The development of organ transplantation has brought new hope to many patients with organ failure and their families， but it has also raised numerous ethical issues. How to balance the rights and interests between organ donors and recipients， as well as ensure the fairness and transparency of the transplantation process has become an urgent problem to be solved. Based on the latest Regulations on Organ Donation and Transplantation and the Working Rules of the Ethics Committee for Human Organ Transplantation， the current difficulties and challenges in organ transplantation ethics were deeply analyzed. Taking the ethical review practice of Shenzhen Third People’s Hospital as an example， this paper explored issues such as full informed consent of both donors and recipients， risk assessment of marginal donors， and the review of relationships between donors and recipients. It also explored and constructed a set of complete ethical review models for organ transplantation through refined management. This model improved the efficiency and quality of ethical review as well as enriched the related knowledge system. It is expected that the implementation of this model can provide a reference for promoting effective ethical review nationwide， advancing the improvement and development of ethical review work in organ transplantation. Meanwhile， more medical ethics experts and practitioners are called upon to focus on and engage in the research and practice of ethical review in organ transplantation， jointly promoting progress in this field.

Metabolic dysfunction-associated fatty liver disease （MAFLD） is a common chronic liver disease with the pathological feature of lipid accumulation in the liver， and it is closely associated with liver metabolic disorders. The latest research has shown that the pathogenesis of MAFLD is associated with the abnormal expression of specific genes， especially the fat mass and obesity-associated （FTO） gene. The abnormal activity of the FTO gene may lead to an imbalance in liver lipid metabolism， which manifests as the increase in fatty acid synthesis and the reduction in fatty acid oxidation， thereby promoting liver fat deposition and inflammatory response. Therefore， regulating the expression or activity of the FTO gene is considered one of the potential strategies for the treatment of MAFLD. At present， drug research targeting the function of the FTO gene has achieved preliminary results， and inhibition of the activity of the FTO gene can help to regulate liver lipid metabolism and alleviate liver inflammatory injury. This article reviews the mechanism of action of the FTO gene in the development and progression of MAFLD， summarizes the advances in drug research on the FTO gene and related metabolic pathways in recent years， and analyzes their application prospect in research and treatment.

The well-known insulin-like growth factor 1 (IGF1)/IGF-1 receptor (IGF-1R) signaling pathway is overexpressed in many tumors, and is thus an attractive target for cancer treatment. However, results have often been disappointing due to crosstalk with other signals. Here, we report that IGF-1R signaling stimulates the growth of hepatocellular carcinoma (HCC) cells through the translocation of IGF-1R into the ER to enhance sarco-endoplasmic reticulum calcium ATPase 2 (SERCA2) activity. In response to ligand binding, IGF-1Rβ is translocated into the ER by β-arrestin2 (β-arr2). Mass spectrometry analysis identified SERCA2 as a target of ER IGF-1Rβ. SERCA2 activity is heavily dependent on the increase in ER IGF-1Rβ levels. ER IGF-1Rβ phosphorylates SERCA2 on Tyr⁹⁹⁰ to enhance its activity. Mutation of SERCA2-Tyr⁹⁹⁰ disrupted the interaction of ER IGF-1Rβ with SERCA2, and therefore ER IGF-1Rβ failed to promote SERCA2 activity. The enhancement of SERCA2 activity triggered Ca²⁺_ER perturbation, leading to an increase in autophagy. Thapsigargin blocked the interaction between SERCA2 and ER IGF-1Rβ and therefore SERCA2 activity, resulting in inhibition of HCC growth. In conclusion, the translocation of IGF-1R into the ER triggers Ca²⁺_ER perturbation by enhancing SERCA2 activity through phosphorylating Tyr⁹⁹⁰ in HCC.

ObjectiveTo explore the mechanism of Gancao Fuzitang （GCFZ）in inhibiting the bone destruction of collagen-induced arthritis （CIA） model in mice. MethodThirty male DBa/1J mice were randomly divided into normal group， CIA group， low-dose GCFZ group （GCFZ-L， 2.4 g·kg^-1）， high-dose GCFZ group （GCFZ-H， 4.8 g·kg^-1）， and methotrexate group （MTX， 1 mg·kg^-1）， with six mice in each group. The CIA model was induced by secondary immunization method. The arthritis index of mice in each group was observed and recorded， and the histopathological changes in ankle joint were observed by hematoxylin-eosin （HE） staining. The damage to ankle cartilage was detected by safranin O-fast green staining. Micro-CT scanning was used to detect the bone destruction of ankle joint， and the expression of nuclear factor-κB p65 （NF-κB p65）， p-NF-κB p65， inhibitory-κB kinase α/β （IKKα/β）， and p-IKKα/β was observed by immunohistochemical staining. ResultCompared with the normal group， the CIA group showed manifest joint swelling and increased arthritis index score （P<0.01）. Compared with the CIA group， the groups with drug intervention could inhibit joint swelling and reduce arthritis index score （P<0.05， P<0.01）. As revealed by HE staining and safranine O-green staining， compared with the CIA group， the groups with drug intervention could inhibit synovial invasion and reduce the destruction of articular cartilage. Micro-CT scanning analysis showed that compared with the CIA group， the GCFZ-H group and the MTX group showed reduced bone destruction scores （P<0.01）. The immunohistochemical results showed that compared with the normal group， the CIA group showed increased optical density values of NF-κB p65， p-NF-κB p65， IKKα/β， and p-IKKα/β（P<0.01）. Compared with the CIA group， the GCFZ-H group and the MTX group showed reduced optical density values of NF-κB p65， p-NF-κB p65， IKKα/β， and p-IKKα/β（P<0.05，P<0.01）. In the GCFZ-L group， only the NF-κB p65 optical density value decreased（P<0.01）. ConclusionGCFZ may inhibit bone destruction in CIA mice by regulating the NF-κB signaling pathway.

Thoracoscopic pulmonary segmentectomy is one of the important treatment methods for early lung cancer. Only the premise of surgical precision can make the radical resection of lesions and maximum reservation of healthy lung tissue be simultaneously guaranteed. As a representative of the precise lung operation, the “cone-shaped lung segmentectomy” focuses on the lesion, and combines the anatomical characteristic of the patient to design individualized operation scheme. The technological core consists of three parts, three dimensional-computed tomography bronchography and angiography (3D-CTBA) surgery path planning, accurate definition of intersegmental demarcation and anatomic dissection of intersegmental borders along the demarcation. This paper aims to explore the technical process and quality control of the key techniques of thoracoscopic precise segmentectomy, so as to standardize the segmentectomy procedure under the principle of radical and minimally invasive therapy.

Objective This study applied " modified inflation-deflation" to identify the intersegmental plane and explored a method to remove pulmonary segments from the lobe on the basis of cone-shaped principle."Cone-shaped" Segmentectomy includes anatomical separation of the hilum(conical tip) and the intersegmental plane(undissociative conical surface).The feasibility was evaluated.Methods We retrospectively reviewed 146 patients with peripheric pulmonary nodules who underwent cone-shaped segmentectomy between September 2013 and August 2016.Under the guidance of preoperative 3D-CTBA (three-dimensional computed tomography bronchography and angiography)the targeted bronchi and arteries were dissected.The intersegmental plane was identified by " modified inflation-deflation" method.The inflation-deflation interface was anatomically separated from hilum to distal region along the intersegmental veins,while leaving 1-2 cm in thickness from far end.The residual intersegmental parenchyma was then dissected using endo staplers.Mean folhow-up was 20.4 months.Results Sixty two single segmentectomies,38 combined segmentectomies,43 subsegmentectomies and 3 subsubsegmentectonies were performed.Twelve diagnoses of benign nodule,15 diagnoses of atypical adenomatous hyperplasia,6 diagnoses of metastatic carcinona and 113 diagnosis of primary puhmonary cancer were confirmed pathologically." Modified inflation-deflation" spent (12.5 ±6.4)minutes to show the clear inflation-deflation line.All the targeted bronchi and arteries were dissected precisely and the intersegmental veins were preserved.All the preserved adjacent segments kept approximately original shape after inflated.The tumor size was(1.4 ±0.7)cm,the surgical margin width was(2.5 ± 1.6)cm.The depth of the separated intersegmental plane was(4.2 ±1.7)cm,and the width of the plane was(6.5 ± 2.2)cm.The operative time was(158.5 ± 42.6)min,the volume of hemorrhage was(25.2 ± 15.7) ml,the postoperative hospital stay was (5.2 ± 2.2) days.The total incidence of complications was 5.5％ (8/146).No death within 30 days occurred.Among 113 primary pulmonary cancers,there were 35 T0 N0M0(adenocarcinoma in situ) and 78 T1a No M0 non-small-cell lung cancers.One patient had local recurrence,and no death occurred during follow-up period.Conclusion Modified inflation-deflation can show clear inflation-deflation line to identify the intersegmental plane.Thoracscopic cone-shaped segmentectomy can achieve a complete anatomical segmentectomy.

Objective: To explore the expression of epidermal growth factor receptor(EGFR) protein during benzo(a)pyrene (BaP) induced carcinogenesis. Methods: This study, we firstly utilized immunofluorescence assay and Western-blot to examine EGFR expression of the BaP which was constructed previously by project team induced malignant transformation human bronchial epithelial cell (BTC) and the control (16HBE cell). Then, we selected 36 healthy SD rats, divided into two groups according to simple random method, 18 rats each group. The constructed rat lung neoplasm model induced by pulmonary injection of BaP (10 mg/ml of BaP solution in 0.2 ml corn oil), contrast group use 0.2 ml corn oil, lung tissue was collected and the EGFR expression of lung tissue was detected by immunofluorescence assay and Western blot. T analysis was used to test the different of EGFR between two groups. Results: Immunofluorescence analysis showed that the EGFR expression in BTC was significantly higher than 16HBE cell. Meanwhile, Western blot also was used to confirmed this result, the relative expression of EGFR protein in the rats of the model group the control group were 1.04±0.13 and 2.32±0.12, respectively, and the difference was statistically significance (t=12.39, P<0.001). In vivo, well-defined tumor was found in the rat with pulmonary injection of BaP, and the lung showed diffuse alveolar septal thickening, alveolar wall destruction and pulmonary alveoli fusion, which suggested that the rat lung neoplasm model was constructive successfully. Furthermore, we found the EGFR expression of lung was increased dramatically in the rat lung neoplasm model by immunofluorescence detection and Western blot. The relative expression of EGFR protein in the rats of the model group the control group were 0.21±0.03 and 1.30±0.07, respectively, and the difference was statistically significance (t=12.84, P<0.001). Conclusion Expression of EGFR protein was increased during BaP carcinogenesis, and EGFR may play an important role in the carcinogenesis of BaP.