Concentrated ultrasound-processed fat (CUPF): More than a mechanically emulsified graft.

INTRODUCTION: Autologous fat grafting is still an evolving technique. Researchers have attempted to increase the survival rate of grafts by concentrating adipose-derived stem cells (ASCs). In this study, we investigate a novel method that combines ultrasonic processing and centrifugation to generate small fat particles termed concentrated ultrasound-processed fat (CUPF) for grafting. METHODS: The standard approach for obtaining CUPF is described. The properties of processed fat, including CUPF, microfat, centrifuged fat, and nanofat, were investigated using histological observation. Comparative analyses were conducted on the cell number, viability, and immunophenotypic profile of stromal vascular fraction cells (SVFs). Cultured ASCs were evaluated for cell proliferation and adipogenic, osteogenic, and chondrogenic potential. The processed fats were transplanted and evaluated using in vivo and histological studies. RESULTS: Compared with microfat, centrifuged fat, and nanofat, CUPF had a condensed tissue content and higher concentration of viable cells in a small tissue structure and could smoothly pass through a 27-gauge cannula. In the CUPF group, SVFs were isolated in great numbers, with high viability and a high proportion of CD29- and CD105-positive cells. ASCs from the CUPF group exhibited high proliferation and multilineage differentiation potential. The grafts from the CUPF group were well preserved, and histological quantification revealed an increase in the abundance of Ki67- and CD31-positive cells in the tissue. CONCLUSIONS: Our study established a new fat processing strategy that combines ultrasonic processing and centrifugation to harvest small particle grafts named CUPF. CUPF concentrated a large number of ASCs and has great potential for regenerative therapy.

Upregulation of microRNA-133a and downregulation of connective tissue growth factor suppress cell proliferation, migration, and invasion in human glioma through the JAK/STAT signaling pathway.

Recently, microRNA-133a (miR-133a) has been found to function in many diseases in previous studies, yet few studies have been focused on its role in glioma. This study aims to investigate the mechanism of miR-133a/CTGF on regulating the malignant phenotypes of glioma cells via the JAK/STAT signaling pathway. Sixty-five human glioma specimens were collected and 30 normal brain tissues were selected as controls. The expression of connective tissue growth factor (CTGF) and miR-133a in tissues was detected, and the relationship between their expression and the clinicopathological features as well as prognosis of glioma was analyzed. MiR-133a and CTGF expression in U87, A172, and HEB cell lines was determined. The expression of CTGF, signaling pathway-, proliferation-, migration-, invasion-, apoptosis- and epithelial-mesenchymal transition (EMT)-related factors was detected. A number of assays were used to detect cell proliferation, migration, invasion, cell cycle, apoptosis, glioma growth, and the targeting site between CTGF and miR-133a. MiR-133a was downregulated and CTGF was upregulated in human glioma tissues and cells. MiR-133a and CTGF expression was related to glioma's WHO staging and size. Downregulated miR-133a and upregulated CTGF caused unfavorable prognosis in glioma. Upregulated miR-133a suppressed CTGF expression and the activation of JAK/STAT signaling pathway, thereby constraining cell colony formation, proliferation, migration and invasion, and promoting apoptosis in glioma. Our study reveals that upregulated miR-133a and downregulated CTGF suppress cell proliferation, migration, and invasion in human glioma through the inhibition of the JAK/STAT signaling pathway.

MicroRNA-98 reduces amyloid ß-protein production and improves oxidative stress and mitochondrial dysfunction through the Notch signaling pathway via HEY2 in Alzheimer's disease mice.

Alzheimer's disease (AD) is a chronic neurodegenerative disease that often occurs at a slow pace yet deteriorates with time. MicroRNAs (miRs) have been demonstrated to offer novel therapeutic hope for disease treatment. The aim of the present study was to investigate the effect of miR­98 on amyloid ß (Aß)­protein production, oxidative stress and mitochondrial dysfunction through the Notch signaling pathway by targeting hairy and enhancer of split (Hes)­related with YRPW motif protein 2 (HEY2) in mice with AD. A total of 70 Kunming mice were obtained and subjected to behavioral assessment. The levels of oxidative stress­related proteins glutathione peroxidase, reduced glutathione, superoxide dismutase, malondialdehyde, acetylcholinesterase and Na+­K+­ATP were measured. Morphological changes in brain tissue, HEY2­positivity levels, neuronal apoptotic index (AI) and neuron mitochondrial DNA (mtDNA) levels were also determined. Subsequently, the levels of miR­98 and the mRNA and protein levels of HEY2, Jagged1, Notch1, Hes1, Hes5, ß­amyloid precursor protein, B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein in tissues and hippocampal neurons were determined by reverse transcription­quantitative polymerase chain reaction and western blot analyses, respectively. Finally, hippocampal neuron viability and apoptosis were determined using an MTT assay and flow cytometry, respectively. The levels of miR­98­targeted HEY2 and miR­98 were low and the levels of HEY2 were high in the AD mice. The AD mice exhibited poorer learning and memory abilities, oxidative stress function, and morphological changes of pyramidal cells in the hippocampal CA1 region. Furthermore, the AD mice exhibited increased protein levels of HEY2 and AI in the CA1 region of brain tissues with reduced mtDNA levels and dysfunctional neuronal mitochondria. miR­98 suppressed hippocampal neuron apoptosis and promoted hippocampal neuron viability by inactivating the Notch signaling pathway via the inhibition of HEY2. In conclusion, the results demonstrated that miR­98 reduced the production of Aß and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice.

A comparative study of high-viscosity cement percutaneous vertebroplasty vs. low-viscosity cement percutaneous kyphoplasty for treatment of osteoporotic vertebral compression fractures.

The clinical effects of two different methods-high-viscosity cement percutaneous vertebroplasty (PVP) and low-viscosity cement percutaneous kyphoplasty (PKP) in the treatment of osteoporotic vertebral compression fractures (OVCFs) were investigated. From June 2010 to August 2013, 98 cases of OVCFs were included in our study. Forty-six patients underwent high-viscosity PVP and 52 patients underwent low-viscosity PKP. The occurrence of cement leakage was observed. Pain relief and functional activity were evaluated using the Visual Analog Scale (VAS) and Oswestry Disability Index (ODI), respectively. Restoration of the vertebral body height and angle of kyphosis were assessed by comparing preoperative and postoperative measurements of the anterior heights, middle heights and the kyphotic angle of the fractured vertebra. Nine out of the 54 vertebra bodies and 11 out of the 60 vertebra bodies were observed to have cement leakage in the high-viscosity PVP and low-viscosity PKP groups, respectively. The rate of cement leakage, correction of anterior vertebral height and kyphotic angles showed no significant differences between the two groups (P>0.05). Low-viscosity PKP had significant advantage in terms of the restoration of middle vertebral height as compared with the high-viscosity PVP (P<0.05). Both groups showed significant improvements in pain relief and functional capacity status after surgery (P<0.05). It was concluded that high-viscosity PVP and low-viscosity PKP have similar clinical effects in terms of the rate of cement leakage, restoration of the anterior vertebral body height, changes of kyphotic angles, functional activity, and pain relief. Low-viscosity PKP is better than high-viscosity PVP in restoring the height of the middle vertebra.