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Article ; Online: Contribution of the serotonergic system to developmental brain abnormalities in autism spectrum disorder.

Wegiel, Jarek / Chadman, Kathryn / London, Eric / Wisniewski, Thomas / Wegiel, Jerzy

Autism research : official journal of the International Society for Autism Research

2024

Abstract: This review highlights a key role of the serotonergic system in brain development and in distortions of normal brain development in early stages of fetal life resulting in cascades of abnormalities, including defects of neurogenesis, neuronal migration, ... ...

Abstract	This review highlights a key role of the serotonergic system in brain development and in distortions of normal brain development in early stages of fetal life resulting in cascades of abnormalities, including defects of neurogenesis, neuronal migration, neuronal growth, differentiation, and arborization, as well as defective neuronal circuit formation in the cortex, subcortical structures, brainstem, and cerebellum of autistic subjects. In autism, defects in regulation of neuronal growth are the most frequent and ubiquitous developmental changes associated with impaired neuron differentiation, smaller size, distorted shape, loss of spatial orientation, and distortion of cortex organization. Common developmental defects of the brain in autism include multiregional focal dysplastic changes contributing to local neuronal circuit distortion, epileptogenic activity, and epilepsy. There is a discrepancy between more than 500 reports demonstrating the contribution of the serotonergic system to autism's behavioral anomalies, highlighted by lack of studies of autistic subjects' brainstem raphe nuclei, the center of brain serotonergic innervation, and of the contribution of the serotonergic system to the diagnostic features of autism spectrum disorder (ASD). Discovery of severe fetal brainstem auditory system neuronal deficits and other anomalies leading to a spectrum of hearing deficits contributing to a cascade of behavioral alterations, including deficits of social and verbal communication in individuals with autism, is another argument to intensify postmortem studies of the type and topography of, and the severity of developmental defects in raphe nuclei and their contribution to abnormal brain development and to the broad spectrum of functional deficits and comorbid conditions in ASD.
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2481338-2
ISSN	1939-3806 ; 1939-3792
ISSN (online)	1939-3806
ISSN	1939-3792
DOI	10.1002/aur.3123
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Article ; Online: Immune Checkpoint Inhibitor Related Rheumatological Complications: Cooperation between Rheumatologists and Oncologists.

Pacholczak-Madej, Renata / Kosałka-Węgiel, Joanna / Kuszmiersz, Piotr / Mituś, Jerzy W / Püsküllüoğlu, Mirosława / Grela-Wojewoda, Aleksandra / Korkosz, Mariusz / Bazan-Socha, Stanisława

International journal of environmental research and public health

2023 Volume 20, Issue 6

Abstract: In cancer, immune checkpoint inhibitors (ICIs) improve patient survival but may lead to severe immune-related adverse events (irAEs). Rheumatic irAEs are a distinct entity that are much more common in a real-life than in clinical trial reports due to ... ...

Abstract	In cancer, immune checkpoint inhibitors (ICIs) improve patient survival but may lead to severe immune-related adverse events (irAEs). Rheumatic irAEs are a distinct entity that are much more common in a real-life than in clinical trial reports due to their unspecific symptoms and them being a rare cause of hospitalization. This review focuses on an interdisciplinary approach to the management of rheumatic irAEs, including cooperation between oncologists, rheumatologists, and immunologists. We discuss the immunological background of rheumatic irAEs, as well as their unique clinical characteristics, differentiation from other irAEs, and treatment strategies. Importantly, steroids are not the basis of therapy, and nonsteroidal anti-inflammatory drugs should be administered in the front line with other antirheumatic agents. We also address whether patients with pre-existing rheumatic autoimmune diseases can receive ICIs and how antirheumatic agents can interfere with ICIs. Interestingly, there is a preclinical rationale for combining ICIs with immunosuppressants, particularly tumor necrosis factor α and interleukin 6 inhibitors. Regardless of the data, the mainstay in managing irAEs is interdisciplinary cooperation between oncologists and other medical specialties.
MeSH term(s)	Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Rheumatologists ; Antineoplastic Agents, Immunological/therapeutic use ; Rheumatic Diseases/drug therapy ; Rheumatic Diseases/diagnosis ; Antirheumatic Agents/adverse effects ; Neoplasms/drug therapy ; Neoplasms/complications ; Oncologists ; Immunotherapy/adverse effects
Chemical Substances	Immune Checkpoint Inhibitors ; Antineoplastic Agents, Immunological ; Antirheumatic Agents
Language	English
Publishing date	2023-03-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph20064926
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Article ; Online: Enhanced accumulation of N-terminally truncated Aβ with and without pyroglutamate-11 modification in parvalbumin-expressing GABAergic neurons in idiopathic and dup15q11.2-q13 autism.

Frackowiak, Janusz / Mazur-Kolecka, Bozena / Mehta, Pankaj / Wegiel, Jerzy

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 58

Abstract: Autism, the most frequent neurodevelopmental disorder of a very complex etiopathology, is associated with dysregulation of cellular homeostatic mechanisms, including processing of amyloid-β precursor protein (APP). Products of APP processing - N- ... ...

Abstract	Autism, the most frequent neurodevelopmental disorder of a very complex etiopathology, is associated with dysregulation of cellular homeostatic mechanisms, including processing of amyloid-β precursor protein (APP). Products of APP processing - N-terminally truncated amyloid-β peptide (N-tr-Aβ) species - are accumulated in autism in neurons and glia in the cortex, cerebellum, and subcortical structures of the brain. This process in neurons is correlated with increased oxidative stress. Because abnormally high levels of N-tr-Aβ are detected in only a fraction of neurons in the prefrontal cortex, we applied immunocytochemical staining and confocal microscopy in autopsy brain material from idiopathic and chromosome 15q11.2-q13 duplication (dup-15) autism to measure the load of N-tr-Aβ in the cells and synapses and to identify the subpopulation of neurons affected by these pathophysiological processes. The peptides accumulated in autism are N-terminally truncated; therefore, we produced a new antibody against Aβ truncated at N-terminal amino acid 11 modified to pyroglutamate to evaluate the presence and distribution of this peptide species in autism. We also quantified and characterized the oligomerization patterns of the Aβ-immunoreactive peptides in autism and control frozen brain samples. We provide morphological evidence, that in idiopathic and dup-15 autism, accumulation of N-tr-Aβ with and without pyroglutamate-11 modified N-terminus affects mainly the parvalbumin-expressing subpopulation of GABAergic neurons. N-tr-Aβ peptides are accumulated in neurons' cytoplasm and nucleus as well as in GABAergic synapses. Aβ peptides with both C-terminus 40 and 42 were detected by immunoblotting in frozen cortex samples, in the form of dimers and complexes of the molecular sizes of 18-24kD and 32-34kD. We propose that deposition of N-tr-Aβ specifically affects the functions of the parvalbumin-expressing GABAergic neurons and results in a dysregulation of brain excitatory-inhibitory homeostasis in autism. This process may be the target of new therapies.
MeSH term(s)	Adolescent ; Adult ; Amyloid beta-Peptides/metabolism ; Autistic Disorder/genetics ; Autistic Disorder/metabolism ; Autistic Disorder/pathology ; Child ; Chromosome Duplication/genetics ; Chromosomes, Human, Pair 15/genetics ; Female ; GABAergic Neurons/metabolism ; GABAergic Neurons/pathology ; Humans ; Male ; Parvalbumins/metabolism ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; Pyrrolidonecarboxylic Acid/metabolism ; Young Adult
Chemical Substances	Amyloid beta-Peptides ; Parvalbumins ; Pyrrolidonecarboxylic Acid (SZB83O1W42)
Language	English
Publishing date	2020-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-00923-8
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Article ; Online: Immune Checkpoint Inhibitor Related Rheumatological Complications

Renata Pacholczak-Madej / Joanna Kosałka-Węgiel / Piotr Kuszmiersz / Jerzy W. Mituś / Mirosława Püsküllüoğlu / Aleksandra Grela-Wojewoda / Mariusz Korkosz / Stanisława Bazan-Socha

International Journal of Environmental Research and Public Health, Vol 20, Iss 4926, p

Cooperation between Rheumatologists and Oncologists

2023 Volume 4926

Abstract	In cancer, immune checkpoint inhibitors (ICIs) improve patient survival but may lead to severe immune-related adverse events (irAEs). Rheumatic irAEs are a distinct entity that are much more common in a real-life than in clinical trial reports due to their unspecific symptoms and them being a rare cause of hospitalization. This review focuses on an interdisciplinary approach to the management of rheumatic irAEs, including cooperation between oncologists, rheumatologists, and immunologists. We discuss the immunological background of rheumatic irAEs, as well as their unique clinical characteristics, differentiation from other irAEs, and treatment strategies. Importantly, steroids are not the basis of therapy, and nonsteroidal anti-inflammatory drugs should be administered in the front line with other antirheumatic agents. We also address whether patients with pre-existing rheumatic autoimmune diseases can receive ICIs and how antirheumatic agents can interfere with ICIs. Interestingly, there is a preclinical rationale for combining ICIs with immunosuppressants, particularly tumor necrosis factor α and interleukin 6 inhibitors. Regardless of the data, the mainstay in managing irAEs is interdisciplinary cooperation between oncologists and other medical specialties.
Keywords	rheumatic adverse events ; immune checkpoint inhibitors ; immune-related adverse events ; cancer immunotherapy ; Medicine ; R
Subject code	616
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Risk factors of contrast-induced nephropathy in patients with acute coronary syndrome.

Rakowski, Tomasz / Dziewierz, Artur / Węgiel, Michał / Siudak, Zbigniew / Zasada, Wojciech / Jąkała, Jacek / Dykla, Dominika / Matysek, Jerzy / Surdacki, Andrzej / Bartuś, Stanisław / Dudek, Dariusz / Wojdyła, Roman

Kardiologia polska

2022 Volume 80, Issue 7-8, Page(s) 760–764

Abstract: Background: Patients with acute coronary syndrome (ACS) are at high risk of contrast-induced nephropathy (CIN), which is associated with prolonged hospitalization, higher morbidity and mortality after angiographic procedures. The occurrence of CIN is ... ...

Abstract	Background: Patients with acute coronary syndrome (ACS) are at high risk of contrast-induced nephropathy (CIN), which is associated with prolonged hospitalization, higher morbidity and mortality after angiographic procedures. The occurrence of CIN is regarded as a transient and reversible condition. However, the persistence of CIN until hospital discharge in patients with ACS has not been thoroughly analyzed. Aims: We aimed to analyze CIN persistent until hospital discharge in contemporary ACS population referred to invasive diagnostics and treatment. Methods: A total of 2638 consecutive patients with ACS were included in a prospective registry. The occurrence of CIN was defined as a 25% increase in serum creatinine from baseline or a 0.5 mg/dl (44 μmol/l) increase in the absolute value. Results: Criteria of CIN at hospital discharge were met in 10.7% of patients. Immediate percutaneous coronary intervention (PCI) after angiography (67% of patients) was associated with higher rates of CIN compared to patients referred for other treatment strategies (P < 0.001). The logistic regression model showed that anemia at baseline (8.7% of patients) was an independent predictor of CIN, which occurred in 17.9% of anemic patients and 10% of patients without anemia (P < 0.001). Also, ST-segment elevation myocardial infarction (STEMI) presentation and immediate PCI were independent predictors of CIN. Conclusions: Despite intravenous fluid administration during the hospital stay, CIN persisted until hospital discharge in more than 10% of patients with ACS. Anemia at baseline, STEMI presentation, and immediate PCI strategy were independent predictors of CIN. Thus, preventive actions should be specially aimed at those groups of patients.
MeSH term(s)	Acute Coronary Syndrome/therapy ; Contrast Media/adverse effects ; Creatinine ; Humans ; Kidney Diseases/chemically induced ; Percutaneous Coronary Intervention/adverse effects ; Risk Factors ; ST Elevation Myocardial Infarction/etiology
Chemical Substances	Contrast Media ; Creatinine (AYI8EX34EU)
Language	English
Publishing date	2022-05-06
Publishing country	Poland
Document type	Journal Article
ZDB-ID	411492-9
ISSN	1897-4279 ; 0022-9032
ISSN (online)	1897-4279
ISSN	0022-9032
DOI	10.33963/KP.a2022.0123
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Article ; Online: Thrombin generation potential is increased in patients with autoimmune inflammatory myopathies.

Kuszmiersz, Piotr / Siwiec-Koźlik, Andżelika / Pacholczak-Madej, Renata / Rams, Anna / Celińska-Lowenhoff, Magdalena / Iwaniec, Teresa / Kosałka-Węgiel, Joanna / Zaręba, Lech / Dziedzic, Radosław / Bazan-Socha, Stanisława / Dropiński, Jerzy

Advances in medical sciences

2022 Volume 67, Issue 2, Page(s) 346–352

Abstract: Purpose: Dermatomyositis and polymyositis (DM/PM) are rare autoimmune inflammatory myopathies, characterized by an increased risk of cardiovascular and thromboembolic events, likely related to the prothrombotic plasma properties. The aim of this study ... ...

Abstract	Purpose: Dermatomyositis and polymyositis (DM/PM) are rare autoimmune inflammatory myopathies, characterized by an increased risk of cardiovascular and thromboembolic events, likely related to the prothrombotic plasma properties. The aim of this study was to assess the in vitro thrombin generation profile as a biomarker of plasma procoagulant properties in DM/PM patients. Methods: In 58 clinically stable DM/PM patients and 67 controls matched for sex, age, body mass index, we measured plasma thrombin generation potential using the Calibrated Automated Thrombinography (CAT) and analyzed its relationship with clinical disease characteristics, including autoantibodies profile. Results: Patients with DM/PM had a 21% increase in endogenous thrombin potential (ETP), 36% higher peak thrombin concentration, and 11% faster thrombin generation, compared to controls (p < 0.001, all, also after adjustment for potential confounders). Interestingly, although both diseases did not differ in thrombin generation potential, heterogenous variables predicted elevated ETPs in both of them. In DM, that was higher fibrinogen, C-reactive protein, and total cholesterol, whereas in PM, presence of arthritis and increased blood platelet count. Surprisingly, thrombin formation capacity remained in a robust inverse relationship with serum troponin (r = -0.67, p < 0.001) in the patient group. Conclusions: DM/PM patients are characterized by an increased thrombin generation potential, suggesting prothrombotic plasma properties in both diseases. However, more studies are needed to verify its rationale and role in DM/PM clinical course and unfavorable clinical outcomes.
MeSH term(s)	Humans ; Dermatomyositis/etiology ; Thrombin ; C-Reactive Protein ; Autoimmune Diseases ; Autoantibodies ; Biomarkers ; Fibrinogen ; Troponin ; Cholesterol
Chemical Substances	Thrombin (EC 3.4.21.5) ; C-Reactive Protein (9007-41-4) ; Autoantibodies ; Biomarkers ; Fibrinogen (9001-32-5) ; Troponin ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2022-09-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2273668-2
ISSN	1898-4002 ; 1896-1126
ISSN (online)	1898-4002
ISSN	1896-1126
DOI	10.1016/j.advms.2022.08.005
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Article ; Online: Developmental deficits and staging of dynamics of age associated Alzheimer's disease neurodegeneration and neuronal loss in subjects with Down syndrome.

Wegiel, Jerzy / Flory, Michael / Kuchna, Izabela / Nowicki, Krzysztof / Wegiel, Jarek / Ma, Shuang Yong / Zhong, Nanbert / Bobrowicz, Teresa Wierzba / de Leon, Mony / Lai, Florence / Silverman, Wayne P / Wisniewski, Thomas

Acta neuropathologica communications

2022 Volume 10, Issue 1, Page(s) 2

Abstract: The increased life expectancy of individuals with Down syndrome (DS) is associated with increased prevalence of trisomy 21-linked early-onset Alzheimer's disease (EOAD) and dementia. The aims of this study of 14 brain regions including the entorhinal ... ...

Abstract	The increased life expectancy of individuals with Down syndrome (DS) is associated with increased prevalence of trisomy 21-linked early-onset Alzheimer's disease (EOAD) and dementia. The aims of this study of 14 brain regions including the entorhinal cortex, hippocampus, basal ganglia, and cerebellum in 33 adults with DS 26-72 years of age were to identify the magnitude of brain region-specific developmental neuronal deficits contributing to intellectual deficits, to apply this baseline to identification of the topography and magnitude of neurodegeneration and neuronal and volume losses caused by EOAD, and to establish age-based staging of the pattern of genetically driven neuropathology in DS. Both DS subject age and stage of dementia, themselves very strongly correlated, were strong predictors of an AD-associated decrease of the number of neurons, considered a major contributor to dementia. The DS cohort was subclassified by age as pre-AD stage, with 26-41-year-old subjects with a full spectrum of developmental deficit but with very limited incipient AD pathology, and 43-49, 51-59, and 61-72-year-old groups with predominant prevalence of mild, moderately severe, and severe dementia respectively. This multiregional study revealed a 28.1% developmental neuronal deficit in DS subjects 26-41 years of age and 11.9% AD-associated neuronal loss in DS subjects 43-49 years of age; a 28.0% maximum neuronal loss at 51-59 years of age; and a 11.0% minimum neuronal loss at 61-72 years of age. A total developmental neuronal deficit of 40.8 million neurons and AD-associated neuronal loss of 41.6 million neurons reflect a comparable magnitude of developmental neuronal deficit contributing to intellectual deficits, and AD-associated neuronal loss contributing to dementia. This highly predictable pattern of pathology indicates that successful treatment of DS subjects in the fourth decade of life may prevent AD pathology and functional decline.
MeSH term(s)	Adult ; Aged ; Aging/pathology ; Alzheimer Disease/complications ; Alzheimer Disease/pathology ; Brain/pathology ; Down Syndrome/complications ; Down Syndrome/pathology ; Female ; Humans ; Male ; Middle Aged ; Nerve Degeneration/pathology ; Neurons/pathology
Language	English
Publishing date	2022-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-021-01300-9
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Article ; Online: Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by Tyr

Im, Eunju / Jiang, Ying / Stavrides, Philip H / Darji, Sandipkumar / Erdjument-Bromage, Hediye / Neubert, Thomas A / Choi, Jun Yong / Wegiel, Jerzy / Lee, Ju-Hyun / Nixon, Ralph A

Science advances

2023 Volume 9, Issue 30, Page(s) eadg1925

Abstract: Lysosome dysfunction arises early and propels Alzheimer's disease (AD). Herein, we show that amyloid precursor protein (APP), linked to early-onset AD in Down syndrome (DS), acts directly via its β-C-terminal fragment (βCTF) to disrupt lysosomal vacuolar ...

Abstract	Lysosome dysfunction arises early and propels Alzheimer's disease (AD). Herein, we show that amyloid precursor protein (APP), linked to early-onset AD in Down syndrome (DS), acts directly via its β-C-terminal fragment (βCTF) to disrupt lysosomal vacuolar (H
MeSH term(s)	Mice ; Humans ; Animals ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Down Syndrome/genetics ; Down Syndrome/metabolism ; Down Syndrome/pathology ; Alzheimer Disease/metabolism ; Adenosine Triphosphatases/metabolism ; Lysosomes/metabolism ; Disease Models, Animal ; Amyloid beta-Peptides/metabolism
Chemical Substances	Amyloid beta-Protein Precursor ; Adenosine Triphosphatases (EC 3.6.1.-) ; Amyloid beta-Peptides
Language	English
Publishing date	2023-07-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adg1925
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Article: Genetic Association between TNFA Polymorphisms (rs1799964 and rs361525) and Susceptibility to Cancer in Systemic Sclerosis.

Kosałka-Węgiel, Joanna / Lichołai, Sabina / Dziedzina, Sylwia / Milewski, Mamert / Kuszmiersz, Piotr / Rams, Anna / Gąsior, Jolanta / Matyja-Bednarczyk, Aleksandra / Kwiatkowska, Helena / Korkosz, Mariusz / Siwiec, Andżelika / Koźlik, Paweł / Padjas, Agnieszka / Sydor, Wojciech / Dropiński, Jerzy / Sanak, Marek / Musiał, Jacek / Bazan-Socha, Stanisława

Life (Basel, Switzerland)

2022 Volume 12, Issue 5

Abstract: Tumor necrosis factor (TNF)-α is a proinflammatory cytokine that plays an important role in the pathogenesis of autoimmune diseases. The aim of the study was to establish an association between TNF-α promoter variability and systemic sclerosis (SSc). The ...

Abstract	Tumor necrosis factor (TNF)-α is a proinflammatory cytokine that plays an important role in the pathogenesis of autoimmune diseases. The aim of the study was to establish an association between TNF-α promoter variability and systemic sclerosis (SSc). The study included 43 SSc patients and 74 controls. Four single nucleotide polymorphisms (rs361525, rs1800629, rs1799724, and rs1799964) located at the promoter of the TNFA gene were genotyped using commercially available TaqMan allelic discrimination assays with real-time PCR. The rs1799724 allele was associated with an increased SSc susceptibility (
Language	English
Publishing date	2022-05-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life12050698
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Article: Endothelial dysfunction in patients with systemic sclerosis.

Pacholczak-Madej, Renata / Kuszmiersz, Piotr / Bazan-Socha, Stanisława / Kosałka-Wêgiel, Joanna / Iwaniec, Teresa / Zarêba, Lech / Kielczewski, Stan / Rams, Anna / Walocha, Jerzy A / Musiał, Jacek / Dropiñski, Jerzy

Postepy dermatologii i alergologii

2020 Volume 37, Issue 4, Page(s) 495–502

Abstract: Introduction: Patients with systemic sclerosis experience endothelial dysfunction and damage even in the absence of clinical manifestations.: Aim: To evaluate various methods for assessing the endothelial function for their applicability to clinical ... ...

Abstract	Introduction: Patients with systemic sclerosis experience endothelial dysfunction and damage even in the absence of clinical manifestations. Aim: To evaluate various methods for assessing the endothelial function for their applicability to clinical practice. Material and methods: Forty-two patients (7 men and 35 women) with systemic sclerosis and 36 controls (11 men and 25 women) matched for age, sex, body mass index, smoking habit, and comorbidities were enrolled in the study. We assessed each participant for typical risk factors for cardiovascular diseases and measured serum levels of vascular cell adhesion molecule-1 (VCAM-1) and thrombomodulin together with flow-mediated dilatation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery using ultrasonography. Results: Patients with systemic sclerosis did not differ from controls in serum levels of VCAM-1 and thrombomodulin, however, the statistical analysis with adjustment for potential confounders revealed increased levels of thrombomodulin in the patients ( Conclusions: Patients with systemic sclerosis present with endothelial dysfunction which may be detected using ultrasonographic methods. The exact mechanism of observed abnormalities is unknown, but it is possibly related to the chronic inflammation and ischemia-reperfusion injury.
Language	English
Publishing date	2020-09-02
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2596142-1
ISSN	1642-395X
ISSN	1642-395X
DOI	10.5114/ada.2019.83501
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