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ABSTRACT: This study aimed to analyze the long-term results of mitral valve replacement and concomitant Cox-Maze III procedure (CMP) in treating rheumatic heart valve disease and associated permanent atrial fibrillation. Outcomes of CMP using a pure "cut-and-sew" method were assessed.
Between 1995 and 2004, 60 patients received mechanical mitral (or mitral plus aortic) valve replacement and concomitant CMP. Among them, 22 underwent classic CMP that included five localized cryoablations, and 38 received a CMP without using cryoablations. All patients received periodic follow-up and oral anticoagulation therapy.
The demographic features of both groups of patients were comparable. A total of 65 mechanic valves were implanted. Operative data and in-hospital outcomes were insignificant except that the immediate sinus conversion rate was higher in the pure cut-and-sew group. At last follow-up, sinus rhythm was 81.1% in the pure cut-and-sew group (median, 112 months) and 72.7% in the classic CMP group (median, 113 months; p = 0.4541). Actuarial freedom from atrial fibrillation was also similar (5 years, 83.8% versus 76.8%; 10 years, 79.1% versus 70.4%; p = 0.6039). In both groups, the late results of left atrium size were significantly reduced, while the proportion of long-term tricuspid regurgitation was still remarkable.
Mitral valve replacement and concomitant CMP is effective in treating rheumatic valve disease and permanent atrial fibrillation with satisfactory results. A complete cut-and-sew method is technically practicable, and is as effective as the classic CMP in the long term.
The Annals of thoracic surgery 06/2010; 89(6):1942-9. · 3.74 Impact Factor
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ABSTRACT: To explore the role and function of stromal cell-derived factor-1 (SDF-1) in stem cells migrating into injured brain area.
Rat-derived nerve stem cells (NSCs) were isolated and cultured routinely. Transwell system was used to observe the migration ability of NSCs into injured nerve cells. Immunocytochemistry was used to explore the expression of chemotactic factor receptor-4 (CXCR-4) in NSCs. In vivo, we applied immunofluorescence technique to observe the migration of NSCs into injured brain area. Immunofluorescence technique and Western blotting were used to test expression level of SDF-1. After AMD3100 (a special chemical blocker) blocking CXCR-4, the migration ability of NSCs was tested in vivo and in vitro, respectively.
NSCs displayed specific tropism for injured nerve cells or traumatic brain area in vivo and in vitro. The expression level of SDF-1 in traumatic brain area increased remarkably and the expression level of CXCR-4 in the NSCs increased simultaneously. After AMD3100 blocking the expression of CXCR-4, the migration ability of NSCs decreased significantly both in vivo and in vitro.
SDF-1 may play a key role in stem cells migrating into injured brain area through specially combining with CXCR-4.
Chinese Journal of Traumatology (English Edition) 10/2009; 12(5):263-8.
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ABSTRACT: To promote stem cells differentiation into neurons and enhance neuromotor function after brain injury through brain-derived neurotrophic factor (BDNF) induction.
Recombinant adenovirus vector was applied to the transfection of BDNF into human-derived umbilical cord mesenchymal stem cells (UCMSCs). Enzyme linked immunosorbent assay (ELISA) was used to determine the secretion phase of BDNF. The brain injury model of athymic mice induced by hydraulic pressure percussion was established for transplantation of stem cells into the edge of injury site. Nerve function scores were obtained, and the expression level of transfected and non-transfected BDNF, proportion of neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP), and the number of apoptosis cells were compared respectively.
The BDNF expression achieved its stabilization at a high level 72 hours after gene transfection. The mouse obtained a better score of nerve function, and the proportion of the NSE-positive cells increased significantly (P<0.05), but GFAP-positive cells decreased in BDNF-UCMSCs group compared with the other two groups (P<0.05). At the site of high expression of BDNF, the number of apoptosis cells decreased markedly.
BDNF gene can promote the differentiation of the stem cells into neurons rather than glial cells, and enhance neuromotor function after brain injury.
Chinese Journal of Traumatology (English Edition) 09/2009; 12(4):195-9.
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Chinese medical journal 09/2006; 119(16):1392-5. · 0.86 Impact Factor
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ABSTRACT: To observe the dynamic changes of alveolar apoptosis in ischemia-reperfusion (IR) induced pulmonary injury, and to evaluate the roles of these two cell death styles, apoptosis and necrosis, in the progress of lung function deterioration in pulmonary IR injury.
Fifty-four Sprague-Dawley rats were made ischemia/reperfusion models by ischemia and reperfusion in situ in single lung. Thirty-six of the 54 rats in the experimental group were re-divided into 6 equal subgroups to undergo detection of partial pressure of oxygen (PaO2) of blood in left atrium, detection of lung tissue wet weight/dry weight ratio, histology of lung by light microscope, examination of ultrastructural changes of cells by transmission electron microscopy, and quantitative detection of apoptotic cells in the right middle lobe by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) 0 h, 0.5 h, 1 h, 2 h, 6 h, and 12 h respectively after the reperfusion (subgroups R0, R(0.5), R1, R2, R6, and R12). Another 18 rats in the experimental group were re-divided into 3 subgroups of 6 rats to undergo insertion of venous catheter into the main pulmonary artery via right ventricle to perfuse trypan blue so as to evaluate the cell death degree. The death index was observed under light microscope and the necrosis index was indirectly calculated by the equation: death index = apoptotic index + necrosis index. Thirty-six rats underwent sham operation. Twelve rats were used as preoperative blank controls.
Proliferation of alveolar type II, but not alveolar type I cell, accompanied by ultrastructural morphological changes were seen 1 h, 2 h, and 6 h after reperfusion, the most prominently 2 h after reperfusion. Apoptotic index was elevated since 1 h after reperfusion, and peaked 2 h after reperfusion. Statistical analysis indicated that, compared with apoptotic index, the necrotic index was of more prominent correlation with blood oxygen partial pressure and wet/dry weight ratio.
Alveolar apoptosis occurs in the early stage of reperfusion, and becomes the most prominent 2 h after reperfusion. Most apoptotic cells are alveolar type II cells. In the two styles of cell death in pulmonary IR injury, alveolar necrosis is more prominently correlated with progress of lung function deterioration.
Zhonghua yi xue za zhi 11/2004; 84(19):1597-600.
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ABSTRACT: The therapeutic mechanism and clinical effect of mild hypothermia in patients with severe head injury were studied.
All 396 patients with severe head injury [Glasgow Coma Scale score (GCS) equal to or less than 8 on admission] were randomly divided into the hypothermic group (198 cases) and the control group (198 cases). Hypothermia was induced within 24 hours of injury. Rewarming began 1 to 7 days (average 62.4 +/- 27.6 h) after the rectal temperature (RT) reached 32.0 to 35.0 degrees C. Meanwhile, the vital signs, intracranial pressure (ICP), blood gas values, blood electrolytes, brain tissue oxygen pressure (P(bt)O2), brain tissue temperature (BT), cerebral blood flow (CBF), and jugular venous oxygen saturation (S(jv)O2) were measured. The rectal temperature of control patients was induced to 36.5 to 37.0 degrees C. According to GOS, the prognosis of the patients was evaluated.
In comparison with control group, during mild hypothermia the high level of ICP, hyperglycemia and blood lactic acid significantly decreased (p < 0.05) and cerebral flow improved dominantly. The vital signs, blood gas values, and blood electrolytes did not change significantly. Decreased mortality and good recovery were also found in hypothermia group.
Mild hypothermia is safe and effective for preventing brain damage on patients with severe head injury, as well as reducing mortality and improving the prognosis. It is important to monitor P(bt)O2, BT, CBF, and S(jv)O2 in hypothermic therapy.
Surgical Neurology 05/2003; 59(5):381-5. · 1.67 Impact Factor
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ABSTRACT: To study the changes of partial pressure of oxygen in brain tissue (P(bt)O(2)) and brain temperature (BT) in patient s in acute phase of severe head injury, and to study the effect of mild hypothermia on P(bt)O(2) and BT.
The P(bt)O(2) and the BT of 18 patients with severe head injury were monitored, and the patients were treated with mild hypothermia within 20 hours after injury. The rectal temperature (RT) of the patients was kept on 31.5-34.9 degrees C for 1-7 days (57.7 hours+/-28.4 hours averagely), simultaneously, the indexes of P(bt)O(2) and BT were monitored for 1-5 days (with an average of 54.8 hours+/-27.0 hours). According to Glasgow Outcome Scale (GOS), the prognosis of the patients was evaluated at 6 months after injury.
Within 24 hours after severe head injury, the P(bt)O(2) was significantly lower (9.6 mm Hg+/-6.8 mm Hg, 1 mm Hg=0.133 kPa) than the normal value (16-40 mm Hg). After treatment of mild hypothermia, the mean P(bt)O(2) increased to 28.7 mm Hg+/-8.8 mm Hg during the first 24 hours, and the P(bt)O(2) was still maintained within the range of normal value at 3 days after injury. The BT was higher than the RT in the patients in acute phase of severe head injury, and the difference between the BT and the RT significantly increased after treatment of mild hypothermia. Hyperventilation (the partial pressure of carbon dioxide in artery (P(a)CO(2)) approximately 25 mm Hg) decreased the high intracranial pressure (ICP) and significantly decreased the P(bt)O(2).
This study demonstrates that P(pt)O(2) and BT monitoring is a safe, reliable and sensitive diagnostic method to follow cerebral oxygenation. It might become an important tool in our treatment regime for patients in the acute phase of severe head injury requiring hypothermia and hyperventilation.
Chinese Journal of Traumatology (English Edition) 03/2002; 5(1):43-5.
