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Zhou J.,University of Electronic Science and Technology of China | Fang L.,Chengdu Medical College | Liao J.,Sixth Hospital | Li L.,Second Hospital | And 3 more authors.
PLoS ONE | Year: 2017

Quercetin, a natural polyphenolic flavonoid compound, can inhibit the growth of several malignant cancers. However, the mechanism still remains unclear. Our previous findings have suggested that quercetin can significantly inhibit HepG2 cell proliferation and induce cell apoptosis in vitro. It can also affect cell cycle distribution and significantly decrease cyclin D1 expression. In this study, we investigated the anti-cancer effect of quercetin on HepG2 tumor-bearing nude mice and its effect on cyclin D1 expression in the tumor tissue. First, the nude murine tumor model was established by subcutaneous inoculation of HepG2 cells, then quercetin was administered intraperitoneally, and the mice injected with saline solution were used as controls. The daily behavior of the tumor-bearing mice was observed and differences in tumor growth and survival rate were monitored. The expression of cyclin D1 in isolated tumor sections was evaluated by immunohistochemistry. We found that HepG2 tumor became palpable in the mice one-week post-inoculation. Tumors in the control group grew rapidly and the daily behavior of the mice changed significantly, including listlessness, poor feeding and ataxia. The mice in quercetin-treated group showed delayed tumor growth, no significant changes in daily behavior, and the survival rate was significantly improved. Finally, we observed increased tumor necrosis and a lighter cyclin D1 staining with reduced staining areas. Our findings thus suggest that quercetin can significantly inhibit HepG2 cell proliferation, and this effect may be achieved through the regulation of cyclin D1 expression. © 2017 Zhou et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


PubMed | Second Hospital, Harbin Medical University, First Hospital and Cardiology and.
Type: | Journal: Journal of neurosurgery | Year: 2016

OBJECTIVE Phosphatidylserine (PS) is a major component of the inner leaflet of membrane bilayers. During cell activation or apoptosis, PS is externalized to the outer membrane, providing an important physiological signal necessary for the release of the microparticles (MPs) that are generated through the budding of cellular membranes. MPs express PS and membrane antigens that reflect their cellular origin. PS exposure on the cell surface and the release of MPs provide binding sites for factor Xa and prothrombinase complexes that promote thrombin formation. Relatively little is known about the role of PS exposure on blood cells and MPs in patients with internal carotid artery (ICA) stenosis who have undergone carotid artery stenting (CAS). The authors aimed to investigate the extent of PS exposure on blood cells and MPs and to define its role in procoagulant activity (PCA) in the 7 days following CAS. METHODS The study included patients with ICA stenosis who had undergone CAS (n = 70), matched patients who had undergone catheter angiography only (n = 30), and healthy controls (n = 30). Blood samples were collected from all patients just before the procedure after an overnight fastand at 2, 6, 24, 48, and 72 hours and 7 days after the CAS procedure. Blood was collected from healthy controls after an overnight fast. Phosphatidylserine-positive (PS+) MPs and blood cells were analyzed by flow cytometry, while PCA was assessed with clotting time analysis, purified coagulation complex assays, and fibrin formation assays. RESULTS The authors found that levels of PS+ blood cells and PS+ blood cell-derived MPs (platelets and platelet-derived MPs [PMPs], neutrophils and neutrophil-derived MPs [NMPs], monocytes and monocyte-derived MPs [MMPs], erythrocytes and erythrocyte-derived MPs [RMPs], and endothelial cells and endothelial cell-derived MPs [EMPs]) were increased in the 7 days following the CAS procedure. Specifically, elevation of PS exposure on platelets/PMPs, neutrophils/NMPs, and monocytes/MMPs was detected within 2 hours of CAS, whereas PS exposure was delayed on erythrocytes/RMPs and EMPs, with an increase detected 24 hours after CAS. In addition, PS+ platelets/PMPs peaked at 2 hours, while PS+ neutrophils/NMPs, monocytes/MMPs, and erythrocytes/RMPs peaked at 48 hours. After their peak, all persisted at levels above baseline for 7 days post-CAS. Moreover, the level of PS+ blood cells/MPs was correlated with shortened coagulation time and significantly increased intrinsic and extrinsic Xase, thrombin generation, and fibrin formation. Pretreatment of blood cells with lactadherin at their peak time point after CAS blocked PS, resulting in prolonged coagulation times, decreased procoagulant enzyme activation, and fibrin production. CONCLUSIONS The results of this study suggest that increased exposure of PS on blood cells and MPs may contribute to enhanced PCA in patients with ICA stenosis who have undergone CAS, explaining the risk of perioperative thromboembolic complications in these patients. PS on blood cells and MPs may serve as an important biomarker for predicting, and as a pivotal target for monitoring and treating, acute postoperative complications after CAS. CLASSIFICATION OF EVIDENCE Type of question: association; study design: prospective cohort trial; evidence: Class I.


News Article | October 29, 2016
Site: www.PR.com

Second Hospital in California and First in Orange County to Receive Prestigious Accreditation from DNV GL. Newport Beach, CA, October 29, 2016 --( "Hoag is honored to receive this distinction, as it demonstrates our team’s expertise and devotion to patient care and safety,” said Michael Brant-Zawadzki, M.D., F.A.C.R., Senior Physician Executive and Ron & Sandi Simon Executive Medical Director Endowed Chair, Hoag Neurosciences Institute. “The Comprehensive Stroke Center certification is a significant accomplishment for the Stroke Program of the Hoag Neurosciences Institute, and solidifies our ranking as a healthcare leader.” The DNV GL Comprehensive Stroke Center Certification is given to esteemed hospitals that have specific abilities to receive and treat the most complex stroke cases from the initial and rapid diagnosis, advanced and state-of-the art treatment, comprehensive rehabilitation program and community wide stroke education - and establishes clear metrics to evaluate outcomes. “It’s essential to receive immediate medical attention from a facility, like Hoag, that is experienced in acute stroke management,” said David M. Brown, M.D., program director, Hoag Neurosciences Institute’s Stroke Program. “Our Stroke Program’s multidisciplinary team utilizes state-of-the-art technology and proven specialized neurological techniques to provide and document the best outcomes for our stroke patients.” Hoag Neurosciences Institute’s Stroke Program ranks among the top five percent in the nation and this certification furthers Hoag’s mission to provide the highest quality care to its patients. About Hoag Memorial Hospital Presbyterian Hoag is an approximately $1 billion nonprofit, regional health care delivery network in Orange County, California, that treats more than 27,000 inpatients and 379,000 outpatients annually. Hoag consists of two acute-care hospitals – Hoag Hospital Newport Beach, which opened in 1952, and Hoag Hospital Irvine, which opened in 2010 – in addition to seven health centers and ten urgent care centers. Hoag is a designated Magnet® hospital by the American Nurses Credentialing Center (ANCC). Hoag offers a comprehensive blend of health care services that includes five institutes providing specialized services in the following areas: cancer, heart and vascular, neurosciences, women’s health, and orthopedics through Hoag’s affiliate, Hoag Orthopedic Institute, which consists of an orthopedic hospital and two ambulatory surgical centers. In 2013, Hoag entered into an alliance with St. Joseph Health to further expand health care services in the Orange County community, known as St. Joseph Hoag Health. Hoag has been named one of the Best Regional Hospitals in the 2016 - 2017 U.S. News & World Report, and Becker’s Hospital Review named Hoag as one of the 2016 “100 Great Hospitals in America” – a designation Hoag has received four times. National Research Corporation has endorsed Hoag as Orange County’s most preferred hospital for the past 20 consecutive years and, for an unprecedented 21 years, residents of Orange County have chosen Hoag as one of the county’s best hospitals in a local newspaper survey. Visit www.hoag.org for more information. About Hoag Neurosciences Institute Delivering a personalized, integrated approach using best-practice guidelines, the most advanced technology, and integration of medical specialists in the most appropriate facilities, Hoag Neurosciences Institute provides the highest quality care for patients with brain and spine disorders including stroke, aneurysms and vascular malformations, brain tumors, epilepsy, movement disorders, memory and cognitive disorders, pain, minimally invasive spine surgery, multiple sclerosis, addiction medicine and sleep disorders, as well as the mind-body interface of behavioral health. Several of Hoag’s neuroscience programs have received high acclaim, including Hoag’s stroke program, which ranks among the top five percent in the nation and was awarded the American Stroke Association’s Get With The Guidelines Stroke Gold Plus Performance Achievement for Hoag’s high standard of stroke care. And as one of the first centers in the U.S. to offer the most advanced radiosurgical treatment system available, Leksell Gamma Knife® Perfexion™, Hoag’s brain tumor program is the largest in Orange County and is also among the top volume programs in the western United States. Newport Beach, CA, October 29, 2016 --( PR.com )-- Hoag Memorial Hospital Presbyterian announced today it has been certified as a Comprehensive Stroke Center by DNV GL Healthcare USA, Inc., reflecting the highest level of competence for treatment of the most serious stroke events. Hoag is the second DNV GL certified hospital in California and the first hospital in Orange County to receive this accreditation."Hoag is honored to receive this distinction, as it demonstrates our team’s expertise and devotion to patient care and safety,” said Michael Brant-Zawadzki, M.D., F.A.C.R., Senior Physician Executive and Ron & Sandi Simon Executive Medical Director Endowed Chair, Hoag Neurosciences Institute. “The Comprehensive Stroke Center certification is a significant accomplishment for the Stroke Program of the Hoag Neurosciences Institute, and solidifies our ranking as a healthcare leader.”The DNV GL Comprehensive Stroke Center Certification is given to esteemed hospitals that have specific abilities to receive and treat the most complex stroke cases from the initial and rapid diagnosis, advanced and state-of-the art treatment, comprehensive rehabilitation program and community wide stroke education - and establishes clear metrics to evaluate outcomes.“It’s essential to receive immediate medical attention from a facility, like Hoag, that is experienced in acute stroke management,” said David M. Brown, M.D., program director, Hoag Neurosciences Institute’s Stroke Program. “Our Stroke Program’s multidisciplinary team utilizes state-of-the-art technology and proven specialized neurological techniques to provide and document the best outcomes for our stroke patients.”Hoag Neurosciences Institute’s Stroke Program ranks among the top five percent in the nation and this certification furthers Hoag’s mission to provide the highest quality care to its patients.About Hoag Memorial Hospital PresbyterianHoag is an approximately $1 billion nonprofit, regional health care delivery network in Orange County, California, that treats more than 27,000 inpatients and 379,000 outpatients annually. Hoag consists of two acute-care hospitals – Hoag Hospital Newport Beach, which opened in 1952, and Hoag Hospital Irvine, which opened in 2010 – in addition to seven health centers and ten urgent care centers. Hoag is a designated Magnet® hospital by the American Nurses Credentialing Center (ANCC). Hoag offers a comprehensive blend of health care services that includes five institutes providing specialized services in the following areas: cancer, heart and vascular, neurosciences, women’s health, and orthopedics through Hoag’s affiliate, Hoag Orthopedic Institute, which consists of an orthopedic hospital and two ambulatory surgical centers. In 2013, Hoag entered into an alliance with St. Joseph Health to further expand health care services in the Orange County community, known as St. Joseph Hoag Health. Hoag has been named one of the Best Regional Hospitals in the 2016 - 2017 U.S. News & World Report, and Becker’s Hospital Review named Hoag as one of the 2016 “100 Great Hospitals in America” – a designation Hoag has received four times. National Research Corporation has endorsed Hoag as Orange County’s most preferred hospital for the past 20 consecutive years and, for an unprecedented 21 years, residents of Orange County have chosen Hoag as one of the county’s best hospitals in a local newspaper survey. Visit www.hoag.org for more information.About Hoag Neurosciences InstituteDelivering a personalized, integrated approach using best-practice guidelines, the most advanced technology, and integration of medical specialists in the most appropriate facilities, Hoag Neurosciences Institute provides the highest quality care for patients with brain and spine disorders including stroke, aneurysms and vascular malformations, brain tumors, epilepsy, movement disorders, memory and cognitive disorders, pain, minimally invasive spine surgery, multiple sclerosis, addiction medicine and sleep disorders, as well as the mind-body interface of behavioral health. Several of Hoag’s neuroscience programs have received high acclaim, including Hoag’s stroke program, which ranks among the top five percent in the nation and was awarded the American Stroke Association’s Get With The Guidelines Stroke Gold Plus Performance Achievement for Hoag’s high standard of stroke care. And as one of the first centers in the U.S. to offer the most advanced radiosurgical treatment system available, Leksell Gamma Knife® Perfexion™, Hoag’s brain tumor program is the largest in Orange County and is also among the top volume programs in the western United States. Click here to view the list of recent Press Releases from Hoag Memorial Hospital Presbyterian


Li X.W.,Second Hospital | Li C.L.,Mudanjiang Medical College | Liang W.D.,Wenzhou Medical College | Bi Y.T.,Wenzhou Medical College | And 2 more authors.
Chinese Medical Journal | Year: 2014

Background Protectin D1 (PD1), derived from docosahexaenoic acid, has been shown to control and resolve inflammation in some experimental models of inflammatory disorders. We investigated the protective roles of protectin D1 in pulmonary inflammation and lung injury induced by lipopolysaccharide (LPS). Methods Mice were randomly assigned to six groups (n=6 per group): sham-vehicle group, sham-PD1 group, sham-zVAD-fmk group, LPS-vehicle group, LPS-PD1 group, and LPS-PD1-zVAD-fmk group. Mice were injected intratracheally with 3 mg/kg LPS or saline, followed 24 hours later by intravenous injection of 200 μg/mouse PD1 or vehicle. At the same time, some mice were also injected intraperitoneally with the pan-caspase inhibitor zVAD-fmk. Seventy-two hours after LPS challenge, samples of pulmonary tissue and bronchoalveolar lavage fluid were collected. Optical microscopy was used to examine pathological changes in lungs. Cellularity and protein concentration in bronchoalveolar lavage fluid were analyzed. Lung wet/dry ratios and myeloperoxidase activity were measured. Apoptosis of neutrophils in bronchoalveolar lavage fluid (BALF) was also evaluated by flow cytometry. Results Intratracheal instillation of LPS increased neutrophil counts, protein concentration in bronchoalveolar lavage fluid and myeloperoxidase activity, it induced lung histological injury and edema, and also suppressed apoptosis of neutrophils in BALF. Posttreatment with PD1 inhibited LPS-evoked changes in BALF neutrophil counts and protein concentration and lung myeloperoxidase activity, with the outcome of decreased pulmonary edema and histological injury. In addition, PD1 promoted apoptosis of neutrophils in BALF. The beneficial effects of PD1 were blocked by zVAD-fmk. Conclusion Posttreatment with PD1 enhances resolution of lung inflammation during LPS-induced acute lung injury by enhancing apoptosis in emigrated neutrophils, which is, at least in part, caspase-dependent.


Lehnus K.S.,University of Portsmouth | Donovan L.K.,University of Portsmouth | Huang X.,Yunnan University | Zhao N.,Second Hospital | And 3 more authors.
International Journal of Oncology | Year: 2013

The cancer stem cell (CSC) marker CD133 is widely expressed in gliomas and employed mostly by use of the CD133/1 antibody which binds the extracellular glycosylated AC133 epitope. CD133 recognition may, however, be affected by its glycosylation pattern and oxygen tension. The present study investigates the effect of oxygen deprivation on CD133 expression and glycosylation status employing a high AC133-expressing glioblastoma multiforme (GBM) cell line, IN699. IN699 cells were cultured under normoxic (21% O2) and hypoxic (3% O2) conditions. CD133 expression was analysed by western blotting (WB), qRT-PCR, immunocytochemistry (ICC) and flow cytometry using the glycosylation-specific antibody CD133/1 and ab19898 which binds the unglycosylated intracellular residues of CD133. By flow cytometry, ab19898 detected 94.1% and 96.2% CD133+ cells under normoxia and hypoxia, respectively. Hypoxia significantly increased the percentage of CD133 + cells from 69% to 92% using CD133/1 (p<0.005). Moreover, a significantly higher geomean fluorescence intensity (GMI) was demonstrated by ab19898 (p<0.005) in CD133+ cells. WB and qRT-PCR results were consistent with flow cytometry data. Furthermore, over a period of 72-h incubation under normoxic and hypoxic conditions after autoMACS sorting, an average of 31.8% and 42.2%, respectively, of CD133-negative IN699 cells became positive using CD133/1. Our data show that a) previously reported CD133- cells may have been misidentified using the glycosylation-specific CD133/1 as constitutive expression of CD133 was detected by the intracellular antibody ab19898; b) hypoxia promotes glycosylation status of CD133, indicating possible involvement of glycosylated CD133 in the process of anti-hypoxia-mediated apoptosis.


Xu S.,Fujian Medical University | Song H.,Peoples Hospital | Huang M.,Fujian Medical University | Wang K.,Second Hospital | And 2 more authors.
International Journal of Molecular Medicine | Year: 2014

The aim of this study was to investigate the inhibition capacity of telmisartan to endothelial inflammation induced by homocysteine (Hcy) and discuss the proposed mechanism in vitro. Human umbilical vein endothelial cells (HUVECs) were prepared by collagenase digestion and cultured in vitro. An increase in monocyte chemoattractant protein-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) as markers of Hcy-induced endothelial inflammation. HL-60 cell adhesion to HUVECs was measured by rose bengal staining. Nuclear, cytosolic and total nuclear transcription factor-κB (NF-κB) p65 levels were analyzed by western blotting. Peroxisome proliferator-activated receptor-δ (PPARδ) expression by HUVECs exposed to Hcy with or without telmisartan pretreatment was analyzed by RT-PCR and western blotting. Hcy significantly increased the levels of MCP-1 mRNA, VCAM-1 mRNA and monocyte binding to HUVECs. These effects were significantly attenuated by pretreatment with telmisartan and PPARδ agonists. The effect of telmisartan was inhibited by PPARδ antagonists. The Hcy-mediated downregulation of PPARδ mRNA and protein of HUVECs was inhibited by telmisartan. Hcy-mediated upregulation of NF-κB p65 protein levels in nuclear extracts was inhibited by telmisartan and PPARδ agonists. In conclusion, telmisartan exerts potent anti-inflammatory effects in endothelial cells, probably via a binary mechanism involving PPARδ activation and inhibition of the nuclear translocation of NF-κB.


Zhao B.,Second Hospital | Wang Q.,Second Hospital | Tao T.,Second Hospital | Li J.,Second Hospital | And 2 more authors.
International Journal of Molecular Medicine | Year: 2013

This study aimed to compare the treatment effects of lentiviral vector-mediated hBMP2 which was overexpressed in the femoral bone marrow stromal cells of osteoporotic rats through genetic infection in vitro and in vivo. Comparison of the two transgenic effects may be crucial to determining the lentivirus infection method to be used. Following a comparison of the rat bone marrow stromal cells (rBMSCs) in osteoporotic (MSCs OVX) and normal (MSCs CON) groups, the lentiviral vector-mediated human bone morphogenetic protein 2 (hBMP2), which overexpressed the BMSCs of osteoporotic rats in vitro (rBMSCs in OE group), was constructed. The osteogenic ability in the overexpressed (OE) group was then compared to that of the MSCs CON. The rBMSCs in the OE group (transplants of genetic infection in vitro) and the lentivirus-containing solution (injected material of genetic infection in vivo) were injected into the femurs. The treatment effect of each group was compared via bone mineral density (BMD) and bone histomorphometry. The hBMP2-modified osteoporosis rBMSCs formed by genetic infection in vitro (n=7) had an ameliorated treatment effect on the femur as compared to that of the in vivo (n=7) (BMD: 0.315 vs. 0.19 g/cm2, P<0.01; bone histomorphometry: For bone trabeculars (Tb.Ar/T.Ar): 0.301 vs. 0.114, P<0.01; for trabecular thickness (Tb.Th): 43.54 vs. 21.39 μm, P<0.01; for trabecular separation (Tb.Sp): 115.7 vs. 304.87 μm, P<0.01). The results showed that the treatment effects of osteoporotic rBMSCs on local osteoporosis performed by genetic infection were improved in vitro as compared to those in vivo.


Liu L.,Shandong University | Liu L.,Karolinska University Hospital | Liu C.,Karolinska University Hospital | Liu C.,Shandong University | And 11 more authors.
Journal of Pathology | Year: 2011

Seminal fluids are involved in the development of cervical cancer but the underlying mechanism is unclear. Because cellular transformation requires telomerase activation by expression of the telomerase reverse transcriptase (hTERT) gene, we examined the role of seminal fluids in telomerase activation. Significantly elevated hTERT mRNA and telomerase activity were observed in cervical cell lines (HeLa, SiHa and Caski) treated with seminal plasma. Normal cervical epithelial cells expressed minimal levels of hTERT mRNA and telomerase activity, and seminal plasma substantially enhanced both expression and activity. The hTERT promoter activity was similarly increased in seminal plasma-treated HeLa cells and this effect was closely correlated with increased Sp1 expression and binding to the hTERT promoter. Cyclooxygenase-2 (COX-2) was simultaneously increased in HeLa cells exposed to seminal plasma, and blockade of COX-2 induction abolished seminal plasma stimulation of the hTERT promoter activity, hTERT expression and telomerase activity. Prostaglandin E2 (PGE2) mimics the effect of seminal plasma, stimulating Sp1 expression, enhancing Sp1 occupancy on the hTERT promoter and promoter activity. Moreover, tumour growth was robustly enhanced when HeLa cells together with seminal plasma were injected into nude-mice. Taken together, seminal plasma stimulates COX-2-PGE2-Sp1- dependent hTERT transcription, which provides insights into the putative mechanism underlying telomerase activation in cervical epithelial and cancer cells. Copyright © 2011 Pathological Society of Great Britain and Ireland. Copyright © 2011 Pathological Society of Great Britain and Ireland.


Wang L.,Second Hospital | Han L.-Y.,Second Hospital | Li H.-L.,Second Hospital
National Medical Journal of China | Year: 2013

Objective: To explore the alteration of collagen infrastructure and content in uterine ligaments and paraurethral tissue and explore whether the alteration may contribute to stress urinary incontinence (SUI) and pelvic organ prolapse (POP). Methods: The cardinal ligament, uterosacral ligament and paraurethral tissue samples were obtained from 90 subjects undergoing hysterectomy. Collagen ultrastructure was examined with transmission electron microscopy. And collagen content and expression of vasoactive intestinal peptide (VIP) were examined with immunohistochemisty. Results: The smooth muscle fascicles were thinner in the patients of SUI and POP. Arrangement of smooth muscle fascicles was disorderly. Fiberoblast was metabolically active. The mean collagen fibril diameters in the SUI and POP groups were larger than that in the control group (P<0.01). The mean contents of collagen I and III in the SUI and POP groups were lower than that in the control group (P<0.01). The expression of VIP was lower (P<0.05). Conclusion: Predominance of collagen degradation during tissue repair may contribute to and promote POP and SUI. The decrease of VIP might be related with nerve damage or degeneration to cause or accelerate the progress of pelvic organ prolapse. Copyright © 2013 by the Chinese Medical Association.


Liang G.,Second Hospital
Chinese Journal of Burns | Year: 2012

Objective: To investigate the feasibility and effect of different types of axial pattern flaps in repairing soft tissue defects of the fingers. Methods: Five types of axial pattern flaps were used to repair soft tissue defects of the fingers of 30 patients admitted to the Second Hospital of Shaoxing Municipality from 2005 to 2010, including distally-based dorsal thumb neurocutaneous vascular flaps in 4 cases, free flaps from the fibular side of the great toe in 6 cases, modified retrograde dorsal metacarpal artery flaps in 8 cases, free flaps based on the radiodorsal septomuscular perforator of the posterior interosseous artery in 6 cases, and free posterior interosseous artery flaps carrying a long segment of the posterior interosseous artery in 6 cases. The flap size ranged from 2.5 cm x 2.0 cm to 8.0 cm x 3.0 cm. The donor sites were sutured directly or covered with skin graft. The condition of flaps was observed. The local feeling, function, and appearance of affected hands were followed up. Results: Twenty-seven flaps grew well without infection. Partial necrosis at the distal portion in two flaps and venous congestion in 1 flap were observed after surgery, and they were healed with suitable treatment. Eighteen patients were followed up for 1 to 12 months. The flaps were found to have good color, texture, and thickness. Satisfactory appearance and function both in the donor sites and in the recipient areas were found in most patients. The sense of two-point discrimination of repaired fingers ranged from 5 to 9 mm. Conclusions: Optimizing the repair method for soft tissue defects in the fingers by taking both the characteristics of various axial pattern flaps and the specific conditions of soft tissue defects into account can achieve expected effect.

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