Acrylamide ; analysis ; Air Pollutants, Occupational ; analysis ; Chromatography, High Pressure Liquid ; methods ; Workplace

Humans ; Indicators and Reagents ; supply & distribution ; Occupational Health

Biopsy ; Brain ; pathology ; Frozen Sections ; methods ; Humans

Acute myeloid leukemia (AML) is a genetic heterogeneous disease in which primordial and juvenile myeloid cells proliferate or accumulate abnormally in bone marrow, peripheral blood and other tissues, resulting in damage to normal hematopoietic function. Studies have shown that about 30% of AML patients have FMS-like tyrosine kinase 3 (FLT3), FLT3 abnormal regulation is closely related to the occurrence and development of AML. At present, FLT3 has become an important target for developing small molecular targeted drugs. Currently, a variety of FLT3 inhibitors and FLT3 degraders have been developed targeting FLT3, and some compounds have exhibited good anti-AML activity. This article summarizes and sorts out the current mainstream drugs for AML therapeutic targeting FLT3, in order to provide a reference for the development and design of AML drugs.

Aim To investigate the relationship between the clinical actions and the serum concentrations of the enantiomers of (?)-trans tramadol and its active metabolite. Methods 20 postoperative patients were divided into two groups and given multiple intravenous doses of (?)-trans tramadol hydrochloride injection, 400 mg?d-1 (group A) or 300 mg?d-1 (group B). The blood samples were taken at 38 h after the initial dose. The concentrations of the enantiomers of (?)-trans tramadol and its active metabolite, (?)-trans O-demethyltramadal were determined with high performance capillary electrophoresis(HPCE). Results The concentrations of the enantiomers of (?)-trans tramadol, the frequency and serious level of adverse reactions were higher in group A than in group B. The concentrations of the enantiomers of (?)-trans O-demethyltramadal, the analgesic effect were similar between group A and group B. Conclusion There is much closer relation between the analgesic effect and the concentration of (+)-O-demethyltramadal. The frequency and serious level of adverse reactions may be attributed to the higher concentrations of the enantiomers of (?)-trans tramadol, which are caused by the saturated metabolism.

Objective To demonstrate high mobility group box chromosomal protein 1(HMGBI) expression in synovium and joint,and to identify the role of HMGB1 in the pathogenesis of synovitis and joint destruction in adjuvant-induced arthritis(AA).Methods AA of 15 male rats were induced in SD rats by intradermal injection of 100?l Freud's complete adjuvant in the foot pad of the left hind paw.All rats were killed at the 18th day.Synovium and joints were collected for histopathology studies and determining the expression of HMGB1 by immunohistochemistry,and serum was collected for determining the expression of HMGB1 by western blotting analysis.Results Immunostaining of specimens from normal rats showed that HMGB1 was primarily confined to the nucleus of synoviocytes with occasional cytoplasmic staining.In contrast, inflammatory synovial tissues from AA rats showed a distinctly different HMGB1 staining pattern.Nuclear HMGBI expression was accompanied by a cytoplasmic staining in many mononuclear cells.The cytoplasmic HMGB1 expression in synovium of AA rats is significantly higher than that of normal rats.Additionally,HMGBI was highly expressed in the nuclei and cytoplasm of the subchondral chondrocytes and inflammatory cells in bone erosion in AA rats(P＜0.01),while fewer positive cytoplasmic staining of HMGB1 was found in chondrocytes and fewer positive nuclear staining was found in bone cells in normal rats.HMGB1 concentration was significantly higher in serum of AA rats than that in normal rats(P＜0.001).Conclusion The cytoplasmic HMGBI expression in synovium and joints is greatly upregulated;the level of HMGB1 in serum is increased in AA rats which suggests a patbogenetic role of HMGB1 in synovitis and bone destruction of adjuvant-induced arthritis.

Child ; Humans ; Lymphoma, T-Cell ; complications ; Panniculitis ; etiology ; Subcutaneous Tissue

Agmatine ; administration & dosage ; pharmacology ; Analgesia ; methods ; Animals ; Injections, Spinal ; Male ; Morphine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; drug effects

The present is aimed at identifying the activation of TRAFs in n asopharyngeal carcinoma (NPC) in vitro. The differential expression of TRAF2\,TRAF3 was not detected in RN A and protein level, whereas the expression of TRAF1 in HNE2-LMP1 cell lines wa s much more abundant than that in HNE2 cell lines, suggesting that TRAF1 may be an inducible molecule; More importantly, TRAF1, TRAF2 or TRAF3 were activated in the HNE2-LMP1 cells, whereas TRAF1, TRAF2 or TRAF3 were not activated in HNE2 cells as detected by the immunoprecipitation-Western blotting assay. These data provide an experimental basis for our study beginning from the signal transduca tion pathway for the eluccidation of the mechanism of LMP1 carcinogenesis in NP C.

Background Oxidative stress plays an important role in the pathogenesis of diabetic complications.Peroxiredoxin 6(Prx6) is a doubly-functional protein.and its ability to eliminate phospholipid hydroperoxides is essential. Objective The aim of this study was to investigate the dynamic expression of Prx6 in the retina of streptozotocin(STZ)-induced diabetes and explore its correlation with the progression of diabetic retinopathy. Methods Diabetes was induced by an intraperitoneal injection of streptozotocin(STZ)in 48 clean Wistar rats.The rats were sacrificed at 1,2,and 4 months after the injection of STZ,and expressions of Prx6 protein and Prx6 mRNA in the retina was determined by immunohistochemistry and reverse transcription polymerase chain reaction.Another 12 matched normal Wistar rats were used as the control group. Results The resuh of immunohistochemistry showed that Prx6 protein was expressed in the cytoplasm of the outer nuclear layer(ONL)and inner nuclear layer(INL)in normal rats,and low expression of Prx6 protein was observed in the ganglion cell layer (GCL).In the first month,Prx6 protein was strongly expressed in the INL and the ONL of diabetic rats.However.two and three months after STZ administration,the expression of Prx6 protein was absent in the retina,showing a considerable difference among different course groups(F=22 967.63,P＜0.05).Furthermore,the expression trend of Prx6 mRNA in the retina was similar to that of the Prx6 protein with a significant difference among different course groups(F=942.84,P＜0.05). Conclusion It is conceivable that normal maintenance of Prx6 expression may be important to the prevention of diabetic retinopathy.We hypothesize that oxidative impairments in the retina that develop over time may partly contribute towards the development of retinal dysfunction,which eventually leads to retinal degeneration during the progressive phase of STZ-induced diabetes in adult rats.