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We aimed to characterize NDM-5-producing我们旨在对中国广州零售水产品中产NDM-5的肠杆菌科细菌进行调查。对2019年采集的196份草鱼肠道样品进行碳青霉烯酶基因筛查，通过药物敏感性试验、接合试验、Illumina HiSeq和Nanopore测序的方法研究

Background Toxoplasma gondii is an intracellular protozoan that can infect humans and other animals, including cattle. Cattle are one of the world’s main sources of meat, and people who consume raw or undercooked meat and milk of cattle infected with T. gondii can become infected. In this study, a total of 5292 dairy cattle serum samples, collected from 17 cities (Henan Province, China) from January 2015 to September 2017, were screened for antibodies against T. gondii. Results Antibodies to T. gondii were found in 1.93% (102/5292) (95% CI, 1.56–2.30) of dairy cattle using a modified agglutination test (cut-off 1:100). The results showed that geographic location and season may be risk factors for T. gondii infection of cattle (P

Abnormal angiogenesis is critical for portal hypertension in cirrhosis. Except for etiological treatment, no efficient medication or regime has been explored to treat the early stage of cirrhosis when angiogenesis is initiated or overwhelming. In this study, we explored an anti-angiogenesis effort through non-cytotoxic drugs octreotide and celecoxib to treat early stage of cirrhotic portal hypertension in an animal model. Peritoneal injection of thioacetamide (TAA) was employed to induce liver cirrhosis in rats. A combination treatment of celecoxib and octreotide was found to relieve liver fibrosis, portal venous pressure, micro-hepatic arterioportal fistulas, intrahepatic and splanchnic angiogenesis. Celecoxib and octreotide exerted their anti-angiogenesis effect via an axis of cyclooxygenase-2/prostaglandin E2/EP-2/somatostatin receptor-2, which consequently down-regulated phosphorylation of extracellular signal-regulated kinase (p-ERK)–hypoxia-inducible factor-1α (HIF-1α)–vascular endothelial growth factor (VEGF) integrated signaling pathways. In conclusions, combination of celecoxib and octreotide synergistically ameliorated liver fibrosis and portal hypertension of the cirrhotic rats induced by TAA via the inhibition of intrahepatic and extrahepatic angiogenesis. The potential mechanisms behind the regimen may due to the inactivation of p-ERK–HIF-1α–VEGF signaling pathway. Electronic supplementary material The online version of this article (doi:10.1007/s10456-016-9522-9) contains supplementary material, which is available to authorized users.

Toxoplasma gondii has a complex life cycle and pathogenic mechanisms. Acute T. gondii infections in mice often result in death, whereas in chronic infections, the parasites may persist in the host tissues as intraneuronal or intramuscular cysts. However, the virulence of T. gondii strains in mice varies with its genetic background. The present study investigated the pathogenicity and pathological lesions of two T. gondii isolates from China: namely, TgCatCHn2 (ToxoDB#17) and TgCatCHn4 (ToxoDB#9). The virulent (ToxoDB#216) and avirulent (VEG) strains were employed as controls. Toxoplasmosis was induced by inoculating BALB/c mice with oocysts of the strains of T. gondii VEG, ToxoDB#216, TgCatCHn2 (ToxoDB#17), and TgCatCHn4 (ToxoDB#9), respectively. As a result, one oocyst of ToxoDB#216 could kill a mouse within 10 days post inoculation (DPI). The survival time of the mice for T. gondii TgCatCHn2 and TgCatCHn4 was >60 DPI for 106/mL oocysts, but this concentration (106/mL oocysts) of VEG strain could kill mice within 11 DPI. Compared with the strains of T. gondii ToxoDB#216 and VEG, the lesions in the small intestines of the strains of TgCatCHn2- and TgCatCHn4-infected mice were significantly smaller (P 0.05). However, the granules in the PCs showed negative lysozyme expression in the intestines of mice infected with T. gondii TgCatCHn2 and TgCatCHn4. Thus, T. gondii strains of TgCatCHn2 (ToxoDB#17) and TgCatCHn4 (ToxoDB#9) were avirulent strains, they triggered an inhibition of lysozyme expression in the granules of PCs of the mouse intestine. These effects may in turn lead to intestinal dysbiosis, which may be related to further parasitic invasion of the intestines. The findings of the present study further expand the spectrum of the pathogenic features of various Chinese isolates of T. gondii.

The felids are the only definitive hosts of Toxoplasma gondii, which could excrete oocysts into the environment and provide an infection source for toxoplasmosis in various warm-blooded animal species, particularly the captive felids that live close to human communities. The infection rate of the captive felids is a perfect standard in detecting the presence of Toxoplasma gondii oocysts in the environment. In this study, sera or tissue samples from zoo (1 young tiger, 2 adult tigers, 6 young lions), farm (10 masked palm civets), and pet hospital (28 cats) from Henan Province (China) were collected. The sera (n = 47) were tested for immunoglobulin G (IgG) antibodies against T. gondii by using modified agglutination test (MAT), whereas the hearts tissue (n = 40) were bioassayed in mice to isolate T. gondii strains. The genotype was distinguished by using PCR-RFLP of 10 loci (SAG1, SAG2, SAG3, GRA6, BTUB, L358, c22-8, PK1, c29-2, and Apico). The detection rate for the T. gondii antibody in captive felids was 21.3% (10/47). One viable T. gondii strain (TgCatCHn4) was obtained from a cat heart tissue, and its genotype was ToxoDB#9. The oocysts of ToxoDB#9 were collected from a T. gondii-free cat. The virulence of TgCatCHn4 was low and no cysts were detected in the brain of mice at 60 days post-inoculation. The finding of the present study suggested a widespread exposure of T. gondii for felids in Henan Province of central China, particularly those from the zoological gardens and homes. ToxoDB#9 was the predominant strain in China. Preventive measures against T. gondii oocyst contamination of various components of the environment should thus be implemented, including providing pre-frozen meat, well-cooked cat food, cleaned fruits and vegetables, monitoring birds and rodents, inactive T. gondii oocysts in felids feces, and proper hygiene.

A steady-state model was established to simulate EDI process for producing ultrapure water (MixEDI), the dilute compartment of which is filled with mixed cation and anion-exchange resins. By calculating the mathematical model which includes water dissociation mechanism, ionic status of ion-exchange resin, concentration polarization status and the concentration distribution of water dissociation products are obtained. The influence of water dissociation on the current efficiency, removal rate and pH value of EDI effluent is investigated. The existence of water dissociation catalyst at anion-exchange membrane (AM) makes the water dissociation current of the AM much larger than that of CM. The result is that the amount of electro-regenerated cation-exchange resins is much larger than that of anion resins. This is the reason why the removal rate of salt cation much larger than that of salt anion in EDI for producing ultrapure water. Thus, at the target percentage removal, water dissociation at AM surface is excessive and the one at CM surface is insufficient. We assume that there is also some water dissociation catalyst at CM surface. It is found that the improved water dissociation at CM could increase the percentage removal of salt anions and the current efficiency.

The epithelial-mesenchymal transition (EMT) of hepatocytes is a key step for hepatic fibrosis and cirrhosis. Long-term administration of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, can ameliorate hepatic fibrosis. This research aimed to examine the effect of celecoxib on the EMT of hepatocytes during the development of liver cirrhosis.Cirrhotic liver model of rat was established by peritoneal injection of thiacetamide (TAA). Thirty-six rats were randomly assigned to control, TAA, and TAA + celecoxib groups. Hepatic expressions of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), COX-2, prostaglandin E2 (PGE2 ), matrix metalloproteinase (MMP)-2 and -9, transforming growth factor-β1 (TGF-β1), Phospho-Smad2/3, Snail1, α-smooth muscle actin (α-SMA), vimentin, collagen I, fibroblast-specific protein (FSP-1), E-cadherin and N-cadherin were quantitated. Hepatic fibrosis was assessed by the visible hepatic fibrotic areas and Ishak's scoring system.Exposed to TAA treatment, hepatocytes underwent the process of EMT during hepatic fibrosis. Compared with those in TAA group, celecoxib significantly downregulated the hepatic expressions of TNF-α, IL-6, COX-2, PGE2 , MMP-2, MMP-9, TGF-β1, Phospho-Smad2/3, Snail1, α-SMA, FSP-1, and vimentin while greatly restoring the levels of E-cadherin. The fibrotic areas and collagen I levels of TAA + celecoxib group were much lower than those in TAA group.Celecoxib could ameliorate hepatic fibrosis and cirrhosis in TAA-rat model through suppression of the mesenchymal biomarkers in the hepatocytes while restoring the levels of their epithelial biomarkers. The inhibitory effect of celecoxib on the EMT of hepatocytes is associated with reduction of intrahepatic inflammation, preservation of normal basement matrix, and inhibition of TGF-β1/Smad pathway.