Objective:To evaluate the correlation between peri-implant probing depth (PPD) and radiographic bone level (rBL) in implants with peri-implantitis.Methods:From January 2019 to December 2022, 24 patients with 30 implants who suffered from peri-implantitis at the Department of Periodontology, Peking University School and Hospital of Stomatology were included in the present research. SPSS 26.0 software was used to simple random sampling select 30 healthy implants from which with electronic examination records in Department of Periodontology, Peking University School and Hospital of Stomatology from January 2007 to June 2023 as the control group. On the premise of retaining the implant prosthesis, PPD (distance between pocket bottom and peri-implant soft tissue margin) was examined using a Williams periodontal probe with a light force (about 0.2 N), and a total of 4 sites were recorded for each implant. Periapical radiography and cone beam CT were applied to measure the rBL (distance between the reference point at the neck of the implant and the apical point of the bone defect) and the width of the bone defect (DW), and the type of the bone defect was recorded. The correlation and consistency between the diagnosis of PPD and rBL were analyzed.Results:PPD was significantly correlated with rBL in a total of 60 implants in 180 sites ( r=0.64, P<0.001). The chi-square test showed an 8.15-fold increase in the detection rate of PD≥6 mm at sites with rBL≥1 mm ( P<0.001). Multivariate logistic regression analysis showed that rBL was still statistically associated with PPD after adjustment for jaw position and examination position of implants. Take rBL <1 mm as reference, the odds ratios ( OR) of 1 mm≤rBL<2 mm, 2 mm≤rBL<3 mm and rBL≥3 mm group with PPD were 6.23 ( P=0.014), 2.77 ( P=0.183) and 10.87 ( P=0.001), respectively. Conclusions:There is a positive correlation between PPD and rBL in implants with peri-implantitis. PPD can be used as a clinical examination index to assist in estimating the level of peri-implant bone under the premise of retaining the prosthesis.

Ferroptosis is a novel form of programmed cell death that relies on the accumulation of intracellular iron ions,causing irreversible damage to cell membranes through extensive lipid peroxidation,ultimately leading to cell death.Ferroptosis is closely associated with various neurodegenerative diseases.The ferroptosis of glial cells can regulate neuronal death by inducing neuroinflammation and affecting oxidative stress,thereby exacerbating the progression of neu-rodegenerative diseases.This review summarizes how ferroptosis occurs in different types of glial cells and its impact on neurons,aiming to deeply understand the effects of glial cell ferroptosis on neurodegenerative diseases and explore the po-tential therapeutic applications of inhibiting this process in treatment.

Objective:To explore the effect of chemotherapy administration sequence combined with programmed cell death protein-1(PD-1)monoclonal antibody on the efficacy and immune-related adverse events(irAEs)in patients with advanced non-small cell lung cancer(NSCLC).Methods:The clinical data of 110 patients with advanced NSCLC treated at The First Affiliated Hospital of Zhengzhou University between November 2019 and January 2022 were retrospectively collected.The factors influencing irAEs were analyzed by univariate and multivariate Logistic regression analyses,while those influencing curative effect were analyzed by Kaplan-Meier curve analysis,Log-rank test,and univariate and multivariate Cox regression analyses.Results:Treatment with PD-1 monoclonal antibody after 2 days of chemotherapy(sequential treatment group,n=36)significantly prolonged progression-free survival(PFS)compared with PD-1 monoclonal antibody admin-istration on the same day of chemotherapy(simultaneous treatment group,n=74)(17.2 months vs.11.3 months,respectively;P＜0.05).The disease control rate(DCR)was better in the sequential treatment group than in the simultaneous treatment group(94.4％vs.79.7％,re-spectively;P=0.045),while the objective response rate(ORR)did not differ significantly(69.4％vs.51.4％,respectively;P=0.072).The Cox re-gression analysis showed that cytokerat in 19 fragment(Cyfra21-1)and d-dimer(D-dimer)affected the efficacy of combination therapy(P＜0.05).The Logistic regression analysis showed that age and lactic dehydrogenase(LDH)influenced the occurrence of irAEs(P＜0.05),while the administration sequence did not significantly affect the occurrence of irAEs(P=0.130).Conclusions:Administration sequence influences the efficacy of combination therapy,and patients with advanced NSCLC who receive sequential therapy may experience better efficacy.Age and LDH are negatively correlated with the occurrence of irAEs.

EGFR tyrosine kinase inhibitor (EGFR-TKI) has been used successfully in clinic for the treatment of solid tumors. In the present study, we reported the discovery of from our in-house diverse compound library, which was validated to be a potent and selective EGFR-TKI. showed excellent inhibitory activities against EGFR (IC = 0.81 nmol/L), EGFR (IC = 1.2 nmol/L) and EGFR (IC = 1.1 nmol/L), but was less effective or even inactive against other nine kinases. also displayed excellent antiproliferative activities against a panel of human cancer cell lines, and exhibited the ability to reduce colony formation and wound healing the same as gefitinib. We found that upon oral administration showed better anti-tumor activity in A431 bearing xenograft mouse models compared to gefitinib. In addition, showed better intestinal absorption than gefitinib and had favorable pharmacokinetic properties and microsomal metabolic stability in different species. These studies indicate that has strong antitumor activity and , and could be used for the development of anti-lung cancer agent targeting EGFR.

Objective To study the role of natural antiox-LDL subclass IgM antibodies in formation of atherclerosis.Methods The macrophages from mice were divded into LDL group,Cuox-LDL group and control group.The macrophages in LDL group and Cuox-LDL group were precultured with LDL and Cuox-LDL.Adhesion experiment was performed in control group.3A6,5G8 and 2H7 were incubated.The macrophages were divided into 3A6 group,5G8 group and 2H7 group.Adhesion experiment was performed by adding the pretreated 125I Cuox-LDL.The binding parameters of macrophages and 125I Cuox-LDL in different groups were recorded.Foam cells were analyzed by cell lipid analysis with oil red O staining.Results The bound 125I Cuox-LDL level was significantly lower in Cuox-LDL group than in control group and LDL group (P＜0.01).No significant difference was found in bound 125I Cuox-LDL level between 5G3 group and 2H7 group (P＞0.05).The bound 125I Cuox-LDL level was significantly lower in 3A6 group than in control group,5G8 group and 2H7 group (P＜0.01).Oil red O staining showed no oil drop in macrophages,but a small number of oil drops in 3A6 group and a large number of oil drops in control group.The cholesterol and TG in macrophages reduced 45％ and the TG reduced 170％ in 3A6 group,which were significantly lower than those in control group (P＜0.01).Conclusion Antiox-LDL IgM subclass antibody 3A6 can effectively prevent the binding of unactivated macrophages to ox-LDL,reduce the occurrence and progression of atherosclerosis.

Objective To investigate the sustained release of BSA from chitosan-OREC/BSA films coated mats in vitro.Methods The negatively charged cellulose acetate (CA) fibrous mats were modified with multilayers of the positively charged chitosan or chitosan-OREC intercalated composites and the negatively charged bovine serum albumin (BSA) via electrostatic layer-by-layer (LBL) self-assembly technique.The adsorption and rinsing steps were repeated until the desired number of deposition bilayers was obtained.The in vitro BSA encapsulation and release experiments demonstrated that OREC could affect the degree of protein loading capacity and release ficiency of the LBL films coating.Results In the pH-gradient release assay,only a small amount of BSA was released from the mats in 1 h.As the time increased,the release rate of BSA of all the samples gradually went up to the maximum data within 8 h.For the samples with identical number of bilayers and record time,obvious increasing of the release amount could be seen in pH 7.4,in comparison with pH 1.2.Besides,doubling bilayers film-coated mats generally.Meanwhile,it was slightly distinguishable between 5 and 5.5 as well as 10 and 10.5 bilayers (t=0.651～ 1.324,P＞0.05).Interestingly,it could be seen that protein release of the chitosan-OREC/BSA films coated mats remarkably increased compared with that of chitosan/BSA films coated mats(t=2.264～ 2.305,P＜0.05).Conclusion The release of protein in the initial time could be controlled by adjusting the number of deposition bilayers,the outmost layer and the composition of coating bilayers.

Objective To evaluate the value of whole body 18F-FDG PET/CT in the detection of recurrence/metastasis of cervical cancer.Methods A retrospective study was performed on 95 patients with cervical cancer who underwent 18F-FDG PET/CT after treatment.The lesion characteristics on 18F-FDG PET/CT were assessed visually and semi-quantitatively.A final diagnosis was confirmed by histopathology,diagnostic treatment and clinical follow-up imaging.The data were analyzed by Kappa test.Results 18 F-FDG PET/CT was positive in 54 patients,including 24 with local recurrence and 30 with distant metastases.The sensitivity,specificity and accuracy of 18F-FDG PET/CT for the detection of recurrence/metastasis of cervical cancer were 98.1％ (52/53),95.2％ (40/42) and 96.8％ (92/95),respectively.The positive predictive and negative predictive value were 96.3％ (52/54) and 97.6％ (40/41),respectively.18F-FDG PET/CT showed concordant results with pathological/clinical follow-up findings (Kappa =0.936,P＜0.05).Conclusion 18F-FDG PET/CT is a sensitive and specific modality for the detection of recurrence/metastasis of cervical cancer and might be useful for further treatment plan.

Objective To analyze the outcome of applying venous flow-through flap in replantation of complex severed finger.Methods From March,2011 to August,2012,15 cases of complex severed fingers were repaired by flow-through flap with two sets of venous system of forearm vein and one stage repair of wound.The time from injury to operation was 1.5-5.5 h (mean 2.5 h).Vascular defect length ranged from 1.5 to 11.0 cm (mean 3.6 cm);and soft tissue defect of 1.5 cm × 3.0 cm to 11.0 cm × 11.0 cm.All digits had severe soft tissue defect and segmental defect of blood vessels.All the finger blood circulation was disorder.Results All flaps and replanted fingers survived completely,except 1 case of postoperative venous crisis occurred which was remission after the vascular transplantation,and 1 case of skin flap necrosis at the distal part which was healed after skin grafting; Fourteen cases were followed-up from 7 to 20 months.At the final followed-up the flaps were of good consistency and appearance.Function of the finger was graded excellent in 7 cases,good in 5 cases,and poor in 2 cases.All flaps and replanted fingers survived completely over a period of 12 to 30 months follow-up.The flaps were of good consistency and appearance.Function of the finger was graded excellent in 7 cases and good in 5 cases.Conclusion With less injury at donor site,and good repair results,venous flow-through flap is well indicated in complex finger replantation with soft tissue defect and vascule defect.

Objective To explore the role and the possible molecular mechanisms of natural anti-oxLDL IgM monoclonal antibody played and involved in pathogenesis of atherosclerosis. Methods Natural anti-oxLDL IgM monoclonal antibody 3A6 was generated by using standard hybridoma production techniques. Influence of 3A6 on formation of foam cells was observed by Oil Red O staining and affinity of Na125I-conjugated oxLDL on the naive and LPS-activated macrophages. After LPS stimulation on macrophages, anti-TLR4 neutralizing mAb, p38MAPK specific inhibitor SB203580, NF-kB specific inhibitor PDTC or RNAi targeting Fcα/μ receptor (Fcamr) were applied, respectively. Results Natural anti-oxLDL IgM monoclonal antibody 3 A6 were found specifically inhibit the binding of CuoxLDL to naive macrophages but not the binding of CuoxLDL to LPS-activated macrophages. It also promoted the formation of CuoxLDL-mediated foam macrophages. 3A6 F(ab')2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. LPS up-regulated the expression of Fcamr in macrophages in a dose- and time-dependent manner, which was attenuated by treatment with anti-TLR4. LPS induced the phosphorylation of p38MAPK and translocation of NF-kB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages. Conclusions Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to naive macrophages in vitro. However, LPS, through the Toll-like receptor (TLR)4 receptor, activated the p38MAPK and NF-kB pathways and up-regulated the expression of Fcα/μ receptor in macrophages, which promoted the binding of 3A6/CuoxLDL complex to macrophages through binding with Fc fragments and the formation of foam macrophages. Therefore, our findings provide a new explanation why bacterial infection deteriorates the pathogenesis of atherosclerosis.

Objective To observe the effects of constant magnetic fields (CMF) on angiotensinⅡ (AngⅡ)-stimulated proliferation of human umbilical arterial vascular smooth muscle cells (VSMC). Methods The experimental proliferation models of cultured human umbilical arterial VSMC stimulated with AngⅡ was establishea. The VSMC were cultured under 1 and 5 mT CMF for 48 hrs. Proliferation of the VSMC was detected by MTT and 3H-TdR incorporation method (A-value and cpm-value), and cell cycle was analyzed by flow cytometry. Results The CMF of 1 and 5 mT may antagonize proliferation of VSMC stimulated with AngⅡ, and hold-back VSMC from static phase (G 0/G 1)to DNA synthetic (S) and mitotic phase (G 2/M). Conclusion The study demonstrates that CMF of 1 and 5 mT can significantly inhibit the human VSMC proliferation.