No abstract

To develop wearable and implantable bioelectronics accommodating the dynamic and uneven biological tissues and reducing undesired immune responses, it is critical to adopt batteries with matched mechanical properties with tissues as power sources. However, the batteries available cannot reach the softness of tissues due to the high Young's moduli of components (e.g., metals, carbon materials, conductive polymers, or composite materials). The fabrication of tissue‐like soft batteries thus remains a challenge. Here, the first ultrasoft batteries totally based on hydrogels are reported. The ultrasoft batteries exhibit Young's moduli of 80 kPa, perfectly matching skin and organs (e.g., heart). The high specific capacities of 82 mAh g−1 in all‐hydrogel lithium‐ion batteries and 370 mAh g−1 in all‐hydrogel zinc‐ion batteries at a current density of 0.5 A g−1 are achieved. Both high stability and biocompatibility of the all‐hydrogel batteries have been demonstrated upon the applications of wearable and implantable. This work illuminates a pathway for designing power sources for wearable and implantable electronics with matched mechanical properties.

With the rapid advances in safe, flexible, and even stretchable electronic products, it is important to develop matching energy storage devices to more effectively power them. However, the use of conventional liquid electrolytes produces volatilization and leakage that are dangerous and requires strict packaging layers that are typically rigid. To this end, solid electrolytes that can overcome these problems have attracted increasing attention in recent decades. In this review article, three main types of solid electrolytes (i.e., inorganic, polymer, and composite electrolytes) are first described and compared in terms of their structures and properties. The advantages of solid electrolytes to make safe, flexible, stretchable, wearable, and self‐healing energy storage devices, including supercapacitors and batteries, are then discussed. The remaining challenges and possible directions are finally summarized to highlight future development in this field.

We have performed a study aimed at investigating the critical concentration of urinary cadmium (UCd) required for the development of renal dysfunction. We studied population groups (totally 790 persons) living in two cadmium exposed areas and one control area in China. UCd, was determined as an indicator of cadmium exposure and accumulation, while the concentrations of N-acetyl-beta-D-glucosaminidase (NAG), its iso-form B (NAG-B), beta2-microglobulin (B2M), retinol binding protein (RBP), and albumin (ALB) in urine were measured as indicators of the renal effects caused by cadmium. There was a significantly increased prevalence of hyperNAGuria, hyperNAG-Buria, hyperB2Muria, hyperRBPuria and hyperALBuria with increasing levels of Cd excretion in urine. We used the benchmark dose (BMD) procedure to estimate the critical concentration of urinary cadmium in this general population. The lower confidence limit of the BMD (LBMD-05) of urinary cadmium for a 5% level of risk above the background level was estimated for each of the renal effect indicators. The BMD-05/LBMD-05 were estimated to be 4.46/3.99, 6.70/5.87, 8.36/7.31, 7.98/6.98 and 15.06/12.18 microg/g creatinine for urinary NAG-B, NAG, B2M, RBP and ALB, respectively. Our findings suggest, based on the present study, that the Lower Confidence Limit of the Population Critical Concentration of UCd (LPCCUCd-05) of tubular dysfunction for 5% excess risk level above the background may be ca. 3-4 microg/g creatinine, and that cadmium concentration in urine should be kept below this level to prevent renal tubular damage. This report is the first to use the BMD method in this field and to define the concept of critical concentration in urine.

To evaluate chronic loss of lung function in cotton dust-exposed workers, a 5-yr follow-up study was performed in Shanghai, China from 1981 to 1986. Workers at a nearby silk thread manufacturing mill were used as a control population. There were 384 cotton textile workers restudied from an original group of 446, and 403 silk workers restudied from the original 468. The presence of byssinosis among retested cotton workers at the time of first survey was 7.3%. The prevalence of byssinosis was 9.7% at the initial survey among those lost to follow-up. No byssinosis was found among control subjects. The mean annual decline in FEV1 was 39.5 ml among cotton workers and 30.6 ml for silk workers (p < 0.05). The greatest annual decrements were found among smoking cotton workers, but nonsmoking cotton workers also lost lung function at a faster rate than silk nonsmokers (annual loss = 33.3 ml versus 24.4 ml, respectively). Autoregressive modeling revealed that after adjustments for age, sex, height, and smoking, cotton dust exposure was significantly associated with decline in FEV1. Moreover, across-shift drop of 5% or more at the time of first survey was predictive of 5-yr decline in FEV1. Cotton workers who had an acute response (5% or greater drop in FEV1 at the time of first survey) suffered a 57.0 ml/yr FEV1 drop compared with a 35.1-ml drop among cotton workers with less acute response at baseline (p < 0.01). Silk workers with or without 5% across-shift drops had similar annual rates of decline (-33.8 ml and -36.1 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Cadmium, an environmental pollutant, can have adverse effects on the human body. The kidney is the critical organ. In order to improve the understanding of the dose-response relationship between cadmium exposure and health effects, and especially renal dysfunction, a study on a general population group in China was performed. This study was therefore concerned with cadmium exposure biomarkers, such as the concentrations in blood (BCd) and urine (UCd), and effect biomarkers of renal dysfunction, such as beta2-microglobulin (beta2m), retinol binding protein (RBP) and albumin (ALB). To improve the evaluation of exposure levels in relation to the adverse health effects of cadmium exposure in the general population, a quality control program was conducted to determine analytical quality in the determination of cadmium in blood and urine and for beta2m, creatinine, ALB and RBP. The measurements showed that analytical quality was adequate. The exposure and effect biomarkers were studied in the population groups living in three areas, namely a control area and two Cd polluted areas. In the highly exposed area, most of the BCd values were higher than 5 microg/l and most of the UCd values were higher than 5 microg/g creatinine. Beta2-microglobulin, retinol binding protein, and albumin in urine were all significantly higher in the population living in the heavily polluted area than in that in the control area. Based on data from all three areas, a marked dose-response relationship between UCd or BCd and the prevalence of renal dysfunction was demonstrated. The number of abnormalities in kidney was related to the level of cadmium exposure. Only one index of renal tubular dysfunction was affected in subjects exposed to low levels of cadmium, but more than two indices of renal function were affected in those exposed to high levels.

No abstract

Urinary beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase have been recommended as sensitive indicators of renal dysfunction induced by cadmium. However, an increase in urinary calcium in early renal damage induced by cadmium has been reported both in humans and in animal experiments. To investigate the feasibility of using urinary calcium as a biomarker of renal dysfunction induced by cadmium, two areas were selected in this study, namely, a polluted area with a 3.71 mg/kg cadmium concentration in rice and a control area with a 0.07 mg/kg cadmium concentration. The total number of participants was 499, made up of 252 in the control group and 247 from the cadmium-polluted area. Urinary cadmium, urinary calcium, and zinc concentrations were measured by atomic absorption spectrometry, and beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase in urine were analyzed. The levels of urinary cadmium and urinary calcium in persons from the exposed area were significantly higher (P < 0.05) than those in the control area for both men and women, but there was no significant difference regarding urinary zinc between the two areas. A significant dose-response relationship between the prevalence of hypercalciuria and the excretion of urinary cadmium was observed, and a significantly increased prevalence of calciuria was found when excretion of urinary cadmium exceeded 2 micrograms/g creatinine. The findings were similar to those for excess urinary secretion of beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. Because cadmium can affect Ca2+ uptake by tubular cells, with decreased renal Ca2+ reabsorption, calciuria may reflect tubular cell damage caused by cadmium. It was concluded that cadmium exposure can result in increased excretion of urinary calcium in a general population and that there is a significant dose-response relationship. Urinary calcium can therefore be used as a biomarker of renal dysfunction induced by cadmium.