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Nanoparticles (NPs) have gained recognition for diagnosis, drug delivery, and therapy in fatal diseases. This review focuses on the benefits of green synthesis of bioinspired NPs using various plant extract (containing various biomolecules such as sugars, proteins, and other phytochemical compounds) and their therapeutic application in cardiovascular diseases (CVDs). Multiple factors including inflammation, mitochondrial and cardiomyocyte mutations, endothelial cell apoptosis, and administration of non-cardiac drugs, can trigger the cause of cardiac disorders. Furthermore, the interruption of reactive oxygen species (ROS) synchronization from mitochondria causes oxidative stress in the cardiac system, leading to chronic diseases such as atherosclerosis and myocardial infarction. NPs can decrease the interaction with biomolecules and prevent the incitement of ROS. Understanding this mechanism can pave the way for using green synthesized elemental NPs to reduce the risk of CVD. This review delivers information on the different methods, classifications, mechanisms and benefits of using NPs, as well as the formation and progression of CVDs and their effects on the body., Competing Interests: Declaration of competing interest The authors declare that they do not have any conflicts of interest., (Copyright © 2023. Published by Elsevier B.V.)

Systemic sclerosis (SSc), the most lethal of rheumatologic conditions, is the cause of death in >50% of SSc cases, led by pulmonary fibrosis followed by pulmonary hypertension and then scleroderma renal crisis (SRC). Multiple other preventable and treatable SSc-related vascular, cardiac, gastrointestinal, nutritional and musculoskeletal complications can lead to disability and death. Vascular injury with subsequent inflammation transforming to irreversible fibrosis and permanent damage characterizes SSc. Organ involvement is often present early in the disease course of SSc, but requires careful history-taking and vigilance in screening to detect. Inflammation is potentially reversible provided that treatment intensity quells inflammation and other immune mechanisms. In any SSc phenotype, opportunities for early treatment are prone to be under-utilized, especially in slowly progressive phenotypes that, in contrast to severe progressive ILD, indolently accrue irreversible organ damage resulting in later-stage life-limiting complications such as pulmonary hypertension, cardiac involvement, and malnutrition. A single SSc patient visit often requires much more physician and staff time, organization, vigilance, and direct management for multiple organ systems compared to other rheumatic or pulmonary diseases. Efficiency and efficacy of comprehensive SSc care enlists trending of symptoms and bio-data. Financial sustainability of SSc care benefits from understanding insurance reimbursement and health system allocation policies for complex patients. Sharing care between recognised SSc centers and local cardiology/pulmonary/rheumatology/gastroenterology colleagues may prevent complications and poor outcomes, while providing support to local specialists. As scleroderma specialists, we offer a practical framework with tools to facilitate an optimal, comprehensive and sustainable approach to SSc care. Improved health outcomes in SSc relies upon recogntion, management and, to the extent possible, prevention of SSc and treatment-related complications., Competing Interests: Declaration of competing interest None of the authors have conflicts of interest to report that are related to the reported content of this paper., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Genetic defects in matriptase are linked to two congenital ichthyoses: autosomal recessive ichthyosis with hypotrichosis (ARIH, OMIM 610765) and ichthyosis, follicular atrophoderma, hypotrichosis, and hypohidrosis (IFAH, OMIM 602400). Mouse models with matriptase deficiency indicate an involvement of matriptase in suprabasal keratinocytes in the maintenance of the epidermal barrier. In contrast to what has been reported for mouse skin, we show that in human skin matriptase is primarily expressed in the basal and spinous keratinocytes, but not in the more differentiated keratinocytes of the granular layer. In addition, matriptase zymogen activation was predominantly detected in the basal cells. Furthermore, by using skin organotypic cultures as a model system to monitor the course of human epidermal differentiation, we found elevated matriptase zymogen activation during early stages of epidermal differentiation, coupled with a loss of matriptase expression in the late stages of this process. We also show here that matriptase deficiency in HaCaT cells modestly reduces cell proliferation and temporally affects calcium-induced expression of differentiation markers. These collective data suggest that, unlike mouse matriptase, human matriptase may be involved in the regulation of keratinocyte growth and early differentiation, rather than terminal differentiation, providing mechanistic insights into the pathology of the two congenital ichthyoses: ARIH and IFAH.

Muslin wrapping is a commonly utilized alternative technique in the treatment of aneurysms that are not amenable to direct clipping. In this case report, we describe two patients from different institutions who both required aneurysm wrapping with gauze/muslin for aneurysm reinforcement. Both patients developed an inflammatory foreign body response to muslin visible on MRI that resulted in a vasculitic stenosis. The onset of TIAs was at 6 months and 1 month postoperatively, respectively. The stenoses rapidly progressed to near occlusion despite antiplatelet therapy, and in one case, an aggressive corticosteroid regimen. One patient eventually developed leptomeningeal collateral flow that allowed tolerance of the stenosis, while the other patient required microsurgical bypass. These cases reports are the first to our knowledge that describe the adverse effects of muslin wrapping without adhesive reinforcement, as well as one of few reports to include follow-up angiographic imaging., (Copyright © 2011 Elsevier B.V. All rights reserved.)