Objective To investigate the effects of dihydroquercetin(DHQ)on retinal ferroptosis and visual function in rats with optic nerve injury(ONI),and to elucidate the underlying mechanisms.Methods Thirty-six 8-12-week-old adult male SD rats were randomly divided into three groups:SHAM group(sham surgery without optic nerve damage,fol-lowed by saline injection at the same time points),ONI group(ONI model established by surgery,followed by saline injec-tion),DHQ+ONI group(ONI model established by surgery,followed by intraperitoneal injection of 50 mg·kg-1DHQ on days 1,3,5,and 7 post-surgery).The ONI model was constructed by optic nerve clamping.After 7 days:Brn3a immuno-fluorescence was used to observe morphological and quantitative changes in retinal ganglion cells(RGCs).Immunohisto-chemistry and Western blot were performed to analyze protein expression of nuclear factor-erythroid 2-related factor 2(Nrf2),phosphorylated protein kinase B(p-AKT),and glutathione peroxidase 4(Gpx4),Flash visual evoked potential(F-VEP)was applied to assess visual function changes.Results Immunofluorescence quantification of Brn3a-positive cells:SHAM group:(61.49±3.84)cells·mm-1,ONI group:(25.24±1.81)cells·mm-1,DHQ+ONI group:(46.50±3.51)cells·mm-1.Compared with SHAM group,ONI group showed decreased Brn3a-positive cells(P＜0.001).Compared with ONI group,DHQ+ONI group showed increased Brn3a-positive cells(P＜0.01).Immunohistochemistry and Western blot:Compared with SHAM group,ONI group showed decreased protein expression of Nrf2,p-AKT,and Gpx4(all P＜0.001).Compared with ONI group,DHQ+ONI group showed increased expression of these proteins(all P＜0.01).F-VEP meas-urements:SHAM group:P1 wave amplitude(49.87±0.81)μV,ONI group:(5.87±0.25)μV,DHQ+ONI group:(36.43±0.21)μV.Compared with SHAM group,ONI group showed reduced P1 amplitude(P＜0.001).Compared with ONI group,DHQ+ONI group showed increased P1 amplitude(P＜0.001).Conclusion DHQ may protect and repair RGCs in ONI rats by inhibiting the ferroptosis-related Nrf2/p-AKT/Gpx4 signaling pathway,thereby ameliorating vision impairment caused by ONI.

This article systematically reviews the regulatory mechanism of SIRT3,an important mitochondrial deacetylase,in the pathogenesis of Alzheimer disease(AD).As a major mitochondrial deacetylase,SIRT3 participates in cerebral energy metabolism,neuroinflammation,and mitochondrial quality control by regulating mitochondrial protein functions.During the pathological process of AD,the downregulated expression of SIRT3 can induce hyperacetylation of mitochondrial proteins.This not only leads to mitochondrial dysfunction(such as impaired ATP synthesis and excessive reactive oxygen species production)but also impairs mitochondrial quality control mechanisms such as mitophagy and fusion/fission balance,thereby promoting mitochondrial damage.In addition,SIRT3 deficiency can activate neuroinflammatory pathways,prompting the release of inflammatory factors and further exacerbating neuronal damage.Future research will aim to undercover the detailed protective mechanisms of SIRT3 in AD,validate its feasibility as a therapeutic target for AD,and develop specific agonists,providing a theoretical basis for the intervention strategies of AD.

This article systematically reviews the regulatory mechanism of SIRT3,an important mitochondrial deacetylase,in the pathogenesis of Alzheimer disease(AD).As a major mitochondrial deacetylase,SIRT3 participates in cerebral energy metabolism,neuroinflammation,and mitochondrial quality control by regulating mitochondrial protein functions.During the pathological process of AD,the downregulated expression of SIRT3 can induce hyperacetylation of mitochondrial proteins.This not only leads to mitochondrial dysfunction(such as impaired ATP synthesis and excessive reactive oxygen species production)but also impairs mitochondrial quality control mechanisms such as mitophagy and fusion/fission balance,thereby promoting mitochondrial damage.In addition,SIRT3 deficiency can activate neuroinflammatory pathways,prompting the release of inflammatory factors and further exacerbating neuronal damage.Future research will aim to undercover the detailed protective mechanisms of SIRT3 in AD,validate its feasibility as a therapeutic target for AD,and develop specific agonists,providing a theoretical basis for the intervention strategies of AD.

Objective To investigate the effects of dihydroquercetin(DHQ)on retinal ferroptosis and visual function in rats with optic nerve injury(ONI),and to elucidate the underlying mechanisms.Methods Thirty-six 8-12-week-old adult male SD rats were randomly divided into three groups:SHAM group(sham surgery without optic nerve damage,fol-lowed by saline injection at the same time points),ONI group(ONI model established by surgery,followed by saline injec-tion),DHQ+ONI group(ONI model established by surgery,followed by intraperitoneal injection of 50 mg·kg-1DHQ on days 1,3,5,and 7 post-surgery).The ONI model was constructed by optic nerve clamping.After 7 days:Brn3a immuno-fluorescence was used to observe morphological and quantitative changes in retinal ganglion cells(RGCs).Immunohisto-chemistry and Western blot were performed to analyze protein expression of nuclear factor-erythroid 2-related factor 2(Nrf2),phosphorylated protein kinase B(p-AKT),and glutathione peroxidase 4(Gpx4),Flash visual evoked potential(F-VEP)was applied to assess visual function changes.Results Immunofluorescence quantification of Brn3a-positive cells:SHAM group:(61.49±3.84)cells·mm-1,ONI group:(25.24±1.81)cells·mm-1,DHQ+ONI group:(46.50±3.51)cells·mm-1.Compared with SHAM group,ONI group showed decreased Brn3a-positive cells(P＜0.001).Compared with ONI group,DHQ+ONI group showed increased Brn3a-positive cells(P＜0.01).Immunohistochemistry and Western blot:Compared with SHAM group,ONI group showed decreased protein expression of Nrf2,p-AKT,and Gpx4(all P＜0.001).Compared with ONI group,DHQ+ONI group showed increased expression of these proteins(all P＜0.01).F-VEP meas-urements:SHAM group:P1 wave amplitude(49.87±0.81)μV,ONI group:(5.87±0.25)μV,DHQ+ONI group:(36.43±0.21)μV.Compared with SHAM group,ONI group showed reduced P1 amplitude(P＜0.001).Compared with ONI group,DHQ+ONI group showed increased P1 amplitude(P＜0.001).Conclusion DHQ may protect and repair RGCs in ONI rats by inhibiting the ferroptosis-related Nrf2/p-AKT/Gpx4 signaling pathway,thereby ameliorating vision impairment caused by ONI.

The article reported a case of 5G remote robot-assisted sleeve gastrectomy completed on December 14,2023,by using the Minimally Invasive Tumai Laparoscopic Surgical Robotic System(MT-1000)and a 5G signal network system in a dual-master-knife mode.The patient's platform was located in the operating room of the Gansu Provincial People's Hospital(GSPH),and the main manipulator's table was located in the operating room of the Lanzhou New District Branch of the Gansu Provincial People's Hospital(straight-line distance between the two being 75.6 km).The total duration of the surgery was 120 min,including 30 min of loading time and 90 min of robotic operation time.The average intraoperative network delay was(55.16±25.33)ms,and the packet loss rate was 0.01％-0.1％.No adverse network events such as network interruption occurred,and the surgery was completed successfully.

The article reported a case of 5G remote robot-assisted sleeve gastrectomy completed on December 14,2023,by using the Minimally Invasive Tumai Laparoscopic Surgical Robotic System(MT-1000)and a 5G signal network system in a dual-master-knife mode.The patient's platform was located in the operating room of the Gansu Provincial People's Hospital(GSPH),and the main manipulator's table was located in the operating room of the Lanzhou New District Branch of the Gansu Provincial People's Hospital(straight-line distance between the two being 75.6 km).The total duration of the surgery was 120 min,including 30 min of loading time and 90 min of robotic operation time.The average intraoperative network delay was(55.16±25.33)ms,and the packet loss rate was 0.01％-0.1％.No adverse network events such as network interruption occurred,and the surgery was completed successfully.

Objective To evaluate the feasibility of establishing canine rectovaginal fistula ani-mal model using magnetic surgery techniques.Methods Ten female Beagle dogs were randomly di-vided into study group(n=5)and control group(n=5).The study group underwent rectovaginal fistula modeling using magnetic surgery technology,while the control group was subjected to sharp puncture of the rectovaginal septum followed by indwelling rubber tube placement to establish the model.Surgical procedure duration and postoperative adverse events were recorded in both groups.Two weeks later,the magnets and rubber tubes were removed.The formation of rectovaginal fistulas in the animals of two groups was observed,and the success rates of model construction of two groups were statistically analyzed.Results Both groups successfully completed the preparation of the recto-vaginal fistula models.The operative time in both groups was less than 2 minutes.No adverse events such as magnet detachment were observed in the study group during the postoperative period.In the control group,the rubber tube dislodged on day 6 post-surgery in one dog,leading to spontaneous healing of the fistula.Two weeks after surgery,the magnets and rubber tubes were removed.Naked-eye observation showed that the rectovaginal fistula formed well in the experimental dogs of the study group,while the rectovaginal fistula formed well in 4 experimental dogs in the control group.The success rate of model construction in the study group was 100％,and was 80％in the control group.Conclusion The construction of a canine rectovaginal fistula model by magnetosurgical techniques has the advantages of simple operation and high success rate.Magnetosurgical techniques may serve as an ideal animal model for constructing and studying the histopathological changes and treatment methods of rectovaginal fistulas.

Objective:To construct a VP8-mRNA vaccine using human rotavirus spike protein VP8 domain as the immunogen and analyze its immunogenicity in mice.Methods:The VP8-mRNA sequence was designed, optimized, and synthesized. The VP8 gene of rotavirus G1P[8] type was used to construct the plasmid pUC57-VP8-Kan-SapⅠ, which was then sequenced. The plasmid confirmed by sequencing was subjected to large-scale amplification and extraction, followed by linearization, in vitro transcription, and capping. The purified capped products were encapsulated with lipid nanoparticles using a microfluidic control apparatus. The encapsulated VP8-mRNA vaccine was administered intramuscularly to mice at 10, 15, and 20 μg. Serum samples were collected for antibody detection by ELISA. Cellular immune responses were detected by flow cytometry and ELISPOT. Statistical analysis was performed using one-way or two-way analysis of variance and Tukey-Kramer test. Results:The encapsulated VP8-mRNA vaccine was rounded and spherical, with a particle size of about 100 nm, a polymer dispersion index of 0.088, and an encapsulation rate of 92.3%. Two doses of VP8-mRNA vaccine immunization could induce a good immune response in mice. The level of IgG antibody induced after immunization in the 15 μg group was comparable to that of the 20 μg group, and there was no statistical difference ( P>0.05), but the antibody levels in the two groups were significantly higher than that in the 10 μg group ( P<0.000 1). VP8-mRNA vaccine could induce neutralizing antibodies against rotavirus G1 and G9 types. The highest level of neutralizing antibodies against rotavirus type G1 was observed in the 15 μg group, which was significantly higher than that in the 10 μg group ( P<0.05). All immunization groups exhibited good neutralizing ability against rotavirus G9 type. The results of ELISPOT showed that lymphocytes from mice in each vaccine group were able to secrete IFN-γ when stimulated with VP8 peptide. Flow cytometry showed that the proportions of CD8 + T cell subsets in the vaccine groups were higher than that in the control group. Conclusion:The VP8-mRNA vaccine has good immunogenicity in mice and can induce good humoral and T-cell immune responses.

Objective: To investigate the feasibility of magnetic anastomosis for uretero-ileal anastomosis using experimental rabbit models. Methods: Six experimental rabbits were used as the models.The lower part of the left ureter was cut with scissors，the daughter magnet (DM) was placed in the middle of the ureter，and the distal end of the ureter was ligated.After that，the ileum wall was opened，the parent magnet (PM) was inserted through it，the positions of the PM and DM were adjusted so that their ends were attracted to each other，and then ileum wall incision was sutured.The operation time，intraoperative blood loss，postoperative complications and magnet discharge time were recorded.Two weeks after operation，left ureterography was performed to obtain the specimens of the uretero-ileal anastomosis，and to observe the patency of the anastomosis.The formation of the anastomosis was observed with naked eyes and light microscope. Results: Uretero-ileal magnetic anastomosis was performed successfully in 6 experimental rabbits.The operation time was 28-39（32.50±3.94） min，and the intraoperative blood loss was less than 5 mL.The rabbits recovered well after operation，and no complications were observed.All animals survived to the end point of observation.The disconnection time of magnet after operation was 9-13(10.83±1.72) days.The gross specimen showed that the anastomosis was patent.The histological observation showed that the mucosa of the anastomosis was continuous and smooth，and the anastomosis was well formed. Conclusion: Magnetic anastomosis is feasible for uretero-ileal anastomosis with simple operation and good anastomosis formation.After further experimental verification，this technique is expected to be used in clinical practice.

Bisphenols (BPs) are extensively used in food packaging, personal care products, and plastics, making them prevalent in both living and working environments, which has raised significant concern. As endocrine-disrupting chemicals, BPs exert toxic effects on the female reproductive system by binding to estrogen receptors, thereby activating or inhibiting the expression of genes related to reproductive functions, which disrupts the normal function of the endocrine system. This paper reviewed the effects of bisphenol A (BPA), bisphenol S (BPS), and bisphenol F (BPF) on female reproductive function, focusing on three key aspects: the effects on the female reproductive organs, the occurrence of associated reproductive disorders, and the mechanisms of toxicity. Specifically, this review highlighted the effects on ovarian function, uterine morphology and function, and fallopian tube function, as well as their correlation with polycystic ovary syndrome, endometriosis, miscarriage, and eclampsia. Additionally, the toxic mechanisms of BPs exposure were summarized, providing a scientific basis for future research on the impact of BPs on the female reproductive system, as well as for the assessment of potential health risks and the development of preventive measures.