Aim To investigate the role and regulatory mechanism of CREB regulated transcription coactivator 2(CRTC2)in cardiomyocyte hypertrophy.Methods A pathological cardiomyocyte hypertrophy model was established in C57BL/6 mice by intraperitoneal injection of isoproterenol(ISO),the expression of CRTC2 in cardiac tissue was detec-ted by Western blot.The CRTC2 knockout mice model was constructed,the cardiac function of mice was detected by small animal echocardiography,the collagen fiber content in mice cardiac tissue was detected by Masson staining,the car-diomyocyte hypertrophy related proteins:skeletal muscle α1-actin(ACTA1)and brain natriuretic peptide(BNP),as well as ferroptosis related proteins:acyl-CoA synthetase long chain family member 4(ACSL4),solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)in mice cardiac tissue were detected by Western blot,the iron ion content in mice cardiac tissue was detected by iron ion kit,to evaluate the correlation between CRTC2 and cardiomyocyte hypertrophy and ferroptosis.H9c2 cells were induced by ISO to construct an in vitro model of cardiomyocyte hypertrophy,the protein expressions of CRTC2,ACTA1,BNP,ACSL4,SLC7A11 and GPX4 were detected after intervention with fer-roptosis inhibitor ferrostatin-1(Fer-1).H9c2 cells with CRTC2 overexpression induced by ISO were used to construct an in vitro model of cardiomyocyte hypertrophy,the related indicators of cardiomyocyte hypertrophy and ferroptosis were detec-ted to explore the mechanism of CRTC2 in cardiomyocyte hypertrophy.Results Compared with the control group,the expression of CRTC2 protein in the cardiac tissue of ISO induced cardiomyocyte hypertrophy mice was increased(P＜0.05).Compared with wild-type mice,CRTC2-/-mice showed worsened cardiac function,manifested as increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),left ventricular posterior wall thickness(LVPWT),heart weight/tibia length(HW/TL)and heart weight/body weight(HW/BW),decreased short axis shortening(FS)and ejection fraction(EF),increased collagen fiber content in cardiac tissue,upregulated ex-pression of cardiomyocyte hypertrophy-related proteins ACTA1 and BNP,increased mRNA and protein expression of ferrop-tosis-related protein ACSL4,decreased mRNA and protein expression of SLC7A11 and GPX4,and elevated iron ion content in cardiac tissue(P＜0.05 or P＜0.01).In vitro experiments showed that compared with ISO group,the ISO+Fer-1 group had no significant change in CRTC2 protein expression(P＞0.05),the expression of ACTA1 and BNP protein decreased,the surface area of cardiomyocyte reduced,the expression of ACSL4 protein decreased,and the expression of SLC7A11 and GPX4 proteins increased(P＜0.05 or P＜0.01).Compared with the ISO group,the LV-CRTC2+ISO group showed a decrease in surface area of cardiomyocytes(P＜0.01),a decrease in ACTA1,BNP and ACSL4 protein ex-pression,an increase in SLC7A11 and GPX4 protein expression,and a decrease in ROS and iron ion content(P＜0.05 or P＜0.01).Conclusion CRTC2 alleviates cardiomyocyte hypertrophy and protect cardiac function by suppressing fer-roptosis in cardiomyocytes.

Aim To investigate the effect and mechanism of angiotensin Ⅱ(Ang Ⅱ)on ferroptosis in white adi-pocytes.Methods The 3T3-L1 preadipocytes were differentiated into white adipocytes by inducer stimulation.The experiment was divided into control group,Ang Ⅱ group,Ang Ⅱ+Fer-1(ferroptosis inhibitor)group and Ang Ⅱ+PFT-α(p53 inhibitor)group.Ang Ⅱ was used to treat cells.RT-qPCR and Western blot were used to detect the expression levels of ferroptosis factors and adipokines.JC-1 kit was used to detect mitochondrial membrane potential(MMP)level.Iron ion kit was used to detect intracellular iron content.Glutathione(GSH)kit was used to detect GSH content.Fer-1 and Ang Ⅱ were added to treat cells to detect the the changes of ferroptosis level.The expression of p53 and spermidine/spermine N1-acetyltransferase 1(SAT1)protein was detected.Subsequently,PFT-α and Ang Ⅱ were added to co-treat cells to detect the changes of p53 and SAT1 protein expression,and to observe the effect of inhibiting p53 expression on the expression levels of ferroptosis factors and adipokines.Results 3T3-L1 cells were successfully differentiated into white adipocytes by stimulator-induced differentiation.Ang Ⅱ induced ferroptosis in white adipocytes.RT-qPCR results showed that compared with control group,the mRNA expression of anti-ferroptosis factor glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11)and iron regulatory protein 1(IRP-1)was down-regulated in Ang Ⅱ group,and the mRNA expression of pro-ferroptosis factor acyl-CoA synthetase of long-chain family member 4(ACSL4)was up-regulated.Western blot results showed that compared with control group,the protein expression of SLC7A11 and GPX4 was down-regulated in Ang Ⅱ group,and the protein expression of ACSL4 was up-regulated.Ang Ⅱ treatment increased the content of intracellular iron ions and decreased the levels of GSH and MMP.Compared with Ang Ⅱ group,the mRNA expression of IRP-1 and SLC7A11 was up-regulated in Ang Ⅱ+Fer-1 group.Ang Ⅱ induced changes in the expression profile of adipokines in white adipocytes.Western blot results showed that compared with control group,the protein ex-pression of pro-inflammatory adipokine leptin(LEP),resistin(RETN),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)was up-regulated in Ang Ⅱ group,and the protein expression of anti-inflammatory adipokine adiponectin(AD-PN)and omentin 1(ITLN1)was down-regulated.In addition,Ang Ⅱ increased the protein expression of p53 and SAT1.Inhibition of p53 expression can improve the level of ferroptosis and adipokine expression in white adipocytes trea-ted with Ang Ⅱ.Western blot results showed that compared with Ang Ⅱ group,the protein expression of p53 and SAT1 was down-regulated in Ang Ⅱ+PFT-α group,the protein expression of SLC7A11 and GPX4 was up-regulated,and the protein expression of ACSL4 was down-regulated.The protein expression of ADPN was up-regulated in Ang Ⅱ+PFT-αgroup,and the protein expression of TNF-α,LEP and RETN was down-regulated.Conclusion Ang Ⅱ induces fer-roptosis in white adipocytes through activating the p53/SAT1 signaling pathway.

Aim To investigate the role and regulatory mechanism of CREB regulated transcription coactivator 2(CRTC2)in cardiomyocyte hypertrophy.Methods A pathological cardiomyocyte hypertrophy model was established in C57BL/6 mice by intraperitoneal injection of isoproterenol(ISO),the expression of CRTC2 in cardiac tissue was detec-ted by Western blot.The CRTC2 knockout mice model was constructed,the cardiac function of mice was detected by small animal echocardiography,the collagen fiber content in mice cardiac tissue was detected by Masson staining,the car-diomyocyte hypertrophy related proteins:skeletal muscle α1-actin(ACTA1)and brain natriuretic peptide(BNP),as well as ferroptosis related proteins:acyl-CoA synthetase long chain family member 4(ACSL4),solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)in mice cardiac tissue were detected by Western blot,the iron ion content in mice cardiac tissue was detected by iron ion kit,to evaluate the correlation between CRTC2 and cardiomyocyte hypertrophy and ferroptosis.H9c2 cells were induced by ISO to construct an in vitro model of cardiomyocyte hypertrophy,the protein expressions of CRTC2,ACTA1,BNP,ACSL4,SLC7A11 and GPX4 were detected after intervention with fer-roptosis inhibitor ferrostatin-1(Fer-1).H9c2 cells with CRTC2 overexpression induced by ISO were used to construct an in vitro model of cardiomyocyte hypertrophy,the related indicators of cardiomyocyte hypertrophy and ferroptosis were detec-ted to explore the mechanism of CRTC2 in cardiomyocyte hypertrophy.Results Compared with the control group,the expression of CRTC2 protein in the cardiac tissue of ISO induced cardiomyocyte hypertrophy mice was increased(P＜0.05).Compared with wild-type mice,CRTC2-/-mice showed worsened cardiac function,manifested as increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),left ventricular posterior wall thickness(LVPWT),heart weight/tibia length(HW/TL)and heart weight/body weight(HW/BW),decreased short axis shortening(FS)and ejection fraction(EF),increased collagen fiber content in cardiac tissue,upregulated ex-pression of cardiomyocyte hypertrophy-related proteins ACTA1 and BNP,increased mRNA and protein expression of ferrop-tosis-related protein ACSL4,decreased mRNA and protein expression of SLC7A11 and GPX4,and elevated iron ion content in cardiac tissue(P＜0.05 or P＜0.01).In vitro experiments showed that compared with ISO group,the ISO+Fer-1 group had no significant change in CRTC2 protein expression(P＞0.05),the expression of ACTA1 and BNP protein decreased,the surface area of cardiomyocyte reduced,the expression of ACSL4 protein decreased,and the expression of SLC7A11 and GPX4 proteins increased(P＜0.05 or P＜0.01).Compared with the ISO group,the LV-CRTC2+ISO group showed a decrease in surface area of cardiomyocytes(P＜0.01),a decrease in ACTA1,BNP and ACSL4 protein ex-pression,an increase in SLC7A11 and GPX4 protein expression,and a decrease in ROS and iron ion content(P＜0.05 or P＜0.01).Conclusion CRTC2 alleviates cardiomyocyte hypertrophy and protect cardiac function by suppressing fer-roptosis in cardiomyocytes.

Aim To investigate the effect and mechanism of angiotensin Ⅱ(Ang Ⅱ)on ferroptosis in white adi-pocytes.Methods The 3T3-L1 preadipocytes were differentiated into white adipocytes by inducer stimulation.The experiment was divided into control group,Ang Ⅱ group,Ang Ⅱ+Fer-1(ferroptosis inhibitor)group and Ang Ⅱ+PFT-α(p53 inhibitor)group.Ang Ⅱ was used to treat cells.RT-qPCR and Western blot were used to detect the expression levels of ferroptosis factors and adipokines.JC-1 kit was used to detect mitochondrial membrane potential(MMP)level.Iron ion kit was used to detect intracellular iron content.Glutathione(GSH)kit was used to detect GSH content.Fer-1 and Ang Ⅱ were added to treat cells to detect the the changes of ferroptosis level.The expression of p53 and spermidine/spermine N1-acetyltransferase 1(SAT1)protein was detected.Subsequently,PFT-α and Ang Ⅱ were added to co-treat cells to detect the changes of p53 and SAT1 protein expression,and to observe the effect of inhibiting p53 expression on the expression levels of ferroptosis factors and adipokines.Results 3T3-L1 cells were successfully differentiated into white adipocytes by stimulator-induced differentiation.Ang Ⅱ induced ferroptosis in white adipocytes.RT-qPCR results showed that compared with control group,the mRNA expression of anti-ferroptosis factor glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11)and iron regulatory protein 1(IRP-1)was down-regulated in Ang Ⅱ group,and the mRNA expression of pro-ferroptosis factor acyl-CoA synthetase of long-chain family member 4(ACSL4)was up-regulated.Western blot results showed that compared with control group,the protein expression of SLC7A11 and GPX4 was down-regulated in Ang Ⅱ group,and the protein expression of ACSL4 was up-regulated.Ang Ⅱ treatment increased the content of intracellular iron ions and decreased the levels of GSH and MMP.Compared with Ang Ⅱ group,the mRNA expression of IRP-1 and SLC7A11 was up-regulated in Ang Ⅱ+Fer-1 group.Ang Ⅱ induced changes in the expression profile of adipokines in white adipocytes.Western blot results showed that compared with control group,the protein ex-pression of pro-inflammatory adipokine leptin(LEP),resistin(RETN),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)was up-regulated in Ang Ⅱ group,and the protein expression of anti-inflammatory adipokine adiponectin(AD-PN)and omentin 1(ITLN1)was down-regulated.In addition,Ang Ⅱ increased the protein expression of p53 and SAT1.Inhibition of p53 expression can improve the level of ferroptosis and adipokine expression in white adipocytes trea-ted with Ang Ⅱ.Western blot results showed that compared with Ang Ⅱ group,the protein expression of p53 and SAT1 was down-regulated in Ang Ⅱ+PFT-α group,the protein expression of SLC7A11 and GPX4 was up-regulated,and the protein expression of ACSL4 was down-regulated.The protein expression of ADPN was up-regulated in Ang Ⅱ+PFT-αgroup,and the protein expression of TNF-α,LEP and RETN was down-regulated.Conclusion Ang Ⅱ induces fer-roptosis in white adipocytes through activating the p53/SAT1 signaling pathway.

Objective To explore the effect of Yunnan specialty rice products on blood sugar by measuring the glycemic index of 5 Yunnan special rice foods:rice noodles,rice cakes,rice rolls,sour rice noodles and dry rice noodles.Methods Following the national standard method to determine the carbohydrate content of 5 Yunnan specialty rice products,and the target amount of the test substance was calculated.Food Glycemic Index Determination Method was used to determine the glycemic index of 5 Yunnan specialty rice products and observe their impact on blood sugar.Results The GI value of Yunnan specialty food rice noodle is 63,rice cake is 64,rice roll is 46,sour rice noodles is 38,and dry rice noodles is 33.Conclusion Yunnan specialty foods rice noodle and rice cake belong to medium GI foods,and diabetes patients should reduce consumption;rice roll,sour rice noodles,and dry rice noodles belong to low GI foods and can be a better staple food source for diabetes patients.

Objective:To investigate the effect of prolonged negative pressure drainage time after parotidectomy and analyze its relationship with the incidence of postoperative salivary fistula.Methods:The clinical data of 94 patients with benign parotid gland tumors who received treatment in the Department of Otolaryngology-Head and Neck Surgery of The First Affiliated Hospital of Xiamen University from July 2021 to June 2022 were retrospectively analyzed. These patients were divided into an observation group and a control group ( n = 47 per group). In the observation group, the negative pressure drainage tube was removed after 1 week of simple negative pressure drainage, while in the control group, conventional local bandaging of the parotid gland was performed for 2 weeks, and negative pressure drainage was given for 2-3 days. Postoperative drainage volume, pain degree, and the incidence of salivary fistula were recorded for each group. Results:The total drainage volume in the observation group was (77.93 ± 23.83) mL, which was significantly greater than (47.06 ± 24.71) mL in the control group ( t = 6.17, P < 0.001). The Visual Analogue Scale score in the observation group was (3.021 ± 1.07) points, which was significantly lower than (7.53 ± 1.27) points in the control group ( t = 18.63, P < 0.001). The incidence of postoperative salivary fistula in the observation group was 2.1% (1/47), which was significantly lower than 17.0% (8/47) in the control group ( χ2 = 4.42, P = 0.035). Conclusion:Simple prolongation of negative pressure drainage time can achieve full drainage, improve the quality of life of patients after parotidectomy and reduce the occurrence of postoperative salivary fistula, which is worthy of clinical promotion.

Objective:To report our experience of treating open comminuted limb fractures caused by gunshots using the Masquelet technique.Methods:Between January 2016 and July 2018, 3 patients were admitted to Institute of Orthopedics, 920 Hospital of Joint Logistic Service of People's Liberation Army for open comminuted limb fractures caused by gunshots.They were all male, aged from 18 to 41 years (average, 30.7 years).Their fractures were complicated with perforating wounds and belonged to Gustilo type ⅢB for open fractures.The bone defects were 5 to 9 cm in length (average, 6.7 cm), located at the proximal femur in 2 cases and at the upper middle humerus in one.They were treated by standard Masquelet technique at 2 stages.The postoperative functions of the hip, knee and shoulder were evaluated according to the Harris hip score, Lowa knee score and Constant-Murley shoulder function score.Results:The 3 patients obtained an average follow-up of 17.3 months.The bone defects were all repaired in the 3 patients without any signs of infection.The 2 patients with femoral defects were rated as both excellent by the Harris hip score, as excellent in one and as good in the other by the Lowa knee score; the patient with humeral defects was rated as excellent by the Constant-Murley shoulder function score.Conclusion:Masquelet technique is a desirable treat-ment of segmental long bone defects caused by gunshots.

Objective　To observe the incidence of white matter hyperintensities （WMHs） and the distribution of right to left shunt （RLS） in migraine patients，and to explore whether WMHs is related to RLS. Methods　106 patients with migraine were selected as the research objects. The basic data and clinical information of migraine were collected. The WMHs were evaluated by cranial MRI. The RLS was diagnosed and graded by transcranial Doppler （TCD） bubbles test. The correlation between WMHs and RLS was analyzed. Results　Among 106 migraine patients，33 （31.1%） were in WMHs+ group and 73 （68.9%） in WMHs- group. The total positive rate of RLS was 48.1% （51/106）. The distribution of different shunt levels was as follows：grade Ⅰ shunt in 27 cases （25.5%），grade Ⅱ shunt in 4 cases （3.8%），grade Ⅲ shunt in 6 cases （5.6%），grade Ⅳ shunt in 14 cases （13.2%）. In "WMHs+" group，there were 5 cases of grade Ⅰ shunt，1 case of grade Ⅱ shunt，3 cases of grade Ⅲ shunt and 10 cases of grade Ⅳ shunt；in "WMHs-" group，there were 22 cases of grade Ⅰ shunt，3 cases of grade Ⅱ shunt，3 cases of grade Ⅲ shunt and 4 cases of grade Ⅳ shunt. Compared with "WMHs+" group and "WMHs-" group，there was no statistical difference in the overall positive rate of bubbles test between the two groups （P>0.05，χ2=1.719），but the large shunt rate of "WMHs+" group was significantly higher than that of "WMHs-" group （P<0.01，χ2=13.188）. Conclusion　There is no significant correlation between WMHs and RLS in migraine patients，but large RLSs will increase the risk of WMHs in migraine patients.

OBJECTIVE To discuss the therapeutic effect of one stage surgical treatment in the multiple primary hypopharyngeal and cervical thoracic esophageal carcinoma.METHODS The thoracoscopy group: dissecting the esophagus and mediastinal lymph node assisted with thoracoscope, and then opened abdominal cavity to make gastric tube. Head and neck group: doing the cervical lymph node dissection, total laryngectomy, total hypopharyngectomy and total esophagectomy, and then anastomosis of the pharynx with gastric tube. All cases were received conventional radiotherapy and chemotherapy after operation.RESULTS All the cases in this group were successfully underwent the one stage operation. The postoperative complications were pulmonary infection in 3 cases, pleural effusion in 2 cases and tracheal tear in one case. No anastomotic fistula or postoperative deaths occurred. The 3 and 5 year survival rates were 63.6% and 50.0% respectively.CONCLUSION It should take necessary examinations of cervical thoracic esophagus to prevent missing the multiple primary carcinoma of the hypopharyngeal carcinoma. The total laryngectomy, total hypopharyngectomy and total esophagectomy, and anastomosis of the pharynx with gastric tube for multiple primary hypopharyngeal and cervical thoracic esophageal carcinoma is a feasible and active treatment method.

Objective To observe whether hepatitis B vaccine enhance the treating effect of cyto-kine induced kill(CIK) cells on hepatitis B virus transgenic(HBV-Tg) mice. Methods The HBV-Tg mice were treated with CIK cells by peritoneal injection and hepatitis B vaccine by hypodermic injection. The HBV DNA level were tested by real-time PCR,T lymphocyte subgroup were detected by flow cytometry and the pathological diversify of hepatic tissue were observed by HE staining. Results The HBV DNA loading in peripheral blood of HBV-Tg mice decreased after CIK cells were treated and CD3~+ , CD4~+ and CD8~+ cells increased which were enhanced after CIK cells combined with hepatitis B vaccine. Conclusion Hepa-titis B vaccine enhanced the treating effect of CIK on HBV-Tg mice which may be implemented by increased the blood level of CD3~+, CD4~+ and CD8~+ cells, especially CD8~+ cells level.