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51.
Microbial inoculants are globally recommended for plant growth promotion and control of plant pathogens. These inoculants require stringent quality checks for sustainable field efficacy. Questionable regulatory frameworks constantly deteriorate the reliability of bio-inoculant technology. Existing global regulations do not involve any rapid molecular technique for the routine inspection of microbial preparations. Sequence characterized amplified region (SCAR) marker offers rapid and precise strain-level authentication of target microbes. Such advanced molecular techniques must be exploited to accurately validate the microbial formulations. Besides, the global dissemination of plant pathogenic microbes has always been an alarming threat to food security. SCAR markers could be used at the plant quarantine centers to rapidly detect catastrophic pathogens, thereby circumventing the import and export of contagious plant materials. The current review is focused on promoting the SCAR marker technology to validate commercial bio-inoculants and predict plant pandemics. 相似文献
52.
Evaluation of the chronic toxicity and oncogenicity of N,N-diethyl-m- toluamide (DEET) 总被引:1,自引:0,他引:1
Schoenig GP; Osimitz TG; Gabriel KL; Hartnagel R; Gill MW; Goldenthal EI 《Toxicological sciences》1999,47(1):99-109
Chronic toxicity and/or oncogenicity studies were conducted in rats, mice,
and dogs with the insect repellent DEET. DEET was mixed in the diet and
administered to CD rats for two years at concentrations that corresponded
to dosage levels of 10, 30 or 100 mg/kg/day for males and 30, 100, or 400
mg/kg/day for females; to CD-1 mice for 18 months at dosage levels of 250,
500, or 1000 mg/kg/day; and to dogs for one year, via gelatin capsules, at
dosage levels of 30, 100, or 400 mg/kg/day. In the rodent studies, each
group consisted of 60 animals of each sex, and two concurrent independent
control groups, each containing 60 animals/sex were included in each study.
Each group in the dog study consisted of four male and four female dogs and
one control group was included in the study. Treatment-related effects were
observed at the highest dose level in all three studies. For rats, the
effects included decreases in body weight and food consumption and an
increase in serum cholesterol in females only. In mice, the effects
observed were decreases in body weight and food consumption in both sexes.
The effects observed in dogs included increased incidences of emesis and
ptyalism, and levels of transient reduction in hemoglobin and hematocrit,
increased alkaline phosphatase (males only), decreased cholesterol, and
increased potassium. One male dog in the high-dose group also exhibited
ataxia, tremors, abnormal head movements, and/or convulsions on several
occasions during the study. The highest no- observed-effect levels (NO-ELs)
for rats, mice and dogs were determined to be 100, 500, and 100 mg/kg/day,
respectively. No specific target organ toxicity or oncogenicity was
observed in any of the studies.
相似文献
53.
Kathrine R?e Lars TG Mikalsen Albert J van der Kogel Johan Bussink Heidi Lyng Anne H Ree Laure Marignol Dag R Olsen 《Radiation oncology (London, England)》2012,7(1):1-13
Background
The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is activated in tumor cells and promotes tumor cell survival after radiation-induced DNA damage. Because the pathway may not be completely inhibited after blockade of PI3K itself, due to feedback through mammalian target of rapamycin (mTOR), more effective inhibition might be expected by targeting both PI3K and mTOR inhibition.Materials and methods
We investigated the effect of two dual PI3K/mTOR (both mTORC1 and mTORC2) inhibitors, NVP-BEZ235 and NVP-BGT226, on SQ20B laryngeal and FaDu hypopharyngeal cancer cells characterised by EGFR overexpression, on T24 bladder tumor cell lines with H-Ras mutation and on endothelial cells. Analysis of target protein phosphorylation, clonogenic survival, number of residual ??H2AX foci, cell cycle and apoptosis after radiation was performed in both tumor and endothelial cells. In vitro angiogenesis assays were conducted as well.Results
Both compounds effectively inhibited phosphorylation of Akt, mTOR and S6 target proteins and reduced clonogenic survival in irradiated tumor cells. Persistence of DNA damage, as evidenced by increased number of ??H2AX foci, was detected after irradiation in the presence of PI3K/mTOR inhibition, together with enhanced G2 cell cycle delay. Treatment with one of the inhibitors, NVP-BEZ235, also resulted in decreased clonogenicity after irradiation of tumor cells under hypoxic conditions. In addition, NVP-BEZ235 blocked VEGF- and IR-induced Akt phosphorylation and increased radiation killing in human umbilical venous endothelial cells (HUVEC) and human dermal microvascular dermal cells (HDMVC). NVP-BEZ235 inhibited VEGF-induced cell migration and capillary tube formation in vitro and enhanced the antivascular effect of irradiation. Treatment with NVP-BEZ235 moderately increased apoptosis in SQ20B and HUVEC cells but not in FaDu cells, and increased necrosis in both tumor and endothelial all cells tumor.Conclusions
The results of this study demonstrate that PI3K/mTOR inhibitors can enhance radiation-induced killing in tumor and endothelial cells and may be of benefit when combined with radiotherapy. 相似文献54.
The paper aims to determine whether the inflammation,a powerful risk factor that has been demonstrated for the development of coronary artery disease,plays a role in no-reflow phenomenon in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI).Methods We prospectively analyzed 656 patients with AMI after primary PCI.Based on post-PCI angiography data,patients were divided into two groups:the no-reflow group (TIMI=2,n =60) and the reflow group (TIMI=3,n =596).Results Our results showed that the inflammatory factors including leukocyte count (×109/L) (10.90±4.04 vs.9.12±2.98 P =0.002),hs-CRP (5.04±0.71 vs.4.70±0.75 P =0.001) and other factor platelet count (×109/L) (210.96±33.42 vs.196.41±46.06 P =0.033) in no-reflow group are significantly higher than those in reflow group,major adverse cardiac events happened in the patients with no-reflow are higher than in reflow patients no matter in hospital or at the end of follow-up.We also found the left ventricular ejection fraction (LVEF) dramatically decreased (58.65±9.34 vs.51.29±11.38,P<0.001) and left ventricular end-diastolic dimension (LVEDD) significantly increased (49.94±6.75 mm vs.54.66±6.68mm,P<0.001) in no-reflow patients at the end of follow-up.Conclusions Our results suggest that inflammation factors function in no-reflow phenomenon,and no-reflow is a serious complication after primary PCI which predicts poor left ventricular systolic functional recovery and mortality in patients with AMI.(J Geriatr Cardiol 2008;5:217-222) 相似文献
55.
V Balachandar J Pahuja V T Maddaiah P J Collipp 《American journal of diseases of children (1960)》1975,129(9):1092-1095
A mildly obese 15-year-old boy had short stature with rounded facies and short, stubby hands and toes. He had the fully expressed syndrome of pseudohypoparathyroidism but was the only member of his family who had all the somatic characteristics of this disease. The serum parathyroid hormone level was substantially elevated. Urinary excretion of cyclic adenosine monophosphate and phosphate failed to increase following intravenous infusion of parathyroid hormone. However, he did not have hypocalcemia. The present entity is probably a transient form of pseudohypoparathyroidism with partial responsiveness of skeletal adenyl cyclase to parathyroid hormone. 相似文献
56.
Protective role of DLalpha-lipoic acid against adriamycin-induced cardiac lipid peroxidation 总被引:3,自引:0,他引:3
The cytoprotective activity of alpha-lipoic acid against free radical toxicity manifested during adriamycin (ADR)-induced cardiotoxicity has been investigated. ADR is a potent antitumour drug known to cause severe cardiotoxicity. Although ADR generates free radicals, the role of these radicals in the development of cardiac toxicity is still not well understood. In the present study, we evaluated the influence of chronic ADR treatment on the cellular defence mechanism against free radicals and the effect of alpha-lipoic acid supplementation on ADR-induced cardiotoxicity in male Wistar rats. The increase in lipid peroxidation (LPO) and activities of serum myocardial enzymes, namely lactate dehydrogenase (LDH) and creatinephosphokinase, associated with the decrease in activities of enzymatic (SOD, CAT, GPx, G6PD and GR) and non-enzymatic (GSH, Vit C and Vit E) antioxidants levels were the salient features observed in ADR-induced cardiotoxicity. Lipoic acid pretreated groups showed significant increase in activities of both enzymatic and non-enzymatic antioxidant levels. These observations highlight the antioxidant property of alpha-lipoic acid and its cytoprotective action against ADR-induced cardiotoxicity. 相似文献
57.
Seventeen out of 21 children with severe asthma had an abnormal increase in urinary Kynurenic (KA) and Xanthurenic (XA) acid following oral tryptophane administration. In a second study 11 asthmatic children had significantly greater increases in XA and KA than nine normal healthy children. A micro-assay of KA and XA by column chromatography was performed. The data suggest the presence of a partial block in the metabolism of tryptophane in some children with bronchial asthma. 相似文献
58.
Dopa-responsive dystonia in British patients: new mutations of the GTP- cyclohydrolase I gene and evidence for genetic heterogeneity 总被引:4,自引:0,他引:4
Bandmann O; Nygaard TG; Surtees R; Marsden CD; Wood NW; Harding AE 《Human molecular genetics》1996,5(3):403-406
Dopa-responsive dystonia (DRD) was originally described in a series of
Japanese patients, but is now increasingly recognized in other countries.
Recently the GTP cyclohydrolase I (GTPCH) gene was isolated as the first
causative gene for dopa-responsive dystonia (DRD). Mutations were
identified in three Japanese families with autosomal dominantly inherited
DRD and in one sporadic Japanese patient. Characterisation of the
exon-intron boundaries of this gene has now allowed the analysis of
mutations at the level of genomic DNA. Amplifying all six exons, we
analyzed the GTPCH gene in nine British families with 33 affected family
members and in three sporadic cases and found six new mutations. Only point
mutations were found, causing a stop codon in one family and an amino acid
change in highly conserved regions of the gene in a further four families
and in one sporadic case. None of these mutations were detected more than
once and none of the mutations previously described were found in our
patients. No mutations were identified in four families and in two sporadic
cases.
相似文献
59.
Anirban Goutam Mukherjee Uddesh Ramesh Wanjari Sandra Kannampuzha Soumik Das Reshma Murali Arunraj Namachivayam Kaviyarasi Renu Gnanasambandan Ramanathan George Priya Doss C. Balachandar Vellingiri Abhijit Dey Abilash Valsala Gopalakrishnan 《Journal of medical virology》2023,95(1):e28206
In addition to the COVID-19 waves, the globe is facing global monkeypox (MPX) outbreak. MPX is an uncommon zoonotic infection characterized by symptoms similar to smallpox. It is caused by the monkeypox virus (MPXV), a double-stranded DNA virus that belongs to the genus Orthopoxvirus (OPXV). MPXV, which causes human disease, has been confined to Africa for many years, with only a few isolated cases in other areas. Outside of Africa, the continuing MPXV outbreak in multiple countries in 2022 is the greatest in recorded history. The current outbreak, with over 10 000 confirmed cases in over 50 countries between May and July 2022, demonstrates that MPXV may travel rapidly among humans and pose a danger to human health worldwide. The rapid spread of such outbreaks in recent times has elevated MPX to the status of a rising zoonotic disease with significant epidemic potential. While the MPXV is not as deadly or contagious as the variola virus that causes smallpox, it poses a threat because it could evolve into a more potent human pathogen. This review assesses the potential threat to the human population and provides a brief overview of what is currently known about this reemerging virus. By analyzing the biological effects of MPXV on human health, its shifting epidemiological footprint, and currently available therapeutic options, this review has presented the most recent insights into the biology of the virus. This study also clarifies the key potential causes that could be to blame for the present MPX outbreak and draw attention to major research questions and promising new avenues for combating the current MPX epidemic. 相似文献
60.
TG Poehlmann UR Markert 《American journal of reproductive immunology (New York, N.Y. : 1989)》2006,55(6):407-407
Preterm birth is a major cause of perinatal morbidity and mortality. Intrauterine infection/inflammation is associated with a majority of preterm labor and birth cases. Despite decades of studies recognizing a strong association between infection/inflammation and preterm birth, no effective method of preventing infection-induced premature labor and delivery is yet available. Importantly, the mechanisms by which intrauterine infection/inflammation may contribute to preterm birth are not known. Based on our observations with human gestational tissue to highlight the role of IL-10 in normal and comprimised pregnancy outcomes, we have performed experiments with syngeneic and allogeneic pregnant IL-10-/- mice or congenic wild type mice. Pregnancy outcomes were assessed in response to i.p. administration of low doses of lipopolysacchade (LPS) on gd 14. The mice were allowed to deliver or were sacrificed on gd 16 for isolation of uterine immune cells for functional studies or collected tissue for histological analysis. Attempts were made to prevent preterm parturition. LPS-treated IL-10-/- , but not wild type mice, displayed a significant acceleration in time of delivery, on gd 16.5 compared to gd 19.6 for wild type controls. The premature delivery observed in LPS-treated IL-10-/- mice was associated with an increase in the number of uterine NK (uNK) cells. These cells also displayed a dramatic infiltration of the placenta with a perivascular localization. uNK cells appear to be responsible for the induction of preterm birth in these mice as depletion of NK cells completely restored normal length of gestation. Moreover, neutralization TNF-α also rescued the premature delivery. Taken together, our results for the first time demonstrate that IL-10 deficiency and uterine NK cell cytotoxic activation link intrauterine inflammation to preterm parturition. 相似文献