The coronavirus disease 2019 (COVID-19) is a pandemic disease, originated in Wuhan City, China. It is caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) and its biology is still poorly understood. Currently, there are no vaccines and drugs/or agents that can reduce severity of this new disease. Recent data suggest that patients with age-related comorbidities, including cardiovascular disease, diabetes, obesity, hypertension, chronic kidney disease, and dementia are highly susceptible to severe respiratory illness due to coronavirus infection. Recent research also revealed that aged individuals with elevated baseline inflammation cause defects in T and B cells, leading to decreased body’s immune response to viral infection. In the current article, we discuss the effects of SARS-CoV-2 on age-related chronic diseases, such as diabetes, obesity, and Alzheimer’s disease. Our article also highlights the interaction between coronavirus and immune cells, and how COVID-19 alters mitochondrial activities in host cells. Based on new and compelling evidence, we propose that mitochondrial fission is inhibited while fusion is promoted, causing mitochondrial elongation and providing a receptive intracellular environment for viral replication in infected cells. Further research is still needed to understand the cross talk between viral replication in mitochondria and disease progression in patients with COVID-19.
Background Although laparoscopic cholecystectomy is one of the most common operations performed, there is no consensus on the best surgical approach when inflammation obscures hepatocystic anatomy in severe cholecystitis. Traditionally, this situation triggered conversion to open cholecystectomy (COC); however, in recent decades, alternative approaches have been described. We compared outcomes of bailout procedures for severe cholecystitis, primarily focusing on COC versus laparoscopic subtotal cholecystectomy (LSTC). Study Design Retrospective review comparing outcomes of intended laparoscopic cholecystectomy cases that were converted to bailout procedures between 2015–2020 at a single institution. Bailout procedures were categorized into LSTC and COC groups. Demographics, clinical presentation, time to surgery, operative indications, operative duration, and post-operative outcomes were compared using independent sample t-tests with Welch-Satterthwaite correction or Wilcoxon rank-sum tests (continuous variables) or Fisher’s exact/χ2 tests. A P-value of less than .05 was considered significant. Results Final analysis included 158 subjects: 55 LSTC and 99 COC. Patient demographics and clinical presentations were similar between groups. LSTC had shorter operative time, fewer ICU admissions, and shorter length of stay than COC ( P < .05). There were 9 (9.2%) cases of ileus, 4 (4.0%) cases of post-operative bleeding, and 2 (2.0%) cases of bile duct injury in COC. There was 1 (1.8%) case of ileus, 1 (1.8%) case of post-operative bleeding, and no bile duct injury in LSTC. Conclusion LSTC was associated with fewer complications than COC, which had higher rates of biliary injury, bleeding, ileus, ICU admission, and longer hospital stay.
Purpose The negative correlation between BPH-size and incidence of prostate cancer (PCa) is well-documented in the literature, however the exact mechanism is not well-understood. The present study uses histo-anatomical imaging to study prostate volume in correlation to prostate capsule thickness, and glandular epithelial cell density within the peripheral zone (PZ). Materials and Methods Specimens were selected from radical prostatectomies ranging from 20 to 160 mL based on ease of anatomical reconstruction by the slides. A total of 60 patients were selected and underwent quantitative measurements of prostate capsule thickness and glandular epithelial density within the PZ using computer-based imaging software. Pearson's correlation and a stepwise multiple linear regression analysis was conducted to determine the relationship between these measured parameters and the clinical characteristic of these patients. Results Pearson's correlation analysis revealed a strongly significant, negative correlation between prostate volume and glandular epithelial cell density (r(58)=−0.554, p<0.001), and a strongly significant, positive correlation between prostate volume and average capsule thickness (r(58)=0.462, p<0.001). Results of multiple regression analysis showed that average glandular epithelial cell density added statistically to this prediction (p<0.05). Conclusions The results suggest that growth of the transition zone in BPH causes increased fibrosis of the PZ, leading to atrophy and fibrosis of glandular cells. As 80% of PCa originates from the glandular epithelium within the PZ, this observed phenomenon may explain the inverse correlation between BPH and PCa that is well-documented in the literature.
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