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Dengue fever is one of the most serious mosquito-borne infectious diseases in the tropical world, causing substantial human morbidity and mortality, yet there is no specific treatment till now, and the main measures preventing dengue fever include applying pesticide to kill adult vector mosquitos and removing standing water to prevent the breeding of mosquitoes etc. Appropriate uses of such approaches can reduce dengue epidemic risk via reducing mosquito density. In fact, vector control using insecticides is the most common method to prevent and control mosquito-borne disease transmission. Nevertheless, recent research has shown that Aedes albopictus and Aedes aegypti, the two key vectors for dengue fever transmission, have rapidly developed high resistance to the most commonly used adult insecticide pyrethroid (deltamethrin and permethrin) and larvicide organophosphate (temephos). Therefore, it is of great significance to obtain a new drug with longer-term efficacy to prevent dengue virus transmission. Pesticides currently used act on adult stage of mosquitoes, typically applying to the environment where mosquito bites (on humans) occur, and very few target on egg or juvenile stages of the mosquitoes in the water environment. Calcium cyanamide (CaCN2), widely used as a fertilizer in many different settings, was recently shown to have potential to prevent tropical diseases by eliminating or inhibiting the growth and development of intermediate hosts. The main compounds of calcium cyanamide (CaCN2) are CaCN2 (50%- 60%) and calcium oxide (15%). The representative products of calcium cyanamide (CaCN2) are PERLKA® from Germany and ROEBON® from China. CaCN2 has recently been recognized to have the fungicidal effect on the pathogens of the soil borne diseases and addition of CaCN2 could benefit the thermophilic phase and the composting could quickly reach the sanitary standard and will contribute to solve the feces disposal problems. According to our team's long-term investigation and research, we found that ROEBON® (50% CaCN2) can be used to eliminate Oncomelania and effectively control the spread of schistosomiasis. In the latest research, we have confirmed that 10 mg/L CaCN2 (20 mg/L ROEBON®) can completely inhibit the emergence of mosquito larvae and the population growth from the perspective of inhibiting development and the efficacy can lasts for three months. Calcium cyanamide is a good candidate drug to control mosquito-borne infectious diseases transmission, especiallly for dengue fever prevention. In 2014, Scientific Committee on Health and Environmental Risks in European Commission promoted preliminary opinion on potential risks to human health and the environment from the utilization of calcium cyanamide as fertilizer, but convincing evidences for the causal connections between the exposure to CaCN2 and human health damages are missed. Given a 96-h acute zebrafish toxicity study, the No Observed Effect Concentration (NOEC) of calcium cyanamide to zebrafish was 100 mg/L CaCN2. In summary, most of the data are based on the evaluation of the effect of CaCN2 as a fertilizer, and the related research as a mosquito inhibitor is still very scarce. The research on toxicity of CaCN2 in mosquitoes needs to be further strengthened.
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Objective To study the morphological change of Schistosoma japonicum eggs processed by calcium cyanamide synthetic drug,so as to provide the basis for further study of the mechanism that calcium cyanamide synthetic drug to schisto?some eggs. Methods The calcium cyanamide synthetic drug was added to the cattle feces containing schistosome eggs and mixed up,and then the cattle feces was stacked as original shape on the marshland. Blank controls were set at the same time. The cattle feces samples were collected and the schistosome eggs were observed under a microscope on the 1st,2nd,3rd,7th day after the experiment. Results By the effect of calcium cyanamide synthetic drug,the color of eggs was deepening gradual?ly,the miracidia were atrophied,and the shells of eggs were thickened. The embryonic membrane of miracidia was no longer completed 3 days later,and the miracidia were deformed severely 7 days later. The atrophy of miracidia was not obvious in the blank controls. Conclusion The schistosome miracidia and embryonic membrane can be damaged by the calcium cyanamide synthetic drug,and worse damaged with time extending.
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Objective To investigate the effect of diuretic (furosemide) therapy on kidney injury induced by melamine and cyanuric acid in rats. Methods 36 male Spragne Dawley rats were random disided into 3 groups. Group A was treated with 2mL of water daily, group B was treated with melamine and cyanuric acid ( each 100 mg/kg) daily for 4 days and then 2ml of water daily, group C was treated with the same as group B at the first 4 days and then treatment with furosemide (20mg/kg) daily. Samples of blood and 24h urine were collected to detective biochemical indexes, and kidney sections were performed on days 4 and 11 ( each end point, n = 6). The kidneys were observed with histopathology and renal crystal deposition scores were determined. Results On the 4th day, group B and group C were resulted in acute kidney injury such as oliguria [ ( 3. 39 ± 1.02 ) ml, ( 3. 20 ± 0. 86 ) ml ] and high serum creatinine [ ( 153.54 ±27. 08)μmol/L, (160. 11 ± 19. 55)μmol/L] and renal melamine cyanurate crystal were found in the renal tissues. On the 11th day, the renal crystal deposition score in the rats was reduced by 9. 52% ( P >0. 05). Compared with those of the 4th day in group B, it reduced by 63.63%( P <0.05) in group C. Urine volume were increased significantly compared with those of the 4th day( P < 0. 05 ) in group C [ from (3.20±0. 86)ml to (25.96 ±5.97)ml] and group B [ from(3. 39 ± 1.02)ml to (8. 57 ± 1.66)ml] , and Urine volume in group C was increased significantly more than that in group B ( P < 0. 05 ). The serum creatinine was obviously reduced as compared with those of the 4th day in group B and C( P <0.05), from[ (153. 54±27.08) μmol/L] to [ ( 106. 10 ±5.53) μmol/L] in group B and from [ ( 160. 11 ± 19. 55) μmol/L] to [ (67. 17 ± 12. 80 ) μmol/L] in group C, but the serum creatinine in group B was still higher than that in group A and C ( P < 0. 05). Conclusions Furosemide can attenuate the damage of acute kidney injury induced by melamine and cyanuric acid.
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Objective To observe the effects of calcium cyanamide (Rongbao) on the histological and morphological changes of Oncomelania hupensis snails in order to explore its molluscicidal mechanisms.Methods The serial snails' slides were fixed after soaking in a concentration of Rongbao leached liquor at different time.The histological and morphological changes of the snails were compared among these slides.Results After soaking in the Rongbao leached liquor for 48 h,the mantle epithelia,respiratory epithelia of the gill,liver cells,and muscle cells of gastropods were injured seriously,which resulted in the death of the snails directly.The death rates of the snails were 96.70% and 100% after soaking in the Rongbao leached liquor for 48 h and 72 h,respectively.Conclusion Rongbao is an effective molluscicide by damaging the several snail tissues.
ABSTRACT
O experimento foi conduzido com o objetivo de verificar a eficiência da combinação de cinco concentraçõesde cianamida hidrogenada (CH) e quatro épocas de poda, na quebra da dormência e antecipação dacolheita da videira Niagara Rosada no município de Ponta Grossa PR. O delineamento experimentalfoi em blocos casualizados no esquema fatorial 4 x 5 (épocas de poda x concentrações de CH) , com 3repetições e 3 plantas por parcela. Foram analisados a porcentagem de brotação, o número de cachos porplanta, a produção por planta e a massa média dos cachos. Houve efeito da aplicação de cianamidahidrogenada no aumento da brotação das gemas apenas para a primeira época de poda (06/08/2007). Aprimeira época de poda antecipou em uma semana a colheita, embora a ocorrência de geadas tenhaprejudicado a produção. O atraso na época de poda proporcionou um maior número de cachos por plantae a maior produção.
This research work had as the aim of verifying the efficiency of five combined concentrations of hydrogencyanamide (CH) in four consecutive pruning times of sprouting vine and harvest anticipation of 'NiagaraRosada' in the county of Ponta Grossa, PR. The experiment had a factorial design (4 x 5) with 3 replicationsand 3 plants per parcel. The analysis were sprouting percentage, number of clusters per plant, rate ofproduction and average weight per cluster. The effect of CH was shown only at the first pruned timewhen sprouting but the occurrence of frosting decreased the yield. The delay in the process of pruningshowed a higher number of cluster per plant, which consequently resulted in yield increase
Subject(s)
Cyanamide , VitisABSTRACT
Aim To investigate the role of mitochondrial aldehyde dehydrogenase 2 ( ALDH2) in the cardio-protection of ischemic postconditioning in isolated rat hearts. Methods Hearts isolated from male Sprague-Dawley rats were perfused on a langendorff apparatus and subjected to 30 min of regional ischemia( occlusion of left anterior descending artery) followed by 120 min reperfusion. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of reperfusion. The ventricular hemodynamic parameters and lactate dehydrogenase ( LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method. The expressions of ALDH2,Bcl-2 and Bax at mRNA level of left anterior myocardium were detected by RT-PCR analysis. Results In contrast to ischemia and reperfusion,ischemic postconditioning improved the recovery of left ventricular developed pressure,rate pressure product during reperfusion,and reduced LDH release and infarct size. The expressions of ALDH2 mRNA level and the ratio of Bcl-2 /Bax were increased. Adminis-tration of ALDH2 antagonist cyanamide at the beginning of reperfusion attentuated the role of ischemic postconditioning. Conclusion Ischemic postconditioning plays a role in the cardioprotection partially through increasing mitochondrial ALDH2 mRNA expression.