We identified a novel plasmid-mediated colistin resistance gene named mcr-7.1 in K. pneumoniae in China. The prevalence of mcr-7.1 in various species of human and animal origin needs to be investigated immediately.

Macrophages are important immune cells in innate immunity, and have remarkable heterogeneity and polarization. Under pathological conditions, in addition to the resident macrophages, other macrophages are also recruited to the diseased tissues, and polarize to various phenotypes (mainly M1 and M2) under the stimulation of various factors in the microenvironment, thus playing different roles and functions. Liver diseases are hepatic pathological changes caused by a variety of pathogenic factors (viruses, alcohol, drugs, etc.), including acute liver injury, viral hepatitis, alcoholic liver disease, metabolic-associated fatty liver disease, liver fibrosis, and hepatocellular carcinoma. Recent studies have shown that macrophage polarization plays an important role in the initiation and development of liver diseases. However, because both macrophage polarization and the pathogenesis of liver diseases are complex, the role and mechanism of macrophage polarization in liver diseases need to be further clarified. Therefore, the origin of hepatic macrophages, and the phenotypes and mechanisms of macrophage polarization are reviewed first in this paper. It is found that macrophage polarization involves several molecular mechanisms, mainly including TLR4/NF-κB, JAK/STATs, TGF-β/Smads, PPARγ, Notch, and miRNA signaling pathways. In addition, this paper also expounds the role and mechanism of macrophage polarization in various liver diseases, which aims to provide references for further research of macrophage polarization in liver diseases, contributing to the therapeutic strategy of ameliorating liver diseases by modulating macrophage polarization.

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Ribonuclease-A (RNase-A) encapsulated PbS quantum dots (RNase-A@PbS Qdots) which emit in the second near-infrared biological window (NIR-II, ca. 1000–1400 nm) are rapidly synthesized under microwave heating. Photoluminescence (PL) spectra of the Qdots can be tuned across the entire NIR-II range by simply controlling synthesis temperature. The size and morphology of the Qdots are examined by transmission electron microscopy (TEM), atomic force microscopy (AFM), and dynamic light scattering (DLS). Quantum yield (Φf) measurement confirms that the prepared Qdots are one of the brightest water-soluble NIR-II emitters for in vivo imaging. Their high Φf (∼17.3%) and peak emission at ∼1300 nm ensure deep optical penetration to muscle tissues (up to 1.5 cm) and excellent imaging contrast at an extremely low threshold dose of ∼5.2 pmol (∼1 μg) per mouse. Importantly, this protein coated Qdot displays no signs of toxicity toward model neuron, normal, and cancer cells in vitro. In addition, the animal’s metabolism results in thorough elimination of intravenously injected Qdots from the body within several days via the reticuloendothelial system (RES), which minimizes potential long-term toxicity in vivo from possible release of lead content. With a combination of attractive properties of high brightness, robust photostability, and excellent biocompatibility, this new NIR-II emitting Qdot is highly promising in accurate disease screening and diagnostic applications.

Diarrhea is a common problem to the whole world and the occurrence of diarrhea is highly associated with gut microbiota, such as bacteria, fungi, and viruses. Generally, diarrheal patients or animals are characterized by gut microbiota dysbiosis and pathogen infections may lead to diarrheal phenotypes. Of relevance, reprograming gut microbiota communities by dietary probiotics or fecal bacteria transplantation are widely introduced to treat or prevent diarrhea. In this review, we discussed the influence of the gut microbiota in the infection of diarrhea pathogens, and updated the research of reshaping the gut microbiota to prevent or treat diarrhea for the past few years. Together, gut microbiota manipulation is of great significance to the prevention and treatment of diarrhea, and further insight into the function of the gut microbiota will help to discover more anti-diarrhea probiotics.

Embryonic stem cells (ESCs) and induced pluripotent stem cells have the potential to differentiate to all cell types of an adult individual and are useful for studying development and for translational research. However, extrapolation of mouse and human ESC knowledge to deriving stable ESC lines of domestic ungulates and large livestock species has been challenging. In contrast to ESCs that are usually established from the blastocyst, mouse expanded potential stem cells (EPSCs) are derived from four-cell and eight-cell embryos. We have recently used the EPSC approach and established stem cells from porcine and human preimplantation embryos. EPSCs are molecularly similar across species and have broader developmental potential to generate embryonic and extraembryonic cell lineages. We further explore the EPSC technology for mammalian species refractory to the standard ESC approaches and report here the successful establishment of bovine EPSCs (bEPSCs) from preimplantation embryos of both wild-type and somatic cell nuclear transfer. bEPSCs express high levels of pluripotency genes, propagate robustly in feeder-free culture, and are genetically stable in long-term culture. bEPSCs have enriched transcriptomic features of early preimplantation embryos and differentiate in vitro to cells of the three somatic germ layers and, in chimeras, contribute to both the embryonic (fetal) and extraembryonic cell lineages. Importantly, precise gene editing is efficiently achieved in bEPSCs, and genetically modified bEPSCs can be used as donors in somatic cell nuclear transfer. bEPSCs therefore hold the potential to substantially advance biotechnology and agriculture.

The mcr-1 gene was detected in 5.11% (58/1136) of Escherichia coli isolates of chicken origin from 13 provinces in China. A novel mcr-1 variant, named mcr-1.3, encoding an Ile-to-Val functional variant of MCR-1 was identified in a sequence type 155 (ST155) strain. An mcr-1.3-containing IncI2 plasmid, pHeN867 (60,757 bp), was identified. The transfer of pHeN867 led to a 32-fold increase in the MIC of colistin in the recipient, exhibiting an effect on colistin resistance that was similar to that of mcr-1. KEYWORDS E. coli, colistin resistance, mcr-1.3, plasmid P olymyxins (polymyxin B and colistin) are a last-resort treatment for infections caused by multidrug-resistant (MDR) Gram-negative bacteria (1). In veterinary use, colistin is administered with food in pig and poultry farming to prevent infections caused by pathogens (2). The mcr-1 gene, which confers plasmid-mediated colistin resistance to Enterobacteriaceae, was identified in an IncI2 plasmid from Escherichia coli and Klebsiella pneumoniae in China in 2016 (3). The mcr-1 gene found in E. coli (4), K. pneumoniae (5), and Salmonella spp. (6) has been proven to disseminate ubiquitously. The transmission of mcr-1-mediated colistin resistance between animals and human has been a threat to human health. It has also been demonstrated that the mcr-1 gene can coexist with bla CTX-M (5), bla NDM (7), and other resistance genes (4), which threatens a return of untreatable infections worldwide. Previous reports described the unique mcr-1 gene sequence compared with that of the originally published sequence (3), which indicates that mcr-1 is relatively conserved. Recently, a point mutation of A¡T at position 8 in mcr-1 was identified in K. pneumoniae (8). To investigate the epidemiology of mcr-1 and its variant, E. coli isolates collected from chickens nationwide in China were assessed.In total, 1,136 nonduplicate E. coli isolates were collected between 2010 and 2015 from sick chickens in 20 provinces and municipalities in China. All of these isolates were preliminarily screened on Mueller-Hinton agar medium with 2 g/ml colistin. Because the cooccurrence of mcr-1 with bla CTX-M may accelerate the transmission of resistance to colistin and cephalosporins, the mcr-1 (3) and bla CTX-M (9) genes were detected by PCR amplification of the isolates with resistance to colistin. The corresponding primers used to amplify the whole mcr-1 gene and parts of the ISApl1 element are listed in Table S1 in the supplemental material. For all of the positive PCR products of mcr-1, Sanger sequencing was performed (Tsingke Biological Technology, Chengdu, China) by using a DNA analyzer (Applied Biosystems, Life Technologies, Carlsbad, CA). We found a total of 58 (5.11%) mcr-1-positive isolates, including one isolate harboring the mcr-1 gene with mutations not found in the originally published gene sequence (3). MICs of colistin