8 results match your criteria: "Barrow Neurological Institute. Phoenix. AZ[Affiliation]"

Mitochondrial fission inhibition protects against hypertension induced by angiotensin II.

Hypertens Res

May 2024

Department of Cardiovascular Science and Sol Sherry Thrombosis Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA.

Article Synopsis
  • Mitochondrial dysfunction plays a role in cardiovascular diseases, especially hypertension, with a focus on the balance of mitochondrial fission and fusion.
  • In a study using C57BL6 mice, the mitochondrial fission inhibitor mdivi1 was shown to reduce hypertension and related vascular changes induced by angiotensin II.
  • Mdivi1 not only limited vessel fibrosis and hypertrophy but also improved mitochondrial structure and reduced cardiac hypertrophy and vascular reactivity associated with angiotensin II treatment, indicating multiple protective mechanisms in the vasculature.
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Intracranial aneurysms (IAs) are rare vascular lesions that are more frequently found in women. The pathophysiology behind the formation and growth of IAs is complex. Hence, to date, no single pharmacological option exists to treat them.

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Background Familial cerebral cavernous alformation (CCM) is an autosomal dominant disease caused by mutations in , , or . Cases typically present with multiple lesions, strong family history, and neurological symptoms, including seizures, headaches, or other deficits. Intracranial hemorrhage (ICH) is a severe manifestation of CCM, which can lead to death or long-term neurological deficits.

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Background Investigations into alternative treatments for hypertension are necessary because current treatments cannot fully reduce the risk for the development of cardiovascular diseases. Chronic activation of unfolded protein response attributable to the endoplasmic reticulum stress has been proposed as a potential therapeutic target for hypertension and associated vascular remodeling. Triggered by the accumulation of misfolded proteins, chronic unfolded protein response leads to downstream signaling of cellular inflammation and dysfunction.

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Introduction: We examined the association between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) and hypothesized that diabetes is associated with an increased pathological burden in clinically and pathologically diagnosed AD.

Methods: All data were obtained from the Uniform Data Set (UDS) v3, the Neuropathology Data Set, and the Researcher's Data Dictionary-Genetic Data from the National Alzheimer's Coordinating Center. The dataset (37 cases with diabetes and 1158 cases without) relies on autopsy-confirmed data in clinically diagnosed AD patients who were assessed for diabetes type in form A5 or D2 during at least one visit.

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Article Synopsis
  • Eculizumab has shown effectiveness in treating AChR-positive generalized myasthenia gravis (gMG) patients, but its impact on MGFA class V gMG patients is not well-studied.
  • Three refractory MGFA class V gMG patients were treated with eculizumab, with two showing significant improvement in symptoms, while the third had a partial response.
  • The findings suggest that eculizumab may be beneficial for class V patients, but more extensive research is needed to confirm its efficacy and understand its role in treatment.
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Article Synopsis
  • Hereditary hemorrhagic telangiectasia (HHT) is a genetic disorder characterized by vascular malformations, caused by mutations in genes like ENG, ACVRL1, and SMAD4.
  • Animal models with ENG and ACVRL1 mutations replicate HHT symptoms, but there has been a lack of models for SMAD4 mutations.
  • This study introduces Smad4-inducible knockout (iKO) mice, which exhibit gastrointestinal bleeding and arteriovenous malformations similar to existing models, confirming the importance of SMAD signaling in vascular formation and offering a new avenue for HHT research.
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Background: Clinical diagnostic criteria for PD rely on rest tremor, bradykinesia, and rigidity. These features are non-specific and neuropathological confirmation remains the gold standard for diagnosis. This study presents data on clinical certainty ratings in autopsy-proven PD.

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