SARS-CoV Infection in a Restaurant from Palm Civet

Contact with food animals was associated with SARS-CoV infection in the People’s Republic of China

Empagliflozin inhibits coronary microvascular dysfunction and reduces cardiac pericyte loss in db/db mice

BackgroundCoronary microvascular dysfunction (CMD) is a pathophysiological feature of diabetic heart disease. However, whether sodium-glucose cotransporter 2 (SGLT2) inhibitors protect the cardiovascular system by alleviating CMD is not known.ObjectiveWe observed the protective effects of empagliflozin (EMPA) on diabetic CMD.Materials and methodsThe mice were randomly divided into a db/db group and a db/db + EMPA group, and db/m mice served as controls. At 8 weeks of age, the db/db + EMPA group was given empagliflozin 10 mg/(kg⋅d) by gavage for 8 weeks. Body weight, fasting blood glucose and blood pressure were dynamically observed. Cardiac systolic and diastolic function and coronary flow reserve (CFR) were detected using echocardiography. The coronary microvascular structure and distribution of cardiac pericytes were observed using immunofluorescence staining. Picrosirius red staining was performed to evaluate cardiac fibrosis.ResultsEmpagliflozin lowered the increased fasting blood glucose levels of the db/db group. The left ventricular ejection fraction, left ventricular fractional shortening, E/A ratio and E/e′ ratio were not significantly different between the three groups. CFR was decreased in the db/db group, but EMPA significantly improved CFR. In contrast to the sparse and abnormal expansion of coronary microvessels observed in the db/db group, the number of coronary microvessels was increased, and the capillary diameter was decreased in the db/db + EMPA group. The number and microvascular coverage of cardiac pericytes were reduced in the db/db mice but were improved by EMPA. The cardiac fibrosis was increased in db/db group and may alleviate by EMPA.ConclusionEmpagliflozin inhibited CMD and reduced cardiac pericyte loss in diabetic mice

Pontibacter diazotrophicus sp. nov., a novel nitrogen-fixing bacterium of the family Cytophagaceae.

Few diazotrophs have been found to belong to the family Cytophagaceae so far. In the present study, a Gram-negative, rod-shaped bacterium that forms red colonies, was isolated from sands of the Takalamakan desert. It was designated H4XT. Phylogenetic and biochemical analysis indicated that the isolate is a new species of the genus Pontibacter. The 16S rRNA gene of H4XT displays 94.2-96.8% sequence similarities to those of other strains in Pontibacter. The major respiratory quinone is menaquinone-7 (MK-7). The DNA G+C content is 46.6 mol%. The major cellular fatty acids are iso-C15∶0, C16∶1ω5c, summed feature 3 (containing C16∶1ω6c and/or C16∶1ω7c) and summed feature 4 (comprising anteiso-C17∶1B and/or iso-C17∶1I). The major polar lipids are phosphatidylethanolamine (PE), one aminophospholipid (APL) and some unknown phospholipids (PLs). It is interesting to see that this bacterium can grow very well in a nitrogen-free medium. PCR amplification suggested that the bacterium possesses at least one type of nitrogenase gene. Acetylene reduction assay showed that H4XT actually possesses nitrogen-fixing activity. Therefore, it can be concluded that H4XT is a new diazotroph. We thus referred it to as Pontibacter diazotrophicus sp. nov. The type strain is H4XT ( = CCTCC AB 2013049T = NRRL B-59974T)

Distribution and Diversity of Aerobic Carbon Monoxide-Oxidizing Bacteria in Geothermal Springs of China, the Philippines, and the United States

Accumulating genomic evidence suggests that a variety of thermophilic bacteria contain cox operons and may be capable of aerobic carbon monoxide (CO) oxidation. However, little is known about the distribution and diversity of the cox-encoding (COXE) bacteria in natural geothermal environments. In this study, we examined coxL gene (encoding the large subunit of carbon monoxide dehydrogenase: CoxL) sequences retrieved from the sediments of 25 geothermal sites located in the Qinghai-Tibetan Plateau (QTP) and Yunnan Province (YP) of China, the Bacon-Manito Geothermal Production Field (BGPF) of the Philippines, and the Great Basin of the United States (USGB). Temperature and pH ranges of the studied hot springs were 22.1 to 90.8°C and 2.7 to 9.4, respectively. Phylogenetic analyses showed that most CoxL sequences were closely related to the classes Actinobacteria, Deinococci, Ktedonobacteria, Thermomicrobia, and Clostridia, and hot springs from different regions hosted different COXE communities. In addition, these hot springs harbored some COXE bacteria that were phylogenetically distinct from those inhabiting nongeothermal ecosystems. This study revealed no significant correlation between temperature or pH and the composition or diversity of COXE communities at the global scale. However, within a given region, temperature was correlated with the COXE bacterial community composition

A review of the microbiology of the Rehai geothermal field in Tengchong, Yunnan Province, China

The Rehai Geothermal Field, located in Tengchong County, in central-western Yunnan Province, is the largest and most intensively studied geothermal field in China. A wide physicochemical diversity of springs (ambient to ∼97 °C; pH from ≤1.8 to ≥9.3) provides a multitude of niches for extremophilic microorganisms. A variety of studies have focused on the cultivation, identification, basic physiology, taxonomy, and biotechnological potential of thermophilic microorganisms from Rehai. Thermophilic bacteria isolated from Rehai belong to the phyla Firmicutes and Deinococcus-Thermus. Firmicutes include neutrophilic or alkaliphilic Anoxybacillus, Bacillus, Caldalkalibacillus, Caldanaerobacter, Laceyella, and Geobacillus, as well as thermoacidophilic Alicyclobacillus and Sulfobacillus. Isolates from the Deinococcus-Thermus phylum include several Meiothermus and Thermus species. Many of these bacteria synthesize thermostable polymer-degrading enzymes that may be useful for biotechnology. The thermoacidophilic archaea Acidianus, Metallosphaera, and Sulfolobus have also been isolated and studied. A few studies have reported the isolation of thermophilic viruses belonging to Siphoviridae (TTSP4 and TTSP10) and Fuselloviridae (STSV1) infecting Thermus spp. and Sulfolobus spp., respectively. More recently, cultivation-independent studies using 16S rRNA gene sequences, shotgun metagenomics, or “functional gene” sequences have revealed a much broader diversity of microorganisms than represented in culture. Studies of the gene and mRNA encoding the large subunit of the ammonia monooxygenase (amoA) of ammonia-oxidizing Archaea (AOA) and the tetraether lipid crenarchaeol, a potential biomarker for AOA, suggest a wide diversity, but possibly low abundance, of thermophilic AOA in Rehai. Finally, we introduce the Tengchong Partnerships in International Research and Education (PIRE) project, an international collaboration between Chinese and U.S. scientists with the goal of promoting international and interdisciplinary cooperation to gain a more holistic and global view of life in terrestrial geothermal springs

IFI16 Inhibits Porcine Reproductive and Respiratory Syndrome Virus 2 Replication in a MAVS-Dependent Manner in MARC-145 Cells

Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-β). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies

Major Vault Protein Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection in CRL2843CD163 Cell Lines and Primary Porcine Alveolar Macrophages

Porcine reproductive and respiratory syndrome (PRRS), a significant viral infectious disease that commonly occurs among farmed pigs, leads to considerable economic losses to the swine industry worldwide. Major vault protein (MVP) is a host factor that induces type Ⅰ interferon (IFN) production. In this study, we evaluated the effect of MVP on PRRSV infection in CRL2843CD163 cell lines and porcine alveolar macrophages (PAMs). Our results showed that MVP expression was downregulated by PRRSV infection. Adenoviral overexpression of MVP inhibited PRRSV replication, whereas the siRNA knockdown of MVP promoted PRRSV replication. In addition, MVP knockdown has an adverse effect on the inhibitive role of MVP overexpression on PRRSV replication. Moreover, MVP could induce the expression of type Ⅰ IFNs and IFN-stimulated gene 15 (ISG15) in PRRSV-infected PAMs. Based on these results, MVP may be a potential molecular target of drugs for the effective prevention and treatment of PRRSV infection

Major Vault Protein Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection in CRL2843^CD163 Cell Lines and Primary Porcine Alveolar Macrophages

Porcine reproductive and respiratory syndrome (PRRS), a significant viral infectious disease that commonly occurs among farmed pigs, leads to considerable economic losses to the swine industry worldwide. Major vault protein (MVP) is a host factor that induces type Ⅰ interferon (IFN) production. In this study, we evaluated the effect of MVP on PRRSV infection in CRL2843CD163 cell lines and porcine alveolar macrophages (PAMs). Our results showed that MVP expression was downregulated by PRRSV infection. Adenoviral overexpression of MVP inhibited PRRSV replication, whereas the siRNA knockdown of MVP promoted PRRSV replication. In addition, MVP knockdown has an adverse effect on the inhibitive role of MVP overexpression on PRRSV replication. Moreover, MVP could induce the expression of type Ⅰ IFNs and IFN-stimulated gene 15 (ISG15) in PRRSV-infected PAMs. Based on these results, MVP may be a potential molecular target of drugs for the effective prevention and treatment of PRRSV infection