Objective     To analyze the clinical efficacy and survival outcome of totally thoracoscopic redo mitral valve replacement and evaluate its efficiency and safety. Methods     The clinical data of patients with totally thoracoscopic redo mitral valve replacement in Guangdong Provincial People’s Hospital between 2013 and 2019 were retrospectively analyzed. Survival analysis was performed using the Kaplan-Meier method. Univariate and multivariate Cox regression analyses were used to determine the risk factors for postoperative death. Results     There were 48 patients including 29 females and 19 males with a median age of 53 (44, 66) years. All the procedures were performed successfully with no conversion to median sternotomy. A total of 15, 10 and 23 patients received surgeries under non-beating heart, beating heart and ventricular fibrillation, respectively. The in-hospital mortality rate was 6.25% (3/48), and the incidence of early postoperative complications was 18.75% (9/48). Thirty-five (72.92%) patients had their tracheal intubation removed within 24 hours after the operation. The 1- and 6-year survival rates were 89.50% (95%CI 81.30%-98.70%) and 82.90%(95%CI 71.50%-96.20%), respectively. Age>65 years was an independent risk factor for postoperative death (P=0.04). Conclusion     Totally thoracoscopic redo mitral valve replacement is safe and reliable, with advantages of rapid recovery, reducing blood transfusion rate, reducing postoperative complications and acceptable long-term survival rate. It is worthy of being widely popularized in the clinic.

An 81-year-old male patient was admitted to Guangdong Provincial People's Hospital due to chest distress and shortness of breath after activity for half a year. Examination after admission revealed severe aortic insufficiency, tricuspid aortic valve and extremely horizontal aorta with an aortic root angulation of 99°. The Society of Thoracic Surgeons score was 7%. And taking the strong demand of the patient and his family into consideration, we decided to perform transapical transcatheter aortic valve replacement after multidisciplinary evaluation. The procedure was successfully performed by means of low deployment land zone and traction of pre-exist Prolene suture. Three-month follow-up confirmed the normal function of aortic prosthetic valve without residual regurgitation. This case provides a reference for the interventional treatment in patients with extremely horizontal aorta.

Objective    To investigate the effectiveness and safety of totally endoscopic transmitral myectomy (TETM) for hypertrophic obstructive cardiomyopathy (HOCM), comparing with traditional sternotomy modified Morrow procedure (SMMP). Methods    Thirty-eight patients with HOCM who needed surgical intervention were selected from our hospital in 2019, including 14 males and 24 females, with an average age of 56 (44-68) years. According to the operation method, they were divided into a TETM group (n=18) and a SMMP group (n=20). Appropriate patients  were screened by propensity matching scores. Finally, the clinical data of two matched groups were compared and

Objective    To determine the clinical efficacy of transapical transcatheter mitral valve-in-valve treatment for patients with deteriorated mitral bioprosthesis after aortic-mitral double valve replacement. Methods    The clinical data of 9 patients who underwent transapical transcatheter mitral valve-in-valve implantation after aortic-mitral double valve replacement due to mitral bioprosthesis deterioration from May 2020 to January 2021 in our hospital were retrospectively analyzed, including 4 males and 5 females with a mean age of 72.44±7.57 years. Results    Surgeries were performed successfully in all patients with no conversion to median sternotomy. The mean procedural time was 101.33±48.49 min, the mechanical ventilation time was 23.11±26.54 h, the ICU stay was 1.89±1.05 d and the postoperative hospital stay was 6.11±2.02 d. Residual mild mitral regurgitation was only observed in 1 patient. Only 1 patient needed postoperative blood transfusion. No major complications were observed in all patients. There was no death in postoperative 90 days. Conclusion    For patients with deteriorated mitral bioprosthesis after aortic-mitral double valve replacement, transapical transcatheter mitral valve-in-valve implantation achieves good clinical results and effectively  improves the hemodynamics without increasing the risk of postoperative left ventricular outflow tract obstruction. The surgery is feasible and effective.

Objective:To explore the early surgical outcomes of Thoracoscopic Transmitral Myectomy(TTM) on patients with hypertrophic obstructive cardiomyopathy(HOCM).Methods:Preoperative echocardiography and cardiac magnetic resonance were used to evaluate the patient's hypertrophy extent, mitral valve morphology and function. Myocardial resection was performed via the trans-mitral approach under total thoracoscopy, and the surgical methods and early results were analyzed.Results:From April 2019 to October 2019, a total of 15 cases of TTM were performed by a single surgeon in our ward. Preoperative imaging evaluation revealed that 6 patients(40.0%) had predominantly hypertrophic basal septum while another 9 patients(60.0%) had concomitant midventricular septal hypertrophy. Two(13.3%) patients were interrogated ruptured posterior mitral chord by preoperative echocardiogram. After myocardial resection, the mitral valve was treated as follows: 11 patients(73.3%) underwent anterior leaflet enlargement, and 3(20.0%) were directly reattached to mitral valve annulus, and 1(6.7%) underwent bioprosthetic mitral replacement. There was no case of perioperative death, ventricular septal perforation, residual left ventricular outflow tract obstruction and complete atrioventricular block. Median aortic crossclamp time, cardiopulmonary bypass time, postoperative ventilator use time, ICU stay time, and postoperative hospital stay were 129.0min(116.0, 147.0), 184.0 min(158.0, 227.0), 22.0 h(9.0, 26.0), 3 days(2, 7) and 9 days(7, 14) respectively. No patient lost to follow up, the median follow-up time was 4 months(2, 5). One patient(6.7%) underwent mitral angioplasty three months after surgery due to a tear in the A3 area; the ventricular septal thickness and left ventricular outflow tract pressure decreased significantly(preoperative vs follow-up), and were(19.3±3.3)mm vs. (8.9±4.4) mm( P=0.001), (90.8±23.2)mmHg vs. (8.9±4.4) mmHg(1 mmHg = 0.133kPa)( P<0.001) respectively; no residual SAM was observed during follow-up. Patients with moderate-to severe mitral regurgitation were decreased from 12(80.0%) before surgery to 1(6.7%) during follow up( P<0.001). Conclusion:TTM is a safe and effective procedure for HOCM patients with appropriate surgical indications, providing better exposure to septum from basal to apical area, eliminating left ventricular outflow tract obstruction and SAM-related mitral regurgitation. The anterior mitral valve leaflet should be carefully treated during surgery to reduce the occurrence of residual mitral regurgitation resulted in inappropriate selection of patch size and suturing technique.

Objective To investigate the cytotoxic effects of differentiated PC12 cells afterinfected by prion protein 106-126 peptide.Methods The PC12 cells were infected by prion protein 106-126peptide after differentiated by nerve growthfactor(NGF).Cell viability andthe morphological changes were observed.The energy metabolize and apoptosis was detected.Results Afterinfected by this peptide,cell viability decreasedfrom(98.1±1.9)% to (69.2±4.7)%,and apoptosis peak Was observed byflow cytometry.Aboutthe process of the cytotoxic effects,afterthe cells affected by PrP106-126,oxidative stress presented and existed continually,and then the intracellular free calcium concentrate increased from (185.74±12.93)nmol/L to (493.00±58.71)nmol/L subsequently,the activity of Ca2+ ATPase decreased from 54.92±4.05 to 34.92±4.86,the mitochondrial membrane potential decreasedto 65%,and also the energy metabolize disorder,the cells presented apoptosisinthe end.The changed Bcl-2/Bax system involvedinthe apoptosis.Conclusions Prion protein106-126 peptide caninduce apoptosisin differentiated PC12 cells and presented cellulartoxicity definitely.It might be a perfect model to study the cellular toxicity of prion protein.Continual oxidative stress could causetheintracellularfree calcium concentrate and disturb the energy metabolize,and the apoptosis might be the end-result.The oxidative stress of might play a startup and important role.

Objective To investigate the genetic association between the inducible nitric oxide synthase (NOS) 2A gene and stroke with a history of coronary artery disease ( CAD). Methods 708 patients with stroke and 235 healthy controls were recruited in this study, and the stroke group was delaminated into 2 subgroups according to the history of CAD. SNP rs28944190, an A to C base change located in intron 22 of the gene, was used as a genetic marker. PCR-based restriction fragment length polymorphism analysis was applied to genotype rs28944190 (Hac Ⅲ site). Results The x2 test showed no association between patients with stroke and healthy controls. Of 708 patients, 94 had a history of CAD and the frequency of allele C of rs28944190 was significantly higher in patients with a history of CAD than those without (23.9% vs 16.6%, x2 =5.629, df= 1, P =0.018, OR = 1.580, 95% CI 1.083—2.306), especially in male patients (x2 = 8. 592, df= 1, P = 0. 003, OR = 1. 983, 95% CI 1. 255—3. 134). The frequency of genotype AA + AC of rs28944190 was significantly higher in patients with a history of CAD than those without such a history (47.9% vs 30. 8%, x2 = 10. 761, df= 1, P = 0. 001, OR = 2. 065, 95% CI 1.34—3.19), especially in male patients (x2 = 15. 762, df= 1, P =0. 000, OR =2. 985, 95% CI 1.74—5. 12). Conclusion The present study suggests that the NOS2A gene is unlikely to contribute to the etiology of stroke.

BACKGROUND: It is proposed that elevated serum homocysteine is an important independent risk factor for ischemic stroke (IS), and 5, 10-methylenetetrahydrofolate reductase (MTHFR) is the key enzyme for homocysteine metabolism. The relationship between genetic mutation of MTHFR and IS remains controversial.OBJECTIVE: To examine the association of hyperhomocysteinemia and two MTHFR gene polymorphisms with IS in Northwest Chinese population.DESIGN: Case-control study.SETTING: Department of Neurology, First Hospital Affiliated to Jilin University, and Department of Neurology, Xijing Hospital, Fourth Military Medical University of Chinese PLA.PARTICIPANTS: Ninety-seven consecutive patients with ischemic stroke (71 males and 26 females) treated between November 2001 and May 2002were recruited, who were diagnosed by CT scan or MRI in the Department of Neurology, Xijing Hospital, Fourth Military Medical University of Chinese PLA. The control group consisted of 94 subjects (58 males and 36 females) without history of ischemic stroke. All the subjects were free of intracranial hemorrhage, cancer, renal dysfunction, and none used multivitamins or estrogen.METHODS: Serum homocysteine was measured by fluorescence polarization immunoassay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP) method was employed to detect the genotype at the two sites of C677T and A1298C in MTHFR gene.MAIN OUTCOME MEASURES: Serum homocysteine levels and the genotypic frequency frequencies of the two mutations of MTHFR.RESULTS: The 677T allele frequency was 59.3% in IS patients and 44.7% in the controls, showing significant differences (P=0.006), but no difference in 1298C allele frequency was detected between the two groups (22.7% vs 19.7%, P ＞ 0.05). Homozygous 677TT genotype was closely associated with hyperhomocysteinemie (P ＜ 0.01). In multivariate logistic regression analysis,677T gene mutation and hyperhomocysteinemie were all associated with the IS, with an OR of 1.870 and 1.031 (P＜ 0.05), respectively.CONCLUSION: Hyperhomocysteinemie is a risk factor of IS, and C677T mutation significantly increases homocysteine levels, and serves also as an independent genetic risk factor of IS.

BACKGROUND: Pathological changes of the brain tissue in patients with dementia of frontal type(DFT) are still controversial. This paper brought forward the pathological alterative characteristics of brain tissue in DFT patients through one pathological case study of the brain tissue in one dead dementia patient.OBJECTIVE: To validate one uncommon neurodegenerative disease complicated with dementia, DFT.DESIGN: A case analysis.SETTING: Department of Neurology of the First Hospital of Jilin University METHODS: Brain anatomy, serials of histological staining and immunohistochemical staining for PrP, tau protein, etc. were performed after 3 hours since the death of one patient with progressive dementia.stainingfrontal lobes. EEG displayed a paroxysmal high-amplitude slow wave with and the brain atrophy was limited to frontal lobe and the temporal lobe loss of neurocyte companied with significant gliosis since the second layer; However, the pyramidal cell was relatively healthy. No abnormality was munohistochemical staining had negative reactions.CONCLUSION: This case was typical DFT. This type of dementia should be considered in future analysis of the neurodegenerative disease complicated with dementia.

Objective To detect point mutations of the PRNP in 10 sporadic Creutzfeldt-Jakob disease (CJD) patients. Methods Priori protein gene open reading frame was amplified by PCR of genomic DNA extracted from peripheral blood leukocytes. Products were sequenced and digested with restriction endonuc lease Nsp I to check the phenotype at codon 129. Results Two CJD patients were confirmed at autopsy. One full sequencing of the PRNP open reading frame revealed normal, but the other revealed a single novel mutation consisting of a cytosine-to-guanine substitution at nucleotide 729, causing asparagine to replace glutamic acid at codon 211. Among 8 probable CJD patients, 2 full sequencing of the PRNP open reading frame revealed anadenine-to-guanine substitution at nucleotide 751, causing lysine to replace glutamic acid at codon 219. The patients were methionine homozygosity at codon 129. Conclusions The E211D mutation was identified in a confirmed CJD patient. The novel point mutation might be associated with familial CJD. However, E219K identified in 2 possible CJD patients was included in polymorphism of the PRNP as well as M129V. Analysis of PRNP plays an important role for diagnose of familial priori disease.