Minimally invasive aortic valve replacement for isolated aortic valve disease: clinical analysis of 101 consecutive patients / 中华外科杂志

<p><b>OBJECTIVE</b>To review the results for minimally invasive aortic valve replacement (AVR) through a 5 cm right anterolateral thoracotomy.</p><p><b>METHODS</b>From July 2009 to September 2011, 101 consecutive patients with isolated aortic valve disease (degenerative in 37 patients, rheumatic in 21 patients, congenital in 37 patients, endocarditic in 3 patients and aorta-arteritis in 1 patients) underwent AVR through the right anterolateral thoracotomy approach in the third intercostal space with a groin incision for femoral connection of cardiopulmonary bypass. The mean age was 45.7 years (ranging from 17 to 71 years). Sixty patients were male.</p><p><b>RESULTS</b>Operations were successfully performed in all but 1 patient (1.0%) who required intraoperative conversion to full sternotomy. Mean duration of cardiopulmonary bypass time and aortic cross-clamp time was (88 ± 24) minutes and (55 ± 18) minutes, respectively. Thirty-day mortality was 1.0% (1/101), this patient was found difficult in weaning off cardiopulmonary bypass and exhibited severe coronary artery plaque, although bypass graft was carried out immediately, the patient died of severe low cardiac output syndrome finally. No blood products were needed in 83.2% patients. Follow-up was performed in all patients at an average of (16 ± 7) months postoperatively. A good recovery was obtained in all patients except one who died of multiple organ failure caused by massive cerebral infarction 38 days after surgery.</p><p><b>CONCLUSIONS</b>Minimally invasive aortic valve replacement though the right anterolateral thoracotomy approach is safe and feasible, with good cosmetic results and rapid postoperative recovery. It is worthy of clinical elective application.</p>

Repair of posterior mitral valve prolapsed: comparative study of three different approaches / 中华外科杂志

<p><b>OBJECTIVE</b>To compared outcomes of robotic mitral valve repair with those of standard sternotomy, and right anterolateral thoracotomy.</p><p><b>METHOD</b>From August 2010 to July 2011, 70 patients with degenerative mitral valve disease and posterior leaflet prolapsed scheduled for elective isolated mitral valve repair were prospectively nonrandomized to undergo mitral valve operation by standard sternotomy (n = 30), right anterolateral thoracotomy (n = 30), or a robotic approach (n = 10). There were 49 male and 21 female patients, aging from 16 to 70 years with a mean of 53.4 years. Outcomes of the three groups were compared.</p><p><b>RESULTS</b>Mitral valve repair was achieved in all patients except 1 patient in the standard group. There were no in-hospital deaths. The median operation time [(300 ± 41) min, (184 ± 20) min and (169 ± 22) min, F = 112.5, P < 0.01], cardiopulmonary bypass time [(139 ± 26) min, (82 ± 20) min and (69 ± 23) min, F = 36.8, P < 0.01], aortic cross-clamping time [(93 ± 23) min, (47 ± 10) min and (38 ± 8) min, F = 75.0, P < 0.01] were longer for robotic than standard sternotomy and right anterolateral thoracotomy. The robotic group had shortest time of mechanical ventilation time [(4.9 ± 2.1) h, (5.3 ± 4.5) h and (14.1 ± 10.2) h, F = 13.2, P < 0.01], ICU time [(15.1 ± 2.1) h, (16.4 ± 5.4) h and (28.7 ± 16.1) h, F = 11.6, P < 0.01], postoperative hospital stay time [(4.6 ± 1.0) d, (5.7 ± 1.7) d and (8.8 ± 5.1) d, F = 8.0, P < 0.01] with the lowest of drainage [(192 ± 200) ml, (215 ± 163) ml and (405 ± 239) ml, F = 7.1, P < 0.01] and ratio of the patients needed blood transfusion (0, 20.0% and 66.7%, χ(2) = 22.7, P < 0.01). Patients were followed up 6 to 17 months, with 100% completed. No patients died during follow-ups, and no moderate or more mitral regurgitation was observed. The robotic group had the shortest time of return to normal activities compared with the other two groups [(2.4 ± 0.7) weeks, (4.2 ± 1.2) weeks and (8.2 ± 1.8) weeks, F = 83.0, P < 0.01].</p><p><b>CONCLUSION</b>This study shows mitral valve repair via the right anterolateral thoracotomy and a robotic approach is safe and feasible, with good cosmetic results and rapid postoperative recovery, and is worthy of clinical selective application.</p>

Hypoxia induces heat shock protein HSP70-2 expression in a HIF-1 dependent manner / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To investigate role of hypoxia inducible factor 1 (HIF-1) in the transcriptional activation of heat shock protein 70-2 (HSP70-2) in hepatocellular carcinoma (HCC) cells under hypoxic conditions.</p><p><b>METHODS</b>HCC cells were exposed to reduced oxygen atmosphere (1% O2), or treated with YC-1 or HIF-1 alpha siRNA, the expression of HIF-1 alpha and HSP70-2 were detected by Western blot analysis. Serial deletions of the HSPA2 promoter were cloned in the reporter pGL3-Basic plasmid. These reporter plasmids were co-transfected with HIF-1 alpha siRNA, and the promoter activities were detected with the dual luciferase assay.</p><p><b>RESULTS</b>Western blot analysis showed that both HIF-1 alpha and HSP70-2 proteins were strongly increased after HCC cells were exposed to hypoxic conditions (1% O2) for 6 h, and the expression level of HSP70-2 was increased in a time-dependent manner. Treatment of HepG2 cells with YC-1 or HIF-1 alpha siRNA significantly inhibited the expression of HIF-1 alpha and HSP70-2. In silico analysis of the HSP70-2 promoter using the Gene2 Promoter software revealed the presence of two putative hypoxic response element (HRE) consensus at -446bp (HRE1) and -238bp (HRE2). Depletion of promoter sequence between -653 and -385 led to a dramatic reduction of promoter activity, whereas further deletion to position -201 did not reduce the activity further. These data suggested that HRE1 plays an important role in hypoxia-induced activation of the HSPA2 promoter. Site-directed mutagenesis further confirmed these results. Mutation of HRE1 but not of HRE2 abrogated the sensitivity of the HSP70-2 promoter to hypoxia.</p><p><b>CONCLUSIONS</b>HSP70-2 expression is up-regulated in response to hypoxia and a HIF-1 binding site (HRE1) in the HSP70-2 promoter is involved in this response.</p>

Role of focal adhesion kinase in the hypoxia-induced invasion of SMMC-7721 cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study focal adhesion kinase (FAK) expression in hypoxia-stressed SMMC-7721 cells and the role of FAK expression in the hypoxia-induced invasion of SMMC-7721 cells.</p><p><b>METHODS</b>SMMC-7721 cells were cultured in 21% O2 or 1% O2. FAK expression was determined by Western blot. The siRNA expression vector pshRNA-FAK targeting to FAK and the control vector pGensil-2 were transfected into SMMC-7721 cells. The hypoxia-induced migration and invasion ability of SMMC-7721 cells transfected with pshRNA-FAK were analyzed. In normoxia, invasion of SMMC-7721 cells transfected with pcDNA3-FAK was analyzed.</p><p><b>RESULTS</b>The expression of FAK was increased significantly in SMMC-7721 cells 24 h after hypoxia stress (P<0.01). The level of FAK protein was decreased by 74.6%+/-5.1% after the pshRNA-FAK transfection in normoxia and hypoxia. The migration and invasion of SMMC-7721 cells was increased in 1% O2 (P<0.01). However, the migration and invasion of SMMC-7721 cells transfected with pshRNA-FAK was decreased in 1% O2 (P<0.05). Overexpression of FAK significantly stimulated the invasion of SMMC-7721 cells.</p><p><b>CONCLUSION</b>Up-regulation of FAK may play an important role in the invasion of SMMC-7721 cells induced by hypoxia.</p>

Inhibition of HSP70-2 expression by RNA interference induces apoptosis of human hepatocellular carcinoma cells / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To determine the effect of short hairpin RNA targeting HSP70-2 on the growth and apoptosis of hepatocellular carcinoma (HCC) cells, and to elucidate its possible mechanisms in mitochondria apoptotic pathway.</p><p><b>METHODS</b>Western blot and immunocytochemistry were used to determine the expression of HSP70-2 in HCC cells and normal hepatocytes. HepG2 and Huh-7 cells were cultured and transfected with HSP70-2 shRNA1 and shRNA2. Cell proliferation was examined by MTT. Cell apoptosis and mitochondria membrane potential were determined by flow cytometry. Western blot was used to analyze the expressions of apoptosis related proteins including Bax, Bcl-2, PARP, caspase-9 and caspase-3.</p><p><b>RESULTS</b>HSP70-2 was expressed at high levels in hepatocellular carcinoma (HCC) cells (SNU-449, HepG2, Huh-7, Hep3B) whereas there were very low levels in normal hepatocytes (L02). Using DNA vector-based RNA interference, we found that knockdown of HSP70-2 inhibited the growth of HCC cells through induction of mitochondria-dependent apoptosis. The mitochondria-dependent apoptosis induced by HSP70-2 knockdown was indicated by cytochrome c release from mitochondria, activation of caspase-9 and caspase-3, and loss of mitochondrial potential. Furthermore, knockdown of HSP70-2 resulted in up-regulation of the pro-apoptotic factor Bax and down-regulation of the pro-survival factor Bcl-2.</p><p><b>CONCLUSIONS</b>Our results indicated that HSP70-2 down-regulation induces apoptosis of HCC cells through the mitochondrial apoptotic pathway, highlighting the importance of HSP70-2 in survival of HCC cells and maintenance of liver function.</p>