Correction: Detection of airborne pathogens with single photon counting and a real-time spectrometer on microfluidics.

Correction for 'Detection of airborne pathogens with single photon counting and a real-time spectrometer on microfluidics' by Ning Yang et al., Lab Chip, 2022, https://doi.org/10.1039/D2LC00934J.

Detection of airborne pathogens with single photon counting and a real-time spectrometer on microfluidics.

The common practice for monitoring pathogenic bioaerosols is to collect bioaerosols from air and then detect them, which lacks timeliness and accuracy. In order to improve the detection speed, here we demonstrate an innovative airflow-based optical detection method for directly identifying aerosol pathogens, and built a microfluidic-based counter composite spectrometer detection platform, which simplifies sample preparation and collection detection from two steps to one step. The method is based on principal component analysis and partial least squares discriminant analysis for particle species identification and dynamic transmission spectroscopy analysis, and single-photon measurement is used for particle counting. Compared with traditional microscopic counting and identification methods, the particle counting accuracy is high, the standard deviation is small, and the counting accuracy exceeds 92.2%. The setup of dynamic transmission spectroscopy analysis provides high-precision real-time particle identification with an accuracy rate of 93.75%. As the system is further refined, we also foresee potential applications of this method in agricultural disease control, environmental control, and infectious disease control in aerosol pathogen detection.

Reliability and validity of a modified 8-item Morisky Medication Adherence Scale in patients with chronic pain.

BACKGROUND: The 8-item Morisky Medication Adherence Scale (MMAS-8) is a simple, economic and easy tool to evaluate the medication compliance of chronic disease. The reliability and validity of the MMAS-8 in patients with chronic pain were unclear. Therefore, we aimed to validate the MMAS-8 for detecting nonadherent patients with chronic pain. METHODS: A modified MMAS-8 was used to assess the medication compliance of patients with chronic pain who were treated at our hospital from July 2018 to October 2018. Cronbach's α was used to evaluate the internal consistency, and a factor analysis was used to examine the construct validity. Convergent validity was assessed by comparing the MMAS-8 and a medication adherence visual analog score (MA-VAS) through Pearson's correlation coefficient. RESULTS: A total of 113 patients were evaluated. The (t-test) results revealed that there was a significant difference in average scores between the low-score group (who scored less than 5 points) and the high-score group (who scored 8 points or above), indicating that the scale displayed a good degree of discrimination. Except for Items 4 and 5, all the other items exhibited a good correlation with the total score (correlation coefficient >0.5; P<0.05). The Cronbach's α coefficient was 0.625, indicating that the scale's internal consistency was relatively satisfactory. Two common factors, which explained 62.978% of the total variance, were extracted by factor analysis to examine the construct validity of the MMAS-8, and the load of the 6 items was greater than 0.4. The Pearson correlation coefficient was 0.845 (P<0.001); thus, convergent validity was high. CONCLUSIONS: The modified MMAS-8 exhibited acceptable reliability and validity in evaluating medication compliance in patients with chronic pain; thus, it can be applied to detect nonadherent patients with chronic pain.

Temperature Tolerance Electric Cell-Substrate Impedance Sensing for Joint Assessment of Cell Viability and Vitality.

Evaluation of the cell health status is critical for drug screening and cell physiological activity investigations. The existing cell health assessment methods are solely devoted to the study of cell vitality or viability, leading to an incomplete evaluation. Herein, we report a convenient and robust method for the joint assessment of cell viability and vitality based on electric cell-substrate impedance sensing (ECIS) supplied with an environmental temperature control. The static value of electric cell-substrate impedance reflects the survival rate of cells, while the temperature tolerance of cells demonstrates the cell vitality. It was found that the cell vitality evaluated by the temperature tolerance of cells was independent of the initial cell numbers, rendering the proposed method easy to utilize in various applications. We compared the temperature tolerance ECIS method with the traditional trypan blue staining method, the methyl thiazolyl tetrazolium assay, and the direct impedance sensing method for joint evaluation of cell viability and vitality in drug screening. The temperature tolerance ECIS method showed comparable results but with a simpler protocol, faster results, and less dependence on the sample conditions. By providing both information on cell viability and cell vitality, the proposed temperature tolerance ECIS method would pave the way in building a simple and robust sensing system for cell health evaluation.

Pyrazinamide Induced Rat Cholestatic Liver Injury through Inhibition of FXR Regulatory Effect on Bile Acid Synthesis and Transport.

Pyrazinamide (PZA) is an indispensable first-line drug used for the treatment of tuberculosis which may cause serious hepatotoxicity; however, the mechanisms underlying these toxicities are poorly understood. Cholestasis plays an important role in drug-induced liver injury. Since there were no previous published works reported cholestasis and PZA hepatotoxicity relationship, this study aimed to identify whether PZA can induce liver injury with characterized evidences of cholestasis and to clarify expression changes of proteins related to both bile acid synthesis and transport in PZA-induced liver injury. PZA (2 g/kg) was administered for 7 consecutive days by oral gavage. Results showed there were 2-fold elevation in both ALT and AST serum levels in PZA-treated rats. In addition, a 10-fold increment in serum total bile acid was observed after PZA administration. The mRNA and protein expressions of bile acid synthesis and transport parameters were markedly altered, in which FXR, Bsep, Mrp2, Mdr2, Ostα/ß, Oatp1a1, Oatp1b2, and Cyp8b1 were decreased (P < .05), while Mrp3, Ntcp, Oatp1a4, and Cyp7a1 were increased (P < .05). Moreover, treatment with the FXR agonist obeticholic acid (OCA) generated obvious reductions in serum ALT, AST, and TBA levels in PZA-treated rats. Those effects were due to transcriptional regulation of pre-mentioned target genes by OCA. Taken together, these results suggested that PZA-induced cholestatic liver injury was related to FXR inhibition, leading to the dysfunction in bile acid synthesis and transport.

Emodin ameliorates hepatic steatosis through endoplasmic reticulum-stress sterol regulatory element-binding protein 1c pathway in liquid fructose-feeding rats.

AIM: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by liquid fructose-feeding in rats and the possible underlying mechanisms. METHODS: Sprague-Dawley rats were divided into the control, fructose-feeding group, and three fructose-feeding groups treated with 40, 80 and 160 mg/kg emodin, respectively. After 4 weeks of feeding, liquid consumption, food intake, bodyweight, liver index, serum triglyceride (TG), glucose and aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), liver TG contents and histology features were examined. The hepatic expression of lipogenic and fatty acid oxidation key enzymes, and an upstream transcriptional factor, sterol regulatory element-binding protein 1c (SREBP1c) were determined. Glucose regulated protein 78 (GRP78), a liver endoplasmic reticulum stress (ERS) marker and the unfolded protein response (UPR) related proteins were also measured. RESULTS: Emodin reduced bodyweight, liver index, serum TG levels of fructose-feeding rats with no significant difference in serum glucose, AST and ALT levels. Emodin improved hepatic steatosis by inhibiting SREBP1c activation and its target genes, and enhancing carnitine palmitoyltransferase 1 expression in fructose-feeding rats. Emodin resolved hepatic ERS and the UPR induced by liquid fructose in rats. CONCLUSION: Emodin is capable of improving the lipid accumulation through the ERS-SREBP1c pathway in fructose-induced non-alcoholic fatty liver disease.