The primary antiphospholipid syndrome and protein S deficiency are known hypercoagulable states predisposing to ischemic strokes. The pathogenesis of those hypercoagulable states has been independently studied and, recently, interaction between them has been proposed. A 48-year-old Hispanic man had generalized seizures 5 months after the acute onset of a left middle cerebral artery infarct. He had a strong family history of strokes. After evaluation for cardiologic, rheumatologic, hematologic and metabolic etiologies for stroke, anticardiolipin antibodies and protein S deficiency were detected. Cerebral angiography was normal. First degree relatives were evaluated and screened for these conditions. Lupus anticoagulant was detected in a sister who reported a transient hemisensory deficit. None of the relatives studied had clinical or laboratory criteria for collagen vascular diseases. Coexistence of the primary antiphospholipid syndrome and protein S deficiency, two known prothrombotic states, has rarely been reported in Hispanic adults in association with ischemic stroke.
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http://dx.doi.org/10.1097/00007611-199803000-00020 | DOI Listing |
Sci Rep
January 2025
Department of Pharmacology and Experimental Therapeutics; MS 1015, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, Health Education Building; Room 282E, 3000 Arlington Ave, Toledo, OH, 43614, USA.
We previously demonstrated that the inability of primary endothelial cilia to sense fluid shear stress can lead to nitric oxide (NO) deficiency and cause hypertension (HTN). Decreased biosynthesis of NO contributes to cerebral amyloid angiopathy in Alzheimer's disease (AD) patients through increased deposition of amyloid beta (Aβ). However, the molecular mechanisms underlying the pathogenesis of HTN and AD are incompletely understood.
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Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Besides the important pathogenic mechanisms of melanoma, including BRAF-driven and immunosuppressive microenvironment, genomic instability and abnormal DNA double-strand breaks (DSB) repair are significant driving forces for its occurrence and development. This suggests investigating novel therapeutic strategies from the synthetic lethality perspective. Poly (ADP-ribose) polymerase 4 (PARP4) is known to be a member of the PARP protein family.
View Article and Find Full Text PDFBlood Cancer J
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Université de Toulouse 3 Paul Sabatier, Cancer Research Centre of Toulouse, UMR1037 Inserm, UMR5077 CNRS, Equipe Labellisée Ligue Nationale Contre le Cancer 2023, Equipe labélisée Institut Carnot Opale, 31037, Toulouse, France.
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View Article and Find Full Text PDFTransfus Apher Sci
January 2025
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Objectives: Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy associated with severe deficiency in ADAMTS13. ADAMTS13 deficiency may be secondary to absent or dysfunctional protein production due to mutations in the ADAMTS13 gene (congenital TTP) or autoantibody-mediated clearance and/or inhibition (immune-mediated TTP). This autoimmunity may, albeit rarely, occur secondary to certain medications (eg, ticlopidine).
View Article and Find Full Text PDFLife Sci Alliance
April 2025
School of Life Sciences, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea
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