Organic fertilizer is a major carrier that stores and transmits antibiotic resistance genes (ARGs). In the environment, due to the application of organic fertilizers in agriculture, the increasing diversity and abundance of ARGs poses a potential threat to human health and environmental safety. In this paper, the microbial community structure and ARGs in different types of organic fertilizer treated with composting were examined. We found that the abundance and diversity of ARGs in earthworm cast organic fertilizer were the lowest and the highest in chicken manure organic fertilizer. Interestingly, the abundance and diversity of ARGs, especially beta-lactam resistance genes, sulfonamide resistance genes, and macrolide-lincosamide-streptogramin B (MLSB) resistance genes, in organic fertilizers were reduced significantly, while composting caused no significant change in mobile genetic elements (MGEs), where antibiotic deactivation and the use of efflux pumps were the two most dominant mechanisms. It was clear that removal of ARGs became more efficient with increasing reduction in the bacterial abundances and diversity of potential ARG hosts, and integron-mediated horizontal gene transfers (HGTs) played an important role in the proliferation of most ARG types. Therefore, the reduction in ARGs was mainly driven by changes in bacterial community composition caused by composting. Furthermore, rather than HGTs, the diversity and abundance of bacterial communities affected by compost physical and chemical properties were the main drivers shaping and altering the abundance and diversity of ARGs, which was indicated by a correlation analysis of these properties, antibiotic residues, microbial community structure, and ARGs. In general, high-temperature composting effectively removed antibiotic residues and ARGs from these organic fertilizers; however, it cannot prevent the proliferation of MGEs. The insights gained from these results may be of assistance in the safe and rational use of organic fertilizers by indicating the changes in microbial community structure and ARGs in different types of organic fertilizer treated with composting.

To compensate radar reflectivity for attenuation effect, a new method for attenuation correction of the radar reflectivity using arbitrary oriented microwave link (referred henceforth to as ACML) is developed and evaluated. Referring to the measurement of arbitrary oriented microwave link, the ACML method optimizes the ratio of specific attenuation to specific differential phase which is a key parameter in attenuation correction schemes. The proposed method was evaluated using real data of a dual-polarization X-band radar and measurements of two microwave links during two rainstorm events. The results showed that the variation range of the optimized ratio was overall consistent with the results of the previous studies. After attenuation correction with the optimal ratios, the radar reflectivity was significantly compensated, especially at long distances. The corrected reflectivity was more intense than the reflectivity corrected by the "self-consistent" (SC) method and closer to the reflectivity of a nearby S-band radar. The effectiveness of the method was also verified by comparing the rain rates estimated by the X-band radar with those derived by rain gauges. It is demonstrated that arbitrary oriented microwave link can be adopted to optimize the attenuation correction of radar reflectivity.

Apparent mineralocorticoid excess is an autosomal recessive form of monogenic disease characterized by juvenile resistant low-renin hypertension, marked hypokalemic alkalosis, low aldosterone levels, and high ratios of cortisol to cortisone metabolites. It is caused by defects in the HSD11B2 gene, encoding the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which is primarily involved in the peripheral conversion of cortisol to cortisone. To date, over 50 deleterious HSD11B2 mutations have been identified worldwide. Multiple molecular mechanisms function in the lowering of 11β-HSD2 activity, including damaging protein stability, lowered affinity for the substrate and cofactor, and disrupting the dimer interface. Genetic polymorphism, environmental factors as well as epigenetic modifications may also offer an implicit explanation for the molecular pathogenesis of AME. A precise diagnosis depends on genetic testing, which allows for early and specific management to avoid the morbidity and mortality from target organ damage. In this review, we provide insights into the molecular genetics of classic and non-classic apparent mineralocorticoid excess and aim to offer a comprehensive overview of this monogenic disease.

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