scholarly journals Trajectories of Functional Health Following Stroke: The Role of Social Resources

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 847-847
Author(s):  
Takeshi Nakagawa ◽  
Taiji Noguchi ◽  
Ayane Komatsu ◽  
Masumi Ishihara ◽  
Tami Saito
Keyword(s):  
Social Participation ◽  
Functional Decline ◽  
Protective Role ◽  
Social Resources ◽  
Stroke Onset ◽  
Functional Health ◽  
Japanese Adults ◽  
Before And After ◽  
Crucial Information

Abstract Stroke is one of the major causes of disability in old age. Predictors for the functional prognosis have been studied, but the role of social resources in recovery has not studied as much. We examined whether social resources available before and after stroke onset improved functional prognoses. Data was derived from longitudinal data collected between 1987 and 2006 from Japanese adults aged 60 years and older. We identified 396 people who had experienced their self- or proxy-reported first stroke during follow-up (age at stroke onset: M = 76.0, SD = 6.9; 74.2% women). Functional health was measured by self- or proxy-reported activities of daily living. Social resources were indexed as residential status, contact with non-coresident children, social participation, and perceived support. Analyses were adjusted for age at stroke onset, gender, and education. A multiphase growth model showed that functional health typically deteriorated surrounding stroke and gradually declined thereafter. There were also individual differences in the trajectories of functional health. Individuals who more frequently participated in social groups prior to stroke and those who came to participate more frequently thereafter exhibited less functional decline immediately following stroke. Our findings indicate that social participation plays a protective role against adverse prognoses following stroke regardless of when individuals start participating. Inclusive communities would enable older adults to remain independent. Our study was limited in that crucial information about stroke, such as objective measures of initial severity, was not available and that individuals with more severe stroke may have dropped out after the onset.

scholarly journals Physical Activity Prevents Cartilage Degradation: A Metabolomics Study Pinpoints the Involvement of Vitamin B6

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1374 ◽  
Author(s):  
Deiana ◽  
Malerba ◽  
Dalle Carbonare ◽  
Cheri ◽  
Patuzzo ◽  
...  
Keyword(s):  
Physical Activity ◽  
Vitamin B6 ◽  
Cartilage Degradation ◽  
Protective Role ◽  
Before And After ◽  
Metabolomics Study ◽  
Cartilage Cells ◽  
First Time ◽  
Chondrosarcoma Cell Line

Osteoarthritis (OA) is predominantly characterized by the progressive degradation of articular cartilage, the connective tissue produced by chondrocytes, due to an imbalance between anabolic and catabolic processes. In addition, physical activity (PA) is recognized as an important tool for counteracting OA. To evaluate PA effects on the chondrocyte lineage, we analyzed the expression of SOX9, COL2A1, and COMP in circulating progenitor cells following a half marathon (HM) performance. Therefore, we studied in-depth the involvement of metabolites affecting chondrocyte lineage, and we compared the metabolomic profile associated with PA by analyzing runners’ sera before and after HM performance. Interestingly, this study highlighted that metabolites involved in vitamin B6 salvage, such as pyridoxal 5’-phosphate and pyridoxamine 5’-phosphate, were highly modulated. To evaluate the effects of vitamin B6 in cartilage cells, we treated differentiated mesenchymal stem cells and the SW1353 chondrosarcoma cell line with vitamin B6 in the presence of IL1β, the inflammatory cytokine involved in OA. Our study describes, for the first time, the modulation of the vitamin B6 salvage pathway following PA and suggests a protective role of PA in OA through modulation of this pathway.

scholarly journals Results of challenge of goats with Staphylococcus aureus into the teat of the udder

2018 ◽  
Vol 67 (4) ◽  
pp. 237
Author(s):  
A. TZORA ◽  
C. VOIDAROU ◽  
A. KARAMOUTSIOS ◽  
J. SKOUFOS
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Role ◽  
Aureus Strain ◽  
Dairy Herds ◽  
Cytological Examination ◽  
Lactating Goats ◽  
Before And After ◽  
Group A ◽  
Group B

Objective of the present study was to study the outcome of inoculation of Staphylococcus aureus into the teat duct of female goats, which simulates mammary natural infections. In total, 22 lactating goats were used in the study; 8 animals were challenged with a S. aureus strain at a depth of 2 mm into one teat duct (group A), 8 animals were challenged with the same strain at 6 mm into one teat duct (group B) and 6 animals were challenged directly into one gland cistern (group C). Challenge dose was always 1300 cfu. Animals were examined clinically before and after challenge; milk samples were collected for bacteriological and cytological examination, and milk yield measurements were also performed. Goats in group A or B developed a significantly milder response than animals in group C. It is concluded that the evidence indicates a protective role of the normal teat of the udder of goats and that the results also underline the significance of maintaining healthy teats for prevention of mastitis in dairy herds.

scholarly journals Dextrose Hydration May Promote Cisplatin-induced Nephrotoxicity in Rats: Gender-related Difference

2019 ◽  
Vol 11 (2) ◽  
pp. 136-44
Author(s):  
Farzaneh Karimi ◽  
Sayyedehnikta Kasaei ◽  
Azar Baradaran ◽  
Farzaneh Ashrafi ◽  
Ardeshir Talebi ◽  
...  
Keyword(s):  
Kidney Tissue ◽  
Serum Levels ◽  
Protective Role ◽  
Female Rats ◽  
Male And Female ◽  
Cisplatin Nephrotoxicity ◽  
Male And Female Rats ◽  
Before And After ◽  
Different Doses

BACKGROUNDS: Cisplatin (CP) as an anticancer drug may affect the plasma glucose level while diabetic subjects are protected against CP-induced nephrotoxicity. In the current study, the role of dextrose hydration during CP therapy on CP-induced nephrotoxicity was evaluated.METHODS: Sixty-nine male and female rats were divided into 12 groups. The rats were hydrated with 15 mL/kg vehicle or different doses of 2%, 10% and 20% dextrose before and after 7.5 mg/kg CP administration. One week later, the biochemical and kidney function markers, and histology finding were determined.RESULTS: All the animals co-treated with CP and 20% dextrose, were dead during one week of the experiment. Administration of CP alone increased kidney tissue damage score (KTDS) and kidney weight (KW). It also elevated the blood urea nitrogen (BUN) and BUN-creatineine ratio (BUN/Cr) levels in the serum. In addition, CP decreased body weight and creatinine (Cr) clearance (ClCr) significantly in both male and female rats (p<0.05). However, 2% and 10% dextrose did not alter the mentioned parameters in male, but 10% dextrose supplement increased the serum levels of BUN, Cr and BUN/Cr ratio, KW and KTDS significantly in female rats (p<0.05).CONCLUSION: Our data suggest that not only do not support the nephro-protective role of dextrose hydration during CP therapy, the dextrose hydration can act as risk factor to promote CP-induced nephrotoxicity in female rats. Prohibition of high carbohydrate (glucose) diet during CP therapy is recommended.KEYWORDS: cisplatin, nephrotoxicity, dextrose, rat, gender

Why Patients with 5q- Syndrome Have Thrombocythemia?

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5533-5533
Author(s):  
Vit Campr ◽  
Jan Stritesky ◽  
Ota Fuchs ◽  
Anna Jonasova ◽  
Zuzana Zemanova ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mrna Level ◽  
Protective Role ◽  
Refractory Anemia ◽  
Glycophorin A ◽  
Erythroid Precursors ◽  
Before And After ◽  
Ribosomal Stress ◽  
E Cadherin

Abstract Introduction. Fli1 (Friend leukemia virus integration 1) together with other transcription factors induces the megakaryocytic differentiation of MEP (megakarycytic and erythroid progenitor). Refractory anemia and thrombocythemia is typical for 5q- syndrome. We found increased mRNA level of Fli1 in mononuclear bone marrow cells of 5q- syndrome patients in comparison with healthy controls (Neuwirtova et al., Ann Hematol 2013). The reason of the elevated Fli1 in 5q- syndrome is haploinsufficiency of microRNA-145, which targets Fli1 mRNA (Kumar et al., Blood 2011). Due to haploinsufficiency of RPS14 in 5q- syndrome non-consumed ribosomal proteins cause ribosomal stress and inactivate HDM2 in erythroblasts. E3 ubiquitin ligase HDM2 regulates p53 level by p53 degradation in proteasome. Inactivated HDM2 in erythroid precursors of 5q- syndrome leads to apoptosis of erythroblasts and to anemia. Why ribosomal stress does not cause thrombocytopenia and ineffective megakaryopoiesis as well? Our previous results support significant role of Fli1 in this process. Fli1 binds to promoter of the HDM2 gene and increases its transcription (Truong et al., Oncogene 2005). The increased activity of HDM2 in megakaryocytes inspite of ribosomal stress maintains p53 regulation and its degradation in proteasome. Megakaryopoiesis remains effective. Why it is not the case in erythroid precursors? To answer this question it was necessary to detect Fli1 as the protein and to determine in which cells Fli1 is present. Material and Methods. Twenty-three control representative bone marrow trephine biopsies of patients from controls (8 negative staging biopsies in lymphoma) and of patients with various hematological diagnoses (7 MDS with normal chromosome 5, 4 MPN, 3 AML and 1 RARS-T) and from 15 patients with 5q- syndrome were examined. In 13 patients with 5q- syndrome, samples taken before and 6 months after lenalidomide (Revlimid) therapy were available. The expression of Fli1 protein was investigated by immunohistochemistry (IHC). Expression of Fli1 on erythroid precursors was studied by double staining IHC procedure utilizing antibodies against Fli1 and either glycophorin A or E-cadherin known as reliable markers for erythroid precursors. Results. Nuclear expression of Fli1 was demonstrated in normal as well as in dysplastic megakaryocytes, in most cells of granulocytic series and lymphocytes. No staining for Fli1 was seen in erythroblasts and proerythroblasts visualized by expression of either glycophorin A or E-cadherin both in 5q- syndrome and controls. There were no significant differences in Fli1 expression between samples taken before and after lenalidomide treatment.The used IHC technique does not permit quantitative analysis of Fli1 protein levels. This fact could explain why we did not find any difference in Fli1 protein labeling in megakaryocytes before and after lenalidomide treatment while Fli1 mRNA level was decreased in majority of 5q- syndrome patients after six months of this therapy. Conclusion. Fli1 expression was found in normal as well as in dysplastic megakaryocytes. However, no Fli1 positivity was found in erythroid precursors in both 5q- syndrome and controls. Negativity of Fli1 expression in erythroid precursors in 5q- syndrome support our hypothesis of protective role of Fli1 against apoptosis under ribosomal stress in megakaryocytes in contrast to erythroblasts lacking Fli1. This protective role of Fli1 in megakaryocytes consists in Fli1 potentiation of expression of the E3 ubiquitine ligase HDM2 (Truong et al., Oncogene 2005). The presence of increased Fli1 in megakaryocytes helps to explain effective megakaryopoiesis in 5q- syndrome and is the answer to the question in the title of our abstract. Supported by Ministry of Health, Czech Republic-conceptual development of research organization Institute of Hematology and Blood Transfusion 00023736, RVO-VFN64165 and PRVOUK P-27/LF1/2. Disclosures No relevant conflicts of interest to declare.

Cardioprotective role of endogenous hydrogen peroxide during ischemia-reperfusion injury in canine coronary microcirculation in vivo

2006 ◽  
Vol 291 (3) ◽  
pp. H1138-H1146 ◽  
Author(s):  
Toyotaka Yada ◽  
Hiroaki Shimokawa ◽  
Osamu Hiramatsu ◽  
Yoshisuke Haruna ◽  
Yoshitaka Morita ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
No Production ◽  
Coronary Vasodilatation ◽  
Before And After ◽  
Nos Inhibitor

We have recently demonstrated that endogenous H2O2 plays an important role in coronary autoregulation in vivo. However, the role of H2O2 during coronary ischemia-reperfusion (I/R) injury remains to be examined. In this study, we examined whether endogenous H2O2 also plays a protective role in coronary I/R injury in dogs in vivo. Canine subepicardial small coronary arteries (≥100 μm) and arterioles (<100 μm) were continuously observed by an intravital microscope during coronary I/R (90/60 min) under cyclooxygenase blockade ( n = 50). Coronary vascular responses to endothelium-dependent vasodilators (ACh) were examined before and after I/R under the following seven conditions: control, nitric oxide (NO) synthase (NOS) inhibitor NG-monomethyl-l-arginine (l-NMMA), catalase (a decomposer of H2O2), 8-sulfophenyltheophylline (8-SPT, an adenosine receptor blocker), l-NMMA + catalase, l-NMMA + tetraethylammonium (TEA, an inhibitor of large-conductance Ca2+-sensitive potassium channels), and l-NMMA + catalase + 8-SPT. Coronary I/R significantly impaired the coronary vasodilatation to ACh in both sized arteries (both P < 0.01); l-NMMA reduced the small arterial vasodilatation (both P < 0.01), whereas it increased ( P < 0.05) the ACh-induced coronary arteriolar vasodilatation associated with fluorescent H2O2 production after I/R. Catalase increased the small arterial vasodilatation ( P < 0.01) associated with fluorescent NO production and increased endothelial NOS expression, whereas it decreased the arteriolar response after I/R ( P < 0.01). l-NMMA + catalase, l-NMMA + TEA, or l-NMMA + catalase + 8-SPT further decreased the coronary vasodilatation in both sized arteries (both, P < 0.01). l-NMMA + catalase, l-NMMA + TEA, and l-NMMA + catalase + 8-SPT significantly increased myocardial infarct area compared with the other four groups (control, l-NMMA, catalase, and 8-SPT; all, P < 0.01). These results indicate that endogenous H2O2, in cooperation with NO, plays an important cardioprotective role in coronary I/R injury in vivo.

Partner Support as a Protection Against Distress During the Transition to Parenthood

2019 ◽  
Vol 40 (9) ◽  
pp. 1107-1125 ◽  
Author(s):  
Aurélie Gillis ◽  
Barbara Gabriel ◽  
Sarah Galdiolo ◽  
Isabelle Roskam
Keyword(s):  
Transition To Parenthood ◽  
Longitudinal Design ◽  
Protective Role ◽  
Partner Support ◽  
Heterosexual Couples ◽  
Third Trimester ◽  
Mothers And Fathers ◽  
The Third ◽  
Before And After

The majority of previous studies focused on mothers’ distress and considered partner support from the father to the mother. The current research studies the level and the course of distress and partner support in new mothers and fathers during the transition to parenthood and tests the protective role of partner support against distress. Data were collected in a two-wave longitudinal design from 53 heterosexual couples. Mothers and fathers completed questionnaires at two measurement occasions, that is, in the third trimester of pregnancy and 3 months after childbirth. The results provided arguments in favor of a dyadic perspective on distress during the transition to parenthood. No difference was displayed between mothers and fathers before and after childbirth. The level of distress decreased in mothers and also in fathers but only for those whose partner’s distress also decreased. The importance of partner support against postpartum distress was highlighted for mothers and fathers.

scholarly journals The influence of Mediterranean diet in acne pathogenesis and the correlation with insulin-like growth factor-1 serum levels: implications and results

2021 ◽  
Author(s):  
Mariabeatrice Bertolani ◽  
Eleonora Rodighiero ◽  
Roberta Saleri ◽  
Giuseppe Pedrazzi ◽  
Simona Bertoli ◽  
...  
Keyword(s):  
Mediterranean Diet ◽  
Serum Levels ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Healthy Population ◽  
Group Score ◽  
Western Group ◽  
Before And After ◽  
The Mediterranean

Acne is a chronic inflammatory disease of the pilosebaceous unit and its etiology is complex and multifactorial. The role of the diet in its pathogenesis is still debated. The purpose of this study was to assess the association between MD and IGF-1 in acne patients and, as secondary objective, the role of systemic treatment on IGF-1 serum levels, in accordance to the patients’ diet. This study included 35 patients aged 14-30 years affected by acne and treated in line with the EDF guidelines. Patients were divided into 2 groups based on a questionnaire score assessing the adherence to the Mediterranean diet: the Mediterranean Group (score ≥ 6) and the Western Group (score < 5). IGF-1 serum levels were measured in all patients before and after treatment and then compared to healthy population. IGF-1 levels were higher in patients than in controls and in the Western group than in the Mediterranean group. We speculate that the Mediterranean diet can have a protective role in the pathogenesis of acne by acting on the systemic route of IGF-1.

scholarly journals Vascular Stiffness in Aging and Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephen F. Vatner ◽  
Jie Zhang ◽  
Christina Vyzas ◽  
Kalee Mishra ◽  
Robert M. Graham ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Protective Role ◽  
Vascular Stiffness ◽  
Calcium Deposition ◽  
Female Sex Hormones ◽  
Age Related ◽  
Before And After ◽  
Males And Females ◽  
Human Primate

The goal of this review is to provide further understanding of increased vascular stiffness with aging, and how it contributes to the adverse effects of major human diseases. Differences in stiffness down the aortic tree are discussed, a topic requiring further research, because most prior work only examined one location in the aorta. It is also important to understand the divergent effects of increased aortic stiffness between males and females, principally due to the protective role of female sex hormones prior to menopause. Another goal is to review human and non-human primate data and contrast them with data in rodents. This is particularly important for understanding sex differences in vascular stiffness with aging as well as the changes in vascular stiffness before and after menopause in females, as this is controversial. This area of research necessitates studies in humans and non-human primates, since rodents do not go through menopause. The most important mechanism studied as a cause of age-related increases in vascular stiffness is an alteration in the vascular extracellular matrix resulting from an increase in collagen and decrease in elastin. However, there are other mechanisms mediating increased vascular stiffness, such as collagen and elastin disarray, calcium deposition, endothelial dysfunction, and the number of vascular smooth muscle cells (VSMCs). Populations with increased longevity, who live in areas called “Blue Zones,” are also discussed as they provide additional insights into mechanisms that protect against age-related increases in vascular stiffness. Such increases in vascular stiffness are important in mediating the adverse effects of major cardiovascular diseases, including atherosclerosis, hypertension and diabetes, but require further research into their mechanisms and treatment.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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