With the rapid development of artificial intelligence technology,Large Language Models(LLMs)have in-creasingly been applied in the medical field,particularly demonstrating significant potential in the prevention and management of medical disputes,patient management,and medical quality control.This article,from the perspective of cooperative governance,summarizes and analyzes the current application of LLMs in the field of medical dispute from the perspectives of the governments,research and development companies,medical staff,patients and all other relevant parties.It delves into the advantages of LLMs in dispute prediction,document writing,quality control,patient management,and case retrieval,and systematically analyzes the challenges faced in data security,privacy protection,professional competence,ethical and legal issues,and personnel utilization.The aim of this article is to provide references and development suggestions for further research and practice of LLMs in the field of medical disputes.

With the rapid development of artificial intelligence technology,Large Language Models(LLMs)have in-creasingly been applied in the medical field,particularly demonstrating significant potential in the prevention and management of medical disputes,patient management,and medical quality control.This article,from the perspective of cooperative governance,summarizes and analyzes the current application of LLMs in the field of medical dispute from the perspectives of the governments,research and development companies,medical staff,patients and all other relevant parties.It delves into the advantages of LLMs in dispute prediction,document writing,quality control,patient management,and case retrieval,and systematically analyzes the challenges faced in data security,privacy protection,professional competence,ethical and legal issues,and personnel utilization.The aim of this article is to provide references and development suggestions for further research and practice of LLMs in the field of medical disputes.

The effects of tumor suppressor in lung cancer-1(TSLC1)upregulation on gene expressions involved in glucose and lipid metabolism in Hepa1-6 cells were investigated.The results showed that TSLC1 overexpression decreased fatty acid synthase and acetyl CoA carboxylase expressions(P<0.05 or P<0.01),increased adipose triglyceride lipase expression(P<0.05),and did not change hormone-sensitive lipase,glucose transporter (GLUT)1,and GLUT4 expressions.These results suggest that TSLC1 overexpression may promote lipolysis and inhibit adipogenesis in liver cells.

The effects of liraglutide on glucose and lipid metabolism, fibroblast growth factor-21 ( FGF-21 )and its receptors (FGFR) in APoE-/-mice with hypoadiponectinemia were investigated.Hypoadiponectinemia facilitated disturbance in glucose and lipid metabolism and insulin resistance. Compared with the control mice, FGF21 mRNA and protein expressions of liver and adipose tissues as well as plasma FGF-21 level were significantly increased in ApoE-/-mice with hypoadiponectinemia, along with lowered expressions of FGFR1 and β-klotho mRNA in adipose tissues, and expressions of FGFR1-3 and β-klotho mRNA in liver. Liraglutide administration improved glucose and lipid metabolism and insulin resistance, and partially reversed the changes of FGF-21 and its receptors induced by hypoadiponectinemia.

Objective To observe the effects of JAZF1 (Juxtaposed with another zinc finger gene 1 ) overexpression on glucose and lipid metabolism in 3T3-L1 adipocytes. Methods The tissue distribution of JAZF1 in healthy C57BL/6J mice was detected by real-time quantitative PCR( RT-QPCR). Expression vector for JAZF1 gene was constructed and transfected into 3T3-L1 adipocytes. The mRNA levels of JAZF1, GLUT1, GLUT4, FAS, ACC, SREBP1, ATGL, and HSL implicated in glucose and lipid metabolism were determined by RT-QPCR; JAZF1 protein level was measured by Western blot. Intracelluar lipid accumulation were measured by oil red O staining method. Results In JAZF1-transfected adipocytes, JAZF1 mRNA and protein levels were significantly higher than control cells after 48 h. The mRNA level of HSL was increased significantly (P<0. 05) in JAZF1 transfection group compared with negative control and empty vector group, and the expressions of FAS, ACC, SREBP1 mRNA were decreased significantly(all P<0.01). However, the mRNA levels of ATGL, GLUT1, GLUT4 were not changed. Intracelluar lipid accumulation was decreased significantly (P<0.05 ) by oil red O staining and colorimetric in JAZF1 -transfected cells compared with negative control and empty vector group. Conclusions There was an extensive expression of JAZF1 in various tissues of C57BL/6J mice,indicating that JAZF1 might play a role in maintaining normal physiological function. These results show that overexpression of JAZF1 in 3T3-L1 cells can reduce lipid synthesis, increase lipolysis, and improve lipid accumulation. JAZF1 might provide a new potential therapeutic target for obesity and diabetes.

Objective The anterior-lateral defect of foot that lost one of the three supporting point of foot can lead to collapse of the lateral longitudinal arch, overload of the first metatarsal heads, and painful callus formation. It is meaningful to investigate the effect of reconstructing the lateral forefoot defect with pedical fibular osteoseptocutaneous flap. Methods From March 1989 to June 2008, there were 38 patients with anterior-lateral defect of foot were constructed. The supporting point with the local distal based pedical fibular osteoseptocutaneous flap was constracted. Results All the 38 flaps survived. All 38 patients had been followed up from 6 months to 10 years (mean 23.5 months) postoperatively. The constructed supporting point of the foot was functional. The patients could walk freely with no pain, and was satisfied with the operation. Assessed with the rating system for foot and ankle established by the American Orthopaedic Foot And Anke Society, 8 patients got a score above 85, 23 patients between 75 to 85, 7 patients between 60 to 75. Conclusion It is effective that transferring local distal based pedical fibular osteoseptocutaneous flap to repair the anterior-lateral defect of foot.

BACKGROUND: Recent researches indicate that ischemia and hypoxia can lead to abnormal brain metabolism and even energy failure, which is an important reason for brain damage and necrosis and identifies energy metabolism disorder as the key event in brain ischemia-reperfusion (IR)injury. Glucose transporter-3 plays the vital role in brain energy metabolism.OBJECTIVE: To observe the changes of cerebral infarct volume and glucose transporter-3 mRNA and protein expressions in cerebral cortical penumbra at different stages of focal cerebral ischemia and reperfusion in rats.DESIGN: Randomized controlled experiment.SETTING: Department of Neurosurgery, Second Hospital Affiliated to Sun Yat-sen University.MATERIALS: This experiment was conducted in the Animal Laboratory of Medical Research Center, Second Hospital Affiliated to Sun Yat-sen University between August and October 2002.Totally 56 SD rats were randomized into 3 groups which were subjected to ① ischemia for 1 hour followed by reperfusion (n=28), ② ischemia for 3 hours followed by reperfusion (n=24), and ③ sham operation (n=4). The rats in the first group were subdivided into 7 subgroups for examination at 1, 3, 6, 12, 24, and 72hours and 1 week after ischemia, with 7 rats in each subgroup; the rats in the second ischemia group were also subdivided in similar manner but without a 1 hour postischemic subgroup. The rats in the sham operation group only received the operation but without arterial occlusion.METHODS: Focal cerebral ischemia-reperfusion (IR) injury model was induced in the rats in the two ischemic groups by means of insertion of suture for arterial occlusion, and the ratio of central ischemic area to cerebral infarct volume in the ischemic penumbra was examined at the specified time points. Reverse transcription-PCR (RT-PCR) was used to detect the expression of glucose transporter-3 mRNA in the cerebral cortex in ischemic penumbra region, and semi-quantitative immunohistochemistry (IHC) employed to detect the level of glucose transporter-3 protein.MAIN OUTCOME MEASURES: Cerebral infarct volume after IR injury, changes of transporter-3 mRNA and protein expressions after IR injury.RESULTS: Totally 56 rats were used in this experiment and all entered result analysis. The post-IR cerebral infarct volume was obviously smaller in 1-hour ischemia group than in 3-hour ischemia group. Glucose transporter-3 mRNA expression began to increase 3 hours after ischemia in 1-hour ischemia group, reaching the peak level at 24 hours and still mainrained higher level than that of the sham operation 1 week; in 3-hour ischemia group, the mRNA expression was slightly decreased at 3 hours but began to increase afterwards till reaching the peak level at 24 hours, followed then by recovery of normal level at 1 week. The changes in glucose transporter-3 protein and mRNA expressions followed almost the same pattern.CONCLUSION: Glucose transporter-3 expression is up-regulated in the ischemic penumbra region, possibly as a protective response to cerebral IR injury.

AIM: To investigate the volume percentage of infarct and expression of glucose transporter-1 (GLUT1) transcription and protein levels at different ischemic time point and different reperfusion time point in rat focal cerebral ischemic penumbra. METHODS: Focal ischemic models of middle cerebral artery occlusion (MCAO) in rats were made by inserting nylon thread. Brain samples were harvested from ischemic penumbra. Infarct volume were analyzed quantitively by Kontron IBAS 2.5 image auto-analyses system. The expressien of GLUT1 mRNA was assessed by RT-PCR, and the expression of GLUT1 protein was assessed by immunohistochemistry. RESULTS: The infarction volume in MCAO 1 h/reperfusion (R) group was obviously smaller than that in MCAO 3 h/R group. GLUT1 increased at (1 h) MCAO 1 h/R group, climbed to climax at 24 h and remained higher than normal at 1 week. In contrast, in the MCAO 3 h/R group, the corresponding index was at 3 h, 24 h and 1 week, but the increasing degree of GLUT1 was slighter than MCAO 1 h/R. GLUT1 protein began to ascend at 1 h, reached climax at 24 h and was higher than normal at 1 week in MCAO 1 h/R group, while in MCAO 3 h/R group, the corresponding index was at 3 h, 24 h and 1 week. CONCLUSION: GLUT1 expression is notably up-regulated in the penumbra region after focal cerebral ischemia, it may be a protective reaction against ischemic injury. [

AIM: To investigate the volume percentage of infarct and expression level of glucose transporter-3 (GLUT3) transcription and protein at different ischemic time points and different reperfusion time points in rat focal cerebral ischemic penumbra. METHODS: Focal ischemic models of middle cerebral artery occlusion (MCAO) in rats were made by inserting nylon thread. Brain samples were harvested from ischemic penumbra. Infarct volume was analyzed quantitatively by Kontron IBAS 2.5 image auto-analyses system. The change of GLUT3 mRNA was assessed by RT-PCR, and the expression of GLUT3 protein was assessed by immunohistochemistry. RESULTS: The infarction volume in MCAO 1 h/R group was obviously smaller than that in MCAO 3 h/R group. GLUT3 began to ascend at 3 h in MCAO 1 h/R group, reached to climax at 24 h and remained higher than normal at 1 week. In contrast, in the MCAO 3 h/R group, GLUT3 had a descent at 3 h. Later on, it ascended rapidly, and reached climax at 24 h. At 1 week, it approached to normal. The expression level of GLUT3 protein corresponds with that of mRNA. CONCLUSION: GLUT3 expression is up-regulated in the penumbra region after focal cerebral ischemia, it may be a protective reaction against ischemia/reperfusion injury. [