[Clinical Effect of Surgical Reconstruction of Extracranial Vertebral Artery].

Objective To evaluate the effect of surgical reconstruction of extracranial vertebral artery and to summarize the experience. Methods The clinical data of 15 patients undergoing surgical reconstruction of extracranial vertebral artery from September 2018 to June 2022 were collected.The operation methods,operation duration,intraoperative blood loss,operation complications,and relief of symptoms were retrospectively analyzed. Results Eleven patients underwent vertebral artery (V1 segment) to common carotid artery transposition,two patients underwent endarterectomy of V1 segment,two patients underwent V3 segment to external carotid artery bypass or transposition.The operation duration,intraoperative blood loss,and blocking time of common carotid artery varied within 120-340 min,50-300 ml,and 12-25 min,with the medians of 240 min,100 ml,and 16 min,respectively.There was no cardiac accident,cerebral hyperperfusion syndrome,cerebral hemorrhage or lymphatic leakage during the perioperative period.One patient suffered from cerebral infarction and three patients suffered from incomplete Horner's syndrome after the operation.During the follow-up (4-45 months,median of 26 months),there was no anastomotic stenosis,new cerebral infarction or cerebral ischemia. Conclusion Surgical reconstruction of extracranial vertebral artery is safe and effective,and individualized reconstruction strategy should be adopted according to different conditions.

Clinical Effect of Surgical Reconstruction of Extracranial Vertebral Artery / 中国医学科学院学报

Objective To evaluate the effect of surgical reconstruction of extracranial vertebral artery and to summarize the experience. Methods The clinical data of 15 patients undergoing surgical reconstruction of extracranial vertebral artery from September 2018 to June 2022 were collected.The operation methods,operation duration,intraoperative blood loss,operation complications,and relief of symptoms were retrospectively analyzed. Results Eleven patients underwent vertebral artery (V1 segment) to common carotid artery transposition,two patients underwent endarterectomy of V1 segment,two patients underwent V3 segment to external carotid artery bypass or transposition.The operation duration,intraoperative blood loss,and blocking time of common carotid artery varied within 120-340 min,50-300 ml,and 12-25 min,with the medians of 240 min,100 ml,and 16 min,respectively.There was no cardiac accident,cerebral hyperperfusion syndrome,cerebral hemorrhage or lymphatic leakage during the perioperative period.One patient suffered from cerebral infarction and three patients suffered from incomplete Horner's syndrome after the operation.During the follow-up (4-45 months,median of 26 months),there was no anastomotic stenosis,new cerebral infarction or cerebral ischemia. Conclusion Surgical reconstruction of extracranial vertebral artery is safe and effective,and individualized reconstruction strategy should be adopted according to different conditions.

Herbal therapy for ameliorating nonalcoholic fatty liver disease via rebuilding the intestinal microecology.

The worldwide prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing, and this metabolic disorder has been recognized as a severe threat to human health. A variety of chemical drugs have been approved for treating NAFLD, however, they always has serious side effects. Chinese herbal medicines (CHMs) have been widely used for preventing and treating a range of metabolic diseases with satisfactory safety and effective performance in clinical treatment of NAFLD. Recent studies indicated that imbanlance of the intestinal microbiota was closely associated with the occurrence and development of NAFLD, thus, the intestinal microbiota has been recognized as a promising target for treatment of NAFLD. In recent decades, a variety of CHMs have been reported to effectively prevent or treat NAFLD by modulating intestinal microbiota to further interfer the gut-liver axis. In this review, recent advances in CHMs for the treatment of NAFLD via rebuilding the intestinal microecology were systematically reviewed. The key roles of CHMs in the regulation of gut microbiota and the gut-liver axis along with their mechanisms (such as modulating intestinal permeability, reducing the inflammatory response, protecting liver cells, improving lipid metabolism, and modulating nuclear receptors), were well summarized. All the knowledge and information presented here will be very helpful for researchers to better understand the applications and mechanisms of CHMs for treatment of NAFLD.

Role of perivascular adipose tissue in nicotine­induced endothelial cell inflammatory responses.

Smoking is considered to be one of the primary causes of atherosclerosis and vascular injury. Previous studies have shown that nicotine in tobacco can lead to vascular inflammation and endothelial dysfunction. Perivascular adipose tissue (PVAT) is known to secrete various types of adipokines to maintain vascular homeostasis. The present study investigated whether nicotine­induced PVAT malfunction can accelerate endothelial inflammation and eventually lead to endothelial dysfunction. The levels of inflammatory adipokines, including nuclear factor (NF)­κB, interleukin (IL)­1ß, IL­6 and tumor necrosis factor (TNF)­α, the ICAM­1 and VCAM­1 adhesion molecules and secretion of adiponectin were assessed in mature adipocytes and endothelial cells cultured alone or in co­culture under nicotine stimulation. It was found that nicotine reduced the secretion of adiponectin and stimulated secretion of the NF­κB, IL­1ß, IL­6 and TNF­α inflammatory adipokines in mature adipocytes. Although nicotine stimulated endothelial cells to secrete IL­1ß and IL­6, no significant increase in the secretion of TNF­α was observed. The co­culture of mature adipocytes with endothelial cells markedly augmented the expression of the NF­κB, IL­1ß, IL­6 and TNF­α inflammatory adipokines and the ICAM­1 and VCAM­1 adhesion molecules, and significantly lowered the levels of adiponectin. These findings suggested that nicotine induced mature adipocyte dysfunction, which caused the abnormal secretion of adiponectin and inflammatory adipokines, and exacerbated endothelial inflammation. These findings also suggested a mechanism whereby nicotine induced the secretion of adiponectin and inflammatory cytokines by adipocytes. The results of the present study elucidated a novel pathway induced by cigarette smoke, which contributed to atherosclerosis and vascular injury.

[Research advances in endotension after endovascular abdominal aneurysm repair].

When more abdominal aortic aneurysms are repaired by endovascular approaches, the post-operative endotension without endoleak increase along with the extended follow-up. An early detection of such endotension and a proper differentiation from endoleaks are particularly important for the treatment decision-making. This article reviews the mechanism, diagnosis, and management of endotension.

[Establishment and functional identification of a stable cell line overexpression heme oxygenase-1].

OBJECTIVE: To establish a stable cell line overexpression heme oxygenase-1 (HO-1) mediated by a modified lentivirus system and identify its function. METHODS: The HO-1 gene was amplified by polymerase chain reaction and cloned into the modified pLentiLox3.7 expression vectors. The recombinant plasmids were transfected into HEK293T cells and the HO-1 was detected by Western blot. The recombinant plasmids were transfected into HEK293T cells to produce the viruses, with the helping plasmids including plp1, plp2, and VSVG. HEK293T cells were infected by the viruses and the cells that can express HO-1 were identified by Western blot. The reactive oxygen species were detected in the HO-1-overexpression HEK293T cells and the normal cells after the adding of hydrogen peroxide. The same experiment was performed with human umbilical vein endothelial cells. RESULTS: The stable cell line that can overexpress HO-1 was established, which was verified by Western blot. The reactive oxygen species in the HO-1-overexpression HEK293T cells and human umbilical vein endothelial cells decreased obviously after exposure to hydrogen peroxide. CONCLUSIONS: The lentivirus-carrying HO-1 was successfully packaged and the stable cell line overexpression HO-1 was established. HO-1 can play a protective role in the course of oxidative damage.

Protective effect of melatonin on cigarette smoke-induced restenosis in rat carotid arteries after balloon injury.

Vascular restenosis after the interventional angioplasty remains the main obstacle to a favorable long-term patency. Many researches suggest cigarette smoking is one of the most important causes of restenosis. This study was designed to investigate whether melatonin could protect against the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury. Three groups of male rats (normal condition, cigarette smoke exposed, cigarette smoke exposed, and melatonin injected) were used in this study. An established balloon-induced carotid artery injury was performed, and the carotid arteries were harvested from these three groups 14 days later. The ratio of intima to media, the infiltration of inflammatory cells, the expression of inflammatory cytokines (NF-κB, IL-1ß, IL-6, TNF-α, MCP-1), adhesion molecules (ICAM-1, VCAM-1), and eNOS were measured. The results showed that cigarette smoke exposure aggravated the stenosis of the lumen, promoted the infiltration of inflammatory cells and induced the expression of the inflammatory cytokines and adhesion molecules after the balloon-induced carotid artery injury. Moreover, cigarette smoke exposure can inhibit the expression of eNOS. Particularly, we surprised that melatonin could minimize this effect caused by cigarette smoke. These results suggested that melatonin could prevent the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury and the mechanism of its protective effect may be the inhibition of the inflammatory reaction. This also implies melatonin has the potential therapeutic applicability in prevention of restenosis after the vascular angioplasty in smokers.

Comparison of endovascular aortic repair and open surgical repair for ruptured abdominal aortic aneurysm.

OBJECTIVE: To compare the clinical efficacies of endovascular aortic repair(EVAR)and open surgical repair(OSR)for ruptured abdominal aortic aneurysm(rAAA). METHODS: The clinical data of 28 rAAA patients undergoing emergent treatment between February 2002 and February 2013 in PUMC Hospital were retrospectively reviewed. Among them 13 cases were treated by EVAR and 15 cases by OSR. RESULTS: Before the surgery,the general conditions,comorbidities,and hemodynamics were not significantly different between these two groups(all P>0.05),although the EVAR group had significantly higher mean age than OSR group(P=0.041). In the perioperative period,the EVAR group showed significantly lower 30-day mortality(P=0.044),less blood loss(P=0.005),less blood transfusion(P=0.003),less infusion quantity(P=0.000),shorter length of procedure(P=0.001),and shorter hospital stay(P=0.020). Also,the EVAR group had no severe perioperative complications and showed superior 1-year follow up survival(P<0.05). CONCLUSIONS: EVAR is an effective treatment for rAAA and can improve the clinical outcomes. EVAR may be adopted as the first-line treatment for rAAA,especially for the aged.

Establishment and functional identification of a stable cell line overexpression heme oxygenase-1 / 中国医学科学院学报

<p><b>OBJECTIVE</b>To establish a stable cell line overexpression heme oxygenase-1 (HO-1) mediated by a modified lentivirus system and identify its function.</p><p><b>METHODS</b>The HO-1 gene was amplified by polymerase chain reaction and cloned into the modified pLentiLox3.7 expression vectors. The recombinant plasmids were transfected into HEK293T cells and the HO-1 was detected by Western blot. The recombinant plasmids were transfected into HEK293T cells to produce the viruses, with the helping plasmids including plp1, plp2, and VSVG. HEK293T cells were infected by the viruses and the cells that can express HO-1 were identified by Western blot. The reactive oxygen species were detected in the HO-1-overexpression HEK293T cells and the normal cells after the adding of hydrogen peroxide. The same experiment was performed with human umbilical vein endothelial cells.</p><p><b>RESULTS</b>The stable cell line that can overexpress HO-1 was established, which was verified by Western blot. The reactive oxygen species in the HO-1-overexpression HEK293T cells and human umbilical vein endothelial cells decreased obviously after exposure to hydrogen peroxide.</p><p><b>CONCLUSIONS</b>The lentivirus-carrying HO-1 was successfully packaged and the stable cell line overexpression HO-1 was established. HO-1 can play a protective role in the course of oxidative damage.</p>

Research advances in endotension after endovascular abdominal aneurysm repair / 中国医学科学院学报

When more abdominal aortic aneurysms are repaired by endovascular approaches, the post-operative endotension without endoleak increase along with the extended follow-up. An early detection of such endotension and a proper differentiation from endoleaks are particularly important for the treatment decision-making. This article reviews the mechanism, diagnosis, and management of endotension.

Comparison of endovascular aortic repair and open surgical repair for ruptured abdominal aortic aneurysm / 中国医学科学院学报

<p><b>OBJECTIVE</b>To compare the clinical efficacies of endovascular aortic repair(EVAR)and open surgical repair(OSR)for ruptured abdominal aortic aneurysm(rAAA).</p><p><b>METHODS</b>The clinical data of 28 rAAA patients undergoing emergent treatment between February 2002 and February 2013 in PUMC Hospital were retrospectively reviewed. Among them 13 cases were treated by EVAR and 15 cases by OSR.</p><p><b>RESULTS</b>Before the surgery,the general conditions,comorbidities,and hemodynamics were not significantly different between these two groups(all P>0.05),although the EVAR group had significantly higher mean age than OSR group(P=0.041). In the perioperative period,the EVAR group showed significantly lower 30-day mortality(P=0.044),less blood loss(P=0.005),less blood transfusion(P=0.003),less infusion quantity(P=0.000),shorter length of procedure(P=0.001),and shorter hospital stay(P=0.020). Also,the EVAR group had no severe perioperative complications and showed superior 1-year follow up survival(P<0.05).</p><p><b>CONCLUSIONS</b>EVAR is an effective treatment for rAAA and can improve the clinical outcomes. EVAR may be adopted as the first-line treatment for rAAA,especially for the aged.</p>

[Relationship between programmed cell death mechanisms and neuronal necrosis induced by seizures].

OBJECTIVE: To clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons. METHODS: Seizure was induced by pilocarpine (P) in Sprague-Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion-fixation. Neuronal death was assessed by light microscopy with the hematoxylin-eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Bax and Bcl-2 protein expression were examined by histochemistry. RESULTS: Twenty-four and 72 hours after seizures, neuronal death in hippocampus CA1 region was morphologically necrotic. TUNEL-positive and morphologically necrotic cells increased in the hippocampal CA1 region at 72 hours after seizures, there was significant difference compared with controls (P < 0.001). Bax expression was also increased in the hippocampal CA1 region at 72 hours after seizures (P < 0.001), but Bcl-2 expression did not increase, while Bcl-2/Bax ratio decreased. CONCLUSION: Seizures induced late-onset neuronal necrosis was accompanied by programmed cell death mechanisms.

Relationship between programmed cell death mechanisms and neuronal necrosis induced by seizures / 中华儿科杂志

<p><b>OBJECTIVE</b>To clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons.</p><p><b>METHODS</b>Seizure was induced by pilocarpine (P) in Sprague-Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion-fixation. Neuronal death was assessed by light microscopy with the hematoxylin-eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Bax and Bcl-2 protein expression were examined by histochemistry.</p><p><b>RESULTS</b>Twenty-four and 72 hours after seizures, neuronal death in hippocampus CA1 region was morphologically necrotic. TUNEL-positive and morphologically necrotic cells increased in the hippocampal CA1 region at 72 hours after seizures, there was significant difference compared with controls (P < 0.001). Bax expression was also increased in the hippocampal CA1 region at 72 hours after seizures (P < 0.001), but Bcl-2 expression did not increase, while Bcl-2/Bax ratio decreased.</p><p><b>CONCLUSION</b>Seizures induced late-onset neuronal necrosis was accompanied by programmed cell death mechanisms.</p>