In vitro evaluation of electrospun polyvinylidene fluoride hybrid nanoparticles as direct piezoelectric membranes for guided bone regeneration.

A polyvinylidene fluoride (PVDF) piezoelectric membrane containing carbon nanotubes (CNTs) and graphene oxide (GO) additives was prepared, with special emphasis on the piezoelectric activity of the aligned fibers. Fibroblast viability on membranes was measured to study cytotoxicity. Osteoprogenitor D1 cells were cultured, and mineralization of piezoelectric composite membranes was assessed by ultrasound stimulation. Results showed that the electrospun microstructures were anisotropically aligned fibers. As the GO content increased to 1.0 wt% (0.2 wt% interval), the ß phase in PVDF slightly increased but showed the opposite trend with the increase in CNT. Excessive addition of GO and CNT hindered the growth of the ß phase in PVDF. The direct piezoelectric activity and mechanical properties showed the same trend as the ß phase in PVDF. Moreover, GO/PVDF with the same nanoparticle content showed better performance than CNT/PVDF composites. In this study, a comparison of the generated piezoelectric specific voltage (unit: 10-3 Vg-1 cm-2, linear stretch, g33) with control PVDF only (0.55 ± 0.16) revealed that the two composites containing 0.8 wt% GO- and 0.2 wt% CNT- with 15 wt% PVDF exhibited excellent piezoelectric voltages, which were 3.37 ± 1.05 and 1.45 ± 0.07 (10-3 Vg-1 cm-2), respectively. In vitro cultures of these two groups in contact with D1 cells showed significantly higher alkaline phosphatase secretion than the PVDF only group within 1-10 days of cell culture. Further application of ultrasound stimulation showed that the piezoelectric membrane differentiated D1 cells earlier than without ultrasound and induced higher proliferation and mineralization. This developing piezoelectric effect is expected to generate voltage through activities to enhance microcurrent stimulation in vivo.

Effect of smoking and genetic polymorphisms interaction on the risk of esophageal squamous cell carcinoma / 上海预防医学

Esophageal squamous cell carcinoma （ESCC） is a malignant tumor caused by both environmental and genetic factors. Epidemiology studies have identified smoking as a major environmental risk factor. In recent years， the advancement of genomics research has led to the recognition of the influence of genetic variation in ESCC. We reviewed the research progress in smoking， genetic polymorphism and their interaction on susceptibility to ESCC. Reducing exposure time to tobacco was found to be the most effective way to reduce the risk. At the genetic level， mutations in DNA repair genes， regulation genes of carcinogen-metabolizing enzymes， cell cycle regulation genes， folate metabolism related genes， and alcohol metabolism related genes were found to significantly increase the risk of ESCC. However， studies on the interaction between smoking and genetic polymorphisms in ESCC risk are still limited， more studies are needed for better screening of the high-risk populations and the prevention.

Effect of smoking and genetic polymorphisms interaction on the risk of esophageal squamous cell carcinoma / 上海预防医学

Esophageal squamous cell carcinoma （ESCC） is a malignant tumor caused by both environmental and genetic factors. Epidemiology studies have identified smoking as a major environmental risk factor. In recent years， the advancement of genomics research has led to the recognition of the influence of genetic variation in ESCC. We reviewed the research progress in smoking， genetic polymorphism and their interaction on susceptibility to ESCC. Reducing exposure time to tobacco was found to be the most effective way to reduce the risk. At the genetic level， mutations in DNA repair genes， regulation genes of carcinogen-metabolizing enzymes， cell cycle regulation genes， folate metabolism related genes， and alcohol metabolism related genes were found to significantly increase the risk of ESCC. However， studies on the interaction between smoking and genetic polymorphisms in ESCC risk are still limited， more studies are needed for better screening of the high-risk populations and the prevention.

Longitudinal change of metabolite profile and its relation to multiple risk factors for the risk of developing hepatitis B-related hepatocellular carcinoma.

Despite considerable knowledge of viral pathogenesis, the pathophysiological changes related to the multifactorial, multistep process of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) development remains unclear. Longitudinal metabolomics study can reveal biological process for disease progression. We performed metabolite profiling with longitudinal prediagnostic plasma samples from two nested case-control studies of hepatitis B surface antigen carriers participating in ultrasound screening for HCC, one within a government employee cohort (870 samples from 109 HCC cases and 107 controls) and the other within a hospital-based cohort (266 samples from 63 HCC cases and 114 controls). Of the 34 measured metabolites, tyrosine, isoleucine, and glutamine were consistently associated with HCC. In analyses combining longitudinal data, a high metabolic risk score based on the three amino acids was robustly associated with increased risk of HCC (OR = 3.71, 95% confidence interval: 2.53-5.42), even after adjustment for clinical factors, or when assessed for different times up to ≥8 years before diagnosis. Similar association was observed in an independent, prospective analysis comprising 633 randomly selected individuals of the government employee cohort. More importantly, this metabolite signature was longitudinally influenced by HBV-infection phase and involved in gradual progression to liver fibrosis and cirrhosis. Furthermore, mediation analysis showed that the score mediated substantial proportions of the associations of key viral factors, insulin resistance, and diabetes status with HCC risk. Our results suggest that an amino-acid dysregulation metabotype may play a role in HBV-related HCC development, and may also be linked to common pathways that mediate increased HCC risks.

Potential-selective fate of 2D chiral crystallization on an electrode surface.

Molecular resolution STM is used to study the spatial structure and chirality of adsorbed Δ4,4-dicyclopenta[2,1-b:3,4-b]-dithiophene (TTE) on an Au(111) electrode, revealing an ordered, racemate adlayer made of homogeneously mixed R- and S-TTE on the (1 × 1) substrate and patches of R- or S-only TTE on the reconstructed Au(111) at more and less positive potentials.

Intracranial Rosai-Dorfman disease.

Rosai-Dorfman disease (RDD) is a rare histioproliferative disorder that only occasionally involves the central nervous system. We present the diagnosis and treatment of five patients with intracranial RDD. The patients were preoperatively misdiagnosed as meningioma or eosinophilic granuloma. All five patients were treated by total or subtotal surgical resection and none of them experienced recurrence. Histopathological examination showed a characteristic emperipolesis, the lymphocytes were engulfed in the S-100 protein and CD68 positive histiocytes, with negative expression of CD1a. Preoperative diagnosis of intracranial RDD is still challenging because the lesion is usually a dural-based lesion that mimics a meningioma. Surgical resection is an effective treatment and radiotherapy, steroid and chemotherapy has not demonstrated reliable therapeutic efficiency.

Isolated Intramedullary Spinal Rosai-Dorfman Disease: A Case Report and Literature Review.

BACKGROUND: Rosai-Dorfman disease (RDD) is a rare histioproliferative disorder that only occasionally involves the central nervous system. CASE DESCRIPTION: We present the diagnosis and treatment of an exceedingly rare case of isolated intramedullary spinal RDD that has been reported only 3 times previously. Moreover, it is the first time that intramedullary spinal RDD has been described in a child. The patient was treated by total surgical resection and experienced no recurrence during the 12-month follow-up. Histopathologic examination showed a characteristic emperipolesis; the lymphocytes were engulfed in the S-100-protein-positive histiocytes with negative expression of CD1a. CONCLUSIONS: Preoperative diagnosis of spinal RDD is still challenging because the lesion usually is a dura-based lesion that mimics a meningioma. Surgical resection is an effective treatment and radiotherapy; and steroid and chemotherapy have not demonstrated reliable therapeutic efficiency.

Rosai-Dorfman Disease of Rare Isolated Spinal Involvement: Report of 4 Cases and Literature Review.

BACKGROUND: Rosai-Dorfman disease (RDD) is a rare histioproliferative disorder that only occasionally involves the central nervous system (CNS). CASE DESCRIPTION: The diagnosis and treatment of 4 patients with isolated spinal RDD are discussed. All 4 patients were treated by total or subtotal surgical resection and none of them experienced recurrence. Histopathologic examination showed a characteristic emperipolesis, and the lymphocytes were engulfed in the S-100-protein-positive histiocytes with no expression of CD1a. CONCLUSIONS: Preoperative diagnosis of spinal RDD is still challenging because the lesion is usually a dura-based lesion that mimics a meningioma. Surgical resection is an effective treatment, and radiotherapy, steroid therapy, and chemotherapy have not shown reliable therapeutic efficiency.

The PD-1/B7-H1 pathway modulates the natural killer cells versus mouse glioma stem cells.

PURPOSE: Glioblastoma multiforme (GBM) is the most malignant primary type of brain tumor in adults. There has been increased focus on the immunotherapies to treat GBM patients, the therapeutic value of natural killer (NK) cells is still unknown. Programmed death-1 (PD-1) is a major immunological checkpoint that can negatively regulate the T-cell-mediated immune response. We tested the combination of the inhibiting the PD-1/B7H1 pathway with a NK-cell mediated immune response in an orthotopic mouse model of GBM. METHODS AND MATERIALS: Mouse glioma stem cells (GL261GSCs) and mouse NK cells were isolated and identified. A lactate dehydrogenase (LDH) assay was perfomed to detect the cytotoxicity of NK cells against GL261GSCs. GL261GSCs were intracranially implanted into mice, and the mice were stratified into 3 treatment groups: 1) control, 2) NK cells treatment, and 3) PD-1 inhibited NK cells treatment group. Overall survival was quantified, and animal magnetic resonance imaging (MRI) was performed to determine tumor growth. The brains were harvested after the mice were euthanized, and immunohistochemistry against CD45 and PCNA was performed. RESULTS: The mouse NK cells were identified as 90% CD3- NK1.1+CD335+ by flow cytometric analysis. In the LDH assay, the ratios of the damaged GL261GSCs, with the E:T ratios of 2.5:1, 5:1, and 10:1, were as follows: 1) non-inhibited group: 7.42%, 11.31%, and 15.1%, 2) B7H1 inhibited group: 14.75%, 18.25% and 29.1%, 3) PD-1 inhibited group: 15.53%, 19.21% and 29.93%, 4) double inhibited group: 33.24%, 42.86% and 54.91%. In the in vivo experiments, the mice in the PD-1 inhibited NK cells treatment group and IL-2-stimulated-NK cells treatment group displayed a slowest tumor growth (F = 308.5, P<0.01) and a slower tumor growth compared with control group (F = 118.9, P<0.01), respectively. The median survival of the mice in the three groups were as follows: 1) conrol group: 29 days, 2) NK cells treatment group: 35 days (P = 0.0012), 3) PD-1 inhibited NK cells treatment group: 44 days (P = 0.0024). Immunologic data of PCNA-positive cell ratios and CD45-positive cell ratios of the tumor specimens in the three groups were as follows: 1) control group: 65.72% (PCNA) and 0.92% (CD45), 2) NK treatment group: 27.66% (PCNA) and 13.46% (CD45), and 3) PD-1 inhibited NK cells treatment group: 13.66% (PCNA) and 23.66% (CD45) (P<0.001). CONCLUSION: The results demonstrated that blockade of PD-1/B7H1 pathway could promote mouse NK cells to kill the GL261GSCs, and the PD-1-inhibited NK cells could be a feasible immune therapeutic approach against GBM.

[Study on effect of snore guard to upper airway structure of normal occlusion people by magnetic resonance imaging].

OBJECTIVE: To investigate the imagery changes of the upper airway and the surrounding soft tissues of local adults with non-apnea who used snore guard and to provide experimental data for the clinical diagnosis and treatment of obstructive sleep apnea syndrome (OSAS). METHODS: Thirty students with non-apnea from Hebei medical university were chosen, and magnetic resonance imaging (MRI) was used to measure the changes of the upper airway and the surrounding soft tissues after snore guards were used. SPSS 105 software was used to analyze statistically. RESULTS: After the snore guard was put into oral cavity, the change of the average section and volume of the nasopharynx, the palatopharynx, the hypopharynx and the glossopharynx were statistically significant. The average sagittal size, the average horizontal size of the nasopharynx, the palatopharynx, the hypopharynx and the glossopharynx were increased statistically. The ratio of sagittal size, the horizontal sizand the in the hypopharynx and the glossopharynx changed statistically important. There was a decrease of the soft palate, the shape, the height, and the length of the tongue, the difference was statistically significant. The results demonstrated that snore guard affected the upper airway mainly by changing the volume and the shape of the upper airway, there was an obvious increase of the pharynx. The results also showed that snore guard could increase the width (both sagittal and horizontal) of the upper airway and could change the shape of the surrounding soft tissues, which caused air way more smooth. Snore guard could make the indexes of soft palate and tongue change decreasingly, resulted in the straight stand up of the tongue and the forwardness of the soft palate. CONCLUSION: Snore guard is an effective and convenient instrument for treating the patients with OSAS.