Objective:To test the periodontal regeneration potential after tooth root replantation combined with in vitro cultured periodontal ligament cells (PDLCs).Methods:The third and fourth mandibular premolars of two mongrel dogs were extracted and the dog PDLCs were in vitro cultured.The autologous roots combined with PDLCs were replanted into the created cavities in the right mandibular edentulous area one month after premolar extraction.Roots replanted without PDLCs on the left mandible served as the controls. The dogs were sacrificed 2 months after the replantation. Paraffin sections were made and stained with hematoxylin & eosin, then examined histologically.Results:In the samples of root combined with PDLCs implantation, some fiber bundles vertical to the surface of bone were embedded in some inner walls of the alveolar socket opposite to the apical root.Conclusion:Cultured PDLCs in vitro retain the capacity of PDL-like tissue formation even in the artificial alveolar socket.

AIM: To investigate the influence of three dimentional printing processes(3DP) on the release of controlled-release helicid tablet. METHODS: Parameters of 3DP,such as skeleton polymer,binder,thickness of powder layering,number of spray painting,subregion ser up and diameter of aperture,were selected in the preparation of donut-shape multilayer controlled-release helicid tablet.Dissolution tests in vitro were carried out to analyse the effect of technological parameters on the release of helicid. RESULTS: Under the condition of fixed subregion and diameter of aperture,the selections of binders and thickness of spray painting were key factors concerning the release period of helicid. CONCLUSION: 3DP processes shows high flexibility and efficacy in the preparation of controlled-release tablets.

Object To study the mechanism of triptolide solid lipid nanoparticle (TP-SLN) for decreasing liver toxicity of triptolide (TP). Methods With ig three doses of TP-SLN to mice for 60 d, the A LT, AST activities in serum and superoxide dismutase (SOD), glutathione peroxida se (GSH-Px) activites and malondialdehyde (MDA) contents in liver were determin ed. Results The activities of ALT, AST, SOD, GSH-Px and conten t of MDA between experimental group and blank group did not have remarkable diff e rence. However, the activites of ALT, AST, SOD, GSH-Px for the middle- (20 ?g /kg) and high-dose (30 ?g/kg) group were higher and the contents of MDA were lower than the experimental group. Conclusion TP-SLN can decrease the liver toxicity of TP.

Purpose　The aim is to sulfonize Hunai polysaccharide fr om p leurotus tuber-rigium(Fr.)Sing. and to evaluate the antioxidative activities of the sulfated po lysaccharide (S-HNP).Methods　S-HNP was prepared by the reacti on of Hunai polysaccharide with chlorosulfonic acid-Pyridine. The antioxidative activities o f S-HNP were evaluated as follows: (1) the inhibition effects on Fe2+- Vc inducing the injury of rat liver mitochondria in vitro, (2) the protectiv e ef fect on CuSO4 -Phen-Vc-H2O2 inducing the damage of DNA, (3) the scaven ging effect on O*-2. Results　 S-HNP could protect mitochondria from lipid peroxidation induced by Fe2+-Vc, i ncluding the inhibitions of the increase of TBARS content, the swelling of mitoc hondria and the decrease of membrane fluidity, and protect DNA from the damage induced by CuSO4-Phen-Vc-H2O2， and scavenge O*-2 generated in the sel f-oxidation of pyrogallic acid. Conclusion　S-HNP exhibi ted marked antioxidative activities.

Objective Inflammation response is involved in the whole pathological process of acute cerebral infarction ( ACI) , but few reports are seen on its clinical implication in ACI patients .The purpose of this study was to investigate the predictive value of the differential count of leukocytes for stroke severity and early clinical outcomes in the acute phase of cerebral infarction . Methods We collected the clinical and laboratory data of 635 patients diagnosed with ACI within 72 hours of symptom onset and eval-uated the association between the differential count of peripheral blood leukocytes and stroke severity at admission and within 3 days af-ter admission as well as the clinical outcomes at discharge .The neural function impairment scores of the patients were obtained with The NIH Stroke Score ( NIHSS) at admission and on the third day after admission , and the therapeutic results evaluated with the modi-fied Rankin Scale ( mRS) , mRS >2 as poor prognosis .Analyses were performed on the correlation of the differential count of leuko-cytes with NIHSS and mRS scores and its influence on the ACI patients . Results At discharge , the mRS related influencing factors included the total count of leukocytes (OR=1.147, 95% CI:1.038-1.268), count of neutrophil cells (OR=1.227, 95% CI:1.00-1.369 ), count of lymphocytes ( OR =0.508, 95% CI:0.342-0.753), and neutrophil to lymphocyte ratio (NLR) (OR=1.150, 95%CI:1.008-1.314).the NIHSSs were correlated with the counts of leucocytes (r=0.078, P=0.024), neutrophil cells (r=0.083, P=0.019), and lymphocytes (r=0.010, P=0.004) at admission, and with the counts of leucocytes ( r =0.238, P <0.001), neutrophil cells (r=0.335, P<0.001), lymphocytes (r=-0.269, P<0.001), and NLR (r=0.423, P<0.001) on the third day after admission. Conclusion In the acute phase of cer-ebral infarction , the differential count of leukocytes and NLR are valuable for predicting the severity of neurologic impairment and early poor functional outcome .

Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it needs analgesics during oncology treatment, particularly in the context of the coronavirus disease, where patients are more susceptible to contract high fever and sore throat.This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression.Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.

Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it needs analgesics during oncology treatment, particularly in the context of the coronavirus disease, where patients are more susceptible to contract high fever and sore throat.This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression.Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.

Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it needs analgesics during oncology treatment, particularly in the context of the coronavirus disease, where patients are more susceptible to contract high fever and sore throat.This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression.Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.

Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it needs analgesics during oncology treatment, particularly in the context of the coronavirus disease, where patients are more susceptible to contract high fever and sore throat.This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression.Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.