The electronic medical record management systems may improve monitoring and control of disease activity in patients with ankylosing spondylitis.

To investigate the impact of an electronic medical record management system (EMRMS) on disease activity and the frequency of outpatient visits among patients with ankylosing spondylitis (AS). We identified 652 patients with AS who were followed up for at least 1 year before and after the first Ankylosing Spondylitis Disease Activity Score (ASDAS) assessment and compared the number of outpatient visits and average visit time within 1 year before and after the initial ASDAS assessment. Finally, we analyzed 201 patients with AS who had complete data and received ≥ 3 continuous ASDAS assessments at an interval of 3 months, and we compared the results of the second and third ASDAS assessments with those of the first. The number of annual outpatient visits increased after ASDAS assessment (4.0 (4.0, 7.0) vs. 4.0 (4.0, 8.0), p < 0.001), particularly among those with a high initial disease activity. The average visit time was reduced within 1 year after ASDAS assessment (6.4 (8.5, 11.2) vs. 6.3 (8.3, 10.8) min, p = 0.073), especially among patients whose with an inactive disease activity was < 1.3 (ASDAS C-reactive protein (CRP) 6.7 (8.8, 11.1) vs. 6.1 (8.0, 10.3) min, p = 0.033; ASDAS erythrocyte sedimentation rate (ESR) 6.4 (8.7, 11.1) vs. 6.1 (8.1, 10.0) min, p = 0.027). Among patients who received at least three ASDAS assessments, the third ASDAS-CRP tended to be lower than the first (1.5 (0.9, 2.1) vs. 1.4 (0.8, 1.9), p = 0.058). The use of an EMRMS increased the frequency of ambulatory visits among AS patients with high and very high disease activity and reduced the visit time among those with an inactive disease. Continual ASDAS assessments may help control the disease activity of patients with AS.

Investigation of changes in ankylosing spondylitis disease activity through 2021 COVID-19 wave in Taiwan by using electronic medical record management system.

We aim to investigate the alteration in disease activity of ankylosing spondylitis (AS) individuals before, during, and after the COVID-19 wave in Taiwan by using electronic medical-record management system (EMRMS). We identified 126 AS individuals from the single center, and gathered data of the three disease activities (Bath Ankylosing Spondylitis Disease Activity Index [BASDAI], Ankylosing Spondylitis Disease Activity Score with erythrocyte sedimentation rate [ASDAS-ESR], and Ankylosing Spondylitis Disease Activity Score with C-Reactive Protein [ASDAS-CRP]) by using EMRMS before (7 February to 1 May, 2021), during (2 May to 24 July, 2021), and after the COVID-19 wave (25 July to 16 October, 2021). We compared the disease activity measures of the three phases through a paired t test. Among the 126 individuals, CRP was significantly higher during the COVID-19 wave (0.2 (0.1, 0.5) mg/dl, p = 0.001) than before the wave (0.2 (0.1, 0.4) mg/dl), ESR (8.0 (4.0, 15.0) mm/h, p = 0.003) and ASDAS-ESR (1.4 (1.0, 1.9), p = 0.032) were significantly higher after the wave than during the wave (6.0 (3.0, 12.0) mm/h and 1.2 (0.9, 1.8) mm/h) e. ESR, CRP, ASDAS-ESR and ASDAS-CRP were all significant higher after COVID-19 wave than before. The disease activities of AS individuals in Taiwan worsened after 2021 COVID-19 wave in Taiwan.

Association between a History of herpes zoster and the risk of Sjögren's syndrome: a nationwide, population-based, case-control study.

OBJECTIVE: Viral infection is an exogenous factor for Sjögren's syndrome (SS). The relationship between herpes zoster infection and the ensuring risk of SS has remained unclear. This study investigated the association between a history of herpes zoster infection and the risk of SS through a nationwide population-based case-control study. DESIGN: Retrospective case-control study. SETTING: General population of Taiwan. DATA SOURCE: 2003-2013 National Health Insurance Research Database of Taiwan. PARTICIPANTS: We identified all patients with newly diagnosed SS between 1 January 2007 and 31 December 2012 without a history of rheumatoid arthritis or systemic lupus erythematosus as the SS group. CONTROLS: We randomly selected patients without SS between 1 January 2003 and 31 December 2012 and matched 1:5 with controls based on index year, age and sex. MAIN OUTCOME MEASURE: Conditional logistic regression analysis to examine the association between a history of herpes zoster and the risk of SS. RESULTS: The study included 5751 patients with SS and 28 755 matched controls. The risk of SS was significantly associated with a history of herpes zoster (model A (adjusted for Charlson Comorbidity Index (CCI) (excluding connective tissue disease, CTD)): OR 1.89; 95% CI 1.71 to 2.08; model B (adjusted for comorbidities used to calculate CCI (excluding CTD)): OR 1.90; 95% CI 1.72 to 2.10), in particular if the interval from the last visit for herpes zoster infection to the index date was <3 months (model A: OR 3.09; 95% CI 2.20 to 4.34; model B: OR 3.13; 95% CI 2.20 to 4.45). Such associations remained robust using various definitions of herpes zoster. CONCLUSION: This nationwide, population-based, case-control study revealed a significant association between a history of herpes zoster and the risk of SS.

Construction of Recombinant Saccharomyces cerevisiae with Ethanol and Aldehydes Tolerance via Overexpression of Aldehyde Reductase.

Furfural and hydroxy-methyl-furfural (HMF) are produced by lignocellulosic biomass during heat or acid pretreatment and are toxic to yeast. Aldehyde reductase is the main enzyme to reduce furfural and HMF. To improve the conversion efficiency of lignocellulosic biomass into ethanol, we constructed Saccharomyces cerevisiae with overexpression of aldehyde reductase (encoded by ari1). The gene of aldehyde reductase (encoded by ari1) was cloned via polymerase chain reaction (PCR) and ligated with the expression vector pGAPZαC. Western blot coupled with anti-His tag confirmed overexpression of the ari1 gene. The growth curves of the wild and ari1-overexpressed strain in the YPD medium were found to be almost identical. Compare to the ari1-overexpressed strain, the wild strain showed a longer doubling time and lag phase in the presence of 20 mM furfural and 60 mM HMF, respectively. The real-time PCR results showed that furfural was much more potent than HMF in stimulating ari1 expression, but the cell growth patterns showed that 60 mM HMF was more toxic to yeast than 20 mM furfural. S. cerevisiae with ari1 overexpression appeared to confer higher tolerance to aldehyde inhibitors, thereby increasing the growth rate and ethanol production capacity of S. cerevisiae in an aldehyde-containing environment.

Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p.

Carbonic anhydrase VIII (CAVIII) is a member of the CA family, while CA8 is the oncogene. Here we observed increased expression of CAVIII with high expression in colorectal cancer tissues. CAVIII is also expressed in more aggressive types of human colorectal cancer cells. Upregulated CAVIII expression in SW480 cell lines increased vascular endothelial growth factor (VEGF) and reduced miRNA16-5p. Conversely, knockdown of the CAVIII results in VEGF decline by up-regulated miRNA16-5p. Moreover, the collection of different grades of CAVIII expression CRC cells supernatant co-culture with endothelial progenitor cells (EPCs) promotes the ability of tube formation in soft agar and migration in the Transwell experiment, indicating that CAVIII might facilitate cancer-cell-released VEGF via the inhibition of miRNA16-5p signaling. Furthermore, in the xenograft tumor angiogenesis model, knockdown of CAVIII significantly reduced tumor growth and tumor-associated angiogenesis. Taken together, our results prove that the CAVIII/miR-16-5p signaling pathway might function as a metastasis suppressor in CRC. Targeting CAVIII/miR-16-5p may provide a strategy for blocking its metastasis.

Endothelin-1-mediated miR-let-7g-5p triggers interlukin-6 and TNF-α to cause myopathy and chronic adipose inflammation in elderly patients with diabetes mellitus.

BACKGROUND: Diabetes and sarcopenia are verified as mutual relationships, which seriously affect the quality of life of the elderly. Endothelin-1 is well investigated, is elevated in patients with diabetes, and is related to muscle cellular senescence and fibrosis. However, the mechanism of ET-1 between diabetes and myopathy is still unclear. The aim of this study was to evaluate the prevalence of sarcopenia in the elderly with diabetes and to clarify its relationship with ET-1 molecular biological mechanism, progress as well as changes in muscle and fat. METHODS: We recruited 157 type 2 diabetes patients over 55 years old and investigated the prevalence of sarcopenia in diabetes patients and examined the association of ET-1 alterations with HbA1c, creatinine, or AMS/ht2. Next, sought to determine how ET-1 regulates inflammation in muscle cells by western blot and qPCR assay. Using XF Seahorse Technology, we directly quantified mitochondrial bioenergetics in 3T3-L1 cells. RESULTS: ET-1 was positively correlated with HbA1c, creatinine levels, and duration of disease, and negatively correlated with AMS/ht2. We found that ET-1 dose-dependently induces tumor necrosis factor-α (TNF-α) and interleukin (IL)-6ß expression through the PI3K/AKT, and NF-κB signaling pathways in C2C12 cells. Also identified that TNF-α, IL-6ß, and visfatin releases were found in co-cultured with conditioned medium of ET-1/C2C12 in 3T3-L1 cells. ET-1 also reduces the energy metabolism of fat and induces micro-environment inflammation which causes myopathy. ET-1 also suppresses miR-let-7g-5p expression in myocytes and adipocytes. CONCLUSION: We describe a new mechanism of ET-1 triggering chronic inflammation in patients with hyperglycemia.

Potential of antiviral drug oseltamivir for the treatment of liver cancer.

Liver cancer is a leading cause of cancer­related mortality globally. Since hepatitis virus infections have been strongly associated with the incidence of liver cancer, studies concerning the effects of antiviral drugs on liver cancer have attracted great attention in recent years. The present study investigated the effects of two anti­hepatitis virus drugs, lamivudine and ribavirin, and one anti­influenza virus drug, oseltamivir, on liver cancer cells to assess alternative methods for treating liver cancer. MTT assays, wound healing assays, Τranswell assays, flow cytometry, immunoblotting, ELISA, immunofluorescence staining and a xenograft animal model were adopted to verify the effects of lamivudine, ribavirin and oseltamivir on liver cancer cells. Treatment with ribavirin and oseltamivir for 24 and 48 h significantly decreased the viability of both Huh-7 and HepG2 cells compared with that of THLE­3 cells in a dose­dependent manner. The subsequent investigations focused on oseltamivir, considering the more serious clinical adverse effects of ribavirin than those of oseltamivir. Significantly decreased migration and invasion were observed in both Huh-7 and HepG2 cells that were treated with oseltamivir for 24 and 48 h. In addition, oseltamivir significantly increased autophagy in Huh­7 cells, as revealed by the significantly higher ratios of LC3­II/LC3­I, increased expression of Beclin­1, and decreased expression of p62, whereas no significant increases in the expression of apoptosis­related proteins, including Apaf­1, cleaved caspase­3, and cleaved PARP­1, were detected. Notably, apoptosis and autophagy were significantly increased in HepG2 cells in the presence of oseltamivir, as revealed by the significant increases in the expression of Apaf­1, cleaved caspase­3, and cleaved PARP­1, the higher ratios of LC3­II/LC3­I, the increased expression of Beclin­1, and the decreased expression of p62. Additionally, significant inhibitory effects of oseltamivir on xenografted Huh­7 cells in athymic nude mice were observed. The present study, for the first time to the best of our knowledge, reported the differential effects of oseltamivir on inducing liver cancer cell death both in vitro and in vivo and may provide an alternative approach for treating liver cancer.

Association between α-glucosidase inhibitor use and psoriatic disease risk in patients with type 2 diabetes mellitus: A population-based cohort study.

AIMS: To investigate the association between the use of alpha-glucosidase inhibitors (AGIs) and the risk of psoriatic disease (ie, psoriasis and psoriatic arthritis) in patients with type 2 diabetes mellitus (T2DM) treated with metformin. METHODS: Using the 1999-2013 Taiwanese Longitudinal Cohort of Diabetes Patients Database, we identified patients with T2DM who initiated hypoglycaemic treatment between 2003 and 2012. After excluding patients with a history of psoriatic disease (International Classification of Disease, Ninth Revision, Clinical Modification codes 696.0-1) before T2DM diagnosis, patients who received antidiabetic treatment for <90 days, and patients aged <20 or >100 years, we identified 1390 patients who received metformin+AGIs (AGI exposure group) and 47 514 patients who received metformin only (comparison group). We matched the two groups at a 1:10 ratio by age, sex, and index date of T2DM drug use. The association between AGI use and psoriatic disease risk was analysed using a Cox proportional hazard mode; time-dependent covariates for factors were reported in terms of hazard ratios (HRs) with 95% confidence intervals (CIs) after age, sex, T2DM duration, and comorbidities were controlled for. RESULTS: After adjusting the AGI exposure and comparison groups for potential confounders, we found that psoriatic disease risk was associated with metformin+AGI use when AGI was discontinued for 30 days (HR, 8.77; 95% CI, 1.58-48.5) and when a high AGI dose was administered; furthermore, the risk declined during AGI discontinuation. CONCLUSIONS: This population-based study reports that AGI use and interruption of AGI use may be associated with increased psoriatic disease risk in treated patients with T2DM.

[Case-control study of risk factors for hip fracture in the elderly].

BACKGROUND: The elderly (> = 65 years of age) accounted for 10.4% of Taiwan's population in 2008. Hip-fracture-related hospitalizations cost the National Health Insurance Bureau around NT$1.3 billion annually. Hip fractures currently account for one-fifth of all fractures, and this proportion has been rising by 2.8 % annually. Hip fracture-associated mortality has been reported as 8.4-36% during the first post-fracture year. Hip fractures in the elderly is an issue that deserves further elucidation and study. PURPOSE: We investigated whether variables including gender, age, body mass index, lifestyle, and medical history were risk factors for elderly hip fractures. METHODS: We used a case control study and collected data via retrospective chart review and telephone questionnaires. Hip fracture risk factor data collected included demographic, lifestyle, and medical history data. RESULTS: Results showed average age in the hip fracture group as significantly higher than the non-hip fracture group and body mass index as significantly lower in the hip fracture than the non-hip fracture group (p < .05). Gender, history of alcoholism, exercise habits, history of stroke, diabetes mellitus, hypertension, depression, and past fractures were identified as significant hip fracture risk factors. CONCLUSIONS / IMPLICATIONS FOR PRACTICE: This study identified critical hip fracture risk factors in the elderly. Results provide a reference for prevention and health education. Reducing hip fractures, in addition to improving daily life quality for elderly individuals, can significantly reduce medical and social expenses.