Mellisa Renteria

Background/Objectives: Cerebral cavernous malformations (CCMs) are neurological disorders that increase the risk of hemorrhagic stroke. The Mexican Hispanic population has a higher prevalence of both CCMs and metabolic syndrome (MetS), defined by the presence of three or more of the following: central obesity, elevated triglycerides, low HDL, dyslipidemia, hypertension, or elevated fasting glucose. MetS is also associated with an increased risk of hemorrhagic stroke. However, the connection between MetS and hemorrhagic stroke in Hispanic CCM patients remains uncertain. Additionally, it is unclear if Hispanic CCM patients have different cardiometabolic profiles compared to controls. Methods: We analyzed a retrospective cohort of Mexican Hispanic adult CCM patients, including age- and gender-matched controls from the NHANES database. Fisher’s exact test or an unpaired Student’s t-test was used to compare risk factors between the CCM cohort and controls. Additionally, we conducted relative risk regression analysis to assess the adjusted association of MetS with hemorrhagic stroke. Results: The CCM cohort showed higher rates of epilepsy (24.6% vs. 1.6%, p < 0.001) and hemorrhagic stroke (36.6% vs. 3.6%, p < 0.001), but a lower prevalence of MetS (14% vs. 54.8%, p < 0.001) compared to age- and gender-matched Mexican Hispanic controls. The adjusted analysis revealed that among CCM patients in the older age group (age ≥ 50 years), MetS was associated with hemorrhagic stroke (RR = 2.38, 95%CI: 1.40–4.02, p = 0.001). Conclusions: This study reveals distinct features of CCMs in the Mexican Hispanic population, indicating a higher risk of hemorrhagic stroke and epilepsy compared to other ethnic groups. To mitigate the risk of hemorrhagic stroke, controlling blood pressure and managing comorbidities like metabolic syndrome (MetS) and epilepsy are essential, particularly in CCM patients aged 50 years and above.

It is well-known that serum and cellular concentrations of zinc are altered in breast cancer patients. Specifically, there are notable zinc hyper-aggregates in breast tumor cells when compared to normal mammary epithelial cells. However, the mechanisms responsible for zinc accumulation and the consequences of zinc dysregulation are poorly understood. In this review, we detailed cellular zinc regulation/dysregulation under the influence of varying levels of sex steroids and breast cancer tumorigenesis to try to better understand the intricate relationship between these factors based on our current understanding of the CmPn/CmP signaling network. We also made some efforts to propose a relationship between zinc signaling and the CmPn/CmP signaling network.