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BACKGROUND The main clinical manifestation of Alzheimer’s disease (AD) is memory loss, which can be accompanied by neuropsychiatric symptoms at different stages of the disease. Amygdala is closely related to emotion and memory. AIM To evaluate the diagnostic value of amygdala on structural magnetic resonance imaging (sMRI) for AD. METHODS In this study, 22 patients with AD and 26 controls were enrolled. Their amygdala volumes were measured by sMRI and analyzed using an automatic analysis software. RESULTS The bilateral amygdala volumes of AD patients were significantly lower than those of the controls and were positively correlated with the hippocampal volumes. Receiver operating characteristic curve analyses showed that the sensitivity of the left and right amygdala volumes in diagnosing AD was 80.8% and 88.5%, respectively. Subgroup analyses showed that amygdala atrophy was more serious in AD patients with neuropsychiatric symptoms, which mainly included irritability (22.73%), sleep difficulties (22.73%), apathy (18.18%), and hallucination (13.64%). CONCLUSION Amygdala volumes measured by sMRI can be used to diagnose AD, and amygdala atrophy is more serious in patients with neuropsychiatric symptoms.

Introduction Spinocerebellar ataxias (SCAs) are a heterozygous group of neurodegenerative disorders. Spinocerebellar ataxia type 5 (SCA5) is a rare autosomal-dominant ataxia with pure cerebellum involvement. The clinical characteristics are limb and gait ataxia, trunk ataxia, sensory deficits, abnormal eye movement, dysarthria, and hyperactive tendon reflexes. Spectrin beta nonerythrocytic 2 gene (SPTBN2), coding β-III spectrin protein, was identified to be associated with SCA5. To date, more than 19 variants of SPTBN2 have been reported. Methods A family and an apparently sporadic patient with ataxia and cerebellar atrophy were recruited from Shandong Province (China). To discover the disease-causing variants, capillary electrophoresis and targeted next-generation sequencing were performed in the proband of the family and the sporadic patient. The candidate variants were verified by Sanger sequencing and analyzed by bioinformatics software. Results In our study, we verified two novel heterozygous variants in SPTBN2 in a SCA pedigree and a sporadic patient. The proband of the pedigree and her mother presented with walking instability and progressively getting worse. The sporadic patient suffered from slurred speech, walking instability, and drinking water choking cough. MRI examination of the proband and sporadic patient both displayed moderate cerebellar atrophy. The variants identified were traditionally conserved and predicted probably damaging and disease-causing by bioinformatics analysis. Conclusion We identified two novel heterozygous variants of SPTBN2 resulting in severe ataxia which further delineated the correlation between the genotype and phenotype of SCA5, and pathogenesis of variants in SPTBN2 should be further researched.

Emerging evidence addresses the link between the aberrant epigenetic regulation of gene expression and numerous diseases including neurological disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). LncRNAs, a class of ncRNAs, have length of 200 nt or more, some of which crucially regulate a variety of biological processes such as epigenetic-mediated chromatin remodeling, mRNA stability, X-chromosome inactivation and imprinting. Aberrant regulation of the lncRNAs contributes to pathogenesis of many diseases, such as the neurological disorders at the transcriptional and post-transcriptional levels. In this review, we highlight the latest research progress on the contributions of some lncRNAs to the pathogenesis of neurodegenerative diseases via varied mechanisms, such as autophagy regulation, Aβ deposition, neuroinflammation, Tau phosphorylation and α-synuclein aggregation. Meanwhile, we also address the potential challenges on the lncRNAs-mediated epigenetic study to further understand the molecular mechanism of the neurodegenerative diseases.

Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma.

Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by excessive accumulation of the amyloid-β peptide (Aβ) in the brain, which has been considered to mediate the neuroinflammation process. Microglial activation is the main component of neuroimmunoregulation. In recent years, exosomes isolated from human umbilical cord mesenchymal stem cells (hucMSC-exosomes) have been demonstrated to mimic the therapeutic effects of hucMSCs in many inflammation-related diseases. In this study, exosomes from the supernatant of hucMSCs were injected into AD mouse models. We observed that hucMSC-exosomes injection could repair cognitive disfunctions and help to clear Aβ deposition in these mice. Moreover, we found that hucMSC-exosomes injection could modulate the activation of microglia in brains of the mice to alleviated neuroinflammation. The levels of pro-inflammatory cytokines in peripheral blood and brains of mice were increased and the levels of anti-inflammatory cytokines were decreased. We also treated BV2 cells with hucMSC-exosomes in culture medium. HucMSC-exosomes also had inflammatory regulating effects to alternatively activate microglia and modulate the levels of inflammatory cytokines in vitro.

Screening procedures for infectious diseases, such as HIV, often involve pooling individual specimens together and testing the pools. For diseases with low prevalence, group testing (or pooled testing) can be used to classify individuals as diseased or not while providing considerable cost savings when compared to testing specimens individually. The pooling literature is replete with group testing case identification algorithms including Dorfman testing, higher-stage hierarchical procedures, and array testing. Although these algorithms are usually evaluated on the basis of the expected number of tests and classification accuracy, most evaluations in the literature do not account for the continuous nature of the testing responses and thus invoke potentially restrictive assumptions to characterize an algorithm’s performance. Commonly used case identification algorithms in group testing are considered and are evaluated by taking a different approach. Instead of treating testing responses as binary random variables (i.e., diseased/not), evaluations are made by exploiting an assay’s underlying continuous biomarker distributions for positive and negative individuals. In doing so, a general framework to describe the operating characteristics of group testing case identification algorithms is provided when these distributions are known. The methodology is illustrated using two HIV testing examples taken from the pooling literature.

Alzheimer disease (AD) is the most common form of dementia. Amyloid β-peptide (Aβ) deposition is a major neuropathologic feature of AD. When unfolded or misfolded proteins accumulate in mitochondria, the unfolded protein responses (UPRmt) is initiated. Numerous lines of evidence show that AD pathogenesis involves mitochondrial dysfunction. However little is known about whether the UPRmt is engaged in the process of AD development. In this study, we investigated the UPRmt in mouse and cell models of AD. We found that UPRmt was activated in the brain of 3 and 9 months old APP/PS1 mice, and in the SHSY5Y cells after exposure to Aβ25–35, Aβ25–35 triggered UPRmt in SHSY5Y cells could be attenuated upon administration of simvastatin or siRNA for HMGCS-1 to inhibit the mevalonate pathway, and or upon knocking down Serine palmitoyltransferase long chain subunit 1 (SPTLC-1) to lower sphingolipid biosynthesis. We observed that inhibition of UPRmt aggravated cytotoxic effects of Aβ25–35 in SHSY5Y cells. Our research suggests that the UPRmt activation and two pathways necessary for this response, and further provides evidence for the cytoprotective effect of UPRmt during the AD process.

Long non-coding RNA (lncRNA) and exosomes are involved in the pathological process of Alzheimer's disease (AD), the pathological changes of which are usually first observed in the entorhinal cortex and hippocampus. The aim of the present study was to determine whether the measurement of plasma exosomal lncRNA combined with image data of the entorhinal cortex and hippocampus could be used as a biomarker of AD. A total of 72 patients with AD and 62 controls were recruited, and the expression levels of several lncRNAs were assessed. Of the recruited participants, 22 patients and 26 controls received brain 3D‑BRAVO sequence magnetic resonance imaging (MRI) scans, which were analyzed using an automated analysis tool. The plasma exosomal β‑site amyloid precursor protein cleaving enzyme‑1‑antisense transcript (BACE1‑AS) levels in patients with AD were significantly higher compared with the controls (P

The study was designed to explore the underlying mechanism of micro ribonucleic acids (miR)-145-5p in the process of hypertrophic scar (HS). The difference in the relative content of miR-145-5p between HS and adjacent normal skin collected from 5 patients was detected via RT-PCR. Expressions of Smad2 and Smad3 with or without TGF-β1 was detected by western blotting. Fibroblasts apoptosis rate was examined by Annexin V/Propidium Iodide double staining. HS fibroblasts (HSFs) were isolated from HS tissues, cultured and then divided into control group, miR-145-5p inhibitor group (transfected with miR-145-5p inhibitor) and miR-145-5p mimic group (transfected with miR-145-5p plasmid) based on different treatment methods. Next, CCK-8 was employed to examine the function of miR-145-5p in HSF proliferation. Luciferase assay was conducted to confirm whether Smad2/3 were direct targets of miR-145-5p, and RT-PCR was done to measure the expression of miR-145-5p, Smad2/Smad3 and fibrosis-related genes of fibroblasts in three groups. Wound injury mice model was established to determine the function of miR-145-5p in regulating scar formation. miR-145-5p was found lowly expressed in HS tissues. Compared with Control group, miR-145-5p mimic decreased the levels of Smad2/3, arrested the activation and proliferation of HSFs and induced HSFs apoptosis. Overexpressing miR-145-5p achieved the contrary results. Smad2/3 was confirmed as the target of miR-145-5p. Moreover, miR-145-5p mimic decreased the recruitment of fibroblasts in vivo and decreased the expression of fibrosis-related genes after wound injury. In conclusion, miR-145-5p arrests the development of fibrogenesis and decreases HS formation by reducing the expression of Smad2/3. miR-145-5p may be an optional novel molecular target for treating HS.

AIM Uterine leiomyomas (UL) are the most common pelvic tumors, and the etiology and pathophysiology are not well understood. We aimed to elucidate the genes responsible for UL development. METHODS Integrated analyses of four datasets of mRNA profiling for UL were performed. Functional annotation of differentially expressed genes (DEG) was used to systematically characterize the global expression profiles. The UL-specific protein-protein interaction network was constructed. RESULTS Integrated analysis led to the discovery of 2167 DEG (1042 upregulated and 1125 downregulated). The aberrant expression of NAV2, KIF5C, DCX, CAPN6, COL4A2, ALDH1A1, and DPT may play important roles in UL tumorigenesis. In addition, the dysregulation of MEST, LGALS3, and TLR3 may be involved in the progression of UL by a common mechanism. Functional annotation showed that extracellular matrix receptor interaction may be more active and cause the extracellular matrix abnormally formed in UL. Moreover, focal adhesion and cell adhesion molecules may play roles in the development of UL. Furthermore, chemokine signaling pathway and cytokine-cytokine receptor interaction were most probably involved in the development of UL. CONCLUSION In conclusion, our study observed that a set of aberrantly expressed genes and the related biochemical pathways may lead to transformation of normal myometrium in pathological focuses.

Unlike activated carbon, graphene sheets are lack of ion pathways on their basal planes and prone to agglomerate or restack unfortunately for their strong π − π interactions between neighboring sheets. All of which will pose significant obstacles for its application in high performance supercapacitors. Herein, we report a simple and fast strategy for the scalable synthesis of hierarchical honeycomb-like porous graphene–carbon nanotubes hybrid (PGCTs) through a simple laser induced self-propagating reaction process and subsequent activation with low amount of KOH without any template. Benefiting from properly integration of large surface area, hierarchical pore structures, in-plane nanopores and CNTs nanospacers, the as-obtained PGCTs based symmetrical supercapacitor exhibits outstanding electrochemical performance with super capacitance, excellent rate capability, and desirable cyclability.

Activated carbon materials have been playing a significant role in addressing the challenges posed with the ever-increasing demand for alternative clean and sustainable energy technologies. In the present study, a facile strategy is proposed for generating porosity in porous carbons by using carton box as the precursor and eutectic NaOH–KOH melt as the activating agent. The prepared carbon materials have a very high specific surface area up to 2731 m2 g−1 with large pore volume of 1.68 cm3 g−1, which is greater than that of only KOH was used at the same mass ratio. Electrochemical studies based on symmetric supercapacitor devices demonstrating that the NaOH–KOH melt activated porous carbon exhibits significantly improved rate capability in the range of 0.5–75 A g−1 despite of the similar specific capacitance with respect to KOH activated carbon at a low current density of 0.5 A g−1. The remarkable deviations in capacitive behavior at high current density for the NaOH–KOH melt activated porous carbon and KOH activated samples highlighting the specific surface area is not the only parameter that determines the capacitive performance especially at high charge–discharge rate.

e13062 Background: Platinum-based chemotherapy is an important treatment for anthracycline- and taxane-resistant metastatic breast cancer(MBC), especially for triple-negative breast cancer(TNBC). Here, we presented the results of a phase IV clinical study of the third-generation platinum compound lobaplatin (LBP) in the treatment of MBC. Methods: Patients(Pts) diagnosed with MBC who had previously received chemotherapies containing anthracycline and/or taxane were recruited. The chemotherapy regimen was decided by the investigator but must include LBP. The primary endpoint was safety, the secondary study endpoints included PFS, OS, ORR, and DCR. Results: 1181 pts were enrolled from 34 research centers, 252 pts of them were TNBC. The main treatment regimens included LBP plus paclitaxel (134, 11.4%), LBP plus docetaxel(263,22.3%), LBP plus gemcitabine(235,19.9%) and LBP plus vinorelbine (404, 34.3%).The overall incidence of AE and grade III/IV(G3-4) incidence of AE were 95.00% and 58.10%, respectively. The most common AE were leukopenia (79.9%, G3-4: 39.5%), neutropenia(75.4%, G3-4: 43.8%), anemia(67.4%, G3-4: 17.8%), and thrombocytopenia(51.1%, G3-4: 17.8%). Creatinine clearance rate (Ccr) was the main influence factor for thrombocytopenia, the incidence of G3-4 thrombocytopenia in pts with Ccr < 60 ml/min were higher than that in pts with Ccr≥60 ml/min. Median follow-up was 36 months. The ORR and DCR were 36.8% and 76.9%, respectively. The mPFS and mOS were 5.5 months and 15.4 months, respectively. The efficacy of LBP combined with taxanes was significantly better than that of other regimens. Different sites of metastasis, ECOG score, clinical stage and age were the main factors influencing for efficacy. Conclusions: LBP-based regimens are effective and safe, and these regimens provide an alternatively treatment option for Chinese MBC pts. Clinical trial information: ChiCTR-ONC-13003471. Clinical trial information: ChiCTR-ONC-13003471 .

Osteosarcoma (OS) is the most common malignant bone tumor in children and young adults, the early symptoms and signs of which are non-specific. The discovery of microRNAs (miRNAs) provides a new avenue for the early diagnosis and treatment of OS. miR-126 has been reported to be highly expressed in vascularized tissues, and is recently widely studied in cancers. Herein, we explored the expression and significance of miR-126 in OS. Using TaqMan RT-PCR analysis, we analyzed the expression of miR-126 in 32 paired OS tumor tissues and 4 OS cell lines and found that miR-126 was consistently under-expressed in OS tissues and cell lines compared with normal bone tissues and normal osteoblast cells (NHOst), respectively. As miR-126 is significantly decreased in OS tissues and cell lines, we sought to compensate for its loss through exogenous transfection into MG-63 cells with a miR-126 mimic. Ectopic expression of miR-126 inhibited cell proliferation, migration and invasion, and induced apoptosis of MG-63 cells. Moreover, bioinformatic prediction suggested that the sex-determining region Y-box 2 (Sox2) is a target gene of miR-126. Using mRNA and protein expression analysis, luciferase assays and rescue assays, we demonstrate that restored expression of Sox2 dampened miR-126-mediated suppression of tumor progression, which suggests the important role of miR-126/Sox2 interaction in tumor progression. Taken together, our data indicate that miR-126 functions as a tumor suppressor in OS, which exerts its activity by suppressing the expression of Sox2.

Background: Several lines of evidence support the clinical use of trimetazidine as an adjunctive therapy in cardioischemic patients. Therefore, we assessed here the efficacy and safety of adjunctive trimetazidine therapy in acute myocardial infarction (MI) patients by a systematic review and meta-analysis of the current literature. Methods: PubMed, the Cochrane Library, and the China National Knowledge Infrastructure databases were searched for clinical studies comparing adjunctive trimetazidine therapy against placebo in adult acute MI patients. Several clinical outcomes [early/short-term all-cause mortality, long-term all-cause mortality, total major adverse cardiac events (MACE), recurrent nonfatal MI, in-hospital adverse events, target vessel revascularization (TVR), and coronary artery bypass graft (CABG)] were analyzed by the intention-to-treat principle. Odds ratios (OR) and their 95% confidence intervals (CI) were derived from the number of outcome events in each study arm to estimate the association between adjuvant trimetazidine administration and the various clinical outcomes. A random-effects model was applied for all meta-analyses. Results: We found that adjunctive trimetazidine therapy showed a significant effect upon total MACE (OR = 0.33, 95% CI = 0.15-0.74; p = 0.007) but showed no significant effect upon early/short-term all-cause mortality, long-term all-cause mortality, recurrent nonfatal MI, in-hospital adverse events, TVR, or CABG (p > 0.05). Conclusions: This is the first meta-analysis to report that adjunctive trimetazidine therapy has a beneficial effect upon total MACE in acute MI patients. Clinical investigators should consider further trials on adjunctive trimetazidine therapy in order to better define its risks and benefits in acute MI patients.

This study investigated the role of alpha 7 nicotinic acetylcholine receptor (α7nAChR) in axonal regeneration after crush injury to the rat sciatic nerve. The time course of α7nAChR expression following injury was assessed by immunohistochemistry and western blotting, and local inflammation, as indicated by the expression of tumor necrosis factor (TNF)-α, was detected by enzyme-linked immunosorbent assay. Axonal regeneration was evaluated by the pinch-test, morphometric analysis, and by measuring growth-associated protein 43 expressions. Local α7nAChR expression increased on day 1, peaked on day 3, and remained elevated on day 5 following nerve injuries. Prominent α7nAChR immunoreactivity was observed in Schwann cells, endothelial cells of the capillaries, and a small number of inflammatory cells. Application of the selective α7nAChR agonist PNU-282987 decreased TNF-α level and enhanced axonal regeneration, but this effect was blocked by concomitant treatment with methyllycaconitine, a α7nAChR antagonist. The results indicate that the local expression of α7nAChR is increased during the early stages of sciatic nerve injury, and application of a α7nAChR agonist promotes axonal regeneration by suppression of TNF-α-mediated inflammation. The α7nAChR can act as a neuroprotective agent and α7nAChR activation may be a useful therapeutic strategy to treat peripheral nerve injury.

Bone grafting is a very useful approach to reconstruction of skeletal defects. However, the clinical use of autografts, allografts, and synthetic products is associated with a number of problems. The use of bone xenotransplantation, on the other hand, is associated with strong immune response, and therefore clear understanding of the mechanisms of immune rejection is essential. In this study, we used rabbit-to-rat xenotransplantation model to investigate the role of IL-17, and the relationship between IL-17, IL-23 and RANKL in inflammatory response during the bone grafting. Rabbit hindlimb bone was transplanted to rats, and half of the xenograft recipient animals received injection of IL-17 neutralizing antibodies before xenotransplantation. Sham control rats did not receive bone transplants. In the xenotransplant group, significant mononuclear cell infiltration and erosion/resorption of graft bone were observed. Administration of IL-17 neutralizing antibodies decreased mononuclear cell infiltration and inhibited bone resorption. The levels of IL-17+, IL-23+, and RANKL+ cells were elevated in xenotransplanted group from compared to the sham control. IL-17+ and RANKL+ cells infiltration was decreased upon administration of IL-17 neutralizing antibodies. No significant difference in the level of IL-23 in xenotransplanted groups with and without IL-17 antibodies was observed. Our results indicate that RANKL, IL-17, and IL-23 participate in the immune rejection of bone xenotransplantion. The IL-17/RANKL pathway may play a very important role in the bone resorption during rejection of fresh bone xenotransplants.

Cinobufacini (Huachansu), a Chinese medicine prepared from the skin of Bufo bufo gargarizans Cantor (Bufonidae), has potent anti-tumor activity in vitro and in vivo. However, the molecular mechanism of cell apoptosis induced by Bufalin remains elusive. Here, we investigated the apoptosis in Bufalin-treated human osteosarcoma MG-63 cells. The results showed that Bufalin could inhibit cell proliferation and induce apoptosis in a dose- and time-dependent manner. Further investigation revealed that a disruption of mitochondrial transmembrane potential (MMP) and an up-regulation of reactive oxygen species (ROS) in Bufalin-treated cells. By western blot analysis, we found that the up-regulation of Apaf-1, cleaved PARP, cleaved caspase-3, cleaved caspase-9, and Bax/Bcl-2, varies with different concentration of Bufalin. These protein interactions may play a pivotal role in the regulation of apoptosis. Taken together, these results overall indicate that Bufalin could be used as an effective anti-tumor agent in therapy of osteosarcoma targets the mitochondrial-dependent signaling pathway.

Osteosarcoma (OS) is the most common malignant bone tumor in children and young adults, the early symptoms and signs of which are non-specific. The discovery of microRNAs (miRNAs) provides a new avenue for the early diagnosis and treatment of OS. miR-126 has been reported to be highly expressed in vascularized tissues, and is recently widely studied in cancers. Herein, we explored the expression and significance of miR-126 in OS. Using TaqMan RT-PCR analysis, we analyzed the expression of miR-126 in 32 paired OS tumor tissues and 4 OS cell lines and found that miR-126 was consistently under-expressed in OS tissues and cell lines compared with normal bone tissues and normal osteoblast cells (NHOst), respectively. As miR-126 is significantly decreased in OS tissues and cell lines, we sought to compensate for its loss through exogenous transfection into MG-63 cells with a miR-126 mimic. Ectopic expression of miR-126 inhibited cell proliferation, migration and invasion, and induced apoptosis of MG-63 cells. Moreover, bioinformatic prediction suggested that the sex-determining region Y-box 2 (Sox2) is a target gene of miR-126. Using mRNA and protein expression analysis, luciferase assays and rescue assays, we demonstrate that restored expression of Sox2 dampened miR-126-mediated suppression of tumor progression, which suggests the important role of miR-126/Sox2 interaction in tumor progression. Taken together, our data indicate that miR-126 functions as a tumor suppressor in OS, which exerts its activity by suppressing the expression of Sox2.

Background The anterolateral thigh (ALT) flap has been widely used in reconstruction of soft tissue defects. The anatomic variations of perforators increase the difficulties of flap elevation. The ABC system has been described for locating the most common three perforators in Western populations. Less evidence has been found regarding whether it is suitable for Chinese population. The purpose of this study is to explore the improvement of preoperative location technology and flap design for Chinese people. Methods Detection for perforator signals on the bilateral thigh surface was perfromed on 50 Chinese adults using handheld Doppler. Define the A-P line as the line between the anterior superior iliac spin (ASIS) and the superolateral corner of the patella (P). We defined a coordinate system on the thigh surface to record the data of each signal point. The A-P line was y-axis in this coordinate system, and the midpoint of the line was the zero point. The data of these signals were recorded in the form of coordinates. Statistics and mathematic methods were used to analyze the regularity of signal distribution and the correlation between body mass index (BMI) and signal distribution. The findings were applied in five patients who underwent the ALT flap transplantation to confirm its clinical value. Results The results showed that most of the signals appeared near the A-P line. Most signals were located 1 cm lateral (mean 0.5 cm lateral) to the A-P line. The mean vertical distance between perforator B and perforators A and C was 4 cm . More perforator signals were detected at the two horizontal level (as shown in the picture above) than other horizontal levels. The rate of accurate preoperative detection was 40% (6 of 15 perforators) and the error rate was 20% (3 of 15 perforators). The mean deviation was 1.34 cm, which is acceptable for clinical application. The mean vertical distance between perforator B and perforators A and C in clinical study (4.81 cm) corresponded to the finding of the Doppler study (4.2 cm), whereas the mean distance between perforators and the A-P line (1.57 cm) was more than the Doppler finding (0.48 cm). Conclusion The A-P line is still a reliable guiding line for Doppler detection and flap design. The ABC system is suitable for the Chinese population but must be adjusted: perforator B is marked first at the midpoint and 0.5 cm lateral to the A-P line and perforators A and C are marked 4 cm distal and proximal to perforator B, respectively. In designing the flap, the region 3 cm around point B and the region between the two horizontal planes at point B and 4 cm lower should both be contained into the flap, no matter what the finding of Doppler detection is.

The effect of oil displacement agents (alkali, surfactant, and polymer) on the stability of the emulsion produced by alkaline surfactant polymer (ASP) flooding can be rapidly and accurately determined using a FORMULACTION (France) stability analyzer. The analyzer detects backscattered light and change in transmittance. We observed that when displacement agents are used, the stability of a water-in-oil emulsion gradually increases with displacement agent concentration and consequently the emulsion dehydration rate gradually decreases, while the stability of an oil-in-water emulsion increases. This is evidence that the oil content in the waste water increases. But the reverse is observed when the alkali content in the water phase is no more than 700 mg/L.

Etomidate is a unique drug used for induction of general anesthesia and sedation, and is usually used through intravenous injection clinically. Before targeting to the receptor, etomidate binds proteins in blood when it comes into veins. Thus to study the interaction of etomidate and serum albumin would be of great toxicological and pharmacological importance. In this study, the interaction between etomidate and human serum albumin (HSA) was studied using fluorescence spectroscopy, UV–vis absorption spectroscopy, Fourier transform infrared spectroscopy (FT-IR), circular dichroism (CD) spectroscopy, site maker displacement and molecular modeling methods. Investigations of the binding constant (K = 3.55 × 105 M−1, 295 K), the number of binding sites (n = 1.16), thermodynamic parameters (ΔG = 3.13 × 104 J·mol−1, ΔS = 364 J·mol−1·K−1 and ΔH = −6.85 × 105 J·mol−1) for the reaction and changes to the binding sites and conformation in HSA in response to etomidate were presented. Results show that etomidate can bind HSA tightly through electrostatic forces, and the protein skeleton conformation and secondary structure changes thereby. This is the first spectroscopic report for etomidate–HSA interactions which illustrates the complex nature of this subject.

An increasing number of microRNAs (miRNAs) have been identified as diagnostic and prognostic biomarkers, as well as additional therapeutic tools, in skeletal diseases. Recent studies have established the pathophysiological role of miR‑214, using human osteoporotic bone specimens. However, miR‑214 expression levels and the underlying regulatory mechanism in human osteosarcoma remain unclear. Quantitative polymerase chain reaction (qPCR) was used to examine the expression of miR‑214 in human osteosarcoma tissues and cells. Transfection of the cells with either a miR‑214 expressing‑plasmid, mimic or inhibitor was performed, in order to investigate the role of miR‑214 in osteosarcoma. In this study, miR‑214 was shown to be significantly increased in the majority of 15 examined osteosarcoma tissues and in the Saos‑2 human osteosarcoma cell line. Overexpression of miR‑214 in Saos‑2 cells induced cell proliferation, while inhibition of miR‑214 promoted Saos‑2 cell apoptosis in vitro. Furthermore, ectopic expression of miR‑214 markedly promoted osteosarcoma development in a subcutaneous xenotransplantation model in BALB/c athymic nude mice. The role of miR‑214 in osteocarcinogenesis was further investigated and phosphatase and tensin homolog (PTEN) was determined to be a direct target of miR‑214 in Saos‑2 cells. The proliferation‑promoting effect of PTEN knockdown was similar to that of miR‑214 overexpression. This study revealed that miR‑214 exerted a crucial role in promoting osteosarcoma progression and this suggests that modulation of miR‑214 levels may provide a novel therapeutic approach in cancer treatment.

To explore the associations between vitamin D receptor (VDR) gene polymorphisms (including Fok I, Bsm I and Apa I) and bone mineral density (BMD) in postmenopausal Asian women.Databases of Medline, Embase and Wangfang were retrieved to identify eligible studies, with update to 1st February 2012. Standardized mean difference (SMD) and 95% confidence intervals were calculated by using fixed- or random-effect model. Best genetic comparison model was determined by using the Thakkinstian method.A total of 14 studies with 3243 healthy postmenopausal Asian women were included in this meta-analysis. Overall, pooled analyses indicated that the f allele of VDR Fok I was significantly associated with decreased BMD in the lumbar spine (ff vs. FF: SMD (95% CI): -0.87 (-1.38, -0.35); P=0.001 for lumbar spine; -0.43 (-0.93, 0.06), P=0.086 for femoral neck). In contrast, we did not observe overall associations between VDR Bsm I and Apa I polymorphisms and BMD in either lumbar spine or femoral neck (Bsm I bb vs. BB: SMD (95% CI): 0.61 (-1.30, 2.53), P=0.531 for lumbar spine; Apa I aa vs. AA: SMD (95% CI): 0.66 (-0.16, 1.48), P=0.113 for lumbar spine). When subgroup analyses were conducted according to countries, Indians carrying the VDR Fok I ff genotype were at risk of low BMD at lumbar spine (ff vs. FF: SMD (95% CI): -0.57 (-0.85, -0.29), P0.001). Sensitivity analyses indicated that no single study had substantial influence on all combined analyses. In addition, no publication bias was identified.This meta-analysis indicated that VDR Fok I, rather than Bsm I and Apa I polymorphisms, is associated with bone mineral density in postmenopausal Asian women (especially for Indian women), and can probably be used with other genetic markers together to identify individuals at high risk of osteoporosis.

Well-defined pyrite FeS2 microcubes and micro-octahedra with high-yield and good uniformity were successfully synthesized by a convenient and simple polymer-assisted hydrothermal method. Employing S as sulfur source and FeCl2·4H2O as the precursor in the presence of polyvinylpyrrolidone (PVP) and polyvinyl alcohol (PVA), cube-shaped and octahedron-shaped pyrite FeS2 crystallites were successfully obtained by simply adjusting the NaOH concentration, and the size of the product can be readily tuned by varying the reaction parameters. The effects of various NaOH concentrations and the polymer dosage on the morphology evolution process were investigated systematically. The phase composition, morphology, structure, and properties of the as-obtained products were studied by X-ray diffraction, field emission scanning electron microscopy, (high-resolution) transmission electron microscopy, Fourier transform-infrared spectroscopy, X-ray photoelectron spectrometry, and UV-Vis spectrometry. It was found that besides the capping effect of the polymer reagents, the “synergistic effect” or “cooperative effect” between the PVA and the PVP also played a crucial role in directing the growth of the FeS2 crystallites. The possible formation mechanism of the FeS2 phase and morphology was tentatively proposed based on a series of contrast experiments. Moreover, the optical properties were also preliminarily studied. This method can be easily controlled and is expected to be extendable to the fabrication of other metal chalcogenides with controlled shape and structure.