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Risk Factor Analysis of Early-Onset Cataracts in Taiwan
No full text[[abstract]]Purpose: According to previous studies, the prevalence rate of cataracts has increased in recent years. This study aims to investigate and analyze the risk factors of early-onset cataracts in Taiwan.
Methods: A total of 71 subjects aged between 20 and 55 were diagnosed with cataracts in a medical center. Participants were divided into three groups: control, early-onset cataract (EOC), and combined (EOC combined with dry eye) groups. Eye examinations including autorefraction, best-corrected visual acuity (BCVA), subjective refraction, axial length, fundus, slit lamp, and reactive oxygen species (ROS, including total antioxidative capacity, TAC; C-reactive protein, CRP; and glutathione peroxidase, GPx) were performed. In addition, a questionnaire on patient information, history, habits, family history, and Depression Anxiety Stress Scales (DASS) was completed before the examination.
Results: 27 non-EOC (control group), 20 EOC, and 24 combined patients participated in the study. Compared with the control group, Body Mass Index (BMI), gender, educational level, hypertension, diabetes, hyperlipidemia, chronic pain, and body-related diseases were significantly different between the three groups. Family history was also significantly different: family heart disease, hypertension, asthma, allergies, stroke, and immune system were also significantly different. In addition, subjects who took hypertensive drugs, antihistamines, and other medications were also significantly different. Statistical analysis indicated that best corrective visual acuity and the spherical equivalent were significantly different between the three groups. Similar results were found in CRP blood analysis.
Discussion and conclusion: According to the results, EOC may result from systemic diseases. The risk corresponded to an increase in ROS blood analysis. Furthermore, eye drops and medicine intake significantly influenced EOC patients. To prevent or defer early-onset cataracts, monitoring physical health, CRP, and GPx analysis may be worth considering in the future
傳承社會資本延續家族企業價值
No full text[[abstract]]家族企業傳承是一件複雜且富有挑戰性的過程，而最大的挑戰在於是否能夠保留、沿用與增加家族現有的有形與無形資源。在此情況下，社會資本乃是家族成員經年累月所投資而形成的一種寶貴資源。在家族企業傳承過程中，若能成功地保留和增加社會資本，將對中小型家族企業的持續發展扮演著關鍵性角色。因此，在家族企業傳承過程中，交棒者如何將社會網絡資源順利轉移給接班人乃是至關重要。本文主要針對國內六家中小型家族企業進行個案訪談研究，並從個人視角來瞭解家族企業傳承時，其社交網絡轉移的實證見解。家族企業的社會資本常因企業負責人不同而有所變動。因此，家族企業在傳承過程中，交棒者和繼任者在家族企業的角色轉變，將會重大影響企業的社會資本。此外，本文還探討有關家族企業的社交網絡資源轉移之相關現象，例如「網絡更新效應」和「世代代溝效應」等，以提出總體研究命題，而這些因素都會影響家族企業傳承的時間和形式。經由實證，本研究認為社會資本確實是家族企業傳承能否成功關鍵因素之一，並左右傳承過程的時間長短與利害關係人的相應行為。[[abstract]]The success of the family business is a complex and challenging process. The biggest challenge is whether to retain, continue and increase social capital of the family. In this context, social capital is a valuable resource that family have invested in over time. During the process of success of family business, if it can successfully retain and increase social capital, it will keep on developing family business. Therefore, it is very important to transfer social network from predecessors to successors smoothly. We conduct interviews on 6 small and medium-sized family business members in Taiwan from individual perspective and understand the empirical insights of the social network transfer during the success of the family business. The social network of a family business often changes depending on who in charge of the family business is. Therefore, in the process of family business success, the change of family business owner will have a significant impact on the social capital of the enterprise. In addition, this paper explores the different modes of social capital transfer in family businesses, such as ?network renewal effect? and ?generation gap effect?, to establish an overall research framework, and these factors will affect the timing and form of family business success. Through empirical evidence, this study believes that social capital is indeed one of the key factors for family business succession
Adjuvant Probiotics of Lactobacillus salivarius subsp. salicinius AP-32, L. johnsonii MH-68, and Bifidobacterium animalis subsp. lactis CP-9 Attenuate Glycemic Levels and Inflammatory Cytokines in Patients With Type 1 Diabetes Mellitus
No full text[[abstract]]Introduction: Type 1 diabetes mellitus (T1DM) is characterized by autoimmune destruction of pancreatic β cells. Previous study has discovered that probiotic strains residing in the gut play essential roles in host immune regulation. However, few clinical results demonstrated probiotic would actually benefit in attenuating glycated hemoglobin (HbA1c) along with inflammatory cytokine levels of the T1DM patients and analyzed their gut microbiota profile at the same time. In this clinical trial, we evaluated the therapeutic efficacy of probiotics on HbA1c along with inflammatory cytokine levels of T1DM patients to determine an alternative administration mode for T1DM medication. The probiotics changed T1DM gut microbiota profile will be measured by next-generation sequencing (NGS).
Research design and methods: A randomized, double-blind, placebo-controlled trial was performed at China Medical University Hospital. T1DM patients between 6 and 18 years of age were enrolled. 27 patients were administered regular insulin therapy plus capsules containing probiotic strains Lactobacillus salivarius subsp. salicinius AP-32, L. johnsonii MH-68, and Bifidobacterium animalis subsp. lactis CP-9 daily for 6 months, and 29 patients were administered insulin therapy without extra probiotic supplement as placebo group. The variations of fasting blood glucose and HbA1c in these patients were analyzed. In addition, serum levels of inflammatory cytokines and anti-inflammatory cytokine were assessed using enzyme-linked immunosorbent assay. Patients' stool microbiota were all subjects to NGS analysis.
Results: NGS data showed elevated populations of Bifidobacterium animalis, Akkermansia muciniphila and Lactobacillus salivarius in the gut of patients with T1DM who were taking probiotics. Patients with T1DM who were administered probiotics showed significantly reduced fasting blood glucose levels compared with the before-intervention levels. The HbA1c levels of the patients also improved after administration of probiotics. The concentrations of IL-8, IL-17, MIP-1β, RANTES, and TNF-α were significantly reduced and were associated with an increased TGF-β1 expression after probiotic intervention. The persistence effect of glycemic control and immunomodulation were observed even 3 months after discontinuation of the probiotics.
Conclusions: Here, we found that conventional insulin therapy plus probiotics supplementation attenuated T1DM symptoms than receiving insulin treatment only. Probiotics supplementation with insulin treatment changed gut microbiota and revealed better outcome in stabilizing glycemic levels and reducing HbA1c levels in patients with T1DM through beneficial regulation of immune cytokines
Adoptive transfer of IL-4 reprogrammed Tc17 cells elicits anti-tumor immunity through functional plasticity
No full text[[abstract]]Ability of IL-17-producing CD8+ T cells (Tc17) to transform into cytotoxic anti-tumour effectors makes them a promising candidate for immune effector cell (IEC) therapy. However, key factors regulating Tc17 reprogramming remain poorly defined, hindering translation of Tc17-based IEC use from bench to bedside. We probed the effects of multiple cytokines and underlying signalling pathways on Tc17 cells and identified pivotal role for IL-4 and PI3K/AKT in promoting Tc17 transformation into cytotoxic IFN-γ-producing IECs, an effect dependent on Eomes expression. IL-4 not only triggered Tc17 cytotoxicity, but also induced cell expansion, which significantly improved the antitumour potential of Tc17 cells compared to that of IFN-γ-producing CD8+ T cells (Tc1) in a murine model. Furthermore, IL-4/AKT signalling drove the upregulation of the T-cell receptor-associated transmembrane adaptor 1 (Trat1) in Tc17 cells to promote IL-4-induced T-cell receptor stabilization and Tc17 cytotoxicity. Finally, we proposed a possible procedure to expand human Tc17 from peripheral blood of cancer patients, and confirmed the function of IL-4 in Tc17 reprogramming. Collectively, these results document a novel IL-4/AKT/Eomes/Trat1 axis that promotes expansion and transformation of Tc17 cells into cytotoxic effectors with a therapeutic potential. IL-4 priming of Tc17 cells should be further explored as a cell therapy engineering strategy to generate IECs to augment anti-tumour responses
Association of SGLT2 inhibitors with lower incidence of death in type 2 diabetes mellitus and causes of death analysis
No full text[[abstract]]Sodium-glucose cotransporter 2 inhibitor (SGLT2i) potentially decrease all-cause and cardiovascular death, however, associations with non-cardiovascular death remain unclear. Therefore, we investigated SGLT2i associations with death and the cause of death. We used the Taiwanese National Health Institutes Research database linked to the National Register of Deaths (NRD). Incident type 2 diabetes mellitus (T2DM) patients and propensity score matched T2DM SGLT2i and Dipeptidyl peptidase 4 inhibitor (DPP4i) users were investigated. The index year was the SGLT2i or DPP4i prescription date from May 2016. Patients were followed-up until death or December 2018. Deaths verified by the NRD and grouped accordingly. Multiple Cox proportional hazards models were used. In total, 261,211 patients were included in the population; 47% of the patients were female and the average age was 62 years. The overall incidence of all-cause death was 8.67/1000 patient-years for SGLT2i and 12.41 for DPP4i users during follow-up. After adjusting for potential risk factors in the propensity score matched population, SGLT2i users were associated with lower risks of all-cause death, cardiovascular death, cancer death, and non-cancer, non-vascular death compared with DPP4i-users. For specific death causes, significantly lower death risks from heart disease, cerebrovascular disease, and accidents were associated with SGLT2i-use. SGLT2i benefits for T2DM patients were not different across subgroups. Compared with DPP4i-use, SGLT2i-use for T2DM was associated with lower disease and death risk
Carboxyl terminus of HSP70-interacting protein attenuates advanced glycation end products-induced cardiac injuries by promoting NFκB proteasomal degradation
No full text[[abstract]]Advanced glycation end products (AGEs), which are highly reactive molecules resulting from persistent high-glucose levels, can lead to the generation of oxidative stress and cardiac complications. The carboxyl terminus of HSP70 interacting protein (CHIP) has been demonstrated to have a protective role in several diseases, including cardiac complications; however, the role in preventing AGE-induced cardiac damages remains poorly understood. Here, we found that elevated AGE levels impaired cardiac CHIP expression in streptozotocin-induced diabetes and high-fat diet-administered animals, representing AGE exposure models. We used the TUNEL assay, hematoxylin and eosin, Masson's trichrome staining, and western blotting to prove that cardiac injuries were induced in diabetic animals and AGE-treated cardiac cells. Interestingly, our results collectively indicated that CHIP overexpression significantly rescued the AGE-induced cardiac injuries and promoted cell survival. Moreover, CHIP knockdown-mediated stabilization of nuclear factor κB (NFκB) was attenuated by overexpressing CHIP in the cells. Furthermore, co-immunoprecipitation and immunoblot assay revealed that CHIP promotes the ubiquitination and proteasomal degradation of AGE-induced NFκB. Importantly, fluorescence microscopy, a luciferase reporter assay, electrophoretic mobility shift assay, and subcellular fractionation further demonstrated that CHIP overexpression inhibits AGE-induced NFκB nuclear translocation, reduced its binding ability with the promoter sequences of the receptor of AGE, consequently inhibiting the translocation of the receptor AGE to the cell membrane for its proper function. Overall, our current study findings suggest that CHIP can target NFκB for ubiquitin-mediated proteasomal degradation, and thereby potentially rescue AGE-induced cardiac damages
Comparison between the analytical sensitivity and clinical performance of two cobas SARS-CoV-2 tests based on high-throughput and point-of-care systems
No full text[[abstract]]Objectives: This study examined analytical sensitivity, specificity, and the clinical performance in detecting SARS-CoV2 of the Cobas SARS-CoV-2 Test based on the high-throughput Cobas 6800 system and the Cobas SARS-CoV-2 & Flu A/
B Test based on the point-of-care cobas Liat system.
Methods: The commercial reagents containing SARS-CoV-2 RNA subgenomes were diluted for assessing the sensitivity of the RT-qPCR assay. 385 nasopharyngeal swab specimens taken from contacts of COVID-19 cases were tested for
the SARS-CoV-2 detection with both Cobas SARS-CoV-2 Tests.
Results: In analytical sensitivity assays, the Cobas SARS-CoV-2 & Flu A/B Test on the Liat system had a lower limit of
detection (12.5e25 copies/mL) than the cobas SARS-CoV-2 Test on the cobas 6800 system (25e50 copies/mL). In clinical
performance assays, the cobas SARS-CoV-2 Test demonstrated 89.36% (42 out of 47) PPA (positive percent agreement)
and 98.82% (334 out of 338) NPA (negative percent agreement) compared to the results of the Cobas SARS-CoV-2 & Flu
A/B test. Among five discordant specimens, four had the positive result of the cobas SARS-CoV-2 test, but the negative
result of the cobas SARS-CoV-2 & Flu A/B Test. Moreover, these discordant specimens had the Ct values of greater than
33 for the cobas SARS-CoV-2 Test, implying a very small number of virions in the samples. Remarkably, four specimens
with a presumptive positive result of the cobas SARS-CoV-2 test had been confirmed by the Cobas SARS-CoV-2 & Flu
A/B Test. Next, the scatter plots of the Ct values showed a highly positive correlation between cobas SARS-CoV-2 & Flu
A/B Test and the cobas SARS-CoV-2 Test (R-squared value ? 0.954e0.962).
Conclusions: Both SARS-CoV2 tests of the cobas 6800 and Liat systems produce reliable high throughput and point-ofcare assays respectively for the early virus detection and the personal care decision-making during COVID-19 pandemic
Cryptotanshinone protects against oxidative stress in the paraquat-induced Parkinson's disease model
No full text[[abstract]]Parkinson's disease (PD) is a common neurodegenerative disorder associated with striatal dopaminergic neuronal loss in the Substantia nigra. Oxidative stress plays a significant role in several neurodegenerative diseases. Paraquat (PQ) is considered a potential neurotoxin that affects the brain leading to the death of dopaminergic neurons mimicking the PD phenotype. Various scientific reports have proven that cryptotanshinone possesses antioxidant and anti-inflammatory properties. We hypothesized that cryptotanshinone could extend its neuroprotective activity by exerting antioxidant effects. This study was designed to evaluate the effects of cryptotanshinone in both cellular and animal models of PQ-induced PD. Annexin V-PI double staining and immunoblotting were used to detect apoptosis and oxidative stress proteins, respectively. Reactive oxygen species kits were used to evaluate oxidative stress in cells. For in vivo studies, 18 B6 mice were divided into three groups. The rotarod data revealed the motor function and immunostaining showed the survival of TH+ neurons in SNpc region. Our study showed that cryptotanshinone attenuated paraquat-induced oxidative stress by upregulating anti-oxidant markers in vitro, and restored behavioral deficits and survival of dopaminergic neurons in vivo, demonstrating its therapeutic potential
Detection of the SARS-CoV-2 D614G mutation using VirSNiP SARS-CoV-2 Spike D614G assay
No full text[[abstract]]Background: At the end of 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly spread worldwide. Until recently, over 190 million cases and nearly four million deaths have been reported globally due to the virus. A point mutation in the SARS-CoV-2 spike protein, the D614G variant, was identified in late February 2020. Studies showed that the D614G mutation is related to higher infectivity. The current study was conducted to determine the validity of VirSNiP SARS-CoV-2 Spike D614G assay to detect the SARS-CoV-2 D614G mutation.
Methods: In this study, the detection of the SARS-CoV-2 D614G mutation was performed using VirSNiP SARS-CoV-2 Spike D614G assay (TIB Molbiol) and by Sanger sequencing. Two plasmids carrying A allele (wild-type) and G allele (mutant type) were designed using GenScript's OptimumGene gene design tool (GenScript Inc., Piscataway, NJ, USA).
Results: It was found that VirSNiP SARS-CoV-2 Spike D614G assay could detect the SARS-CoV-2 D614G mutation. The specific mutation is easily distinguishable in the melting peaks. All of the samples were confirmed using Sanger sequencing.
Conclusions: In summary, it was shown that VirSNiP SARS-CoV-2 Spike D614G assay is a rapid, accurate, and reliable method for identifying the SARS-CoV-2 D614G mutation. In contrast, Sanger sequencing is time consuming and labor intensive. We strongly believe that VirSNiP SARS-CoV-2 Spike D614G assay will provide more information on the prevalence of the D614G mutation in Taiwanese populations
Edible folic acid and medicinal folinic acid produce cardioprotective effects in late-stage triple-transgenic Alzheimer's disease model mice by suppressing cardiac hypertrophy and fibrosis
No full text[[abstract]]Some clinical studies have indicated the patients with Alzheimer's disease (AD) display an increased risk of cardiovascular disease (CVD). Here, to examine the relationship between AD and CVDs, we investigated the changes in heart function in triple-transgenic late-stage AD model mice (3× Tg-AD; APPSwe, PS1M146V, and tauP301L). We fed the AD mice folic acid (FA) or folinic acid (FN) and analyzed the protective effects of the compounds on the heart; specifically, 20-month-old triple-transgenic AD mice, weighing 34-55 g, were randomly allocated into three groups-the AD, AD + FA, and AD + FN groups-and subject to gastric feeding with FA or FN once daily at 12 mg/kg body weight (BW) for 3 months. Mouse BWs were assessed throughout the trial, at the end of which the animals were sacrificed using carbon dioxide suffocation. We found that BW, whole-heart weight, and left-ventricle weight were reduced in the AD + FA and AD + FN groups as compared with the measurements in the AD group. Furthermore, western blotting of excised heart tissue revealed that the levels of the hypertrophy-related protein markers phospho(p)-p38 and p-c-Jun were markedly decreased in the AD + FA group, whereas p-GATA4, and ANP were strongly reduced in the AD + FN group. Moreover, the fibrosis-related proteins uPA, MMP-2, MEK1/2 and SP-1 were decreased in the heart in both AD + FN group. In summary, our results indicate that FA and FN can exert anti-cardiac hypertrophy and fibrosis effects to protect the heart in aged triple-transgenic AD model mice, particular in FN