Objective To evaluate whether 6-gingerol(6G)can inhibit fibrosis and improve the cardiac and renal function and in rats with cardiorenal syndrome.Methods In the in vitro experiments of this study,the incorporation of isotope-labeled amino acids was used to detect the intervention of 6-gingerol on normal rat kidney-49F(NRK-49F)and normal rat kidney-52E(NRK-52E)cells.68 male SD rats weighing 200～250 g were used to establish a rat model of cardiorenal syndrome by ligating the left anterior descending coronary artery and performing 5/6 nephrectomy.The rats were randomly divided into a control group,a model group,a low dose 6-gingerol group(6 mg/kg),a high dose 6-gingerol group(30 mg/kg),and a losartan potassium group(20 mg/kg).The 6-gingerol group received intraperitoneal injection of 6-gingerol,while the control group and model group received intraperito-neal injection of an equal amount of physiological saline.The losartan group received oral administration of losartan potassium for a total of 6 weeks.After successful modeling,blood samples were taken for biochemical and cardiac ultrasound examinations.After the experiment,blood,heart,and kidney samples were taken for Masson,immuno-histochemistry,and Western blot.Results 6-gingerol 20 μmol/L can reduce NRK-49F collagen synthesis and inhibit NRK-52E protein synthesis.Biochemical results showed that the serum creatinine,urea nitrogen,and brain natriuretic peptide(BNP)levels of rats in the low and high dose 6-gingerol groups and the losartan group were all reduced,with high dose 6-gingerol groups and losartan group showing the most significant decrease(P<0.05).Echocardiographic parameters showed that the 6-gingerol group and losartan potassium group improved cardiac contractile function and ventricular remodeling in rats(P<0.05).Masson staining and Western Blot showed renal collagen deposition,with reduced expression of collagen I and α-SMA(P<0.05).Immunofluorescence showed a decrease in the expression of renal collagen deposition I,α-SMA,and TGF-β1(P<0.05).Conclusion 6-Gin-gerol may improve the cardiac and renal function and renal fibrosis in rats with cardiorenal syndrome.

Objective To investigate the role of circular RNAs(circRNA)in Alzheimer's disease(AD)and its potential mechanism.Methods Six-month-old APP/PS1 mouse model of AD and wild type(WT)mice were subjected and then randomly divided into WT group,WT+circ-Olfm1 knockout group,AD group(transgenic APP/PS1 mice),AD+circ-Olfm1 knockout group,AD+FOXO3a knockout group,with 3 mice in each group.① The total RNA of mouse brain was extracted,and the differential expression of circRNAs and mRNAs between the AD mice and WT mice was detected,and the obtained circRNAs and mRNAs were analyzed with gene ontology(GO)analysis.② RT-qPCR was used to detect the expression of the top 10 up-regulated and down-regulated circRNAs,as well as the expression of circ-Olfm1 and miR-330-5p.③ Lentiviral vectors were prepared and stereotaxically injected into the cortex or hippocampus of WT and AD mice to knock out circ-Olfm1 gene.Water maze test was used to evaluate the effect of circ-Olfm1 knockout on cognitive function,and immunofluorescence assay was employed to observe the deposition of amyloid β(Aβ)plaque in the brain.④ The interaction between circ-Olfm1 and miR-330-5p was verified by double luciferase reporter gene analysis.⑤ The protein levels of AMPK and FOXO3a were detected by Western blotting.⑥ Transmission electron microscopy was utilized to observe the mitochondria of the hippocampus.⑦ The levels of inflammatory factors IL-6,IL-1β and TNF-α were detected by ELISA.Results There were totally 52 differentially expressed circRNAs identified between the AD and WT mice,including 28 up-regulated and 24 down-regulated(fold change>1.5,P<0.05).These differentially expressed genes are mainly involved in signal transduction,learning and memory and other functions.circ-Olfm1 was identified as the most significantly differentially expressed circRNA,which is highly expressed in the neurons and up-regulated in the cerebral cortex and hippocampus of the AD mice.Knockout of circ-Olfm1 reduced the number of Aβ plaques in the cerebral cortex and hippocampus of AD mice(P<0.01).In starBase database,there are complementary sequences observed between circ-Olfm1 and miR-330-5p.Western blotting showed that the addition of Aβ42 significantly increased the expression of AMPK and FOXO3a in the neuronal cells(P<0.01).And silencing circ-Olfm1 led to decreased expression of AMPK and FOXO3a in neuronal cells+Aβ42(P<0.01).ELISA revealed that knockout of FOXO3a significantly increased the levels of inflammatory factors IL-6,IL-1β,and TNF-α(P<0.01).Transmission electron microscopy displayed that knocking FOXO3a out significantly aggravated mitochondrial damage(P<0.01).Conclusion circ-Olfm1 is up-regulated in the brain tissue and neurons+Aβ42 of AD rats,and the mechanism of cognitive impairment in AD rats may be through its regulating FOXO3a protein.

Left atrial appendage closure(LAAC)is an important intervention method for preventing thromboembolic events in patients with non-valvular atrial fibrillation(NVAF).However,incomplete endothelialization following the procedure can impact its long-term efficacy and safety.This article proposes the view of qi flourishment promoting tissue regeneration based on the traditional Chinese medicine(TCM)theory of qi and blood,and explores diagnostic and therapeutic strategies for post-LAAC incomplete endothelialization by examining the theoretical connotation of qi flourishment promoting tissue regeneration and the relationship between qi and vascular endothelial cells.It is proposed that the primary pathogenesis in patients after LAAC is due to qi deficiency.Guided by the view of qi flourishment promoting tissue regeneration,therapeutic approaches such as tonifying qi to promote granulation,supplementing qi to activate blood circulation,and harmonizing the viscera can be employed to address incomplete endothelialization in NVAF patients following LAAC.Clinically,the qi-supplementing and blood-activating classic formula Neituo Shengji San,mainly composed of Astragali Radix,Glycyrrhizae Radix et Rhizoma,Olibanum,Myrrha,Paeoniae Radix Alb,Trichosanthis Radix,Salviae Miltiorrhizae Radix et Rhizoma,etc.,is usually utilized for modified use.Depending on the specific symptom patterns or pathogenesis characteristics of patients with incomplete endothelialization,this basic formula may be used by combining with Shengmai San or augmented with qi-supplementing and blood-activating herbs such as Chuanxiong Rhizoma,Fici Simplicissimae Radix,and Notoginseng Radix et Rhizoma to promote endothelialization.Diagnosing and treating post-LAAC incomplete endothelialization in NVAF patients following the view of qi flourishment promoting tissue regeneration,it is expected to offer a novel TCM perspective and therapeutic strategy to enhance post-LAAC outcomes and address the challenge of incomplete endothelialization.This approach can further serve as a reference for TCM clinicians to manage endothelialization issues following implantation procedures.

Objective To evaluate whether 6-gingerol(6G)can inhibit fibrosis and improve the cardiac and renal function and in rats with cardiorenal syndrome.Methods In the in vitro experiments of this study,the incorporation of isotope-labeled amino acids was used to detect the intervention of 6-gingerol on normal rat kidney-49F(NRK-49F)and normal rat kidney-52E(NRK-52E)cells.68 male SD rats weighing 200～250 g were used to establish a rat model of cardiorenal syndrome by ligating the left anterior descending coronary artery and performing 5/6 nephrectomy.The rats were randomly divided into a control group,a model group,a low dose 6-gingerol group(6 mg/kg),a high dose 6-gingerol group(30 mg/kg),and a losartan potassium group(20 mg/kg).The 6-gingerol group received intraperitoneal injection of 6-gingerol,while the control group and model group received intraperito-neal injection of an equal amount of physiological saline.The losartan group received oral administration of losartan potassium for a total of 6 weeks.After successful modeling,blood samples were taken for biochemical and cardiac ultrasound examinations.After the experiment,blood,heart,and kidney samples were taken for Masson,immuno-histochemistry,and Western blot.Results 6-gingerol 20 μmol/L can reduce NRK-49F collagen synthesis and inhibit NRK-52E protein synthesis.Biochemical results showed that the serum creatinine,urea nitrogen,and brain natriuretic peptide(BNP)levels of rats in the low and high dose 6-gingerol groups and the losartan group were all reduced,with high dose 6-gingerol groups and losartan group showing the most significant decrease(P<0.05).Echocardiographic parameters showed that the 6-gingerol group and losartan potassium group improved cardiac contractile function and ventricular remodeling in rats(P<0.05).Masson staining and Western Blot showed renal collagen deposition,with reduced expression of collagen I and α-SMA(P<0.05).Immunofluorescence showed a decrease in the expression of renal collagen deposition I,α-SMA,and TGF-β1(P<0.05).Conclusion 6-Gin-gerol may improve the cardiac and renal function and renal fibrosis in rats with cardiorenal syndrome.

Objective To investigate the effect of galangin on cardiac remodeling and cardiac func-tion after myocardial infarction(MI).Methods A total of 32 male C57/BL6 mice(8-10 weeks old)were subjected for MI modeling,and finally 24 mice were assigned into control group[sham operation+hydroxycellulose sodium(CMC-Na)],model group(MI+CMC-Na),and experimental group(MI+galangin),with 8 mice in each group.After MI modeling,the mice of the experimen-tal group were given 40 mg/kg galangin by gavage for 4 weeks,and those of the control group and the model group were given the same volume(0.4 ml)of CMC-Na solution.HE staining was used to observe the size of the infarct area.The mRNA levels of inflammatory factors in the heart were detected by qRT-PCR,and protein levels of related signaling pathway proteins were measured with Western blotting.Immunofluorescence(IF)assay was applied to detect the infiltration of in-flammatory cells in the infarct border zone.TUNEL staining was employed to detect cell apoptosis in the infarct border zone.Results At 4 weeks after modeling,larger infarct size,enhanced expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,elevated apoptotic rate,decreased cardiac function indicators such as FS and LVEF,and reduced Bcl-2 expression level were observed in the model group than the control group(P＜0.05).The experimental group had sig-nificant smaller myocardial infarct size[(11.64±0.64)％vs(21.84±1.94)％],less CD3 positive T cells[(3.10±0.46)％vs(6.28±0.24)％],F4-80 positive macrophages[(1.98±0.50)％vs(5.35±0.62)％]and LY6G positive neutrophils[(6.33±0.67)％vs(11.33±1.77)％],decreased expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,reduced apoptotic rate[(21.45± 1.62)％vs(35.68±0.88)％],and increased FS and LVEF values and Bcl-2 expression level when compared with the model group(P＜0.05).Conclusion Galangin improves myocardial remode-ling and cardiac dysfunction after MI by inhibiting inflammatory response and cell apoptosis.

Objective:To compare the effectiveness and safety profile of tenofovir amibufenamide (TMF) and tenofovir alafenamide (TAF), especially the effects on lipid metabolism in the treatment of chronic hepatitis B.Methods:A retrospective study was conducted on the virological response rate, biochemical response rate, renal function indicators, and lipid metabolism status of 159 cases with chronic hepatitis B (72 cases with TMF and 87 cases with TAF) after 48 weeks of antiviral treatment. The effects of the two drugs on lipid metabolism were further explored through cell and animal experiments.Results:There were no statistically significant differences in baseline age, gender ratio, treatment-na?ve and treatment-experienced proportions, hepatitis B virus (HBV) DNA and aminotransferase levels, renal function indicators, and serum lipid levels between the two groups. The levels of HBV DNA and transaminase were significantly reduced after 48 weeks of treatment in both groups. However, there were no statistically significant differences in virological response (84.2% vs. 75.8%, χ2=0.733, P=0.392) and biochemical response rate (86.1% vs. 85.1%, χ2=0.035, P=0.851) between the two groups. There was no significant change in the renal function index levels before and after treatment between the two groups of patients. Triglyceride [TG, 1.30 (0.93, 1.81) mmol/L vs. 1.30 (0.82, 1.84) mmol/L, Z=-0.196, P=0.844], total cholesterol [TC, 4.53 (3.91, 5.15) mmol/L vs. 4.55 (3.88, 5.24) mmol/L, Z=-1.131, P=0.258], high-density lipoprotein [HDL-C, 1.04 (0.90, 1.3) mmol/L vs. 1.08 (0.94, 1.30) mmol/L, Z=-0.811, P=0.417], low-density lipoprotein [LDL-C, 2.68 (2.04, 3.29) mmol/L vs. 2.57 (1.99, 3.49) mmol/L, Z=-1.716, P=0.086] and the ratio of total cholesterol to high-density lipoprotein [TC/HDL-C, 4.52 (3.10, 5.23) vs. 4.30 (3.27, 5.01), Z=-0.410, P=0.682] had not statistically significant differences in the TMF group before and after treatment. TG [1.24(0.95, 1.98) mmol/L vs. 1.42(1.09, 2.21) mmol/L, Z=-2.895, P=0.004], TC [4.44(3.74, 5.26) mmol/L vs. 4.68(4.07), 5.46) mmol/L, Z=-2.825, P=0.005], low-density lipoprotein (LDL-C) [2.74 (2.05, 3.58) mmol/L vs. 2.87 (2.34, 3.50) mmol/L, Z=-2.419, P=0.016] , and TC/HDL-C [3.89(3.13, 4.82) vs. 4.39(3.70, 5.40), Z=-4.478, P<0.001] levels were increased after TAF treatment, while HDL-C levels were decreased [1.19 (0.98, 1.35) mmol/L vs. 1.04 (0.90, 1.33) mmol/L, Z=-3.070, P=0.002]. The absolute values comparison changes had no statistically significant differences in TG [-0.04(-0.37, 0.46) mmol/L and 0.18 (-0.14, 0.46) mmol/L, Z=-1.853, P=0.064], TC [0.06(-0.38, 0.63) mmol/L vs. 0.23(-0.21, 0.65) mmol/L, Z=-1.010, P=0.312] and LDL-C level [-0.19(-0.33, 0.18) mmol/L vs. 0.18 (-0.13, 0.58) mmol/L, Z=-0.523, P=0.601] before and after treatment between the two groups of patients. The TMF group had higher HDL-C [0.06 (-0.16, 1.84) mmol/L vs. -0.12 (-0.26,0.04) mmol/L, Z=-2.890, P=0.004], but lower TC/HDL-C [-0.04(-0.67, 0.44) vs. 0.40(-0.14, 1.33), Z=-3.959, P<0.001] than the TAF group. HepG2 cells were interfered with 10 μg/ml TMF and TAF for 72 hours, respectively. Microscopic examination revealed that in the TMF group [12 196 (10 740, 14 345) vs. 4 029 (3 086, 5 425) cells, Z=-4.815, P<0.001] and TAF group [12 484 (11 176, 15 824) vs. 4 029 (3 086, 5 425), Z=-4.815, P<0.001], the number of intracellular lipid droplets was higher than that in the control group after Oil Red O staining, but the difference between the two groups was not statistically significant. Ten-week-old C57/BL6J male mice were given 3.8 mg/kg TMF or TAF by continuous gavage for 12 weeks. The liver tissue was stained with Oil Red O. The number of lipid droplets was higher in the liver tissue of mice in the TAF group than that of the control group [30 647 (28 050, 34 821) and 27 614 (25 214, 29 176), Z=-2.529, P=0.011], while the difference between the TMF group and control group was not statistically significant. The serum TG levels were higher in the TAF group mice [1.17 (1.11, 1.19) μmol/L vs. 1.06 (1.04, 1.09) μmol/L, Z=-2.060, P=0.039], TC [2.58 (2.55, 2.80) μmol/L L vs. 2.33 (2.18, 2.54) μmol/L, Z=-2.084, P=0.037] than those of the control group after drug administration, while HDL-C levels were lower than those of the control group [1.14 (1.13, 1.16) μmol/L vs. 1.29 (1.28, 1.32) μmol/L, Z=-2.313, P=0.021] and TMF group [1.14 (1.13, 1.16) μmol/L vs. 1.30 (1.28, 1.38) μmol/L, Z=-2.795, P=0.005]. However, there was no statistically significant difference in TG, TC, and HDL-C levels between the TMF and the control group. Conclusion:Both TMF and TAF can effectively inhibit HBV replication and promote liver function recovery, with no significant impact on renal function. However, TAF may generate an adverse effect on lipid metabolism in the body, while TMF has no obvious effect.

Objective:To compare the effectiveness and safety profile of tenofovir amibufenamide (TMF) and tenofovir alafenamide (TAF), especially the effects on lipid metabolism in the treatment of chronic hepatitis B.Methods:A retrospective study was conducted on the virological response rate, biochemical response rate, renal function indicators, and lipid metabolism status of 159 cases with chronic hepatitis B (72 cases with TMF and 87 cases with TAF) after 48 weeks of antiviral treatment. The effects of the two drugs on lipid metabolism were further explored through cell and animal experiments.Results:There were no statistically significant differences in baseline age, gender ratio, treatment-na?ve and treatment-experienced proportions, hepatitis B virus (HBV) DNA and aminotransferase levels, renal function indicators, and serum lipid levels between the two groups. The levels of HBV DNA and transaminase were significantly reduced after 48 weeks of treatment in both groups. However, there were no statistically significant differences in virological response (84.2% vs. 75.8%, χ2=0.733, P=0.392) and biochemical response rate (86.1% vs. 85.1%, χ2=0.035, P=0.851) between the two groups. There was no significant change in the renal function index levels before and after treatment between the two groups of patients. Triglyceride [TG, 1.30 (0.93, 1.81) mmol/L vs. 1.30 (0.82, 1.84) mmol/L, Z=-0.196, P=0.844], total cholesterol [TC, 4.53 (3.91, 5.15) mmol/L vs. 4.55 (3.88, 5.24) mmol/L, Z=-1.131, P=0.258], high-density lipoprotein [HDL-C, 1.04 (0.90, 1.3) mmol/L vs. 1.08 (0.94, 1.30) mmol/L, Z=-0.811, P=0.417], low-density lipoprotein [LDL-C, 2.68 (2.04, 3.29) mmol/L vs. 2.57 (1.99, 3.49) mmol/L, Z=-1.716, P=0.086] and the ratio of total cholesterol to high-density lipoprotein [TC/HDL-C, 4.52 (3.10, 5.23) vs. 4.30 (3.27, 5.01), Z=-0.410, P=0.682] had not statistically significant differences in the TMF group before and after treatment. TG [1.24(0.95, 1.98) mmol/L vs. 1.42(1.09, 2.21) mmol/L, Z=-2.895, P=0.004], TC [4.44(3.74, 5.26) mmol/L vs. 4.68(4.07), 5.46) mmol/L, Z=-2.825, P=0.005], low-density lipoprotein (LDL-C) [2.74 (2.05, 3.58) mmol/L vs. 2.87 (2.34, 3.50) mmol/L, Z=-2.419, P=0.016] , and TC/HDL-C [3.89(3.13, 4.82) vs. 4.39(3.70, 5.40), Z=-4.478, P<0.001] levels were increased after TAF treatment, while HDL-C levels were decreased [1.19 (0.98, 1.35) mmol/L vs. 1.04 (0.90, 1.33) mmol/L, Z=-3.070, P=0.002]. The absolute values comparison changes had no statistically significant differences in TG [-0.04(-0.37, 0.46) mmol/L and 0.18 (-0.14, 0.46) mmol/L, Z=-1.853, P=0.064], TC [0.06(-0.38, 0.63) mmol/L vs. 0.23(-0.21, 0.65) mmol/L, Z=-1.010, P=0.312] and LDL-C level [-0.19(-0.33, 0.18) mmol/L vs. 0.18 (-0.13, 0.58) mmol/L, Z=-0.523, P=0.601] before and after treatment between the two groups of patients. The TMF group had higher HDL-C [0.06 (-0.16, 1.84) mmol/L vs. -0.12 (-0.26,0.04) mmol/L, Z=-2.890, P=0.004], but lower TC/HDL-C [-0.04(-0.67, 0.44) vs. 0.40(-0.14, 1.33), Z=-3.959, P<0.001] than the TAF group. HepG2 cells were interfered with 10 μg/ml TMF and TAF for 72 hours, respectively. Microscopic examination revealed that in the TMF group [12 196 (10 740, 14 345) vs. 4 029 (3 086, 5 425) cells, Z=-4.815, P<0.001] and TAF group [12 484 (11 176, 15 824) vs. 4 029 (3 086, 5 425), Z=-4.815, P<0.001], the number of intracellular lipid droplets was higher than that in the control group after Oil Red O staining, but the difference between the two groups was not statistically significant. Ten-week-old C57/BL6J male mice were given 3.8 mg/kg TMF or TAF by continuous gavage for 12 weeks. The liver tissue was stained with Oil Red O. The number of lipid droplets was higher in the liver tissue of mice in the TAF group than that of the control group [30 647 (28 050, 34 821) and 27 614 (25 214, 29 176), Z=-2.529, P=0.011], while the difference between the TMF group and control group was not statistically significant. The serum TG levels were higher in the TAF group mice [1.17 (1.11, 1.19) μmol/L vs. 1.06 (1.04, 1.09) μmol/L, Z=-2.060, P=0.039], TC [2.58 (2.55, 2.80) μmol/L L vs. 2.33 (2.18, 2.54) μmol/L, Z=-2.084, P=0.037] than those of the control group after drug administration, while HDL-C levels were lower than those of the control group [1.14 (1.13, 1.16) μmol/L vs. 1.29 (1.28, 1.32) μmol/L, Z=-2.313, P=0.021] and TMF group [1.14 (1.13, 1.16) μmol/L vs. 1.30 (1.28, 1.38) μmol/L, Z=-2.795, P=0.005]. However, there was no statistically significant difference in TG, TC, and HDL-C levels between the TMF and the control group. Conclusion:Both TMF and TAF can effectively inhibit HBV replication and promote liver function recovery, with no significant impact on renal function. However, TAF may generate an adverse effect on lipid metabolism in the body, while TMF has no obvious effect.

Objective:To investigate the genetic safety of allogeneic bone marrow mesenchymal stem cells (BMSCs) transplantation in traumatic brain injury (TBI).Methods:(1) In vivo experiment: BMSCs from male SD rats were isolated and cultured. Moderate TBI models were prepared by implanting and fixing micro-drug injection cannula into the left ventricle of 12 female SD rats, and 3 d after that, striking the right cerebral cortex of the rats with pneumatic precision percussion device was performed. Four h, and 3, 6, 9, and 12 d after modeling, TBI rats were given a single/multiple BMSCs infusion (2.5×10 5/time, total volume 10 μL) by cannula; 48 and 72 h, and 10 and 14 d after modeling, brain tissues of TBI rats (3 at each time point) were prepared into paraffin specimens. Immunofluorescent staining was used to detect the microglia activation, and RNAscope ? technology was used to detect the co-localization of astrocytes, neurons, microglia and transplanted BMSCs to observe whether the allogeneic BMSCs were integrated with the host brain cells after transplantation into TBI host. (2) In vitro experiment: the frozen and revived microglial cell line BV2 was transfected with green fluorescent protein (GFP)-positive lentiviral particles, and then, BMSCs prelabeled with pHrodo RED probe and BV2 cells pretreated with lipopolysaccharide were co-cultured in a certain ratio (BV2:BMSCs=1:1, 1:2, 2:1); after 36 and 72 h of co-culture, the phagocytosis between the 2 kinds of cells was observed under confocal fluorescence inverted microscope to observe the specific action forms of microglia on BMSCs. Results:(1) In vivo experiment: 48 and 72 h, and 10 and 14 d after modeling, no colocalization of transplanted BMSCs with astrocytes or neurons was found in paraffin sections of brain tissue in TBI rats; however, 10 and 14 d after modeling, microglia in TBI rats were obviously activated and migrated to the left lateral ventricle and choroid plexus, and co-localization of microglia with transplanted BMSCs was observed. (2) In vitro experiment: phagocytosis occurred after co-culture of BV2 cells at different proportions with BMSCs for 36 and 72 h. Conclusion:After transplantation, allogeneic BMSCs do not integrate with astrocytes or neurons of the TBI host, but they could be phagocytosed by microglia, indicating that allogeneic BMSCs transplantation for TBI is genetically safe.

[摘 要] 目的：采用基于中国人群单核苷酸多态性位点开发的同源重组缺陷（HRD）检测工具评估云南地区卵巢癌患者的HRD状态和BRCA1/2基因突变频率并探讨其临床意义。方法：共纳入2021年1月至2023年5月间在云南省肿瘤医院收治的卵巢癌患者248例，HRD状态采用基因组瘢痕评分法（GSS）（主要依据拷贝数的长度、类型、位置及基因组断片）或HRD评分法（杂合性缺失、端粒等位基因失衡及大片段移位等基因组不稳定事件的总和）进行评估，当组织样本的GSS≥50分或HRD评分≥42分者或检测到有害的BRCA1/2基因突变时HRD被定义为阳性。分析患者HRD状态与临床病理特征的关系。结果：248名卵巢癌患者中70.97%的患者HRD呈阳性，其中BRCA1/2基因突变率为30.65%。Ⅲ~Ⅵ期、高级别浆液腺癌的卵巢癌患者具有更高的HRD阳性率（均P<0.01），HRD评分更高的患者其合并其他基因突变的频率也越高（P<0.05）。HRD状态与卵巢癌的病理类型、临床分期和其他基因突变均有关联（均P<0.01）。结论：云南地区卵巢癌患者HRD阳性率较高，HRD阳性的卵巢癌患者可以从聚ADP核糖聚合酶（PARP）抑制剂治疗中获得更大的收益。

Objective:To establish a calculation model for the operational efficiency and resource allocation of clinical departments in hospitals, for references for hospitals to optimize resource allocation.Methods:The informations including hospitalization time, nursing grade, etc. of inpatients admitted by 32 clinical departments in a tertiary public hospital from January to December in 2021 were extracted. A data envelopment analysis method was conducted on the operation efficiency and input edundancy of the departments. The K-means algorithm was used to divide inpatients into 3 categories according to the level of medical workload. Taking the numbers of doctors, nurses and beds as the input indicators, and the numbers of patients in the 3 categories as the output indicators, a BCC model 1 was established to evaluate the efficiency of resources invested by clinical departments into professional human value. At the same time, a BCC model 2 was established with the total number of patients admitted and medical income as the output indicators to evaluate the efficiency of resources invested by clinical departments into economic benefits.Results:A total of 38 147 inpatients were enrolled. There were 14 departments with overall technical efficiency (OTE) =1.000 in the BCC model 1, 10 departments with OTE=1.000 in the BCC model 2, and 8 departments with OTE=1.000 in the 2 models. As for the input redundancy, 6 departments had high input redundancy in the BCC model 1, 11 departments had high input redundancy in the BCC model 2, and 4 departments had high input redundancy in both models.Conclusions:The model established by this study could effectively evaluate the operational efficiency and input redundancy of clinical departments, identify departments with high workload and low economic benefits, and provide reference for the rational allocation of medical resources in hospitals.