Alzheimer's disease (AD) is the most common cause of dementia, and contributes to a huge burden of disease worldwide. Observational studies have found that tissue plasminogen activator (t-PA) inhibits the development of AD, but little is known about urokinase plasminogen activator (u-PA) and plasminogen activator inhibitor-1 (PAI-1). At present, the causal relationship is not clear. Therefore, this study intends to explore the relationship between plasminogen activators and their inhibitors with Alzheimer's disease through Mendelian randomization method, so as to provide reference for the prevention and control of Alzheimer's disease.To investigate causal pathways, we conducted a two-sample Mendelian randomization study using pooled statistics from genome-wide association studies. IVW, MR-Egger, Weighted-median, MR-PRESSO and MR-RAPS methods were used to evaluate the robustness of the results.In the outcome of AD (more controls excluded), the IVW effect of PAI-1 OR (95%CI) was found as follows: 1.543 (1.010-2.356), whose interval does not include 1 and P=0.0448, which suggested that PAI-1 was positively correlated with the risk of AD (more controls excluded). The IVW model, Weighted median, MR-PRESSO and MR-RAPs all showed similar results (all ORs >1), and the two outcomes were consistent.Our results showed that gene-predicted PAI-1 in Mendelian stochastic analysis was associated with an increased risk of AD.
阿尔茨海默病（AD）是导致痴呆症的最常见病因，给全世界造成了巨大的疾病负担。观察性研究发现，组织纤溶酶原激活剂（t-PA）可抑制阿尔茨海默病的发展，但人们对尿激酶纤溶酶原激活剂（u-PA）和纤溶酶原激活剂抑制剂-1（PAI-1）知之甚少。目前，两者之间的因果关系尚不明确。因此，本研究拟通过孟德尔随机方法探讨纤溶酶原激活剂及其抑制剂与阿尔茨海默病的关系，从而为阿尔茨海默病的防治提供参考。为了探究因果关系途径，我们利用全基因组关联研究的集合统计数据进行了双样本孟德尔随机研究。我们使用了IVW、MR-Egger、加权中值、MR-PRESSO和MR-RAPS方法来评估结果的稳健性。在AD结果中（排除了更多对照），PAI-1 OR的IVW效应（95%CI）如下：1.543（1.010-2.356），其区间不包括1，P=0.0448，这表明PAI-1与AD风险呈正相关（排除更多对照）。我们的结果表明，孟德尔随机分析中基因预测的 PAI-1 与 AD 风险增加有关。
{"title":"Causal association of plasminogen activators and their inhibitors with Alzheimer's disease: a Mendelian randomization study","authors":"Xin Guo, Fangyu Gao, Baolong Pan, Feng Gao, Jingsi Zhang, Shanshan Wang, Qiao Niu","doi":"10.5114/aoms/192049","DOIUrl":"https://doi.org/10.5114/aoms/192049","url":null,"abstract":"Alzheimer's disease (AD) is the most common cause of dementia, and contributes to a huge burden of disease worldwide. Observational studies have found that tissue plasminogen activator (t-PA) inhibits the development of AD, but little is known about urokinase plasminogen activator (u-PA) and plasminogen activator inhibitor-1 (PAI-1). At present, the causal relationship is not clear. Therefore, this study intends to explore the relationship between plasminogen activators and their inhibitors with Alzheimer's disease through Mendelian randomization method, so as to provide reference for the prevention and control of Alzheimer's disease.To investigate causal pathways, we conducted a two-sample Mendelian randomization study using pooled statistics from genome-wide association studies. IVW, MR-Egger, Weighted-median, MR-PRESSO and MR-RAPS methods were used to evaluate the robustness of the results.In the outcome of AD (more controls excluded), the IVW effect of PAI-1 OR (95%CI) was found as follows: 1.543 (1.010-2.356), whose interval does not include 1 and P=0.0448, which suggested that PAI-1 was positively correlated with the risk of AD (more controls excluded). The IVW model, Weighted median, MR-PRESSO and MR-RAPs all showed similar results (all ORs >1), and the two outcomes were consistent.Our results showed that gene-predicted PAI-1 in Mendelian stochastic analysis was associated with an increased risk of AD.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141924598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Maciej Banach, Martyna Fronczek, T. Osadnik, A. Gach, D. Strapagiel, M. Słomka, M. Lejawa, Anna Goc, E. Boniewska-Bernacka, Anna Pańczyszyn, G. Lip, P. Toth, P. Penson, J. Jóźwiak
Classical risk factors such as hypertension, hypercholesterolemia, pre-diabetes, diabetes and obesity can predict adverse cardiovascular events, but they are less prognostic in patients age <60 years. Polygenic risk scores (PRS) can be effective in predicting adverse coronary events in younger and middle-aged patients. Our main aim is to assess the utility of new PRS created for the Polish population in predicting mortality during an 8-year follow-up in a nationwide LIPIDOGEN2015 population.All DNA samples of 1779 patients were genotyped using Infinium Global Screening Array-24+ v3.0 Kit microarrays. The samples were amplified, fragmented, and hybridized to BeadChips. The BeadChips were scanned using iScan and converted to genotypes using Genome Studio 2.0.We will develop a PRS based on the marked single nucleotide polymorphisms (SNPs) in the LIPIDOGEN2015 project's studied population and determine the analyzed group's risk of death due to cardiovascular diseases (CVD) based on data obtained from 8-years of patient-follow-up. Based on the developed PRS scale and biochemical analyses, we will assess the effectiveness of lipid-lowering therapy with statins in patients with high and low genetic risk of sudden CVD events (secondary endpoints).The developed PRS scale, combined with clinical covariates, will facilitate the creation of an algorithm to predict long-term mortality. This will enable us to stratify CVD risk more precisely, which may result in earlier implementation of lifestyle changes and dietary adjustments and potentially initiate earlier pharmacotherapy for at-risk individuals.
{"title":"Risk of adverse cardiovascular events based on common genetic variants in 8-year follow-up of the LIPIDOGEN2015 population using the polygenic risk score (PRS) - study design and methodology.","authors":"Maciej Banach, Martyna Fronczek, T. Osadnik, A. Gach, D. Strapagiel, M. Słomka, M. Lejawa, Anna Goc, E. Boniewska-Bernacka, Anna Pańczyszyn, G. Lip, P. Toth, P. Penson, J. Jóźwiak","doi":"10.5114/aoms/192147","DOIUrl":"https://doi.org/10.5114/aoms/192147","url":null,"abstract":"Classical risk factors such as hypertension, hypercholesterolemia, pre-diabetes, diabetes and obesity can predict adverse cardiovascular events, but they are less prognostic in patients age <60 years. Polygenic risk scores (PRS) can be effective in predicting adverse coronary events in younger and middle-aged patients. Our main aim is to assess the utility of new PRS created for the Polish population in predicting mortality during an 8-year follow-up in a nationwide LIPIDOGEN2015 population.All DNA samples of 1779 patients were genotyped using Infinium Global Screening Array-24+ v3.0 Kit microarrays. The samples were amplified, fragmented, and hybridized to BeadChips. The BeadChips were scanned using iScan and converted to genotypes using Genome Studio 2.0.We will develop a PRS based on the marked single nucleotide polymorphisms (SNPs) in the LIPIDOGEN2015 project's studied population and determine the analyzed group's risk of death due to cardiovascular diseases (CVD) based on data obtained from 8-years of patient-follow-up. Based on the developed PRS scale and biochemical analyses, we will assess the effectiveness of lipid-lowering therapy with statins in patients with high and low genetic risk of sudden CVD events (secondary endpoints).The developed PRS scale, combined with clinical covariates, will facilitate the creation of an algorithm to predict long-term mortality. This will enable us to stratify CVD risk more precisely, which may result in earlier implementation of lifestyle changes and dietary adjustments and potentially initiate earlier pharmacotherapy for at-risk individuals.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141929028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01eCollection Date: 2024-01-01DOI: 10.5114/aoms/190607
Edyta Matusik, Kamila Czepczor-Bernat, Barbara Lewicka, Sylwia Chmiel-Szajner
Introduction: The aim of the study was to determine predictors of sexual activity and function in patients with multiple sclerosis (MS).
Material and methods: A total of 134 MS patients were included in the study. Sexual activity and function were assessed by the Changes in Sexual Functioning Questionnaire (CSFQ). Symptoms of sexual dysfunction related to multiple sclerosis (the Multiple Sclerosis Intimacy and Sexuality Questionnaire-19; MSISQ-19), disability status in multiple sclerosis (the Expanded Disability Status Scale; EDSS), gender and age were also taken into account.
Results: This analysis indicated that all predictors (gender, age, EDSS score, and all three MSISQ-19 subscales) were significantly associated with the explained variable (sexual activity and function) in the expected direction. Finally, hierarchical regression showed that significant predictors of sexual activity and function were: (a) male gender, (b) age (negative relationship), and (c) primary sexual dysfunction symptoms (negative relationship).
Conclusions: Sexual activity and function can be predicted by using the MSISQ-19, which makes it a useful tool for communication between clinicians and patients.
{"title":"Predictors of sexual activity and function in women and men with multiple sclerosis - a preliminary study.","authors":"Edyta Matusik, Kamila Czepczor-Bernat, Barbara Lewicka, Sylwia Chmiel-Szajner","doi":"10.5114/aoms/190607","DOIUrl":"https://doi.org/10.5114/aoms/190607","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of the study was to determine predictors of sexual activity and function in patients with multiple sclerosis (MS).</p><p><strong>Material and methods: </strong>A total of 134 MS patients were included in the study. Sexual activity and function were assessed by the Changes in Sexual Functioning Questionnaire (CSFQ). Symptoms of sexual dysfunction related to multiple sclerosis (the Multiple Sclerosis Intimacy and Sexuality Questionnaire-19; MSISQ-19), disability status in multiple sclerosis (the Expanded Disability Status Scale; EDSS), gender and age were also taken into account.</p><p><strong>Results: </strong>This analysis indicated that all predictors (gender, age, EDSS score, and all three MSISQ-19 subscales) were significantly associated with the explained variable (sexual activity and function) in the expected direction. Finally, hierarchical regression showed that significant predictors of sexual activity and function were: (a) male gender, (b) age (negative relationship), and (c) primary sexual dysfunction symptoms (negative relationship).</p><p><strong>Conclusions: </strong>Sexual activity and function can be predicted by using the MSISQ-19, which makes it a useful tool for communication between clinicians and patients.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11493024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-30eCollection Date: 2024-01-01DOI: 10.5114/aoms/190516
Petra Macounová, Katka Bobčíková, Hana Tomášková, Marcel Mitták, Ľubica Argalášová
Introduction: This prospective study aimed to evaluate the functional status and risk factors in patients undergoing lung resection.
Methods: Functional status defined by the parameters of spirometry (VC, FVC, FEV1, FEV1/FVC) and whole-body plethysmography (TLC) examination was assessed before lung resection, at hospital discharge, 3 weeks after surgery, and 3 months after surgery.
Results: The sample comprised 24 participants who were observed from 5/2021 to 10/2022. The functional status worsened significantly after the surgery, but the lung function values improved over time.
Conclusions: Lung functions dropped sharply after the surgery but improved over time.
{"title":"Functional status in patients undergoing lung resection.","authors":"Petra Macounová, Katka Bobčíková, Hana Tomášková, Marcel Mitták, Ľubica Argalášová","doi":"10.5114/aoms/190516","DOIUrl":"https://doi.org/10.5114/aoms/190516","url":null,"abstract":"<p><strong>Introduction: </strong>This prospective study aimed to evaluate the functional status and risk factors in patients undergoing lung resection.</p><p><strong>Methods: </strong>Functional status defined by the parameters of spirometry (VC, FVC, FEV<sub>1</sub>, FEV<sub>1</sub>/FVC) and whole-body plethysmography (TLC) examination was assessed before lung resection, at hospital discharge, 3 weeks after surgery, and 3 months after surgery.</p><p><strong>Results: </strong>The sample comprised 24 participants who were observed from 5/2021 to 10/2022. The functional status worsened significantly after the surgery, but the lung function values improved over time.</p><p><strong>Conclusions: </strong>Lung functions dropped sharply after the surgery but improved over time.</p>","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11493037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Ebrahim, Asmaa M Almohanna, A. Shati, Mohammed A. Alshehri, T. M. A-Elgadir, Hailah M. Almohaimeed, M. Haidara, Sara Adel Hosny, A. Dawood, Asmaa M. ShamsEldeeen
Background: Diabetes stands as the predominant etiology behind end-stage kidney disease, commonly referred to as renal failure. The intricate interplay among oxidative stress, inflammation, and renal fibrotic changes in diabetes-induced nephropathy, particularly in instances involving and not involving the administration of mesenchymal stem cells (MSCs), remains a subject less explored in existing research.Methods: Twenty-four male Wistar rats (180 and 200 grams) were randomly assigned to one of three groups (n = 8). The control group received standard laboratory chow, and the groups with T2DM received a single dose of streptozotocin, 45 mg/kg, after three weeks of pretreatment with a high-fat diet (HFD). Rats with T2DM were split into the T2DM model group and Bone marrow (BM) mesenchymal stem cells (MSCs) treated group (T2DM+MSCs) eight weeks after DM was confirmed. BM-MSCs were injected systemically at 2 × 106 cells/rat doses.Results: Diabetes significantly altered oxidative stress (MDA, SOD), inflammation (TNFα, IL-6), and kidney injury (KIM-1, NAGAL) biomarkers, a modulation that was mitigated by MSCs (p < 0.0001). Furthermore, diabetes-induced kidney fibrosis showed a noteworthy reduction in the presence of MSCs. A notable correlation emerged between body weight, systolic blood pressure (SBP), oxidative stress, inflammation, fibrosis, the PKC/NF-KB/STAT-3 axis, and hyperglycemia.Conclusions: Our results suggest that diabetes was associated with elevated oxidative stress, inflammation, biomarkers of kidney injury, upregulation of the renal PKC/NF-KB/STAT-3 pathway, and hypertension, all countered by MSCs intervention.
{"title":"Mesenchymal Stem Cells Suppress Kidney Injury molecule-1 Associated with Inhibition of Renal PKC/ NF-Kβ / STAT3 Fibrotic Signaling Pathway in Rats with Diabetic Nephropathy","authors":"H. Ebrahim, Asmaa M Almohanna, A. Shati, Mohammed A. Alshehri, T. M. A-Elgadir, Hailah M. Almohaimeed, M. Haidara, Sara Adel Hosny, A. Dawood, Asmaa M. ShamsEldeeen","doi":"10.5114/aoms/190868","DOIUrl":"https://doi.org/10.5114/aoms/190868","url":null,"abstract":"Background: Diabetes stands as the predominant etiology behind end-stage kidney disease, commonly referred to as renal failure. The intricate interplay among oxidative stress, inflammation, and renal fibrotic changes in diabetes-induced nephropathy, particularly in instances involving and not involving the administration of mesenchymal stem cells (MSCs), remains a subject less explored in existing research.Methods: Twenty-four male Wistar rats (180 and 200 grams) were randomly assigned to one of three groups (n = 8). The control group received standard laboratory chow, and the groups with T2DM received a single dose of streptozotocin, 45 mg/kg, after three weeks of pretreatment with a high-fat diet (HFD). Rats with T2DM were split into the T2DM model group and Bone marrow (BM) mesenchymal stem cells (MSCs) treated group (T2DM+MSCs) eight weeks after DM was confirmed. BM-MSCs were injected systemically at 2 × 106 cells/rat doses.Results: Diabetes significantly altered oxidative stress (MDA, SOD), inflammation (TNFα, IL-6), and kidney injury (KIM-1, NAGAL) biomarkers, a modulation that was mitigated by MSCs (p < 0.0001). Furthermore, diabetes-induced kidney fibrosis showed a noteworthy reduction in the presence of MSCs. A notable correlation emerged between body weight, systolic blood pressure (SBP), oxidative stress, inflammation, fibrosis, the PKC/NF-KB/STAT-3 axis, and hyperglycemia.Conclusions: Our results suggest that diabetes was associated with elevated oxidative stress, inflammation, biomarkers of kidney injury, upregulation of the renal PKC/NF-KB/STAT-3 pathway, and hypertension, all countered by MSCs intervention.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141797086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mallorie L. Huff, Ranju Gupta, Rahul Gupta, Kelly C. Schadler, Shae Duka, Vienna Histon-Figliolini, Joshua Kalter, Amogh M Joshi, Nadeem V Ahmad, W. Aronow, Deborah W Sundlof
Background: Trastuzumab and anthracyclines are mainstays of chemotherapy in breast cancer and lymphoma patients. We aimed to assess the relationship between obesity and the risk of developing chemotherapy-associated cardiotoxicity.A retrospective chart review was conducted of all patients who received trastuzumab or anthracyclines at our tertiary care center. Bivariate analyses were conducted to determine the association between demographic and clinical variables with cardiotoxicity status. Two multivariate logistic regression models were generated to assess whether BMI was independently associated with cardiotoxicity.Of the 368 patients receiving either trastuzumab or anthracyclines, 16 patients developed cardiotoxicity. Demographically, age, race, BMI, BSA, and weight did not differ between the patients who developed cardiotoxicity and those who did not. The mean dose of anthracycline and trastuzumab did not differ between the patients who developed cardiotoxicity and those who did not. Obesity was not found to increase the odds of developing cardiotoxicity and was slightly protective. A non-significant decrease in the odds of developing cardiotoxicity was found for every one-unit increase in BMI. In a multivariable model using BMI as a continuous predictor and controlling for BMI, age, hypertension, chemotherapy type and coronary artery disease, the only significant predictor of cardiotoxicity was a previous history of arrhythmia.Obesity was not a significant risk factor for patients developing cardiotoxicity from trastuzumab or anthracycline based chemotherapy and may be a protective factor for cardiotoxicity. Additional studies with greater statistical power are needed to further evaluate this effect and independently evaluate obesity as a risk factor for cardiotoxicity.
{"title":"A Retrospective Analysis of the Association of Obesity with Anthracycline and Trastuzumab-Induced Cardiotoxicity in the Treatment of Breast Cancer and Lymphoma","authors":"Mallorie L. Huff, Ranju Gupta, Rahul Gupta, Kelly C. Schadler, Shae Duka, Vienna Histon-Figliolini, Joshua Kalter, Amogh M Joshi, Nadeem V Ahmad, W. Aronow, Deborah W Sundlof","doi":"10.5114/aoms/190869","DOIUrl":"https://doi.org/10.5114/aoms/190869","url":null,"abstract":"Background: \u0000Trastuzumab and anthracyclines are mainstays of chemotherapy in breast cancer and lymphoma patients. We aimed to assess the relationship between obesity and the risk of developing chemotherapy-associated cardiotoxicity.A retrospective chart review was conducted of all patients who received trastuzumab or anthracyclines at our tertiary care center. Bivariate analyses were conducted to determine the association between demographic and clinical variables with cardiotoxicity status. Two multivariate logistic regression models were generated to assess whether BMI was independently associated with cardiotoxicity.Of the 368 patients receiving either trastuzumab or anthracyclines, 16 patients developed cardiotoxicity. Demographically, age, race, BMI, BSA, and weight did not differ between the patients who developed cardiotoxicity and those who did not. The mean dose of anthracycline and trastuzumab did not differ between the patients who developed cardiotoxicity and those who did not. Obesity was not found to increase the odds of developing cardiotoxicity and was slightly protective. A non-significant decrease in the odds of developing cardiotoxicity was found for every one-unit increase in BMI. In a multivariable model using BMI as a continuous predictor and controlling for BMI, age, hypertension, chemotherapy type and coronary artery disease, the only significant predictor of cardiotoxicity was a previous history of arrhythmia.Obesity was not a significant risk factor for patients developing cardiotoxicity from trastuzumab or anthracycline based chemotherapy and may be a protective factor for cardiotoxicity. Additional studies with greater statistical power are needed to further evaluate this effect and independently evaluate obesity as a risk factor for cardiotoxicity.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Doroszko, M. Trocha, Krzysztof Kujawa, Jędrzej Machowiak, Anna Jodkowska, Piotr Rola, Jarosław Sowizdraniuk, Paweł Lubieniecki, Mariusz Koral, Agata Stanek, J. Sokołowski, E. A. Jankowska, K. Madziarska
Since the beginning of SARS-CoV-2-pandemic, intensive efforts have been made to identify predictors of COVID-19 outcomes. Individual components of the C2HEST-scale, used to predict the risk of atrial fibrillation, reflect comorbidities presences. Therefore, we hypothesized that the score could predict unfavorable clinical COVID-19-outcomes.2184-medical-records of subjects hospitalized at the medical-university-center due to COVID-19 from February 2020 to June 2021 were retrospectively analyzed . The subjects were categorized into low/medium/high-risk categories according to the C2HEST scale. Measured outcomes included: in-hospital-, 3-month- and 6-month-all-cause-mortality, the non-fatal hospitalization endpoints and other adverse in-hospital events.A total of 598 deaths (27.4%), including 326 in-hospital (15%) were reported. All three types of mortality were highest in the high-risk C2HEST-stratum (35.4%, 54.4, and 56.9%), ,and lowest in the low-risk-stratum: (8.4%, 15%, and 37.5%), respectively. The receiver-operating characteristics revealed that C2HEST allows one to predict 1-month mortality with AUC30=70.7 and maintained at a similar level after 3- and 6-month-observation(AUC90=72.0 and AUC180=67). The p-value for the Log-rank test comparing survival curves was <0.0001. An increase of one C2HEST-point raised the overall death rate 1.4-fold. A change from the low- to medium category increased the death rate 3.4 times, while between the low- and high-risk-stratum the hazard-ratio was 5.0. The C2HEST-score also revealed predictive value for pneumonia, sepsis, cardiogenic-shock, myocardi-injury, acute heart failure, kidney/liver-injury, stroke, gastrointestinal-bleedings.The C2HEST-score is usefull in predicting adverse COVID-19-outcomes in hospitalized subjects. The simplicity of this scale, based on the presence of comorbidities, may address medical needs in risk stratification of COVID-19- patients.
{"title":"The C2HEST score on admission to hospital may successfully predict the clinical outcomes of COVID-19 in all-comers population","authors":"A. Doroszko, M. Trocha, Krzysztof Kujawa, Jędrzej Machowiak, Anna Jodkowska, Piotr Rola, Jarosław Sowizdraniuk, Paweł Lubieniecki, Mariusz Koral, Agata Stanek, J. Sokołowski, E. A. Jankowska, K. Madziarska","doi":"10.5114/aoms/190744","DOIUrl":"https://doi.org/10.5114/aoms/190744","url":null,"abstract":"Since the beginning of SARS-CoV-2-pandemic, intensive efforts have been made to identify predictors of COVID-19 outcomes. Individual components of the C2HEST-scale, used to predict the risk of atrial fibrillation, reflect comorbidities presences. Therefore, we hypothesized that the score could predict unfavorable clinical COVID-19-outcomes.2184-medical-records of subjects hospitalized at the medical-university-center due to COVID-19 from February 2020 to June 2021 were retrospectively analyzed . The subjects were categorized into low/medium/high-risk categories according to the C2HEST scale. Measured outcomes included: in-hospital-, 3-month- and 6-month-all-cause-mortality, the non-fatal hospitalization endpoints and other adverse in-hospital events.A total of 598 deaths (27.4%), including 326 in-hospital (15%) were reported. All three types of mortality were highest in the high-risk C2HEST-stratum (35.4%, 54.4, and 56.9%), ,and lowest in the low-risk-stratum: (8.4%, 15%, and 37.5%), respectively. The receiver-operating characteristics revealed that C2HEST allows one to predict 1-month mortality with AUC30=70.7 and maintained at a similar level after 3- and 6-month-observation(AUC90=72.0 and AUC180=67). The p-value for the Log-rank test comparing survival curves was <0.0001. An increase of one C2HEST-point raised the overall death rate 1.4-fold. A change from the low- to medium category increased the death rate 3.4 times, while between the low- and high-risk-stratum the hazard-ratio was 5.0. The C2HEST-score also revealed predictive value for pneumonia, sepsis, cardiogenic-shock, myocardi-injury, acute heart failure, kidney/liver-injury, stroke, gastrointestinal-bleedings.The C2HEST-score is usefull in predicting adverse COVID-19-outcomes in hospitalized subjects. The simplicity of this scale, based on the presence of comorbidities, may address medical needs in risk stratification of COVID-19- patients.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Akhtayeva, Lyazzat Kosherbayeva, A. Imamatdinova, K. Šmigelskas
Recent research show the rise of the prevalence of the autism spectrum disorder (ASD) worldwide. At the same time, care for ASD children was found to affect the psychological health of parents or guardians of ASD children. The aim was to identify the wellbeing of parents raising the ASD children and to explore the experiences of primary care (PHC) psychologists in providing support to them.We conducted a cross-sectional study. Parents of ASD children took part in the survey. Wellbeing was assessed using Parental Well-Being Scale including physical and emotional health, stress, social support, and quality of life. Ten primary care psychologists were also interviewed.327 parents of ASD children participated in our study. Mean wellbeing score for all parents was 52.6±15.65 pts. The highest aspect of wellbeing was enjoyment in looking after child (mean 7.29 pts) and quality of life (mean 6.87 pts). The strongest predictor of parental wellbeing was presence of disability diagnosis for ASD child related (6.33 pts), lower parental wellbeing (Beta=0.20, p<0.001). The interview results show the insufficient competence of psychologists to work with parents of children with ASD.On the parental well-being scale, the highest scores are observed for enjoyment in looking after child and quality of life. Insufficient work is carried out by PHC psychologists with parents of children with ASD. There is a need for future training of psychologists in the management of children with ASD and their parents
{"title":"Wellbeing of parents raising the children with autism spectrum disorder and the role of psychologists","authors":"N. Akhtayeva, Lyazzat Kosherbayeva, A. Imamatdinova, K. Šmigelskas","doi":"10.5114/aoms/190772","DOIUrl":"https://doi.org/10.5114/aoms/190772","url":null,"abstract":"Recent research show the rise of the prevalence of the autism spectrum disorder (ASD) worldwide. At the same time, care for ASD children was found to affect the psychological health of parents or guardians of ASD children. The aim was to identify the wellbeing of parents raising the ASD children and to explore the experiences of primary care (PHC) psychologists in providing support to them.We conducted a cross-sectional study. Parents of ASD children took part in the survey. Wellbeing was assessed using Parental Well-Being Scale including physical and emotional health, stress, social support, and quality of life. Ten primary care psychologists were also interviewed.327 parents of ASD children participated in our study. Mean wellbeing score for all parents was 52.6±15.65 pts. The highest aspect of wellbeing was enjoyment in looking after child (mean 7.29 pts) and quality of life (mean 6.87 pts). The strongest predictor of parental wellbeing was presence of disability diagnosis for ASD child related (6.33 pts), lower parental wellbeing (Beta=0.20, p<0.001). The interview results show the insufficient competence of psychologists to work with parents of children with ASD.On the parental well-being scale, the highest scores are observed for enjoyment in looking after child and quality of life. Insufficient work is carried out by PHC psychologists with parents of children with ASD. There is a need for future training of psychologists in the management of children with ASD and their parents","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sheng Li, Libing Zhou, Tielin Wu, Jianting Xu, Huimin Long, Lin Cao
We conducted bidirectional two-sample Mendelian Randomization (MR) analysis to investigate the causal relationship between 91 inflammatory cytokines and prostate cancer (PCa).The Inverse Variance Weighted (IVW) model served as the primary two-sample MR analysis method, utilized to estimate the causal effect of exposure on the outcome. The Weighted Median (WM) and MR Egger methods were additionally employed to complement the IVW model. Sensitivity analyses were performed using Cochran's Q test for both the IVW and MR Egger methods. To assess the presence of horizontal pleiotropy, the instrumental variables (IVs) were subjected to the MR-Egger intercept test.Following Bonferroni correction, the IVW analysis revealed positive correlations between PCa and the levels of C-C motif chemokine 20 (CCL20), C-C motif chemokine 23 (CCL23), fibroblast growth factor 19 (FGF19), fibroblast growth factor 23 (FGF23), and interleukin-6 (IL-6). Notably, IL-6 exhibited the strongest positive association effect (odds ratio [95% confidence interval]: 1.0076 [1.0014, 1.0139]), followed by CCL-20 (1.0067 [1.0004, 1.0129]) and FGF23 ([1.0002, 1.0119]). Reverse MR analysis indicated a negative causal relationship between PCa and interleukin-22 receptor subunit alpha-1 levels (IL22RA1) (0.4852 [0.2390, 0.9847]).This study proposes that there exists a positive correlation between the levels of CCL20, CCL23, FGF19, FGF23, and IL-6 and the occurrence of PCa. Furthermore, we found evidence to support the causal relationship between decreased levels of IL22RA1 and the development of PCa. These findings unveil novel biomarkers and pathways that could potentially be targeted for the prevention and clinical treatment of PCa.
{"title":"Association between inflammatory cytokines and prostate cancer","authors":"Sheng Li, Libing Zhou, Tielin Wu, Jianting Xu, Huimin Long, Lin Cao","doi":"10.5114/aoms/190828","DOIUrl":"https://doi.org/10.5114/aoms/190828","url":null,"abstract":"We conducted bidirectional two-sample Mendelian Randomization (MR) analysis to investigate the causal relationship between 91 inflammatory cytokines and prostate cancer (PCa).The Inverse Variance Weighted (IVW) model served as the primary two-sample MR analysis method, utilized to estimate the causal effect of exposure on the outcome. The Weighted Median (WM) and MR Egger methods were additionally employed to complement the IVW model. Sensitivity analyses were performed using Cochran's Q test for both the IVW and MR Egger methods. To assess the presence of horizontal pleiotropy, the instrumental variables (IVs) were subjected to the MR-Egger intercept test.Following Bonferroni correction, the IVW analysis revealed positive correlations between PCa and the levels of C-C motif chemokine 20 (CCL20), C-C motif chemokine 23 (CCL23), fibroblast growth factor 19 (FGF19), fibroblast growth factor 23 (FGF23), and interleukin-6 (IL-6). Notably, IL-6 exhibited the strongest positive association effect (odds ratio [95% confidence interval]: 1.0076 [1.0014, 1.0139]), followed by CCL-20 (1.0067 [1.0004, 1.0129]) and FGF23 ([1.0002, 1.0119]). Reverse MR analysis indicated a negative causal relationship between PCa and interleukin-22 receptor subunit alpha-1 levels (IL22RA1) (0.4852 [0.2390, 0.9847]).This study proposes that there exists a positive correlation between the levels of CCL20, CCL23, FGF19, FGF23, and IL-6 and the occurrence of PCa. Furthermore, we found evidence to support the causal relationship between decreased levels of IL22RA1 and the development of PCa. These findings unveil novel biomarkers and pathways that could potentially be targeted for the prevention and clinical treatment of PCa.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pan Liu, Tairan Hu, Bing Gao, Ran Xia, Xiaohua Dai, Jing Wang
In China, Yanggan-Yishui granules (YGYSG) have been used to treat hypertensive renal damage (HRD) for over 20 years. Network pharmacology was used to determine whether YGYSG affects HRD via the autophagy pathway, which was verified using in vitro experiments.Common targets of YGYSG, HRD, and the autophagy pathway were screened using network pharmacology, and effective compounds, core targets, and signaling pathways were identified. The affinity of the compounds for the core targets was evaluated using molecular docking simulations. Angiotensin II (Ang II) was used to generate an in vitro renal podocyte model using MPC-5 cells. Morphological changes in the autophagosomes were observed using transmission electron microscopy (TEM). The expression levels of autophagy-related and pathway proteins were detected using western blotting and reverse transcription quantitative real-time PCR (PCR).Network pharmacology and molecular docking analyses identified eight autophagy-related core targets and ten core components in the YGYSG treatment of HRD. These targets are mainly involved in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway and autophagy-related biological processes. In vitro experiments showed that Ang II-stimulated renal podocytes exhibited abnormal autophagy, and YGYSG protected renal podocytes from abnormal autophagy. In addition, YGYSG reversed abnormal autophagy and improved HRD by activating the PI3K/AKT/mTOR signaling pathway.YGYSG may regulate abnormal autophagy in renal podocytes by activating the PI3K/AKT/mTOR signaling pathway and may play a role in improving HRD.
{"title":"Network pharmacology and in vitro experiments reveal the autophagy mechanism of Yanggan-Yishui granules in improving hypertensive renal injury","authors":"Pan Liu, Tairan Hu, Bing Gao, Ran Xia, Xiaohua Dai, Jing Wang","doi":"10.5114/aoms/190794","DOIUrl":"https://doi.org/10.5114/aoms/190794","url":null,"abstract":"In China, Yanggan-Yishui granules (YGYSG) have been used to treat hypertensive renal damage (HRD) for over 20 years. Network pharmacology was used to determine whether YGYSG affects HRD via the autophagy pathway, which was verified using in vitro experiments.Common targets of YGYSG, HRD, and the autophagy pathway were screened using network pharmacology, and effective compounds, core targets, and signaling pathways were identified. The affinity of the compounds for the core targets was evaluated using molecular docking simulations. Angiotensin II (Ang II) was used to generate an in vitro renal podocyte model using MPC-5 cells. Morphological changes in the autophagosomes were observed using transmission electron microscopy (TEM). The expression levels of autophagy-related and pathway proteins were detected using western blotting and reverse transcription quantitative real-time PCR (PCR).Network pharmacology and molecular docking analyses identified eight autophagy-related core targets and ten core components in the YGYSG treatment of HRD. These targets are mainly involved in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway and autophagy-related biological processes. In vitro experiments showed that Ang II-stimulated renal podocytes exhibited abnormal autophagy, and YGYSG protected renal podocytes from abnormal autophagy. In addition, YGYSG reversed abnormal autophagy and improved HRD by activating the PI3K/AKT/mTOR signaling pathway.YGYSG may regulate abnormal autophagy in renal podocytes by activating the PI3K/AKT/mTOR signaling pathway and may play a role in improving HRD.","PeriodicalId":8278,"journal":{"name":"Archives of Medical Science","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141796489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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