The leaves of sensitive maize variety may show symptoms of chlorosis and shrinking 7 d after applying nicosulfuron. The weeding efficiency of nicosulfuron herbicide is related to weed species, leaf age and how long it is applied after rain.. Meanwhile, the resistance of plant to nicosulfuron depends on its metabolic rate, Mechlorethamine hydrochloride sensitivity to ALS, and nicosulfuron dosage. However, there is few paper reporting the application of postemergence herbicide controlling many grasses and broadleaf weeds in Radix Isatidis fields. It is shown that rational application of trifluralin, pendimethalin and glyphosate at preemergence stage can control weeds effectively in Radix Isatidis fields. It is also reported that clethodim and quizalofop-pethyl at post-emergence stage can be used for grassy weed control in Radix Isatidis fields. Primary mode of action of the ALS-inhibiting herbicides that interfere with the activity of ALS enzyme seems no longer in doubt. But, secondary effects of ALS inhibition, such as decreased photosynthesis, disturbed respiration, and synthesis of branched chain amino acids, etc., need to be investigated, which have also been implicated in the mechanism of plant death. Detection of chlorophyll fluorescence dynamics is a rapid and non-invasive 
probe of researching plant photosynthetic functions, which has been widely applied to study the effects of herbicides in plants. The safety of herbicides on plants may be represented through agronomic traits and physiological indexes. In this study, nicosulfuron at the recommended usage was not safe to Radix Isatidis seedlings, which was reflected by reduced biomass. It was coincident with Yuan et al., mesosulfuron-iodosulfuron was unsafe to Radix Isatidis seedlings and decreased the leaf area and fresh weight significantly. The probands in this study presented with an early onset neuromuscular disorder characterized by severe exercise-induced weakness. The lack of specific morphological changes in muscle and peripheral nerve biopsies excluded an underlying congenital myopathy or neuropathy. Electrodiagnostic findings and decreased AChR concentration in the muscle indicated a disorder of neuromuscular transmission. The autoimmune disease myasthenia gravis was eliminated based on the early age of onset and an absence of AChR antibodies in serum and AChR-bound antibodies in the muscle. The clinical Alprostadil diagnosis in the Labrador Retrievers was CMS. While clinical signs and electrophysiological findings are generally similar between presynaptic, synaptic, and postsynaptic forms of CMS, a notable observation in the affected puppies was a worsening of the phenotype upon administration of an AChE inhibitor. This response indicates desensitization of the AChRs from overexposure to ACh and is consistent with a synaptic form of CMS referred to as end-plate AChE deficiency. EAD accounts for 10% to 15% of all human cases of CMSs and is always caused by mutations in COLQ. COLQ encodes a collagen strand that homotrimerizes to form the tail subunit of asymmetric AChE. ColQ anchors AChE to the basal lamina where the enzyme hydrolyzes ACh, thereby limiting the length of the synaptic response. In the absence of ColQ, ACh accumulates, causing prolonged muscle contraction and eventually the desensitization of AChR. Through the examination of SNP allele frequencies in the Labrador Retriever family, we identified 2 chromosomes harboring CMS candidate genes that showed an inheritance pattern consistent with autosomal recessive transmission.