Feasibility of cortical bone trajectory screws for bridging fixation in revision surgery for lumbar adjacent segment degeneration.

BACKGROUND: To investigate the feasibility of using cortical bone trajectory (CBT) screws for bridging fixation in revision surgery for lumbar adjacent segment degeneration and to provide a reference for clinical practice. METHODS: Computed tomography scans of the lumbar spines of 36 patients in our hospital were used. Sixteen males and 20 females with an average age of 65.5 ±â€Š10.5 years (range: 46 to 83 years) were included. Three-dimensional reconstruction was performed using computer software. Screws with appropriate sizes were selected for the L1 to L5 vertebral segments, and traditional pedicle screws were placed using the standard method. After completing screw placement, simulated placement of CBT screws was performed separately. No overlap occurred between the two screws in the process of CBT screw placement, and the placement point and direction were adjusted until screw placement completion. After all screw placement simulations were complete, according to the contact area of the cortical bone of the screw trajectory and the screw puncture position and distance through the trajectory, the screw placement results were categorized as excellent, good, general, and failure. Excellent and good ratings were considered successful, while a general rating was regarded as acceptable. Then, the success rate and acceptable rate of each segment of the lumbar spine were calculated. RESULTS: Three hundred and sixty screw placement simulations were performed in lumbar pedicles, and 72 CBT screws were implanted in each vertebral body of the lumbar spine. The success rates in the L1 to L5 segments were 73.6%, 80.6%, 83.3%, 88.9%, and 77.8%, respectively, and the acceptable rates were 91.7%, 97.2%, 97.2%, 100%, and 91.7%, respectively. The overall success rate and acceptable rate of CBT screw placement in the lumbar spine were 80.8% and 95.6%, respectively. CONCLUSION: CBT screws are feasible for bridging fixation in lumbar adjacent segment degeneration revision surgery, and the accuracy of screw placement in different lumbar vertebrae varies.

Anatomical study of the ideal cortical bone trajectory in the lumbar spine.

BACKGROUND: To explore the ideal trajectory of lumbar cortical bone trajectory screws and provide the optimal placement scheme in clinical applications. METHODS: Lumbar computed tomography (CT) data of 40 patients in our hospital were selected, and the cortical vertebral bone contour model was reconstructed in three dimensions (3D). Depending on the different regions of the screw through the entrance and exit of the pedicle, 9 trajectories were obtained through combinational design: T-Aa, T-Ab, T-Ac, T-Ba, T-Bb, T-Bc, T-Ca, T-Cb, and T-Cc. Cortical bone trajectory (CBT) screws with appropriate diameters were selected to simulate screw placement and measure the parameters corresponding to each trajectory (screw path diameter, screw trajectory length, cephalad angle, and lateral angle), and then determine the optimal screw according to the screw parameters and screw safety. Then, 23 patients in our hospital were selected, and the navigation template was designed based on the ideal trajectory before operation, CBT screws were placed during the operation to further verify the safety and feasibility of the ideal trajectory. RESULTS: T-Bc and T-Bb are the ideal screw trajectories for L1-L2 and L3-L5, respectively. The screw placement point is located at the intersection of the inner 1/3 vertical line of the superior facet joint and the bottom 1/3 horizontal line of the outer crest of the vertebral lamina (i.e., 2-4 mm inward at the bottom 1/3 of the outer crest of the vertebral lamina). CBT screws were successfully placed based on the ideal screw trajectory in clinical practice. During the operation or the follow-up period, there were no adverse events. CONCLUSION: CBT screw placement based on the ideal screw trajectory is a safe and reliable method for achieving effective fixation and satisfactory postoperative effects.

[Pollution Characteristics and Health Risk Assessment of Volatile Organic Compounds in Baiyangdian Lake].

In order to survey the present pollution from volatile organic compounds in Baiyangdian Lake, 15 water samples were collected in March 2016, and analyzed for 54 VOCs by purge and trap gas chromatography-mass spectrometry. The distribution characteristics and health risk assessments were investigated, and the pollution from the VOCs was evaluated by a comprehensive pollution index. The survey showed that:① a total of 14 VOCs were detected in Baiyangdian water, with a 100% detection rate for dichloromethane, benzene, toluene, ethylbenzene, xylene, and 1,3,5-trimethylbenzene; xylene had the highest concentration with an average concentration of 564.9 ng ·L-1; and trichloroethylene had the lowest concentration with an average concentration of 3.3 ng ·L-1 and a detection rate of only 13.3%; ② the total concentration of VOCs in Baiyangdian water was between 423.0 and 4207.8 ng ·L-1, and benzene was the main pollutant, with its main source coming from the effluent from the upstream sewage treatment plant, the industrial wastewater, and the exhaust emissions of motor vehicles in the city; and ③the health risk assessment showed that VOCs in Baiyangdian Lake did not produce carcinogenic and non-carcinogenic risks to humans, and the VOC comprehensive pollution index shows that the VOCs in the Baiyangdian Lake were at a clean level.

[Effects of cardiac resynchronization therapy in patients with advanced congestive heart failure evaluated by real-time 3-dimensional echocardiography].

OBJECTIVE: To quantitatively assess the effects of cardiac resynchronization therapy (CRT) in patients with advanced congestive heart failure by real-time 3-dimensional(3D) echocardiography (RT-3DE). METHODS: Eighteen patients with advanced congestive heart failure underwent CRT with New York Heart association(NYHA) class III and IV and wide QRS complex (>120 ms) were included (17 dilated cardiomyopathy and 1 ischemic cardiomyopathy). Before CRT and 8 months after CRT, the clinical and RT-3DE parameters and outcome were analyzed. RESULTS: The biventricular pacemaker was successfully implanted in 17 patients (94.4%). Compared with before CRT, NYHA class of patients decreased by 1.5 class (P < 0.01), left ventricular ejection fraction increased by 25% (P < 0.01), left ventricular end systolic volume decreased by 38% (P < 0.01), left ventricular systolic dyssynchrony index (SDI) improved significantly (14.2% before CRT vs. 9.8% after CRT, P < 0.01 ) post CRT. Change in SDI and change in LVEF was positively correlated (r = 0.62, P < 0.01) . The procedure complications and outcome during and after CRT included coronary sinus dissection (n = 1), left ventricular lead dislodgement (n = 1), phrenic nerve stimulation (n = 1), sudden cardiac death (n = 1). Three non-response patients were complicated with atrial fibrillation, nonspecific intraventricular block and dilated cardiomyopathy with postero-lateral scar tissue. CONCLUSIONS: CRT could improve the cardiac function, correct the mechanical desynchronization and reverse left ventricular remodeling in patients with congestive heart failure, and SDI quantification by RT-3DE could predict increase of LVEF after CRT, however, there were complications related to the implantation procedure and possibilities of non-response.

Hypothyroid patient with Brugada electrocardiographic waveforms: case report.

We report a 46-year-old man who presented with hypothyroidism. An electrocardiogram obtained at the time of the first examination revealed Brugada electrocardiographic (Brugada-ECG) waveforms in leads V1 to V3. The patient and his family had no history of arrhythmia and syncopal attack. The Brugada-ECG waveforms disappeared with the normalization of thyroid function. The case suggested that hypothyroidism could lead to secondary Brugada-ECG waveforms because of its effect on myocardial ion channels.

[Dynamic changes of electrical remodeling in midmyocardium of rabbit left ventricle during the early stage of chronic pressure-overload.].

In the previous study, we had found that the action potential duration (APD) of midmyocardial (M) cells was gradually prolonged and M cells were easier to produce early after-depolarization (EAD) in the rabbit left ventricle during the early stage of chronic pressure-overload. The present study was performed to investigate the dynamic changes and significance of ionic current remodeling in M cells of rabbit left ventricle during the early stage of chronic pressure-overload. Sixty-four New Zealand rabbits were randomly divided into constriction groups and sham groups. The rabbit models with chronic pressure-overload were prepared by partial constriction of suprarenal abdominal aorta at the site proximal 5-10 mm away from the left renal artery. At 2 and 8 weeks after operation, the single cardiomyocytes were isolated by enzymatic digestion method. The midmyocardium from the anterolateral free wall of left ventricle was obtained by removing the epicardial and endocardial surfaces. Whole-cell patch-clamp technique was used to record the slowly activating delayed rectifier potassium current (I(Ks)), transient outward potassium current (I(to)), L-type calcium current (I(Ca-L)) of M cells. At 2 weeks after the constriction operation, compared with the sham group, I(Ks) tail current (I(Ks,tail)) and I(to) densities of M cells from constriction group significantly decreased by 33.3% and 51.5%, respectively. There was no significant difference in I(Ca-L) density between the two groups. At 8 weeks after operation, compared with the sham group, I(Ks,tail) and I(to) densities of M cells from constriction group significantly decreased by 37.0% and 49.2%, respectively. There was still no significant difference in I(Ca-L) density between the two groups. These results suggest that during the early phase of chronic pressure-overload, the electrical remodeling of M cells in rabbit left ventricle has developed, representing as the down regulations of I(Ks) and I(to) that can lead to the prolongation of APD, which might be a risk factor for the occurrence of malignant arrhythmia.

[Eukaryotic expression vector pcDNA3-HERG transfection inhibits angiotensin II induced neonatal rabbit ventricular myocyte hypertrophy in vitro].

OBJECTIVE: To explore the effects of eukaryotic expression vector pcDNA3-HERG transfection on angiotensin II (Ang II) induced myocyte hypertrophy in cultured neonatal rabbit ventricular myocytes. METHODS: Neonatal rabbit ventricular myocytes and eukaryotic expression vector pcDNA3-HERG transfected ventricular myocytes were cultured in Dulbecco's-modified Eagle medium (DMEM), containing 1% fetal bovine serum (FBS) for 6 h, then stimulated with Ang II (10(-7) mol/L) for 48 h. Control ventricular myocytes were cultured in Dulbecco's-modified Eagle medium (DMEM), containing 1% fetal bovine serum (FBS) for 54 h. At 6 and 54 h, myocyte hypertrophic parameters including myocyte volume, total protein content and membrane capacitance, action potential duration (APD) and Calcineurin (CaN) activity were measured. RESULTS: Compared to control myocytes, APD at 90% repolarization (APD(90)) was prolonged by 19.8% (P < 0.01), without signs of myocyte hypertrophy at 6 h post Ang II stimulation, APD(90) was prolonged by 22.1% (P < 0.01), myocyte volume, total protein content and membrane capacitance and CaN activity were significantly increased by 40.4%, 40.4%, 38.2% and 114.7% respectively (all P < 0.01) at 48 h after Ang II stimulation. HERG gene transfection upregulated I(HERG) tail current (3.6-fold higher than I(Kr)-rapidly activating delayed rectifier potassium current, P < 0.01). HERG gene transfection also accelerated and repolarization and a shortened APD(90) and inhibited myocyte hypertrophy and CaN activation induced by Ang II. CONCLUSIONS: Ang II induced prolongation of APD(90) is directly associated with myocyte hypertrophy by increasing the Ca(2+) influx and resulting in the increment of intracellular Ca(2+) and activation of CaN reaction pathway.

[Functional expression of congenital long QT syndrome related HERG mutation A561V in vitro].

OBJECTIVE: To investigate the functional expression of HERG mutation A561V detected in a Chinese congenital long QT syndrome family. METHODS: The mutation gene A561V was cloned into eukaryotic expressive vector pcDNA3 by quick site-directed mutagenesis PCR and restriction enzymes. The wild-type HERG, heterozygous type HERG and HERG mutation A561V were respectively cotransfected with pRK5-GFP into HEK293 cells by Suprefact transfection regent. The protein expression was measured by immunofluorescence method and Western blot. The electrophysiological characteristics of transfected cells were determined by whole cell patch-clamp technique. RESULTS: Direct sequence analyses revealed a C to T transition at position 1682. A561V mutation was correctly combined to eukaryotic expressive vector pcDNA3 and expressed in HEK293 cells. The protein expression of mutation and heterozygosis were located in cytoplasm and cellular membrane. 155 kDa and 135 kDa protein bands were detected in wild type HERG channel while only 135 kDa protein band was shown in heterozygous and mutational channels. Significant HERG tail-current was recorded in wild type HERG channel but not in mutation and heterozygosis channels. CONCLUSION: This study evidenced a functional dominant-negative current suppression in HEK293 cells transfected with HERG mutation A561V.

[Construction of eukaryotic expression vector of congenital long QT syndrome related HERG gene A561V mutation and its expression in HEK293 cells].

OBJECTIVE: To investigate the protocol of the construction of HERG gene mutations, an A561V mutation which was detected in a Chinese congenital long QT syndrome (LQTS) family had been constructed and expressed in vitro. METHODS: The A561V cloning vector PGEM-HERG-A561V was constructed by quick site-directed mutagenesis PCR. The A561V expressive vector pcDNA3-HERG-A561V was constructed by restriction enzymes. pRK5-GFP was cotransfected with pcDNA3-HERG-A561V or wild type pcDNA3-HERG into HEK293 cells by Superfect transfection reagent. The protein was measured by immunofluorescence. RESULTS: Direct sequence analyses revealed a C to T transition at position 1682. The A561V mutation was correctly combined to eukaryotic expressive vector pcDNA3 and expressed in HEK293 cells. The protein of mutation was expressed in cytoplasm and cellular membrane while the wild type gene was expressed only on cellular membrane. CONCLUSION: The protocol can be used successfully to construct and express HERG A561V mutation and it forms the basement of the further study on functions of mutation.

[Association of the polymorphism of platelet membrane glycoprotein I a gene with myocardial infarction].

OBJECTIVE: Platelet membrane glycoprotein (GP) Ia/IIa complex is the major collagen receptor on platelets. Platelet activation by GP Ia/ IIa dependent adhesion leads to cellular events that catalyze prothrombin conversion and fibrin clot formation. Correlation between the polymorphism of platelet membrane GP Ia gene and myocardial infarction (MI) was explored. METHODS: A total of 137 patient s with myocardial infarction and 175 controls with no history of coronary heart disease, thrombogenic and hemorrhagenic diseases were studied by case-control. Platelet GP I a gene 807 C/T polymorphisms were checked by polymerase chain reaction-sequence specific primers. RESULTS: There were significant differences in the distribution of T and C alleles between MI and control groups (T:42.70% vs 32.00%, C:57.30% vs 68.00%, P<0.001). No matter among all subjects or among subjects aged