Strategy of schistosomiasis elimination and its effects in Jinhu County, Jiangsu Province / 中国血吸虫病防治杂志

Objective To understand the strategy of schistosomiasis elimination and its effects in Jinhu County, Jiangsu Province. Methods The data of schistosomiasis control in Jinhu County at different stages from 1970 to 2017 were collected and analyzed. Results From 1970 to 2017, there were three stages of schistosomiasis control, including transmission control, transmission interruption, and monitoring and elimination stages in Jinhu County. The main measures included Oncomelania hupensis snail control, infectious source control, and health education. A total of area of 290 691.78 hm2 was detected in Jinhu County, and the area with snails was 3 420.98 hm2. There were 8 729.37 hm2 area with snails was controlled. Since 2014, no O. hupensis snails were found. A total of 525 377 person-times were examined for schistosomiasis, with 2 815 schistosomiasis patients identified, and 2 844 person-times were treated by chemotherapy. In addition, 977 cases received the expand chemotherapy. Since 1990, no local schistosome-infected persons were found. In 2017, the awareness rate of schistosomiasis control knowledge and the correct rate of health behavior were increased by 54.59% and 14.23% respectively compared with those in 1992. Conclusions The comprehensive schistosomiasis control measures implemented in Jinhu County at different periods have achieved remarkable outputs and accelerated the schistosomiasis elimination process. However, the precise control measures should be implemented in the future to consolidate the prevention and control achievements.

Strategy of schistosomiasis elimination and its effects in Jinhu County, Jiangsu Province / 中国血吸虫病防治杂志

Objective To understand the strategy of schistosomiasis elimination and its effects in Jinhu County, Jiangsu Province. Methods The data of schistosomiasis control in Jinhu County at different stages from 1970 to 2017 were collected and analyzed. Results From 1970 to 2017, there were three stages of schistosomiasis control, including transmission control, transmission interruption, and monitoring and elimination stages in Jinhu County. The main measures included Oncomelania hupensis snail control, infectious source control, and health education. A total of area of 290 691.78 hm2 was detected in Jinhu County, and the area with snails was 3 420.98 hm2. There were 8 729.37 hm2 area with snails was controlled. Since 2014, no O. hupensis snails were found. A total of 525 377 person-times were examined for schistosomiasis, with 2 815 schistosomiasis patients identified, and 2 844 person-times were treated by chemotherapy. In addition, 977 cases received the expand chemotherapy. Since 1990, no local schistosome-infected persons were found. In 2017, the awareness rate of schistosomiasis control knowledge and the correct rate of health behavior were increased by 54.59% and 14.23% respectively compared with those in 1992. Conclusions The comprehensive schistosomiasis control measures implemented in Jinhu County at different periods have achieved remarkable outputs and accelerated the schistosomiasis elimination process. However, the precise control measures should be implemented in the future to consolidate the prevention and control achievements.

Advances of bacterial flora in mites parasitizing on animals and human / 中国人兽共患病学报

A large number of bacteria were carried by mites parasitizing on animals and human,which including symbiotic and pathogenic bacteria.Mites were an important transmission media and could spread pathogenic bacteria.A total of 184 literatures were collected from database to analye diversity of bacteria carried by mites.There were about 105 species bacteria were carried by 94 mites.These bacteria belong to 9 phylums,22 orders,40 families and 55 genuses(including 17 pathogen and 20 opportunistic pathogen).In this paper,we reviewed the diversity of mites-associated bacteria,which could offer some data for investigation on the relationship between mites and mites-associate bacteria.

Atorvastatin reduces myocardial fibrosis in a rat model with post-myocardial infarction heart failure by increasing the matrix metalloproteinase-2/tissue matrix metalloproteinase inhibitor-2 ratio / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The cholesterol-lowering statin drugs have some non-lipid-lowering effects, such as inhibiting myocardial remodeling. However, the underlying mechanism is still unclear.</p><p><b>METHODS</b>The left anterior descending coronary artery was ligated to establish a rat model of heart failure, and the rats were divided into a sham operation (SO) group, myocardial infarction model (MI) group, and MI-atorvastatin group. Changes in hemodynamic parameters were recorded after the final drug administration. Histological diagnosis was made by reviewing hematoxylin and eosin (HE) stained tissue. Real-time quantitative polymerase chain reaction (PCR) was performed to determine the expressions of type I and type III collagen, matrix metalloproteinase-2 (MMP-2), and tissue matrix metalloproteinase inhibitor-2 (TIMP-2). Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation.</p><p><b>RESULTS</b>The model of heart failure was established and the results of HE staining and Masson's trichrome staining revealed that the rats in the heart failure group showed obvious hyperplasia of fibrotic tissue, which was significantly reduced in the atorvastatin group. Real-time quantitative PCR showed that the MI group showed a significantly increased expression of type I and type III collagen, MMP-2, and TIMP-2, but a significantly reduced MMP-2/TIMP-2 ratio. Compared with the MI group, the atorvastatin group showed significantly reduced expression of type I and III collagen, unchanged expression of MMP-2, significantly reduced expression of TIMP-2, and an increased MMP-2/TIMP-2 ratio. We further found that atorvastatin significantly inhibited the Ang II-induced fibroblast proliferation and the expression of type I and type III collagen in cardiac fibroblasts while increasing the MMP-2/TIMP-2 ratio.</p><p><b>CONCLUSIONS</b>These data suggest that atorvastatin can inhibit cardiac fibroblast proliferation and enhance collagen degradation by increasing the MMP-2/TIMP-2 ratio, thereby inhibiting the formation of myocardial fibrosis in rats with heart failure after myocardial infarction.</p>

Lipopolysaccharide induced activin A-follistatin imbalance affects cardiac fibrosis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Inflammation plays a pivotal role in cardiac remodeling, especially in myocardial fibrosis. Abnormal growth of cardiac fibroblasts is critically involved in the pathophysiology of cardiac hypertrophy/remodeling. Previous study has demonstrated that many inflammation stimulating factors trigger transforming growth factor-β (TGF-β) induction and reactive myocardial fibrosis. Activin A (ACT A) is a member of TGF-β superfamily, and follistatin (FS) is an activin-binding protein, i.e. an antagonist of ACT A. Our previous studies have shown that ACT A-FS imbalance occurs in rats with heart failure (HF), and overexpression of ACT A can lead to ventricular remodeling, and resultant HF. Low expression of FS after myocardial infarction further exacerbated HF. The pathogenic change resulting from overexpression of ACT A is consistent with that of overexpression of angiotensin II (AngII). Ventricular remodeling includes cardiocyte remodeling and myocardial interstitial collagen deposition and fibrosis. Therefore, the present study was designed to investigate the effects of inflammatory factors on the ACT A-FS and the secretions of cardiac fibroblasts in order to explore in depth the mechanism of myocardial fibrosis.</p><p><b>METHODS</b>A rat model with HF was established, and the results showed that there was a greater degree of cardiac fibrosis in HF rats. In addition, we found that there was an imbalance of the ACT A/FS system in HF rats, which was characterized by increased levels of ACT A. Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of the inflammatory factor-bacterial endotoxin lipopolysaccharide (LPS) on cardiac fibroblast proliferation.</p><p><b>RESULTS</b>The results showed that LPS can stimulate the cardiac fibroblasts to proliferate in a dose-dependent manner. Cellular immunohistochemical staining showed that the rat cardiac fibroblasts themselves could express ACT A and FS proteins, and stimulation by LPS could apparently promote the cultured primary rat cardiac fibroblasts to secrete ACT A, but inhibit the secretion of FS. The results also showed that ACT A promoted, in a dose-dependent manner, the proliferation of the cultured primary rat cardiac fibroblasts, and the expression of collagen types I and III. Moreover, ACT A promoted, in a dose dependent manner, the cardiac fibroblasts to secrete nitric oxide (NO), and unregulated the expression of inducible nitric oxide synthase (iNOS) mRNA.</p><p><b>CONCLUSIONS</b>These results suggest that the inflammatory mediator LPS can promote ACT A-FS imbalance in cardiac fibroblasts, mainly overexpression of ACT A. Overexpression of ACT A promotes the proliferation and the secretion of collagens in cardiac fibroblasts through autocrine/paracrine stimulation of NO, and is involved in the pathological process of myocardial fibrosis.</p>

Expression of inflammatory factors in myocardium following coronary microembolization and effect of NF-kB inhibitor on the expression in rats / 第二军医大学学报

Objective To investigate the expression of inflammatory factors in myocardium following coronary microembolization (CME) and effect of NF-kB inhibitor on the expression. Methods CME models were created in 64 rats by injecting homologous microthrombotic particle suspension into the left ventricle with the ascending aorta clamped. The model rats were equally divided into untreated group and pyrrolidine dithiocarbamate (PDTC) treatment group; the animals were sacrificed at 1, 3, 7, and 14 days after operation. Another 24 SD rats served as sham controls. The distribution and dynamic changes of TNF-α, IL-6 and ICAM-1 mRNA expressionin myocardium were determined by in situ hybridization and immunohistochemistry. Results CME associated inflammation was not limited to the surroundings of the microembolization; it also involved a great deal of "innocent" myocardium, producing bystander effect. Myocardium expression of TNF-α, IL-6, and ICAM-1 in CME group was significantly higher than that in the sham control group (P<0.05). NF-kB inhibitor PDTC significantly inhibited TNF-α, IL-6 and ICAM-1 expression after CME (P<0.05). Conclusion CME can produce amplified myocardial inflammation, and NF-kB inhibitor PDTC can markedly ameliorate myocardial inflammation.

Molecular mechanisms of Glanzmann thrombasthenia caused by alpha II b L721R and Q860X compound heterozygous mutation / 中华血液学杂志

<p><b>OBJECTIVE</b>To explore the molecular mechanisms of Glanzmann thrombasthenia caused by alpha II b L721R and Q860X compound heterozygous mutation.</p><p><b>METHODS</b>All exons and exon-intron boundaries of alpha II b and beta3 gene were amplified by PCR and analyzed by direct DNA sequencing. Gene polymorphisms were excluded by direct DNA sequencing. Alpha II b L721R and Q860X mutants expressing vectors were constructed by in vitro site-directed mutagenesis. The expression of alpha II b L721R and Q860X mutants on transfected cell membrane were analyzed by flow cytometry and the whole expression level was confirmed by Western blot. The subcellular localizations of alpha II b L721R and Q860X mutants were determined by immunofluorescent confocal scanning microscopy.</p><p><b>RESULTS</b>The alpha II b compound heterozygous mutations, T2255G (L721R) and C2671T (Q860X), were identified in the proband, the former being inherited from the maternal side and the latter the paternal side. The 293T cells cotransfected with mutated alpha II b L721R and wild-type beta3 expression plasmids expressed 2.1% of normal amount of alpha II b on the cell surface as shown by FACS, in contrast to 31.9% of normal amount of alpha II b on the cells cotransfected with cDNAs of mutated alpha II b Q860X and wildtype beta3 expression plasmids. Western blot of the cell lysates showed no detectable mature alpha II b in cells lysates with L721R mutant. While, truncated alpha II b protein was detected in cell lystes with Q860X mutant. Immunofluorescence studies demonstrated that both L721R and Q860X mutant pro-alpha II bbeta33 complex colocalized in endoplasmic reticulum, but a little in Golgi.</p><p><b>CONCLUSIONS</b>The L721R and Q860X mutations of alpha II b prevent transport of the pro-alpha II bbeta3 complex from the endoplasmic reticulum to the Golgi, hindering its maturation and surface expression. The impaired alpha II bbeta3 transport is responsible for the thrombasthenia.</p>

Granulocyte colony stimulating factor attenuated myocardial apoptosis via Janus kinase 2/signal transducer and activator of transcription signal transduction pathway in rats with coronary microembolization / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of granulocyte colony stimulating factor (G-CSF) on myocardial apoptosis following coronary microembolization (CME) and possible role of Janus kinase/singnal transducer and activator of transcription (JAK/STAT) pathway in this process.</p><p><b>METHODS</b>A total of 92 male Sprague Dawley rats were randomized into CME (n = 24), G-CSF (100 microg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), JAK2 inhibitor AG490 (G-CSF plus AG490, 5 mg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), all rats received left ventricular injection of homologous microthrombotic particle suspension post clamping the ascending aorta. Sham-operated group (n = 20) served as control. The rats were sacrificed at day 3, 7, 14 and 28 after operation. The myocardial mRNA expressions of Bcl-2, Bax, Fas, FasL and GAPDH which was used as the intercomparison, were evaluated by real time PCR. The ratio of Bcl-2/Bax was compared. The protein expression of Caspase-3, cleaved PARP, t-JAK2, p-JAK2, t-STAT3 and p-STAT3 were detected by western blot. Myocardial apoptosis were examined by TUNEL staining.</p><p><b>RESULTS</b>Compared with Sham rats, the mRNA of Bcl-2, Bax, Fas and FasL significantly increased whereas the ratio of Bcl-2/Bax (0.28 +/- 0.04 vs. 2.98 +/- 0.49) significantly decreased and the protein expression of Caspase-3 (0.762 +/- 0.129 vs. 0.133 +/- 0.027), PARP (0.992 +/- 0.146 vs. 0.386 +/- 0.074) and the myocardial apoptosis index (17.2 +/- 1.9 vs. 1.2 +/- 0.6) significantly increased in CME hearts (all P < 0.05). rhG-CSF significantly attenuated CME induced changes and cotreatment with JAK2 inhibitor AG490 abolished the effects of rhG-CSF. The protein expressions of t-JAK2 and t-STAT3 among the groups were similar. P-JAK2 and p-STAT3 protein expressions were significantly increased in G-CSF group compared to other groups (P < 0.05).</p><p><b>CONCLUSION</b>G-CSF attenuated myocardial apoptosis induced by CME via JAK2/STAT3 pathway.</p>

Time course of myocardial NF-kappaB activation post coronary microembolization / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the time course of myocardial NF-kappaB activation and association with cardiac function and other pro-inflammation cytokines following coronary microembolization (CME).</p><p><b>METHODS</b>CME was induced by homologous microthrombotic particle suspension injection into left ventricle with simultaneous short-term ascending aorta clamping. The CME rats were randomized to untreated group and pyrrolidine dithiocarbamate (PDTC, a specific NF-kappaB inhibitor) treated group (n = 32 respectively). The rats were sacrificed on day 1, 3, 7 and 14 post-operationally (n = 8 each). Twenty-four rats were sham-operated and served as controls. NF-kappaB DNA-binding activity was evaluated by electrophoretic mobility shift assay (EMSA), protein expressions of TNFalpha, IL-6 and ICAM-1 were analyzed by Western blotting, the dynamic alterations of TNFalpha, IL-6 and ICAM-1 mRNA were quantitatively assessed by Real-time PCR post hemodynamic measurements.</p><p><b>RESULTS</b>NF-kappaB DNA-binding activity in CME group was significantly increased than that of sham group on day 1, peaked at day 3 and was similar as that in sham rats on day 14. The protein and mRNA expressions of TNFalpha, IL-6 and ICAM-1 were significantly increased in CME group at various time points compared those in sham rats. NF-kappaB DNA-binding activity positively correlated with mRNA expressions of TNFalpha, IL-6, ICAM-1, respectively (r = 0.72, P < 0.05; r = 0.94, P < 0.01; r = 0.62, P < 0.05). PDTC significantly suppressed protein and mRNA expressions of TNFalpha, IL-6 and ICAM-1 (P < 0.05) and improved left ventricular function.</p><p><b>CONCLUSION</b>NF-kappaB activation post CME could upregulate the gene transcriptions of TNFalpha, IL-6, ICAM-1 and enhance inflammatory responses and aggravate left ventricular dysfunction.</p>

The research on the efficacy and safety of recombinant human brain natriuretic peptide treating patients with de- compensated acute heart failure / 中国实用内科杂志

Objective To compare the efficacy and safety of intravenous infusion of recombinant human brain natriuretic peptide(rhBNP)versus Sodium Nitroprusside on treating patients with decompensated acute heart failure.Discuss rhBNP 's effect on connective tissue of heart.Methods A total of 44 patients characterized of decompensated acute heart failure were enrolled in this study.The patients were randomLy allocated to rhBNP group who receive rhBNP(1.5?g/kg bolus intravenous injection followed by 0.0075?g/(kg?min)for 24 hours,n=23)and Sodium Nitroprusside group(10 ?g/ rain for 24 hours,n=21 ).Blood pressure,heart rate,dyspnea grade,24 hours fluid in-and-output and improvement in patient symptoms and signs were evaluated and adverse events were documented.Results Dyspnea and symptom im- provements were much more significant in rhBNP group compared to Sodium Nitroprusside group(P

RECOMMENDATION OF A KIND OF SYNTHETIC MEINTENANCE LIQUOR TO PRESERVE BACTERIUM LONG / 微生物学通报

This Synthetic Meintenance Liquor contains all kinds of nutritive substance that subsist the bacterium, and can preserve the bacterium for nearly ten years by providing energy needed by metabolism. It is a favorable culture medium to preserve bacterum long.