Objective:To introduce the reform and practice of diagnosis and treatment mode in a hospital, analyze the output results, and put forward the characteristics, advantages and disadvantages of online medical care.Methods:The hospital launched the " online consultation" service for the first time in July 2019, and continuously accelerated the function construction of the Internet hospital, gradually transforming the traditional offline diagnosis and treatment mode into a new full-cycle diagnosis and treatment mode integrating online inquiry, billing, self payment, drug mailing, inspection appointment, self admission and chronic disease follow-up. The operation data of hospital online outpatient service from January to June in 2020 were analyzed.Results:From January 1st to June 21st, 2020, the Internet hospital has received over 318 000 patients. Most of the online outpatients suffered from chronic diseases, while the diseases that needed further treatment were mainly in the offline outpatient department, such as the first diagnosis and acute diseases. Among the online outpatient expenses, the drug cost accounted for the highest proportion(80.52%), and the registration cost accounted for the least(4.04%).Conclusions:The change of medical treatment mode will force the continuous reform of public hospitals, but the current policy environment for Internet hospital development needs to be in place. In the future, we should further clarify the functional orientation of Internet hospitals and promote the rapid integration of online and offline services.

Objective:To investigate the dosimetric effects of prone immobilization devices combined with a belly board (PIDBBs) in the intensity-modulated radiotherapy (IMRT) for gynecologic cancers.Methods:A total of 20 patients with cervical or endometrial cancer treated with radiotherapy in the Third Affiliated Hospital of Sun Yat-sen University from August 2020 to June 2021 were retrospectively analyzed. Two sets of body contours were outlined for each patient. One set of body contours did not contain the immobilization devices, and the other contour set included the immobilization devices. For each patient, doses were calculated for the two sets of contours using the same 7-field IMRT plan and were recorded as Plan without and Plan with. The dosimetric difference caused by the immobilization devices was assessed by comparing the parameter values in the dose-volume histograms (DVHs) and by plan subtraction. The Gafchromic EBT3 film and anthropomorphic phantom were used to verify the calculated doses. Results:The target coverage and average dose of Plan with were lower than those of Plan without. Specifically, the V50 Gy, V49 Gy, and Dmean of planning target volume (PTV) decreased by 19.75%, 7.99%, and 2.54% ( t = 8.96, 10.49, 22.09, P < 0.01), respectively. The V40 Gy, V30 Gy, V20 Gy, V15 Gy, and Dmean of skins increased by 51.79%, 51.05%, 45.72%, 33.63% and 10.80% ( t = -2.54, -5.63, -15.57, -24.06, -13.88, P < 0.01), respectively. Doses to other organs at risk (OARs) showed no significant differences. As indicated by the EBT3 measurements, the doses to skins of the abdomen and pelvis on the anthropomorphic phantom increased by approximately 37.24% ( t = 10.86, P<0.01). Conclusions:Although PIDBBs can effectively reduce the low dose to the small intestine, the radiation attenuation caused by them can reduce the PTV coverage of radiotherapy plans and increase the doses to abdominal and pelvic skins sharply, especially for patients requiring irradiation of the groin and perineum.

Phosphoinositide 3-kinase (PI3K) is considered as a promising therapeutic target for rheumatoid arthritis (RA) because of its involvement in inflammatory processes. However, limited studies have reported the involvement of PI3KC2γ in RA, and the underlying mechanism remains largely unknown. Therefore, we investigated the role of PI3KC2γ as a novel therapeutic target for RA and the effect of its selective inhibitor, PBT-6. In this study, we observed that PI3KC2γ was markedly increased in the synovial fluid and tissue as well as the PBMCs of patients with RA. PBT-6, a novel PI3KC2γ inhibitor, decreased the cell growth of TNF-mediated synovial fibroblasts and LPS-mediated macrophages. Furthermore, PBT-6 inhibited the PI3KC2γ expression and PI3K/AKT signaling pathway in both synovial fibroblasts and macrophages. In addition, PBT-6 suppressed macrophage migration via CCL2 and osteoclastogenesis. In CIA mice, it significantly inhibited the progression and development of RA by decreasing arthritis scores and paw swelling. Three-dimensional micro-computed tomography confirmed that PBT-6 enhanced the joint structures in CIA mice. Taken together, our findings suggest that PI3KC2γ is a therapeutic target for RA, and PBT-6 could be developed as a novel PI3KC2γ inhibitor to target inflammatory diseases including RA.

KRAS activating mutations, which are present in more than 90% of pancreatic cancers, drive tumor dependency on the RAS/ mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT signaling pathways. Therefore, combined targeting of RAS/MAPK and PI3K/AKT signaling pathways may be required for optimal therapeutic effect in pancreatic cancer.However, the therapeutic efficacy of combined MAPK and PI3K/AKT signaling target inhibitors is unsatisfactory in pancreatic cancer treatment, because it is often accompanied by MAPK pathway reactivation by PI3K/AKT inhibitor. Therefore, we developed an inRas37 antibody, which directly targets the intra-cellularly activated GTP-bound form of oncogenic RAS mutation and investigated its synergistic effect in the presence of the PI3K inhibitor BEZ-235 in pancreatic cancer. In this study, inRas37 remarkably increased the drug response of BEZ-235 to pancreatic cancer cells by inhibiting MAPK reactivation. Moreover, the co-treatment synergistically inhibited cell proliferation, migration, and invasion and exhibited synergistic anticancer activity by inhibiting the MAPK and PI3K pathways. The combined administration of inRas37and BEZ-235 significantly inhibited tumor growth in mouse models. Our results demonstrated that inRas37 synergistically increased the antitumor activity of BEZ-235 by inhibiting MAPK reactivation, suggesting that inRas37 and BEZ-235 co-treatment could be a potential treatment approach for pancreatic cancer patients with KRAS mutations.