ABSTRACT: Lamb diarrhea seriously restricts the development of the sheep industry. Infectious pathogens often cause diarrhea, and E. coli isolates are highly distributed in infectious diarrhea. The study aimed to investigate the prevalence of pathogenic E. coli in diarrhea lambs and determine the distribution of virulence genes, antibiotic resistance genes, and antibiotic resistance. One hundred seventy-eight E. coli isolates were isolated from the feces of 204 diarrhea lambs. The virulence genes mdh, hlyF, iss, ompA, fimC, iucD, st, lt, stx1, stx2, and antibiotic resistance genes including tetA, tetB, aac (6′)-II, blaCMY-2, qnr, aadA1, sul1, blaTEM, blaCTX-M were detected by polymerase chain reaction (PCR). Antibiotic resistance was determined by Kirby-Bauer Disc Diffusion method. There were 109 (61.24%, 109/178) enterotoxigenic E. coli (ETEC), 119 (66.85%, 119/178) Shiga toxin-producing E. coli (STEC), and 95 (53.37%, 95/178) hybrid STEC/ETEC isolates. The highest prevalent virulence genes were ompA (80.90%, 144/178) and fimC (67.98%, 121/178), and the lowest was iucD (8.99%, 16/178). The most commonly detected antibiotic resistance genes were tetA/tetB (92.70%, 165/178), qnr (75.84%, 135/178), and sul1 (62.92%, 112/178), no blaTEM or blaCTX-M genes were detected. All isolates had high antibiotic resistance to lincomycin (96.63%, 172/178), tetracycline (88.76%, 158/178), and co-trimoxazole (80.34%, 143/178), and the multidrug resistant (MDR) rate reached 93.82% (167/178). The high prevalence of ETEC and STEC indicates that E. coli is one of the critical pathogenic agents leading to diarrhea in lambs in the region, and its high antibiotic resistance, especially MDR, should be brought to our attention. ABSTRACT industry E seventyeight seventy eight 20 mdh hlyF iss st lt stx1 stx stx2 tetA tetB 6′II, 6II II 6′ II, 6 (6′)-II blaCMY2, blaCMY2 blaCMY 2, 2 blaCMY-2 aadA1 aadA sul blaCTXM blaCTX M PCR. PCR . (PCR) KirbyBauer Kirby Bauer method 10 61.24%, 6124 61 24 (61.24% 109/178 109178 178 ETEC, , (ETEC) 11 66.85%, 6685 66 85 (66.85% 119/178 119178 toxinproducing toxin producing STEC, (STEC) 9 53.37%, 5337 53 37 (53.37% 95/178 95178 STECETEC 80.90%, 8090 80 90 (80.90% 144/178 144178 144 67.98%, 6798 67 98 (67.98% 121/178, 121178 121/178 121 121/178) 8.99%, 899 8 99 (8.99% 16/178. 16178 16/178 16 16/178) tetAtetB 92.70%, 9270 92 70 (92.70% 165/178, 165178 165/178 165 165/178) 75.84%, 7584 75 84 (75.84% 135/178, 135178 135/178 135 135/178) 62.92%, 6292 62 (62.92% 112/178, 112178 112/178 112 112/178) 96.63%, 9663 96 63 (96.63% 172/178, 172178 172/178 172 172/178) 88.76%, 8876 88 76 (88.76% 158/178, 158178 158/178 158 158/178) cotrimoxazole co trimoxazole 80.34%, 8034 34 (80.34% 143/178, 143178 143/178 143 143/178) MDR (MDR 9382 93 82 93.82 167/178. 167178 167/178 167 (167/178) region attention 6′II blaCMY- (PCR 1 61.24% 612 (61.24 109/17 10917 17 (ETEC 66.85% 668 (66.85 119/17 11917 (STEC 53.37% 533 5 3 (53.37 95/17 9517 80.90% 809 (80.90 144/17 14417 14 67.98% 679 (67.98 12117 121/17 12 8.99% 89 (8.99 1617 16/17 92.70% 927 7 (92.70 16517 165/17 75.84% 758 (75.84 13517 135/17 13 62.92% 629 (62.92 11217 112/17 96.63% 966 (96.63 17217 172/17 88.76% 887 (88.76 15817 158/17 15 80.34% 803 (80.34 14317 143/17 938 93.8 16717 167/17 (167/178 61.24 (61.2 109/1 1091 66.85 (66.8 119/1 1191 53.37 (53.3 95/1 951 80.90 (80.9 144/1 1441 67.98 (67.9 1211 121/1 8.99 (8.9 161 16/1 92.70 (92.7 1651 165/1 75.84 (75.8 1351 135/1 62.92 (62.9 1121 112/1 96.63 (96.6 1721 172/1 88.76 (88.7 1581 158/1 80.34 (80.3 1431 143/1 93. 1671 167/1 (167/17 61.2 (61. 109/ 66.8 (66. 119/ 53.3 (53. 95/ 80.9 (80. 144/ 67.9 (67. 121/ 8.9 (8. 16/ 92.7 (92. 165/ 75.8 (75. 135/ 62.9 (62. 112/ 96.6 (96. 172/ 88.7 (88. 158/ 80.3 143/ 167/ (167/1 61. (61 66. (66 53. (53 80. (80 67. (67 8. (8 92. (92 75. (75 62. (62 96. (96 88. (88 (167/ (6 (5 ( (9 (7 (167 (16 (1

Abstract In order to explore the effect of different the welding heat input on microstructure and impact properties in coarse grain zone in heat affected zone (CGHAZ) of ultra-low carbon bainitic steel welded joint. In this paper, Gleeble-3500 thermal simulation testing machine was used to simulate different heat input, to study the effect of linear energy on the microstructure and impact toughness of the CGHAZ of Q420qEN steel joint. The scanning electron microscope (SEM), oscillographic impact microscope and transmission electron microscope (TEM) were used. The results show that the microstructure of CGHAZ is mainly the lath bainite and granular bainite. When the welding heat input is 30kJ•cm-1, the CGHAZ grains have obvious growth phenomenon. With the increase of the welding heat input, the grain size also grows. Meanwhile, as the welding heat input increases from 18kJ•cm-1 to 30kJ•cm-1, the impact toughness of the CGHAZ of joint increases first and then decreases at -20°C.

RESUMO OBJETIVO O diabetes é um fator de risco para a lesão renal aguda (LRA). No entanto, seu mecanismo de patogênese não foi elucidado. O objetivo do estudo foi investigar o papel da inflamação e do receptor Toll-like 7 (TLR7) na LRA isquêmica no diabetes. MÉTODOS Um modelo de hipóxia-reoxigenação de células epiteliais tubulares renais humanas (HK-2) na presença de concentrações altas de glicose foi utilizado para gerar LRA induzida por isquemia-reperfusão em diabetes. A atividade das células foi medida pelo ensaio Cell Counting Kit-8 (CCK-8) e pela atividade da lactato desidrogenase (LDH). As citocinas inflamatórias foram avaliadas por ensaio imunoenzimático (Elisa). A expressão de TLR7, do fator de diferenciação mieloide 88 (MyD88) e do fator de transcrição nuclear-κB (NF-κB) foi examinada por Western blotting. A apoptose foi avaliada por citometria de fluxo. RESULTADOS Os grupos glicose alta e glicose baixa foram submetidos à hipóxia-reoxigenação. O grupo de baixa glicose desenvolveu apenas danos celulares ligeiros, apoptose e uma resposta inflamatória. Em contraste, no grupo de alta glicose, uma lesão equivalente de hipóxia-reoxigenação provocou danos celulares graves, apoptose e uma resposta inflamatória. A expressão de TLR7 e suas proteínas relacionadas foi medida no grupo de alta glicose antes e após a hipóxia-reoxigenação. O grupo de alta glicose exibiu maiores aumentos na expressão de TLR7 após hipóxia-reoxigenação do que o grupo de baixa glicose. Além disso, a expressão de TLR7 e suas proteínas relacionadas após a hipóxia-reoxigenação foi maior no grupo com alto nível de glicose do que no grupo com baixo nível de glicose. A inibição do TLR7 fornece proteção significativa contra a lesão isquêmica no diabetes. CONCLUSÃO Nossos resultados sugerem que o diabetes aumenta a vulnerabilidade à lesão renal induzida por isquemia. Essa vulnerabilidade acrescida tem por origem uma resposta inflamatória aumentada envolvendo a via de transdução de sinal do TLR7.

SUMMARY OBJECTIVE Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS A high glucose hypoxia-reoxygenation model of human renal tubular epithelial (HK-2) cells was used to generate AKI induced by ischemia-reperfusion in diabetes. The activity of cells was measured by CCK-8 assay and LDH activity. Inflammatory cytokines were assessed by ELISA. TLR7, MyD88, and NF-κB expressions were examined by western blotting. Apoptosis was evaluated by flow cytometry. RESULTS The high glucose group and low glucose group were subjected to hypoxia-reoxygenation. The low glucose group developed only mild cell damage, apoptosis, and inflammatory response. In contrast, an equivalent hypoxia-reoxygenation injury provoked severe cell damage, apoptosis, and inflammatory response in the high glucose group. Expression of TLR7 and its related proteins were measured in the high glucose group before and after hypoxia-reoxygenation. The high glucose group exhibited more significant increases in TLR7 expression following hypoxia-reoxygenation than the low glucose group. In addition, the expression of TLR7 and its related proteins after hypoxia-reoxygenation were higher in the high glucose group than in the low glucose group. Inhibition of TLR7 provides significant protection against ischemic injury in diabetes. CONCLUSION Our results suggest that diabetes increases the vulnerability to ischemia-induced renal injury. This increased vulnerability originates from a heightened inflammatory response involving the TLR7 signal transduction pathway.

A new method using nonanoic acid-coated magnetic Fe3O4 nanoparticles as adsorbent has been developed for the single-step extraction and preconcentration of lead and copper in tobacco samples. Transmission electron microscopy and X-ray diffraction spectrometry were used to characterize the adsorbent. The experimental parameters affecting extraction efficiency, including amount of nanoparticles, volume of chelating reagents, sample pH, ultrasonic time and desorption conditions were investigated. The analytes desorbed from nanoparticles were determined by flame atomic absorption spectrometry. Under the optimum conditions, good linearity was obtained in the range of 2-400 µg L-1 for copper and 5-800 µg L-1 for lead (r > 0.998, p < 0.05). The limits of detection for copper and lead were 0.2 and 0.5 µg L-1, with enrichment factors of 45 and 52, respectively. The method was successfully employed to tobacco sample analysis and got excellent recoveries between 89.2 and 100.7% with relative standard deviations (n = 6) of 4.5-5.9%.

Abstract Purpose: To investigate whether modulating NRG1 could attenuate diabetic neuropathic pain and analyze the underlying mechanism. Methods: Male SD rats were randomly divided into control group, diabetic group, NRG1 intervention group. After STZ-induced 2 weeks, NRG1 intervention daily for consecutive 7 days. 4 weeks after NRG1 intervention, both the mechanical withdrawal threshold and the morphological changes of the dorsal root ganglion and sural nerve were observed. Meanwhile, the expression of NGF, IL-1β, TNF-α in spinal cord were determined. Results: Compared with the diabetic group, NRG1 treatment improved the mechanical withdrawal threshold in diabetic rats, pathological changes of dorsal root ganglion and sural nerve were alleviated by NRG1 treatment with electron microscopy imagine. Moreover, compared with the control group, the expression of NGF was significantly decreased and the production of IL-1β, TNF-α were markedly induced in diabetic group. Furthermore, NRG1 treatment could normalized the above effect as compared to diabetic group. Conclusion: NRG1 exerted positive effects on the behavioral and pathological changes of rats with STZ-induced diabetic neuropathic pain, the underlying mechanism might be related to the promotion of NGF excretion and the inhibition of inflammatory cytokines excretion.

ABSTRACT PURPOSE: To evaluate the role of low molecular chitosan containing sepia ink (LMCS) in ethanol-induced (5 ml/kg) gastric ulcer in rats. METHODS: Animals were divided into four groups (n = 12): normal group (Normal), negative control group (Con), experiment group (LMCS) and positive control Omeprazole group (OMZ). Gastric empty rate was detected in the first 7 days. Rats were sacrificed at 7, 14 and 21 day for histology and ELISA detections. RESULTS: Gastric empty was no significant differences among the groups (P > 0.05). Histological observation showed gastric mucosal LMCS treated had better healing effect. Hydroxyproline (Hyp) was significantly increased from 7 day (P < 0.05). LMCS significantly inhibited malondialdehyde (MDA) generation for lipid peroxidation from 7 day (P < 0.05). LMCS significantly promoted the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) at the earlier stage (P < 0.05). OMZ had the similar effects above. As for myeloperoxidase (MPO), LMCS significantly decreased and restored it to normal levels from 7 day (P < 0.05), it is earlier than OMZ which is from 14 day. CONCLUSION: LMCS can improve gastric mucosa tissue repair, exert significant influences on oxidative and antioxidant enzyme activities and neutrophil infiltration.