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  1. Article ; Online: COVID-19 and Dysfunctional Endothelium: The Mexican Scenario.

    Alvarado-Moreno, Jose Antonio / Majluf-Cruz, Abraham

    Archives of medical research

    2020  Volume 51, Issue 6, Page(s) 587–588

    Keywords covid19
    Language English
    Publishing date 2020-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1156844-6
    ISSN 1873-5487 ; 0188-4409 ; 0188-0128
    ISSN (online) 1873-5487
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2020.05.004
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  2. Article ; Online: Cell Contact with Endothelial Cells Favors the In Vitro Maintenance of Human Chronic Myeloid Leukemia Stem and Progenitor Cells.

    Torres-Barrera, Patricia / Moreno-Lorenzana, Dafne / Alvarado-Moreno, José Antonio / García-Ruiz, Elena / Lagunas, Cesar / Mayani, Hector / Chávez-González, Antonieta

    International journal of molecular sciences

    2022  Volume 23, Issue 18

    Abstract: Chronic Myeloid Leukemia (CML) originates in a leukemic stem cell that resides in the bone marrow microenvironment, where they coexist with cellular and non-cellular elements. The vascular microenvironment has been identified as an important element in ... ...

    Abstract Chronic Myeloid Leukemia (CML) originates in a leukemic stem cell that resides in the bone marrow microenvironment, where they coexist with cellular and non-cellular elements. The vascular microenvironment has been identified as an important element in CML development since an increase in the vascularization has been suggested to be related with poor prognosis; also, using murine models, it has been reported that bone marrow endothelium can regulate the quiescence and proliferation of leukemic stem and progenitor cells. This observation, however, has not been evaluated in primary human cells. In this report, we used a co-culture of primitive (progenitor and stem) CML cells with endothelial colony forming cells (ECFC) as an in vitro model to evaluate the effects of the vascular microenvironment in the leukemic hematopoiesis. Our results show that this interaction allows the in vitro maintenance of primitive CML cells through an inflammatory microenvironment able to regulate the proliferation of progenitor cells and the permanence in a quiescent state of leukemic stem cells.
    MeSH term(s) Animals ; Bone Marrow ; Chronic Disease ; Endothelial Cells ; Hematopoiesis ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Mice ; Neoplastic Stem Cells ; Tumor Microenvironment
    Language English
    Publishing date 2022-09-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms231810326
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  4. Article ; Online: COVID-19 and Dysfunctional Endothelium

    Alvarado-Moreno, Jose Antonio / Majluf-Cruz, Abraham

    Archives of Medical Research

    The Mexican Scenario

    2020  Volume 51, Issue 6, Page(s) 587–588

    Keywords General Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 1156844-6
    ISSN 0188-4409 ; 0188-0128
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2020.05.004
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Factor XII Deficiency in Mexico: High Prevalence in the General Population and Patients with Venous Thromboembolic Disease.

    Dominguez-Reyes, Víctor Manuel / Hernandez-Juarez, Jesus / Arreola-Diaz, Rodrigo / Majluf-Cruz, Karim / Reyes-Maldonado, Elba / Alvarado-Moreno, José Antonio / Ruiz, Luis Antonio Moreno / Majluf-Cruz, Abraham

    Archives of medical research

    2023  Volume 55, Issue 1, Page(s) 102913

    Abstract: Introduction: Thrombosis is one of the leading causes of morbidity and mortality worldwide. Venous thromboembolic disease (VTD) is considered a new epidemic. FXII deficiency is supposed to be a cause of thrombosis. To search for unknown causes of ... ...

    Abstract Introduction: Thrombosis is one of the leading causes of morbidity and mortality worldwide. Venous thromboembolic disease (VTD) is considered a new epidemic. FXII deficiency is supposed to be a cause of thrombosis. To search for unknown causes of thrombosis in our population, our aim was to determine if FXII deficiency can be considered a risk factor for VTD.
    Methods: Young adult Mexican patients with at least one VTD episode and healthy controls were included in this prospective, observational, controlled study. Liver and renal function tests, blood cytometry, and blood coagulation assays were performed. Plasma FXII activity and its concentration were evaluated.
    Results: Over a two-year period, 250 patients and 250 controls were included. FXII activity was significantly lower in the control group compared to patients with VTD (p = 0.005). However, percentage of patients and controls with FXII deficiency was 8.8 and 9.2%, respectively (p = 1.000). No significant association was found between FXII deficiency and VTD (p = 1.0). FXII plasma concentration was lower in controls vs. patients with VTD: 4.05 vs. 6.19 ng/mL (p <0.001). Percentage of patients with low FXII plasma concentration was 1.6% and 6.0% in patients and controls, respectively (p = 0.010).
    Conclusions: FXII deficiency is a frequent finding in patients with VTD and controls in Mexico. Some patients with FXII deficiency had normal APTT result, an effect not described above. FXII plasma concentration was lower in patients with low activity.
    MeSH term(s) Humans ; Young Adult ; Factor XII Deficiency/complications ; Factor XII Deficiency/epidemiology ; Mexico/epidemiology ; Prevalence ; Prospective Studies ; Thrombosis ; Factor XII/metabolism
    Chemical Substances Factor XII (9001-30-3)
    Language English
    Publishing date 2023-12-07
    Publishing country United States
    Document type Observational Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1156844-6
    ISSN 1873-5487 ; 0188-4409 ; 0188-0128
    ISSN (online) 1873-5487
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2023.102913
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  6. Article ; Online: Self-regulation of TNF-α Induces Dysfunction of Endothelial Colony-forming Cells from Patients with Venous Thromboembolic Disease.

    Moreno-Lorenzana, Dafné / Torres-Barrera, Patricia / Flores-Lopez, Gabriela / Chávez-González, María Antonieta / Isordia-Salas, Irma / Yoder, Mervin C / Majluf-Cruz, Abraham / Alvarado-Moreno, José Antonio

    Archives of medical research

    2022  Volume 53, Issue 7, Page(s) 680–687

    Abstract: Background: Endothelial colony-forming cells (ECFCs) contribute to postnatal vasculogenesis. In venous thromboembolic disease (VTD), they are functionally abnormal and produce high concentrations of TNF-α.: Objective: To analyze the TNF-α signaling ... ...

    Abstract Background: Endothelial colony-forming cells (ECFCs) contribute to postnatal vasculogenesis. In venous thromboembolic disease (VTD), they are functionally abnormal and produce high concentrations of TNF-α.
    Objective: To analyze the TNF-α signaling pathway and its relationship with the expression of cell-cycle regulators.
    Methods: Mononuclear cells (MNCs) were collected from the peripheral blood of 20 healthy human volunteers (controls) and 30 patients with VTD matched by age (20-50 years) and sex to obtain ECFCs. We analyzed the relative quantification of the gene transcripts of TNF, NFkB1, PLAU, HMOX1, GSS, eNOS, CDKN1A, and CDKN1B through quantitative RT-PCR (qRT-PCR assays). Identification of NF-κB and activated targets of each pathway: NF-κB (Ser536); IκBα (Ser32/Ser36); p38 (Thr180/Tyr182) JNK (Thr183/Tyr185), p53 and cell-cycle regulators: p16, p18, p21, p27, p57, Cyclin D, Cyclin E, Cyclin A, Cyclin B, CDK2, CDK4; cell-cycle status was determined by KI-67 and 7-AAD. Cells were analyzed with flow cytometry and the FlowJo vX software.
    Results: In ECFCs from VTD patients, TNF-α receptor and NFkB were overexpressed and hyper-phosphorylated; eNOS and HMOX1 were down-regulated; cell-cycle regulators (p53, p18, p21) were elevated. In addition, the cell cycle was locked in the G2 phase.
    Conclusions: Our results strongly suggest that these molecular alterations in the pathway of TNF-α and cell cycle regulation induce endothelial dysfunction, reduced proliferation potential and vascular regeneration, and consequently, the occurrence of new thrombotic events.
    MeSH term(s) Humans ; Young Adult ; Adult ; Middle Aged ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Tumor Suppressor Protein p53/metabolism ; Endothelial Cells/metabolism ; Self-Control
    Chemical Substances Tumor Necrosis Factor-alpha ; NF-kappa B ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2022-10-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1156844-6
    ISSN 1873-5487 ; 0188-4409 ; 0188-0128
    ISSN (online) 1873-5487
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2022.10.002
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  7. Article ; Online: Morphological and functional alterations in endothelial colony-forming cells from recovered COVID-19 patients.

    Alvarado-Moreno, José Antonio / Davila-Moreno, Jorge / Dominguez-Reyes, Victor / Arreola-Diaz, Rodrigo / Isordia-Salas, Irma / Chavez-Gonzalez, Antonieta / Majluf-Cruz, Abraham

    Thrombosis research

    2021  Volume 206, Page(s) 55–59

    MeSH term(s) COVID-19 ; Cell Proliferation ; Endothelial Cells ; Humans ; SARS-CoV-2
    Language English
    Publishing date 2021-08-13
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 121852-9
    ISSN 1879-2472 ; 0049-3848
    ISSN (online) 1879-2472
    ISSN 0049-3848
    DOI 10.1016/j.thromres.2021.08.007
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  8. Article: [Polimorfismos asociados a disfunción endotelial y a un estado protrombótico en jóvenes mexicanos con infarto cerebral].

    Isordia-Salas, Irma / Jiménez-Alvarado, Rosa María / Cerda-Mancillas, Megan Carolina / Alvarado-Moreno, José Antonio / Hernández-Juárez, Jesús / Santiago-Germán, David / Leaños-Miranda, Alfredo / Majluf-Cruz, Abraham

    Gaceta medica de Mexico

    2018  Volume 154, Issue Supp 2, Page(s) S15–S21

    Abstract: Objective: To examine the contribution the polymorphisms G20210A, G1691A and G10976A in the coagulation factors FII, FV, FVII, respectively; Glu298Asp and C677T in eNOS and 5,10 MTHFR in young Mexican population with cerebral infarction (CI).: Methods! ...

    Abstract Objective: To examine the contribution the polymorphisms G20210A, G1691A and G10976A in the coagulation factors FII, FV, FVII, respectively; Glu298Asp and C677T in eNOS and 5,10 MTHFR in young Mexican population with cerebral infarction (CI).
    Methods: 224 patients ≤ 45 years of age with CI and 224 controls matched by age and gender were recruited from 2006 and 2014. The polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism.
    Results: We identified a significant difference in the genotype distribution of Glu298Asp (p = 0.001) and C677T (p = 0.01) polymorphisms between CI patients and control groups. The genotype distribution in the FII G20210A, FV G1691A and FVII G10976A polymorphisms were similar. There were independent factors for ischemic stroke: Glu298Asp and C677T polymorphisms, smoking; hypertension, and familial history of thrombotic disease.
    Conclusions: The Glu298Asp and C677T, but not FII G20210A, FV G1691A and FVII G10976A polymorphisms were associated with CI. Our results suggest that endothelial dysfunction and the synergist interaction with other factors such as smoking and hypertension contribute to CI in young individuals.
    MeSH term(s) Adult ; Brain Ischemia/genetics ; Cerebral Infarction/genetics ; Factor V/genetics ; Factor VII/genetics ; Female ; Genotype ; Humans ; Hypertension/epidemiology ; Male ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Mexico ; Nitric Oxide Synthase Type III/genetics ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Prothrombin/genetics ; Smoking/epidemiology ; Stroke/genetics
    Chemical Substances Factor V (9001-24-5) ; Factor VII (9001-25-6) ; Prothrombin (9001-26-7) ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; MTHFR protein, human (EC 1.5.1.20) ; Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20)
    Language Spanish
    Publishing date 2018-12-05
    Publishing country Mexico
    Document type Journal Article
    ZDB-ID 425456-9
    ISSN 0016-3813
    ISSN 0016-3813
    DOI 10.24875/GMM.18004574
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  9. Article ; Online: Genetic Polymorphisms Associated with Thrombotic Disease Comparison of Two Territories: Myocardial Infarction and Ischemic Stroke.

    Isordia-Salas, Irma / Martínez-Marino, Manuel / Alberti-Minutti, Paolo / Ricardo-Moreno, María Tania / Castro-Calvo, Ricardo / Santiago-Germán, David / Alvarado-Moreno, José Antonio / Calleja-Carreño, Cristian / Hernández-Juárez, Jesús / Leaños-Miranda, Alfredo / Majluf-Cruz, Abraham

    Disease markers

    2019  Volume 2019, Page(s) 3745735

    Abstract: Background and purpose: The thrombin-activatable fibrinolysis inhibitor (TAFI) is an important inhibitor of fibrinolysis and plays a critical role in the pathogenesis of arterial thrombosis; genetic polymorphisms of the TAFI gene affect its activity and ...

    Abstract Background and purpose: The thrombin-activatable fibrinolysis inhibitor (TAFI) is an important inhibitor of fibrinolysis and plays a critical role in the pathogenesis of arterial thrombosis; genetic polymorphisms of the TAFI gene affect its activity and increase the risk of thrombosis. Moreover, studies in young patients are still scarce. The aim was to examine the contribution of the Thr325Ile and Ala147Thr polymorphisms with ST acute myocardial infarction (STEMI) or idiopathic ischemic stroke (IIS) in the young Mexican population.
    Methods: A total of 244 patients with STEMI ≤45 years of age and 244 controls. In a second study, 250 patients with IIS ≤45 years of age were recruited, including 250 controls. In both studies, cases and controls were matched by age and sex. The polymorphisms were determined in all participants by PCR-RFLP.
    Results: There was significant difference in the Thr325Ile genotype distribution (
    Conclusions: The Thr325Ile polymorphism, but no Ala147Thr polymorphism, represents an independent risk factor for STEMI in the young Mexican population.
    MeSH term(s) Adult ; Biomarkers ; Brain Ischemia/genetics ; Brain Ischemia/pathology ; Case-Control Studies ; Female ; Follow-Up Studies ; Histone Acetyltransferases/genetics ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Prognosis ; Risk Factors ; ST Elevation Myocardial Infarction/genetics ; ST Elevation Myocardial Infarction/pathology ; Stroke/genetics ; Stroke/pathology ; TATA-Binding Protein Associated Factors/genetics ; Transcription Factor TFIID/genetics
    Chemical Substances Biomarkers ; TATA-Binding Protein Associated Factors ; Transcription Factor TFIID ; Histone Acetyltransferases (EC 2.3.1.48) ; TATA-binding protein associated factor 250 kDa (EC 2.7.11.1)
    Language English
    Publishing date 2019-10-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604951-5
    ISSN 1875-8630 ; 0278-0240
    ISSN (online) 1875-8630
    ISSN 0278-0240
    DOI 10.1155/2019/3745735
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  10. Article ; Online: Gene polymorphisms of angiotensin-converting enzyme and angiotensinogen and risk of idiopathic ischemic stroke.

    Isordia-Salas, Irma / Santiago-Germán, David / Cerda-Mancillas, Megan Carolina / Hernández-Juárez, Jesús / Bernabe-García, Mariela / Leaños-Miranda, Alfredo / Alvarado-Moreno, José Antonio / Majluf-Cruz, Abraham

    Gene

    2018  Volume 688, Page(s) 163–170

    Abstract: Objective: The renin-angiotensin system (RAS) is a hormonal signaling mechanism implicated in the atherosclerosis and regulation of blood pressure. Angiotensin-converting enzyme (ACE) a key enzyme in the RAS, plays important roles in vascular remodeling ...

    Abstract Objective: The renin-angiotensin system (RAS) is a hormonal signaling mechanism implicated in the atherosclerosis and regulation of blood pressure. Angiotensin-converting enzyme (ACE) a key enzyme in the RAS, plays important roles in vascular remodeling atherosclerosis, and ischemic stroke. The aim of this study was to examine the possible contribution of the I/D in the ACE gene, M235T and T174M in the angiotensinogen (AGT) gene polymorphisms with ischemic stroke in young Mexican population.
    Materials and methods: A total of 224 patients with diagnosis of idiopathic ischemic stroke ≤45 years of age, and 224 controls matched by age and gender, were recruited from 2006 and 2016. The I/D, M235T and T174M polymorphisms were determined in all participants by PCR-RFLP.
    Results: There was a significant difference in the M235T genotype distribution (p = 0.01) and allele frequency between two groups (p = 0.01). Also, we found a significant difference in the T174M genotype distribution (p = 0.01) and the allele frequency between groups; (p = 0.02). In contrast, in I/D polymorphism, there was a similar genotype distribution; (p = 0.20) and allele distribution (p = 0.20). There were independent factors for ischemic stroke: M235T and T174M polymorphisms, smoking, hypertension, and familial history of atherothrombotic disease. The AGT levels were increased in the group of patients with stroke compared with the control group, but the AGT levels were not influenced by the allele or genotype in each polymorphism.
    Conclusions: The M235T and T174M polymorphisms represented an increased risk for stroke in young Mexican individuals. In contrast, the I/D was not associated with in the same group of patients. The AGT levels were higher in the acute phase of stroke, but it was not determined by the polymorphisms.
    MeSH term(s) Adult ; Alleles ; Angiotensinogen/genetics ; Blood Pressure/genetics ; Brain Ischemia/genetics ; Case-Control Studies ; Female ; Gene Frequency/genetics ; Genotype ; Humans ; Hypertension/genetics ; Male ; Mexico ; Peptidyl-Dipeptidase A/genetics ; Polymorphism, Genetic/genetics ; Polymorphism, Restriction Fragment Length/genetics ; Renin-Angiotensin System/genetics ; Risk Factors ; Stroke/genetics
    Chemical Substances AGT protein, human ; Angiotensinogen (11002-13-4) ; ACE protein, human (EC 3.4.15.1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1)
    Language English
    Publishing date 2018-12-04
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2018.11.080
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