ABSTRACT
Introduction: Myocardial infarction with non-obstructive coronary arteries (MINOCA) has become an increasingly recognized subgroup in patients with acute myocardial infarction, with a recent cohort study reporting a prevalence of 8.8%. This report describes a patient who presented with non-ST-segment elevation myocardial infarction (NSTEMI) due to an incidental anterior mediastinal mass. Case presentation: An 80-year-old woman presented to our emergency department with a chief complaint of progressive shortness of breath associated with retrosternal chest pain for one day duration. Computed tomography (CT) angiogram of the chest was conducted, which revealed an anterior mediastinal mass. Upon admission, the patient developed an acute episode of recurrent severe chest pain, which was diagnosed as an NSTEMI. Emergent cardiac catheterization was performed because of unstable vital signs; however, the results showed no evidence of atherosclerotic changes in the major coronary arteries, compatible with the diagnosis of MINOCA. The mediastinal mass was later confirmed to be a type A thymoma on CT-guided biopsy. Conclusion: Myocardial infarction in patent coronary arteries due to an anterior mediastinal mass is rare. Further studies are needed to standardize the diagnosis and management protocols for the potential etiologies of MINOCA.
ABSTRACT
As the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus continues to infect patients globally, vaccination remains one of the primary methods to combat this prolonged pandemic. However, there are growing reports of coronavirus disease 2019 (COVID-19) vaccines possibly triggering autoimmunity, irrespective of the vaccine's design. This phenomenon has been observed in patients with vitiligo, with a rising number of cases reporting new-onset or worsening vitiligo following COVID-19 vaccinations. In this study, the authors present the most extensive case series of COVID-19 vaccine-associated vitiligo to date, along with a systematic review of the literature. The aim is to assist physicians in the clinical evaluation of patients with vitiligo with regard to future vaccinations.
Subject(s)
COVID-19 , Hypopigmentation , Vitiligo , Humans , Vitiligo/chemically induced , COVID-19 Vaccines/adverse effects , Cross-Sectional Studies , Tertiary Care Centers , COVID-19/epidemiology , COVID-19/prevention & control , SARS-CoV-2 , Vaccination/adverse effectsABSTRACT
Transient receptor potential canonical 7 (TRPC7) has been reported to mediate aging-associated tumorigenesis, but the role of TRPC7 in cancer malignancy is still unclear. TRPC7 is associated with tumor size in patients with lung adenocarcinoma and the present study further evaluated the underlying mechanism of TRPC7 in the regulation of cancer progression. The clinicopathological role of TRPC7 was assessed using immunohistochemistry staining and the pathological mechanism of TRPC7 in lung adenocarcinoma cells was determined using cell cycle examination, invasion and calcium response assays, and immunoblot analysis. The results indicated that high TRPC7 expression was associated with a lower 5-year survival rate compared with low TRPC7 expression, which suggested that TRPC7 expression was inversely associated with overall survival in patients with lung adenocarcinoma. TRPC7 serves a pathological role by facilitating the enhancement of cell growth and migration with increased phosphorylation of Ca2+/calmodulin-dependent protein kinase II, AKT and ERK. TRPC7 knockdown in lung adenocarcinoma cells restrained cell cycle progression and cell migration by interrupting the TRPC7-mediated Ca2+ signaling-dependent AKT and MAPK signaling pathways. These findings demonstrated for the first time a role of oncogenic TRPC7 in the regulation of cancer malignancy and could provide a novel therapeutic molecular target for patients with lung adenocarcinoma.
ABSTRACT
Aging, cancer, and longevity have been linked to intracellular Ca2+ signaling and nociceptive transient receptor potential (TRP) channels. We found that TRP canonical 7 (TRPC7) is a nociceptive mechanoreceptor and that TRPC7 channels specifically mediate the initiation of ultraviolet B (UVB)-induced skin aging and tumor development due to p53 gene family mutations. Within 30 min after UVB irradiation, TRPC7 mediated UVB-induced Ca2+ influx and the subsequent production of reactive oxygen species in skin cells. Notably, this function was unique to TRPC7 and was not observed for other TRP channels. In TRPC7 knockout mice, we did not observe the significant UVB-associated pathology seen in wild-type mice, including epidermal thickening, abnormal keratinocyte differentiation, and DNA damage response activation. TRPC7 knockout mice also had significantly fewer UVB-induced cancerous tumors than did wild-type mice, and UVB-induced p53 gene family mutations were prevented in TRPC7 knockout mice. These results indicate that TRPC7 activity is pivotal in the initiation of UVB-induced skin aging and tumorigenesis and that the reduction in TRPC7 activity suppresses the UVB-induced aging process and tumor development. Our findings support that TRPC7 is a potential tumor initiator gene and that it causes cell aging and genomic instability, followed by a change in the activity of proto-oncogenes and tumor suppressor genes to promote tumorigenesis.
