Hip Displacement in Cerebral Palsy: The Role of Surveillance

IntroductionHip displacement is common in cerebral palsy (CP) and is related to the severity of neurological and functional impairment. It is a silent, but progressive disease, and can result in significant morbidity and decreased quality of life, if left untreated. The pathophysiology of hip displacement in CP is a combination of hip flexor-adductor muscle spasticity, abductor muscle weakness, and delayed weight-bearing, resulting in proximal femoral deformities and progressive acetabular dysplasia. Due to a lack of symptoms in the early stages of hip displacement, the diagnosis is easily missed. Awareness of this condition and regular surveillance by clinical examination and serial radiographs of the hips are the key to early diagnosis and treatment.Hip surveillance programmesSeveral population-based studies from around the world have demonstrated that universal hip surveillance in children with CP allows early detection of hip displacement and appropriate early intervention, with a resultant decrease in painful dislocations. Global hip surveillance models are based upon the patients’ age, functional level determined by the Gross Motor Function Classification system (GMFCS), gait classification, standardized clinical exam, and radiographic indices such as the migration percentage (MP), as critical indicators of progressive hip displacement.ConclusionDespite 25 years of evidence showing the efficacy of established hip surveillance programmes, there is poor awareness among healthcare professionals in India about the importance of regular hip surveillance in children with CP. There is a need for professional organizations to develop evidence-based guidelines for hip surveillance which are relevant to the Indian context.     

Aortoiliac remodeling and 5-year outcome of an ultralow-profile endograft

BackgroundRemodeling of the aortoiliac anatomy is a challenge to the long-term performance of stent grafts for endovascular aneurysm repair. Changes in vessel diameter and length can result in loss of seal at attachment sites, limb disunion, or kinking, with the development of high-pressure endoleaks, migration, or limb occlusion. The aim of this study was to assess the durability and conformability of the ultralow-profile INCRAFT AAA endograft (Cordis Corporation, Milpitas, Calif) during 5-year follow-up.MethodsFrom 2010 to 2011, there were 60 patients (median age, 74 years; range, 60-94 years) with intact abdominal aortic aneurysms who were enrolled in the INNOVATION trial to evaluate the safety, effectiveness, and durability of the INCRAFT AAA device. Clinical and technical success was assessed with protocol-specified, monitored follow-up clinic visits and core laboratory-assessed computed tomography (CT) at 1 month, 6 months, and 12 months after implantation and annually through 5 years thereafter. Diameter and angulation changes at the proximal aortic neck and diameter changes at the iliac attachment zones were measured in addition to the standard CT assessments.ResultsSignificant aortoiliac remodeling was observed throughout long-term follow-up after endovascular aneurysm repair. Proximal aortic neck diameter 15 mm below the lowest main renal artery increased from 23.5 ± 2.5 mm at 1 month to 27.3 ± 2.8 mm at 5 years (P = .002). Neck dilation >5 mm was observed in 8 of 38 patients with 5-year CT studies (21%). The aortic neck straightened, with angulation decreasing from 34 ± 14 degrees preoperatively to 31 ± 11 degrees at 1 month (P < .001) and to 20 ± 12 degrees at 5 years (P = .018). Straightening of the neck was most prominent in patients who presented with a high degree of preoperative angulation (r = 0.61; P < .001). Between 1 month and 5 years, iliac attachment zone diameter increased from 13.5 ± 1.9 mm to 15.0 ± 2.4 mm on the right (P = .002) and from 13.9 ± 2.3 mm to 16.8 ± 2.7 mm on the left (P < .001). During 5 years, 9 of 72 (13%) iliac arteries enlarged >5 mm. There was a significant relationship between main body oversizing and aortic neck enlargement (r = 0.42; P = .009). No similar association was observed between iliac limb oversizing and iliac dilation over time (r = 0.10 and P = .549, right side; r = 0.14 and P = .400, left side). There were no aneurysm-related deaths in the series. There were two type IA endoleaks, both of which were present on the 1-month CT scan and associated with challenging aortic neck anatomy. No patient experienced endograft migration or rupture through 5 years. Type IB endoleaks occurred in two patients, both accompanied by iliac artery dilation and loss of seal. Stent fracture occurred in two struts of the bare transrenal stent of one patient, without loss of fixation or seal. One patient experienced graft limb occlusion and was observed without intervention. There were three patients (5%) with aneurysm sac enlargement (>5 mm) through 5 years, each of whom had type II endoleak.ConclusionsSignificant aortoiliac remodeling occurs after endograft implantation, including proximal aortic neck dilation, straightening of the neck, and iliac artery enlargement. The ultralow-profile INCRAFT device adapted well to these changes, with acceptably low 5-year rates of device-related endoleaks, endograft migration, and limb occlusion.     

miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there was an inverse correlation between the expression of miR-150 and MYB in melanoma tissues. We also showed that MYB was upregulated in melanoma tissues and cell lines. Through functional experiments, we found that restoration of MYB in miR-150-overexpressed melanoma cells rescued the proliferation, migration, and invasion. Therefore, our findings demonstrated that miR-150 suppressed the proliferation, migration, and invasion of melanoma cell by downregulating MYB.     

The oncogenic impact of RNF2 on cell proliferation,invasion and migration through EMT on mammary carcinoma

Mammary carcinoma (MC) is one of most common malignancy in women, and ring finger protein 2 (RNF2) possesses various roles in vast human tumors. In MC tissues as well as in cell lines RNF2 exhibited high expression, had significant association with tumor size, lymph node status, TNM stage, patients’ poor survival, and promoted cell proliferation, colony formation, cell migration and invasion of MC cell lines which was mediated by downregulation of E-cadherin protein. These data reveal that RNF2 protein plays a vital role in the development of MC and may be a potential therapy target of MC.     

肿瘤相关巨噬细胞促进宫颈癌侵袭转移的机制研究

 目的 研究肿瘤相关巨噬细胞（tumor-associated macrophages, TAMs）对宫颈癌侵袭转移的影响及分子机制。方法 免疫组织化学法检测宫颈病变组织TAMs的浸润情况。对人单核巨噬细胞系THP1进行体外诱导分化，使其转化为M2型TAMs。取TAMs上清液刺激宫颈癌细胞SiHa和C33a。划痕法、Transwell法分别检测TAMs对宫颈癌细胞系迁移和侵袭能力的影响。Western blot检测刺激后宫颈癌细胞上皮间质转化进程及MMP-9的表达。结果 TAMs浸润数目与宫颈病变进展呈正相关。TAMs上清液刺激后，SiHa和C33a细胞出现间质样改变，而且迁移和侵袭能力显著增强（均P<0.5）。TAMs可下调E-Cadherin的表达，上调N-Cadherin、Vimentin及MMP-9的表达。结论 TAMs浸润与宫颈上皮恶性转化和进展密切相关，TAMs可能通过上调MMP-9的表达促进宫颈癌细胞侵袭转移。     

Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell viability, migration, invasion, and apoptosis were assessed. The results revealed that UCA1 expression was relatively higher in MHCC97 cells than in MG63, hFOB1.19, and OS-732 cells. Knockdown of UCA1 reduced cell viability, inhibited migration and invasion, and promoted cell apoptosis. However, the effect of UCA1 knockdown on cell growth and migration was blocked by miR-301a overexpression, whose expression was regulated by UCA1. We also found that miR-301a positively regulated CXCR4 expression. CXCR4 inhibition reversed the effect of miR-301a overexpression on cell growth and migration. Moreover, miR-301a activated the Wnt/ -catenin and NF- B pathways via regulating CXCR4. The present study demonstrated that UCA1 inhibition exerted an antigrowth and antimigration role in MHCC97 cells through regulating miR-301a and CXCR4 expression.     

miR-363-3p Inhibits Osteosarcoma Cell Proliferation and Invasion via Targeting SOX4

miR-363-3p has been shown to suppress tumor growth and metastasis in various human cancers. However, the function of miR-363-3p in osteosarcoma (OS) has not been determined. In our study, we found that the expression of miR-363-3p was significantly downregulated in OS tissues compared with adjacent normal tissues. miR-363-3p expression was associated with the poor overall survival rate of OS patients. Moreover, we found that overexpression of miR-363-3p markedly inhibited the proliferation, migration, and invasion of U2OS and MG63 cells. Moreover, we found that SOX4 was a direct target of miR-363-3p in OS cells. Overexpression of miR-363-3p significantly inhibited the expression of SOX4. Expression levels of miR-363-3p and SOX4 were negatively correlated in OS tissues. Finally, we found that restoration of SOX4 attenuated the suppressive effects of miR-363-3p on the proliferation, migration, and invasion of U2OS and MG63 cells. Therefore, our findings demonstrated that miR-363-3p served as a tumor suppressor in OS tissues by targeting SOX4.     

miR-30c Impedes Glioblastoma Cell Proliferation and Migration by Targeting SOX9

miR-30c has been acknowledged as a tumor suppressor in various human cancers, such as ovarian cancer, gastric cancer, and prostate cancer. However, the role of miR-30c in glioblastoma (GBM) needs to be investigated. In our study, we found that the expression of miR-30c was significantly downregulated in GBM tissues and cell lines. We found that overexpression of miR-30c inhibited cellular proliferation of GBM cells in vitro and in vivo. More GBM cells were arrested in the G₀ phase after miR-30c overexpression. Moreover, we showed that miR-30c overexpression suppressed the migration and invasion of GBM cells. Mechanistically, we found that SOX9 was a direct target of miR-30c in GBM cells. Overexpression of miR-30c inhibited the mRNA and protein levels of SOX9 in GBM cells. Moreover, there was a negative correlation between the expression of miR-30c and SOX9 in GBM tissues. Finally, we showed that restoration of SOX9 in GBM cells reversed the proliferation, migration, and invasion of GBM cells transfected with miR-30c mimic. Collectively, our results demonstrated that miR-30c suppressed the proliferation, migration, and invasion of GBM cells via targeting SOX9.