A Rule of Thumb for Evaluating Surface Areas of Chronic Wounds.

BACKGROUND: Rapid estimation of the area of chronic wounds is clinically important. A simple method using the thumb was investigated for universal physical measurement, particularly of small and multiple wounds; the thumb surface area (TSA) was then compared with the total body surface area (TBSA). METHODS: A cross-sectional observational study and random sampling were used to obtain the characteristics of 343 participants. Data related to handprint surface area of the thumb and palm were collected using a scanner and laptop and assessed using image software. The TSA as a percentage of TBSA was confirmed based on the traditional rule that regards palmar surface area as 1% of TBSA. Information on factors potentially influencing measurement was gathered with questionnaires to analyze correlations. RESULTS: The left and right TSAs were on average 4.27% and 4.28%, respectively, of the palmar surface area for all participants. Multiple linear regression analysis found that male and older participants had higher TSA:TBSA proportions (sex, P = .0020; age, P < .0001). The TSA:TBSA proportion increased by age for both males (by age group, 0.0418%, 0.0426%, 0.0432%, and 0.0460%, respectively) and females (0.0400%, 0.0409%, 0.0427%, and 0.0430%, respectively). CONCLUSIONS: Thumb size is relatively stable in relation to TBSA, lending itself to a universal method for estimating the size of chronic wounds as a percentage of TBSA. It therefore represents a convenient physical measurement for assessing the area of burns and other wounds.

Klotho-derived peptide KP1 ameliorates SARS-CoV-2-associated acute kidney injury.

Introduction: The severe cases of COVID-19, a disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), often present with acute kidney injury (AKI). Although old age and preexisting medical conditions have been identified as principal risk factors for COVID-19-associated AKI, the molecular basis behind such a connection remains unknown. In this study, we investigated the pathogenic role of Klotho deficiency in COVID-19-associated AKI and explored the therapeutic potential of Klotho-derived peptide 1 (KP1). Methods: We assessed the susceptibility of Klotho deficient Kl/Kl mice to developing AKI after expression of SARS-CoV-2 N protein. The role of KP1 in ameliorating tubular injury was investigated by using cultured proximal tubular cells (HK-2) in vitro and mouse model of ischemia-reperfusion injury (IRI) in vivo. Results: Renal Klotho expression was markedly downregulated in various chronic kidney disease (CKD) models and in aged mice. Compared to wild-type counterparts, mutant KL/KL mice were susceptible to overexpression of SARS-CoV-2 N protein and developed kidney lesions resembling AKI. In vitro, expression of N protein alone induced HK-2 cells to express markers of tubular injury, cellular senescence, apoptosis and epithelial-mesenchymal transition, whereas both KP1 and Klotho abolished these lesions. Furthermore, KP1 mitigated kidney dysfunction, alleviated tubular injury and inhibited apoptosis in AKI model induced by IRI and N protein. Conclusion: These findings suggest that Klotho deficiency is a key determinant of developing COVID-19-associated AKI. As such, KP1, a small peptide recapitulating Klotho function, could be an effective therapeutic for alleviating AKI in COVID-19 patients.