Phthalate esters belong to the group of environmental hormones,which are ubiquitous environmental pollutants and they can damage the human health through breathing to get into the body.The recent researches on the analysis of phthalate esters in the air such as sampling,pretreatment and determination were reviewed and some related issues were discussed in the paper.It would be reference for the further study of phthalate esters.

Animals ; Benchmarking ; methods ; statistics & numerical data ; Dose-Response Relationship, Drug ; Humans ; Models, Statistical ; No-Observed-Adverse-Effect Level ; Risk Assessment ; methods ; statistics & numerical data ; Toxicology ; methods

AIM: In order to explore the pathogenesis of ulcerative colitis (UC), an experimental colitis in mouse was induced by the hapten dinitrochlorobenzene (DNCB), and the activity of leukocyte migration inhibitory factor (LMIF) was measured at the same time. METHODS: 67 BALB/c mice were randomly divided into control (60% ethanol) and DNCB groups. After they were sensitized by smearing 3.3% DNCB on the abdominal skin, they were challenged with DNCB at concentration of 0.1%, 0.2% and 0.4% respectively by instillation once a day. The weight, stool viscosity and hematochezia were observed and accumulated as disease active index (DAI) score. The pathological changes in colon tissue were judged macropathologically and by means of microscope. LMIF activity was determined by the absorbance (A) of migrated leukocytes. RESULTS: Compared to control group, the increases in DAI accumulate score, pathologic score, and LMIF activity in DNCB groups were observed. CONCLUSION: Mouse colitis was induced by DNCB, which was accompanied by an increase in LMIF activity. [

Objective To construct RNAi combinant adenoviral expressive vectors specific to p65 subunit of NF-?B and to observe their gene silencing effect on p65 subunit.Methods Three pairs of complementary. single-strand DNA oligos targeting three various sites of p65 mRNA were designed and synthesized.Annealling was used to generate double-strand oligos(ds-oligos),and then the ds-oligos were cloned into pENTR~TM/u6 to generate the entry clone named pENTR.Recombination reaction in vitro with the pENTR and pAd/BLOCK-iT~TM- DEST was used to creat the adenovirus plasmid which contains the RNAi cassette.Then,the adenovirus plasmids digested with PacI were transfected into HEK293A cells to product adenovirus,and latter infected the HEK293A cells to amplify the adenoviral stock.Plaque forming assay was used to titer the adenoviral stock.The p65 gene silencing effect induced by the RNAi adenovirus was detected by Western blot and immunocytochemistry assay in ECV304 cells.Results The RNAi adenovirus specific to p65 subunit of NF-?B were produced with titer of 3.0 x 10~9pfu/ml to 2.5?10~10pfu/ml.The expression of p65 protein in ECV304 cells could be down-regulated efficiently by the RNAi adenovirus 48-72 h after infection,which would last for more than 6 days after infection.Conclusion RNAi adenovirus is an important tool inhibiting the expression of target gene efficiently.

Objective To study morphological changes of rabbit artery endothelial cell injury and atherosclerosis caused by high fluoride and the role of selenium. Methods Twenty healthy male New Zealand white rabbits, body weight (2.0 ± 0.5)kg, were randomly divided into control group(drinking deionized water, fed basic diet), fluoride group(drinking fluoride 100 mg/L deionized water, fed basic diet), selenium group(drinking selenium 1 mg/L deionized water, fed basic diet), fluoride plus selenium group(drinking fluoride 100 mg/L deionized water, selenium 1 mg/L of deionized water, fed basic diet). The experimental period was 6 months. At 0, 3, 6 months of the experiment, serum fluorine and selenium levels were determined. At the end of the experiment,thoracic aorta was collected to observe its pathology and ultrastructural changes. Results Serum fluoride was significantly higher at the 3rd and the 6th month of experiment(all P ＜ 0.01 ) in fluoride group[ (0.589 ± 0.146),(0.772 ± 0.175)mg/L] and fluoride plus selenium group[ (0.502 ± 0.094), (0.693 ± 0.158)mg/L] than in control group[ (0.174 ± 0.002), (0.208 ± 0.031 )mg/L] and serum fluoride was significantly higher at 6 months than at 3 months(P ＜ 0.05 ) in fluoride group. Serum selenium was significantly higher at the 3rd and the 6th month of experiment (all P ＜ 0.01 ) in selenium group[ (0.252 ± 0.022), (0.319 ± 0.052)mg/L] and fluoride plus selenium group[ (0.239 ±0.016), (0.294 ± 0.018)mg/L] than in control group[(0.135 ± 0.014), (0.167 ± 0.019)mg/L], and serum selenium was significantly higher at the 6th month than at 3rd month of experiment in selenium group(P ＜ 0.05). Endothelial cell apoptosis indices were (4.92 ± 1.32)%, (30.30 ± 6.80)%, (6.57 ± 2.14)% and (14.29 ± 2.99)%, respectively in control group, fluoride group, selenium group and fluoride plus selenium group. Their main effect of fluorine and selenium was statistically significant (F = 106.833,20.082, all P ＜ 0.01 ). There were antagonistic effect between fluoride and selenium(F = 30.402, P ＜ 0.01 ). Pathological changes of rabbit aortic endothelial cells in fluoride group included endothelial with attached fibrin and red blood cells, and structural of the cells changed, with serious vascular injury; in fluoride plus selenium group apoptosis of endothelial cells decreased, with reduced number of attached red blood cells and fibrin, endothelial cell structure normal, the extent and scope of vascular damage significantly reduced. Conclusions Appropriate amount of selenium inhibits the apoptosis of endothelial cells induced by high fluoride, reduces aortic structural damage caused by high fluoride, and maintains the integrity of endothelial cells, thereby antagonizes the vascular damage and atherosclerosis induced by high fluoride.

AIM To investigate the anti-neuroinflammation effects of 4-hydroxybenzyl aldehyde (4-HBAL) from Gastrodia elata Blume on acute cerebral ischemic injury in rats and its nechanism of action.METHODS The rat model of acute cerebral ischemic injury was induced by injecting arachidonic acid via intracarotid artery.Brain tissue samples were taken from the animals 3 h after the model of acute cerebral ischemic injury.Tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) were detected in brain tissue to evaluate the effects of 4-HBAL in vivo.Lipopolysaccharid (LPS)-induced activation of BV-2 microglia cells model was used to explore the anti-neuroinflammation mechanism of 4-HBAL.RESULTS The experimental results showed that 4-HBAL had a significant protective effect on acute cerebral ischemic injury.It could significandy decrease the contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β),and obviously inhibit the production of nitric oxide (NO),prostaglandin E2 (PGE2) and TNF-α in LPS-stimulated BV-2 cell,and increase the production of interleukin-10 (IL-10) and transforming growth factors-β (TGF-β) in BV-2 cell.CONCLUSION The mechanism of 4-HBAL may be related to the suppression of the excessive activation of microglia after cerebral ischemia and the promotion of the transformation of microglia into anti-inflammatory phenotype.

Objective To summarize the experience of intraoperative care for the patients undergoing microsurgery via retrosigmoid keyhole approach, so as to improve the treatment effect and minimize complications. Method The clinical records on the intraoperative care of 100 patients undergoing microsurgery via retrosigmoid keyhole approach were retrospectively analyzed. Result Using the keyhole technique and small incision, the cerebellopontine angle lesions were exposed clearly. Moreover, the proper intraoperational cooperation shortened the duration of operation, reduced bleeding and minimized postoperative complications such as cerebrospinal fluid otorrhea, intracranial infection, intracranial hemorrhage, and subcutaneous hydrops. Conclusion Proper operational postures and intraoperative cooperation can make full use of the limited space of the microsurgery via retrosigmoid keyhole approach and ensure the success of the operation.

Objective To investigate the apoptosis inducing effects of oridonin on leukemic THP-1 cells and its mechanisms of action. Methods THP-1 cells in culture medium in vitro were given different concentrations of oridonin (16～56 μmol/L) for 24, 48 and 72 h. The inhibitory rate of the cells were measured by MTT assay, apoptotic morphology was observed by Hoechst 33258 staining, and Annexin V/PI staining was used to detect cell apoptosis by flow cytometry (FCM). Caspase-3 and poly (ADP-ribose) polymerase (PARP) expression were detected by Western blotting. Results Oridonin (over 32 μmol/L) could inhibit the growth of THP-1 cells and cause apoptosis remarkably, the suppression was both in time-and dose-dependentmanner. Marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Hoechst 33258 staining, and Annexin V/PI staining showed that apoptotic cells gradually increased after the cells treated with oridinon. Western blotting showed cleavage of the caspase-3 zymogen protein (32×103), with the appearance of its 20×103 subunit, and a cleaved 89×103 fragment of 116×103 PARP was also found. Conclusion Oridonin can inhibit cell growth and induce apoptosis in THP-1 cells via activation of caspase-3. The results indicated that oridonin might be an important potential anti-leukemia reagent.

Objective To investigate the apoptosis inducing effect of peroxisome proliferator-activated receptor r(PPARr)agomst on leukemic K562 cells and its mechanisms of action.Methods K562 cells in culture medium in vitro were given different concentrations of PPARragonist rosiglitazone(RGZ)(20-80 umol/L)for O,24,48 and 72h The inhibitory rate of the cells were measured by MTT assay,cell apoptosis was detected by Annexin V/PI staining,and the expression of P53 protein as well as the activity of caspase-3 were also detected.Results RGZ(over 40umoL/L)could inhibit the growth of K562 cells and cause apopto-sis remarkably,the suppression Was both in time-and dose-dependent manner.The expression of P53 pmtein was upregulated and the activity of caspase-3 Was increased concomitantly after the cells werle treated by RGZ.Conclusion PPARr agonist RGZ(over 40 umol/L)can induce apoptosis on K562 cells signifieantly,upregu-lation the expression of P53 protein as well as increasing caspase-3 activity may be one of its most important mechamisms.

Objective:To investigate the clinical features, risk factors, treatment and prognosis of dermatomyositis (DM) patients with positive anti-melanoma differentiation associated gene 5(MDA5) antibody with rapidly progressive interstitial lung disease (RPILD).Methods:The clinical data of 88 DM patients from June 2019 to June 2020, at the rheumatology department of Guangdong Provincial People's Hospital were collected and retrospectively analyzed. T-test, non-parametric Mann-Whitney U test, Chi-squared test, Fisher exact probability and Logistics regression analysis were used for data analysis. Results:① 37%(36/88) DM patients were positive for anti-MDA5 antibody. The frequency of ulcerative rash, Gottron's sign, arthritis, clinically amyopathic dermatomyositis (CADM), and erythrocyte sedimentation rate (ESR) was significantly higher in patients with anti-MDA5 antibody ( P<0.05). The cell count of white blood cell, neutrophil, lymphocyte, and serum creatine kinase (CK) level were significantly lower in the anti-MDA5 antibody positive group than those in the negative group ( P<0.05). Of anti-MDA5 antibody positive DM patients, 100% developed ILD, 34% (11/32)developed RP-ILD, 16%(5/32) died, which were significantly higher than those of anti-MDA5 antibody negative patients ( P<0.05). ② Of anti-MDA5 antibody positive DM patients, the C reactive protein (CRP) level, positive rate of anti-Ro-52 antibody and mortality rate were significantly higher RPILD group than those in the non-RPILD group [15.70(4.49, 29.00) vs 3.22 (1.66, 7.15), Z=-2.440, P=0.014; 91% vs 43%, P=0.011; 46% vs 0, P=0.002]. Logistics regression analysis indicated that positive anti-Ro-52 antibody [ OR=4.561, 95% CI (1.797, 11.580), P=0.001] might be a risk factor for anti-MDA5 antibody positive DM-RPILD. ③ Among patients with anti-MDA5 antibody with RPILD, serum ferritin and D-dimer level was significantly higher and oxygenation index was significantly lower in the non-survival group than those in the survival group [1 931 (1 377, 7 379) vs 638(196, 876), Z=-2.556, P=0.009; 2 760(1 995, 4 854) vs 985(533, 1 588), Z=-2.379, P=0.017; 230(140, 256) vs 309(262, 382), Z=2.191, P=0.030]. In addition, the delayed intensive treatment time was significantly longer in the non-survival group than those in the survival group [(14.0±2.6) vs (4.5±1.4), t=7.899, P<0.01]. Furthermore, the proportion of combined therapy with two disease modifying antirheumatic drug (DMARDs) was significantly lower in the non-survival group than those in the survival group (0 vs 83%, P=0.015). Conclusion:Anti-MDA5 antibody may be associ-ated with characteristic clinical manifestations of DM, ILD, RPILD and high mortality rate. Positive anti-Ro-52 antibody may be a risk factor for anti-MDA5 antibody positive DM-RPILD. High serum ferritin and D-dimer level and low oxygenation index in RPILD patients may be associated with poor prognosis. Early treatment with two DMARDs may improve the prognosis of RPILD.