Objective To investigate the effect ofnarrow-band ultraviolet-B(NB-UVB)(311 nm)on dendrite formation in B16 melanoma cells.Methods B16 melanoma cells were irradiated with various doses of NB-UVB(0,25,50,100,200,300 mJ/cm2).Atier additional culture of varying durations,irradiated cells were harvested and subjected to the observation of morphological changes and cell cytoskeleton F-actin microfilaments by phase contrast microscopy and laser scanning confocal microscopy(LSCM).respectively,and to the detection of cell proliferation bv MTT colorimetric assay.Pull down assay was performed to detect the activity of GTP-RhoAA and GTP-Rac1 in B16 cells before and after UVB irradiation.Results Twenty-four hours after irradiation with UVB of 100 mJ/cm2.an increase was observed in the cell body of B16 cells which appeared in sphericity,as well as in the number of dendrites(P＜0.01)which showed a branch-like appearance.compared with non-irradiated cells which had 2-3 dendrites and obscure branches.LSCM revealed that F-actin microfilaments in B16 cells were well organized with clear textures before irradiation;after irradiation wim NB-UVB of 100 mJ/cm2.stress fibers were disassembled and disrupted and the texture became unclear,which was observed as early as 30 minutes and became more and more evident,and at 6 hours the stress fibers displayed a clumping appearance with obscure textures.Following the irradiation with NB-UVB of 100 mJ/cm2,the expression level of GTP-Rac 1 protein increased at l 5 minutes,and.at 30minutes,reached 2 times of that observed in nonirradiated cells,then decreased a liale,but still remained elevated at 60 minutes and 120 minutes,compared to unirradiated cells;meanwhile.the level of GTP-RhoA dropped a little at 30 minutes,then gradually increased and,at 120 minutes.reached 1.6 times of that observed in unirradiated cells.Conclusion Narrow-band UVB(311 nm)can promote dendrite formation.likely via regulating the expression of GTP-Racl and GTP-RhoA in B16 melanoma cells.

Increasing attention has been focused on the antitumor activity of artemisinin derivatives in recent years, for artemisinin had been reported to have cytotoxic effects against HL-60, P388 and MCF-7 tumor cells. We report here the synthesis and evaluation for antitumor activity of a series of artemisinin-ether derivatives bearing tetrahydropyrrole, morpholine, piperidine, substituted piperidines and azoles with various linkers. Sixteen 10-O-substituted dihydroartemisinin derivatives were designed and synthesized, all of which have never been reported in literatures and whose antiproliferative effects on human breast cancer MCF-7, MCF-7/Adr and HL-60 cells were determined by MTT assay or direct cell counting. Each of these artemisinin derivatives possessed better effects than dihydroartemisinin evidently against HL-60 and MCF-7 cells growth, while less potent than doxorubicin. All target compounds exhibited significantly improved potency compared to DHA and doxorubicin on the doxorubicin-resistant MCF-7/Adr cells, so did they in their sensitive counterparts MCF-7 cells. Among them, compounds GF02, GH04 and ZH04 showed strong activity against these three cell lines growth. Further research is undergoing.

Objective To investigate the differences of X-ray findings of skeletal fluorosis between coal-burning type endemic fluo-rosis and industrial fluorosis.Methods The patients were randomly selected as research objects including 60 cases of coal-burning type endemic osteofluorosis and 60 cases of industrial osteofluorosis.The X-ray findings on the left forearm,crus and pelvic radio-graphs of these patients were analyzed retrospectively to find out the differences between skeletal fluorosis of coal-burning type endemic fluorosis and industrial fluorosis.Results X-ray features are no significant statistical differences between coal-burning type endemic fluorosis and industrial fluorosis,except these of interosseous membrane ossification of forearm and crus (forearmχ2=10.909,P<0.05;crusχ2=8.547,P<0.05),obturator membrane ossification of pelvis (χ2=36.554,P<0.05),periosteal proliferation outside bone of crus (χ2=4.937,P<0.05),and ossification of soleus (χ2=4.904,P<0.05).Conclusion The X-ray signs of endemic osteofluorosis and industrial skeletal fluorosis are almost similar,but there are some differences between them.

OBJECTIVE:To systematically review the clinical effect of blood flow restriction training on rehabilitation after anterior cruciate ligament reconstruction to provide a reference for clinical practice. METHODS:Databases including CNKI,WanFang,PubMed,Web of Science and EBSCO were searched to collect randomized controlled trials of blood flow restriction training in the intervention of anterior cruciate ligament reconstruction from inception to August 10,2022.Outcomes included knee muscle strength,knee muscle mass,and knee function evaluation,all of which were continuous variables.Two reviewers independently screened the literature and extracted data.Cochrane bias risk assessment tool and Physiotherapy Evidence Database Scale were used to evaluate the bias risk of the included articles.Meta-analysis was then performed using RevMan 5.4 software. RESULTS:A total of 9 publications were included,including 226 subjects,114 in the trial group and 112 in the control group.Meta-analysis results showed that compared with conventional resistance training,the blood flow restriction training group could significantly improve knee muscle strength[SMD=0.54,95%CI(0.29,0.79),P＜0.01],muscle mass[SMD=0.26,95%CI(0.06,0.46),P=0.01]and knee joint function[SMD=1.17,95%CI(0.53,1.80),P＜0.01].Subgroup analysis showed that only when the intervention time was more than 4 weeks,there were significant improvements in knee joint muscle strength[SMD=0.68,95%CI(0.38,0.97),P＜0.01]and muscle mass[SMD=0.38,95%CI(0.09,0.68),P=0.01]. CONCLUSION:Current evidence shows that blood flow restriction training can improve muscle strength and knee function in patients with anterior cruciate ligament reconstruction and reduce muscle atrophy.It is recommended that the postoperative intervention time should be more than 4 weeks to achieve better muscle strength and muscle mass improvement.

Background: The mitogen-activated extracellular signal-regulated kinase 1/2 (MEK1/2) inhibitor trametinib has shown promising therapeutic effects on melanoma, but its efficacy on colorectal cancer (CRC) is limited. Synthetic lethality arises with a combination of two or more separate gene mutations that causes cell death, whereas individual mutations keep cells alive. This study aimed to identify the genes responsible for resistance to trametinib in CRC cells, using a synthetic lethal short hairpin RNA (shRNA) screening approach. Methods: We infected HT29 cells with a pooled lentiviral shRNA library and applied next-generation sequencing to identify shRNAs with reduced abundance after 8-day treatment of 20 nmol/L trametinib. HCT116 and HT29 cells were used in validation studies. Stable ring finger protein 183 (RNF183)-overexpressing cell lines were generated by pcDNA4-myc/his-RNF183 transfection. Stable RNF183-knockdown cell lines were generated by infection of lentivi-ruses that express RNF183 shRNA, and small interference RNA (siRNA) was used to knock down RNF183 transiently. Quantitative real-time PCR was used to determine the mRNA expression. Western blotting, immunohistochemical analysis, and enzyme-linked immunosorbent assay (ELISA) were used to evaluate the protein abundance. MTT assay, colony formation assay, and subcutaneous xenograft tumor growth model were used to evaluate cell proliferation. Results: In the primary screening, we found that the abundance of RNF183 shRNA was markedly reduced after treatment with trametinib. Trametinib induced the expression of RNF183, which conferred resistance to drug-induced cell growth repression and apoptotic and non-apoptotic cell deaths. Moreover, interleukin-8 (IL-8) was a downstream gene of RNF183 and was required for the function of RNF183 in facilitating cell growth. Additionally, elevated RNF183 expression partly reduced the inhibitory effect of trametinib on IL-8 expression. Finally, xenograft tumor model showed the synergism of RNF183 knockdown and trametinib in repressing the growth of CRC cells in vivo. Conclusion: The RNF183-IL-8 axis is responsible for the resistance of CRC cells to the MEK1/2 inhibitor trametinib and may serve as a candidate target for combined therapy for CRC.