the dermis of psoriatic lesional skin. Treating these animals with anti-IL-23 or anti-IL-17 antibodies improved pathological score and immune imbalance, mitigated skin inflammation and downregulated ACT1, TRAF6, TAK1, NF-κB, and pNF-κB in skin. Our results suggest that skin inflammation mediated by the IL-23/IL-17 immune axis in psoriasis involves activation of the ACT1/TRAF6/TAK1/NF-κB pathway in keratinocytes and macrophage.

Intestinal barrier injury is a common complication of severe acute pancreatitis (SAP), which is often accompanied by intestinal mucosal barrier injury and results in serious consequences. However, the exact mechanism remains unclear. We aimed to investigate whether angiotensin II type 1 receptor (AT1)-mediated oxidative stress is involved in SAP intestinal barrier injury and assessed the effects of inhibiting this pathway. The SAP model was established by retrograde bile duct injection of sodium taurocholate (5%). The rats were divided into three groups: the control group (SO), the SAP group (SAP), and the azilsartan intervention group (SAP + AZL). Serum amylase, lipase, and other indexes were measured to evaluate SAP severity in each group. Histopathological changes in the pancreas and intestine were evaluated by HE staining. The oxidative stress of intestinal epithelial cells was detected by superoxide dismutase and glutathione. We also detected the expression and distribution of intestinal barrier-related proteins. The results showed that the serum indexes, the severity of tissue damage, and the level of oxidative stress in the SAP + AZL group were significantly lower than in the SAP group. Our study provided hitherto undocumented evidence of AT1 expression in the intestinal mucosa, confirming that AT1-mediated oxidative stress is involved in SAP intestinal mucosal injury, and inhibiting this pathway could effectively reduce intestinal mucosal oxidative stress injury, providing a new and effective target for the treatment of SAP intestinal barrier injury.

In our previous retrospective study, we found that using the strabismus surgery dosages established by western strabismus mentors tends to result in undercorrection of Taiwanese exotropia (XT) patients compared with those in western populations. We also discovered that the location of extraocular muscle (EOM) insertion could vary by ethnicity. In this study, using a generalized estimation equation model, we compared the XT surgery outcome between augmented and original strabismus surgery dosages in Taiwanese patients. We also conducted an observational study to investigate the horizontal EOM insertion location in a Taiwanese population and compared the data with Dr. Apt L.'s study. For Taiwanese XT patients, augmented surgical dosages resulted in significantly better outcome at 6 months and 1 year postoperatively compared with original surgical dosages (p = 0.003 and p < 0.001, respectively). The distance from the lateral recuts muscle (LR) insertion location to the limbus was significantly shorter in Taiwanese than in white Americans (6.5 vs. 6.9 mm, respectively, p = 0.0001). Furthermore, the medial rectus muscle and LR insertion locations differed significantly between males and females (p < 0.001 and p = 0.023, respectively). The patients' sex did not affect the surgery outcome. Augmented surgery doses modified from western strabismus mentors produce better surgery outcome for Taiwanese XT patients. Surgeons may require country-specific guidelines for strabismus surgery dosage. We also demonstrated a simple method for young ophthalmologists to establish their own normograms to improve their surgical success rate. Our study confirms that LR insertion locations differ between Taiwanese and White Americans.

Nonalcoholic fatty liver disease (NAFLD) is a hepatic metabolic syndrome with a rapidly increasing prevalence globally. Plantamajoside (PMS), a phenylethanoid glycoside component extracted from Plantago asiatica, has various biological properties. However, its effect on NAFLD remains unknown. The study aimed to explore the effect and mechanism of PMS on NAFLD in the high-fat diet (HFD)-feeding rats. PMS induced a decrease in body and liver weight, and the amelioration in the blood lipid parameters and pathological symptoms in HFD-feeding rats. The increase in the serum concentrations and the relative protein expressions of proinflammatory factors was decreased by the PMS treatment in HFD-induced NAFLD rats. Additionally, PMS reduced the excessive lipid vacuoles, and modified the relative expressions of proteins involved in the fatty acid synthesis and uptake in HFD-feeding rats. Mechanically, the downregulation of AMPK/Nrf2 pathway in HFD-feeding rats was restored by the PMS treatment. Inhibition of AMPK pathway reversed the PMS-induced the increase in the level of inflammatory factors, pathological symptoms, excessive lipid vacuoles, and the relative expression of proteins involved in the fatty acid synthesis and uptake. Collectively, PMS ameliorated immune dysregulation and abnormal hepatic lipid metabolism by activating AMPK/Nrf2 pathway in rats with NAFLD.