Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid

AIM: Acute kidney injury (AKI) is common following deliberate self-poisoning with a combination washing powder containing oxalic acid (H2C2O4) and potassium permanganate (KMnO4). Early and rapid increases in serum creatinine (sCr) follow severe poisoning. We investigated the relationship of these increases with direct nephrotoxicity in an ongoing multicenter prospective cohort study in Sri Lanka exploring AKI following poisoning. METHODS: Multiple measures of change in kidney function were evaluated in 48 consenting patients who had serial sCr and serum cystatin C (sCysC) data available. RESULTS: Thirty-eight (38/48, 79%) patients developed AKI (AKIN criteria). Twenty-eight (58%) had AKIN stage 2 or 3. Initial increases in urine creatinine (uCr) excretion were followed by a substantial loss of renal function. The AKIN stage 2 and 3 (AKIN2/3) group had very rapid rises in sCr (a median of 118% at 24 h and by 400% at 72 h post ingestion). We excluded the possibility that the rapid rise resulted from the assay used or muscle damage. In contrast, the average sCysC increase was 65% by 72 h. CONCLUSIONS: In most AKI, sCysC increases to the same extent but more rapidly than sCr, as sCysC has a shorter half-life. This suggests either a reduction in Cystatin C production or, conversely, that the rapid early rise of sCr results from increased production of creatine and creatinine to meet energy demands following severe oxidative stress mediated by H2C2O4 and KMnO4. Increased early creatinine excretion supports the latter explanation, since creatinine excretion usually decreases transiently in AKIN2/3 from other causes.NHMRC Project grant 101177

Recent progresses in wearable triboelectric nanogenerators

Integrating electronics with clothing and the human body to support people's lifestyle is quickly becoming a reality. Some of these electronics, including health sensors, communication devices, and personal electronics, contain the potential to revolutionize life in the future. One of the most demanding aspects of such electronic designs is their power supply systems, which necessitate not only a continuous power supply, but also wearable characteristics and durability, which many conventional power-supply methods have failed to fulfill. The triboelectric nanogenerator (TENG), which depends on static charging between materials, can convert mechanical vibrations into electricity. TENGs are foreseen as a leading candidate to power wearable electronics due to their advantages such as high instantaneous power outputs and efficiency, low cost, ease of fabrication, lightweight, and wearability. This paper is a comprehensive review on the most prominent wearable TENG categories; textiles-based TENGs for clothing applications, footwear-incorporated TENG designs, and other TENG accessories. Herein, the most important developments in these categories, with a focus on their materials, fabrication, features, advantages, and drawbacks, are examined. Finally, a detailed analysis is provided on the main challenges impeding the progress of wearable TENGs with the insights into potential improvement techniques, targeting the widespread commercialization of this technology

Cardiac-specific overexpression of aldehyde dehydrogenase 2 exacerbates cardiac remodeling in response to pressure overload

Pathological cardiac remodeling during heart failure is associated with higher levels of lipid peroxidation products and lower abundance of several aldehyde detoxification enzymes, including aldehyde dehydrogenase 2 (ALDH2). An emerging idea that could explain these findings concerns the role of electrophilic species in redox signaling, which may be important for adaptive responses to stress or injury. The purpose of this study was to determine whether genetically increasing ALDH2 activity affects pressure overload-induced cardiac dysfunction. Mice subjected to transverse aortic constriction (TAC) for 12 weeks developed myocardial hypertrophy and cardiac dysfunction, which were associated with diminished ALDH2 expression and activity. Cardiac-specific expression of the human ALDH2 gene in mice augmented myocardial ALDH2 activity but did not improve cardiac function in response to pressure overload. After 12 weeks of TAC, ALDH2 transgenic mice had larger hearts than their wild-type littermates and lower capillary density. These findings show that overexpression of ALDH2 augments the hypertrophic response to pressure overload and imply that downregulation of ALDH2 may be an adaptive response to certain forms of cardiac pathology. Keywords: Heart failure, Hypertrophy, Oxidative stress, Aldehydes, Cardiac remodeling, Hormesi