Thiamethoxam belongs to the second-generation neonicotinoid insecticides, mainly acting on nicotinic acetylcholine receptors (nAChR) . Severe poisoning cases can lead to respiratory failure, shock, and even death. There are relatively few reports on thiamethoxam poisoning, and few literature reports on concurrent rhabdomyolysis cases have been found so far. This article reviews the treatment process of a case of oral thiamethoxam poisoning. The patient developed mild rhabdomyolysis (CK: 1581 U/l) and renal dysfunction (creatinine: 127 μmol/L) immediately after taking the medication, reaching its peak on the second day (CK: 16329 U/l) . After active treatment (such as Blood purification, drainage, gastrointestinal decompression and organ support) , the symptoms of rhabdosis gradually improved and the patient was discharged. It is suggested that when treating thiamethoxam poisoning, the occurrence of rhabdomyolysis syndrome should be concerned.

Thiamethoxam belongs to the second-generation neonicotinoid insecticides, mainly acting on nicotinic acetylcholine receptors (nAChR) . Severe poisoning cases can lead to respiratory failure, shock, and even death. There are relatively few reports on thiamethoxam poisoning, and few literature reports on concurrent rhabdomyolysis cases have been found so far. This article reviews the treatment process of a case of oral thiamethoxam poisoning. The patient developed mild rhabdomyolysis (CK: 1581 U/l) and renal dysfunction (creatinine: 127 μmol/L) immediately after taking the medication, reaching its peak on the second day (CK: 16329 U/l) . After active treatment (such as Blood purification, drainage, gastrointestinal decompression and organ support) , the symptoms of rhabdosis gradually improved and the patient was discharged. It is suggested that when treating thiamethoxam poisoning, the occurrence of rhabdomyolysis syndrome should be concerned.

Objective To construct in the extracellular matrix metalloproteinase inducer (EMMPRIN)glycosylation single point mutation plasmid,and to explore its relationship with tumor cell proliferation.Methods PCR point mutantion technology was used to construct the mutantion plasimid of EMMPRIN glycosylation single point.After successful mutation, the function of mutantion plasmids were detected. Western blotting was used to detect the expression of EMMPRIN protein,immunofluorescence method was used to detemine the morphological changes of the cells,and MTT assay was performed to detect the relationship between mutantion pasmid and tumor cell proliferation.Results Confirmed by restriction enzyme digestion and sequencing,the 44th,the 152th,and the 186th Asn were successfully mutated to Gln in the sequence of EMMPRIN;EMMPRIN/GFP (N44Q), EMMPRIN/GFP(N152Q),and EMMPRIN/ GFP (N186Q)glycosylation single point mutation plasmids were constructed.Compared with wild-type,thel morphology of the cells was significantly changed,the core division of mutant-type cells was significantly reduced, the number of filopodia was reduced. The results of MTT assay showed that the survival rate of the cells in wild-type group were significantly increased compared with control group (P<0.05 );the survival rates of the cells in EMMPRIN (N44Q) group, EMMPRIN (N152Q) group and EMMPRIN(N186Q)were significantly decreased compared with wild-type group(P<0.05).Conclusion Mutant-type EMMPRIN can inhibit the proliferation of tumor cells;with the duration increasing, the inhibitory effect is weakened.There is a correlation between EMMPRIN glycosylation and proliferation of tumor cells.

We synthesized the superparamagnetic paclitaxel nanoparticles from modified chitosan tangling around Fe3O4 ferrofluid and taxol, and observed the nanoparticles with transmission electronic microscopy (TEM). Then we evaluated the paramagnetism of the particles by vibration specimen magnetometer (VSM) and tested their cytotoxicity with flow cytometry (FCM). The prepared nanoparticle solution was black without any floccule or sediment and appeared transparent after diluted. The nanoparticles were spherical and dispersed in water with mean diameter of 15 nm under TEM and showed superparamagnetic character. FCM test showed the nanoparticles had significant toxic effects against malignant astrocytoma U251 cell lines, equal to taxol alone. These results showed that the superparamagnetic nanoparticle not only enhanced the solubility of paclitaxel in water, but also was superparamagnetic and cytotoxic, which make suitable tools for magnetic targeting chemotherapy of brain gliomas.
Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Brain Neoplasms ; pathology ; Cell Line, Tumor ; Chitosan ; pharmacology ; Drug Carriers ; chemistry ; Drug Compounding ; methods ; Ferric Compounds ; Glioma ; pathology ; Humans ; Magnetics ; Metal Nanoparticles ; chemistry ; Nanoparticles ; Paclitaxel ; pharmacology

Objective To explore the role of transcription factors such as nuclear factor-kappa B(NF-?B) and glucocorticoid receptor(GR) in the pathogenesis of Adriamycin(ADM)-induced nephrosis in rats and the therapeutic effects of dexamethasone(Dex) and cyclosporin(CsA) on these animals.Methods The DNA-binding abilities of NF-?B and GR in cortex of kindey were examined with electrophoretic mobility shift assay(EMSA) and isotopic radioautography on the 7th,14th,21th and 28th day after a single intravenous injection of ADM,and the therapeutic effects of Dex and CsA were estimated.The biochemistry parameters from blood and urine of rats and the urine protein excretion were also measured.Results The NF-?B DNA-binding ability was significantly increased after 7 days and achieved maximum after 28 days(P0.05).Conclusion The DNA-binding ability of NF-?B is abnormally increased and that of GR is decreased in cells from cortex of kindey in Adriamycin-induced nephrotic rats.The NF-?B DNA-binding ability can be inhibited and the urine protein excretion is decreased by the treatment of CsA.