Publications by authors named "Ruyi Huang"

18 Publications

  • Page 1 of 1

The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation.

Immunity 2021 Jun 25;54(6):1168-1185.e8. Epub 2021 May 25.

Department of Hepatobiliary Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, Jiangsu Province, China; Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China. Electronic address:

Chronic inflammation plays a central role in hepatocellular carcinoma (HCC), but the contribution of hepatocytes to tumor-associated inflammation is not clear. Here, we report that the zinc finger transcription factor Miz1 restricted hepatocyte-driven inflammation to suppress HCC, independently of its transcriptional activity. Miz1 was downregulated in HCC mouse models and a substantial fraction of HCC patients. Hepatocyte-specific Miz1 deletion in mice generated a distinct sub-group of hepatocytes that produced pro-inflammatory cytokines and chemokines, which skewed the polarization of the tumor-infiltrating macrophages toward pro-inflammatory phenotypes to promote HCC. Mechanistically, Miz1 sequestrated the oncoprotein metadherin (MTDH), preventing MTDH from promoting transcription factor nuclear factor κB (NF-κB) activation. A distinct sub-group of pro-inflammatory cytokine-producing hepatocytes was also seen in a subset of HCC patients. In addition, Miz1 expression inversely correated with disease recurrence and poor prognosis in HCC patients. Our findings identify Miz1 as a tumor suppressor that prevents hepatocytes from driving inflammation in HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.immuni.2021.04.027DOI Listing
June 2021

Dairy foods, calcium, and risk of breast cancer overall and for subtypes defined by estrogen receptor status: a pooled analysis of 21 cohort studies.

Am J Clin Nutr 2021 May 8. Epub 2021 May 8.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA.

Background: Epidemiologic studies examining the relations between dairy product and calcium intakes and breast cancer have been inconclusive, especially for tumor subtypes.

Objective: To evaluate the associations between intakes of specific dairy products and calcium and risk of breast cancer overall and for subtypes defined by estrogen receptor (ER) status.

Method: We pooled the individual-level data of over 1 million women who were followed for a maximum of 8-20 years across studies. Associations were evaluated for dairy product and calcium intakes and risk of incident invasive breast cancer overall (n = 37,861 cases) and by subtypes defined by ER status. Study-specific multivariable hazard ratios (HRs) were estimated and then combined using random-effects models.

Results: Overall, no clear association was observed between the consumption of specific dairy foods, dietary (from foods only) calcium, and total (from foods and supplements) calcium, and risk of overall breast cancer. Although each dairy product showed a null or very weak inverse association with risk of overall breast cancer (P, test for trend >0.05 for all), differences by ER status were suggested for yogurt and cottage/ricotta cheese with associations observed for ER-negative tumors only (pooled HR = 0.90, 95% CI: 0.83, 0.98 comparing ≥60 g/d with <1 g/d of yogurt and 0.85, 95% CI: 0.76, 0.95 comparing ≥25 g/d with <1 g/d of cottage/ricotta cheese). Dietary calcium intake was only weakly associated with breast cancer risk (pooled HR = 0.98, 95% CI: 0.97, 0.99 per 350 mg/d).

Conclusion: Our study shows that adult dairy or calcium consumption is unlikely to associate with a higher risk of breast cancer and that higher yogurt and cottage/ricotta cheese intakes were inversely associated with the risk of ER-negative breast cancer, a less hormonally dependent subtype with poor prognosis. Future studies on fermented dairy products, earlier life exposures, ER-negative breast cancer, and different racial/ethnic populations may further elucidate the relation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/ajcn/nqab097DOI Listing
May 2021

Machine learning classifies predictive kinematic features in a mouse model of neurodegeneration.

Sci Rep 2021 Feb 17;11(1):3950. Epub 2021 Feb 17.

Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, 300 Stein Plaza, Ste. 536, Los Angeles, CA, 90095-6901, USA.

Motor deficits are observed in Alzheimer's disease (AD) prior to the appearance of cognitive symptoms. To investigate the role of amyloid proteins in gait disturbances, we characterized locomotion in APP-overexpressing transgenic J20 mice. We used three-dimensional motion capture to characterize quadrupedal locomotion on a treadmill in J20 and wild-type mice. Sixteen J20 mice and fifteen wild-type mice were studied at two ages (4- and 13-month). A random forest (RF) classification algorithm discriminated between the genotypes within each age group using a leave-one-out cross-validation. The balanced accuracy of the RF classification was 92.3 ± 5.2% and 93.3 ± 4.5% as well as False Negative Rate (FNR) of 0.0 ± 0.0% and 0.0 ± 0.0% for the 4-month and 13-month groups, respectively. Feature ranking algorithms identified kinematic features that when considered simultaneously, achieved high genotype classification accuracy. The identified features demonstrated an age-specific kinematic profile of the impact of APP-overexpression. Trunk tilt and unstable hip movement patterns were important in classifying the 4-month J20 mice, whereas patterns of shoulder and iliac crest movement were critical for classifying 13-month J20 mice. Examining multiple kinematic features of gait simultaneously could also be developed to classify motor disorders in humans.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-021-82694-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7889656PMC
February 2021

Mitochondrial genome of the Boulenger's Slug-eating snake (Serpentes: Pareidae).

Mitochondrial DNA B Resour 2020 Aug 12;5(3):3161-3162. Epub 2020 Aug 12.

Huangshan Noah Biodiversity Institute, Huangshan, China.

The Boulenger's Slug-eating snake is a species of snake in the family Pareidae. The complete mitochondrial genome sequence (mitogenome) of this species was determined by shotgun sequencing. The total length of mitogenome is 16,778 bp and contains 13 protein-coding genes, 22 tRNA genes, two ribosome RNA genes, and two control regions (CR). Its base composition was 31.6% for A, 24.6% for T, 14.5% for G and 29.3% for C. All the protein-coding genes in . were distributed on the H-strand, except for the ND6 subunit gene and eight tRNA genes which were encoded on the L-strand. The phylogenetic tree of . and 13 other related species was reconstructed using the maximum-likelihood (ML) method. The DNA data presented here will be useful to study the evolutionary relationships of . .
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/23802359.2020.1804471DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782912PMC
August 2020

Design, synthesis and biological evaluation of new ganglioside GM3 analogues as potential agents for cancer therapy.

Eur J Med Chem 2020 Mar 13;189:112065. Epub 2020 Jan 13.

Sorbonne Université, CNRS, IPCM, UMR 8232, 4 place Jussieu, 75005, Paris, France; Institute for Interdisciplinary Research, Jianghan University, Wuhan Economic and Technological Development Zone, Wuhan, 430056, China. Electronic address:

Ganglioside GM3 is well known as a tumor-associated carbohydrate antigen on several types of tumors. Many studies have demonstrated that GM3 plays roles in cells proliferation, adhesion, motility and differentiation, which is involved in the process of cancer development. In the present study, we developed methods to synthesize GM3 analogues conveniently. By enzymatic hydrolysis and chemical procedures, two novel analogues and two known analogues were synthesized, containing lactose and glucosamine. Then anti-proliferation and anti-migration activities were evaluated by cytotoxicity assays and wound healing tests, and the data demonstrated that these analogues exhibited anticancer activities. Based on our previous studies, the structure-activity relationships were discussed. This study could provide valuable sight to find new antitumor agents for cancer therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ejmech.2020.112065DOI Listing
March 2020

A Bioinspired Platform for Effective Delivery of Protein Therapeutics to the Central Nervous System.

Adv Mater 2019 May 25;31(18):e1807557. Epub 2019 Feb 25.

Department of Chemical and Biomolecular Engineering, University of California, Los Angeles, CA, 90095, USA.

Central nervous system (CNS) diseases are the leading cause of morbidity and mortality; their treatment, however, remains constrained by the blood-brain barrier (BBB) that impedes the access of most therapeutics to the brain. A CNS delivery platform for protein therapeutics, which is achieved by encapsulating the proteins within nanocapsules that contain choline and acetylcholine analogues, is reported herein. Mediated by nicotinic acetylcholine receptors and choline transporters, such nanocapsules can effectively penetrate the BBB and deliver the therapeutics to the CNS, as demonstrated in mice and non-human primates. This universal platform, in general, enables the delivery of any protein therapeutics of interest to the brain, opening a new avenue for the treatment of CNS diseases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/adma.201807557DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6701476PMC
May 2019

Programmed Cell Death Protein-1 Predicts the Recurrence of Breast Cancer in Patients Subjected to Radiotherapy After Breast-Preserving Surgery.

Technol Cancer Res Treat 2018 01;17:1533033818793425

1 Department of Surgery, Division of Thyroid and Mammary Surgery, the Affiliated Wuxi People's Hospital of Nanjing Medical University, China.

Radiotherapy is the most important component of the comprehensive treatment of breast cancer, and immunocompromised patients respond with lower response rate. However, the role of programmed cell death protein-1, a critical immune molecule, in recurrence of breast cancer subjected to radiotherapy is unknown. A retrospective analysis was designed to explore the relevance. A number of 42 patients with early-stage breast cancer undergoing breast-conserving surgery and postoperative radiotherapy (18 recurrence and 24 nonrecurrence) were recruited, and clinical data were obtained. Immunohistochemistry was employed to detect programmed cell death protein-1, and Kaplan-Meier curves were used to analyze recurrence-free survival. The expression of programmed cell death protein-1 was higher in the recurrence group than recurrence-free group ( P < .05). Meanwhile, the recurrence-free mean survival was significantly longer in programmed cell death protein-1 low-expression group (68 months) than that in programmed cell death protein-1 high-expression group (56 months). In addition, the levels of T lymphocytes were obviously lower in patients with breast cancer than healthy group, and natural killer showed an opposite tendency. CD4 decreased significantly after 1 week radiotherapy and recovered rapidly 3 weeks after radiotherapy. Compared to recurrence-free group, the increment of T lymphocytes were inadequate in recurrence group. These experimental results indicated that the expression of programmed cell death protein-1 in tumor-infiltrating lymphocytes is related to immune disorder and recurrence of patients undergoing breast-preserving surgery and radiotherapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1533033818793425DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102752PMC
January 2018

Prognostic Value of Phosphotyrosine Phosphatases in Hepatocellular Carcinoma.

Cell Physiol Biochem 2018 4;46(6):2335-2346. Epub 2018 May 4.

Liver Transplantation Center of the First Affiliated Hospital and Department of Hepatobilliary Surgery of Drum Tower Clinical Medical College, Nanjing Medical University, Nanjing, China.

Background/aims: During the occurrence and progression of hepatocellular carcinoma (HCC), phosphotyrosine phosphatases (PTPs) are usually described as tumor suppressors or proto-oncogenes, and to some degree are correlated with the prognosis of HCC.

Methods: A total of 321 patients from the Cancer Genome Atlas (TCGA) database and 180 patients from our validated cohort with hepatocellular carcinoma were recruited in this study. Kaplan-Meier, univariate and multivariate Cox proportional hazards model were used to evaluate the risk factors for survival. Quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) were applied to detect the expression levels of PTP genes.

Results: After screening the data of TCGA, we identified five PTPs as HCC overall survival related PTP genes, among which only three (PTPN12, PTPRN, PTPN18) exhibited differential expression levels in our 180 paired HCC and adjacent tissues (P< 0.001). Further analysis revealed that expression of PTPN18 was positively, but PTPRN was negatively associated with prognosis of HCC both in TCGA cohort and our own cohort. As to PTPN12, results turned out to be opposite according to HBV status. In detail, higher expression of PTPN12 was associated with better outcome in HBV group but worse prognosis in Non-HBV group.

Conclusion: Our results suggested that PTPN12, PTPRN and PTPN18 were independent prognostic factors in HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000489625DOI Listing
August 2018

14-3-3ζ delivered by hepatocellular carcinoma-derived exosomes impaired anti-tumor function of tumor-infiltrating T lymphocytes.

Cell Death Dis 2018 02 7;9(2):159. Epub 2018 Feb 7.

Liver Transplantation Center of the First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, 210029, China.

Increasing evidence shows that the anti-tumor functions of tumor-infiltrating T lymphocytes (TILs) were inhibited significantly, but the underlying mechanisms remain not fully understood. In this study, we found that 14-3-3ζ expression was up-regulated in hepatocellular carcinoma (HCC) cells and in TILs. TILs with 14-3-3ζ high-expression (14-3-3ζ) exhibited impaired activation (CD69), proliferation (Ki67) and anti-tumor functions compared to 14-3-3ζ low expression (14-3-3ζ) TILs. Flow cytometry assay showed that compared with 14-3-3ζ CD8T cells, 14-3-3ζ ones exhibited higher frequency of exhausted phenotypes as measured by inhibitory receptors such as PD-1, TIM-3, LAG3, and CTLA-4. 14-3-3ζ overexpression inhibited the activity and proliferation of peripheral blood CD3 T cells, deviated the differentiation of naive T cells from effector T cells to regulatory T cells. Moreover, we found that 14-3-3ζ expression levels in TILs correlated positively with those in HCC cells. Naive T cells co-cultured with HCC cells or the visible components of culture medium of HCC cells exhibited increased 14-3-3ζ expression. Stochastic optical reconstruction microscopy (STORM) and confocal assay showed that 14-3-3ζ-containing exosomes derived from HCC cells could be swallowed by T cells, suggesting that 14-3-3ζ might be transmitted from HCC cells to TILs at least partially through exosomes. In conclusion, our study for the first time demonstrated that 14-3-3ζ is up-regulated in and inhibited the anti-tumor functions of tumor-infiltrating T cells in HCC microenvironment and that 14-3-3ζ might be transmitted from HCC cells to T cells at least partially through exosomes.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41419-017-0180-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5833352PMC
February 2018

Improving agricultural straw preparation logistics stream in bio-methane production: experimental studies and application analysis.

3 Biotech 2017 Oct 16;7(5):283. Epub 2017 Aug 16.

Biogas Institute of Ministry of Agriculture (BIOMA), Chengdu, 610041 People's Republic of China.

Long-term production in commercial straw biogas plants has been rare in China due to inefficiencies in the logistics stream. Biomass densification could be a potential solution to this issue. Therefore, we conducted a study to evaluate whether biomass densification is a more efficient and sustainable option. We performed methane production experiments to investigate fermentation characteristics of briquettes (with a new pretreatment, model II) and rubs (with a common pretreatment, model I). A 3000-m biogas plant was used to conduct a comparative analysis with solar eMergy joules. Results showed that the methane yield of briquettes of corn stover was 66.74% higher than that of rubs, and the briquettes had better digestion performance in terms of CH content, VFA, and alcohol. The two models required almost the same eMergy investment input, while model II obtained a greater quantity of net eMergy (16.5% higher) in comparison with model I. The net eMergy yield ratio (EYR) (biogas only) of model I and model II was 0.99 and 1.67, respectively, showing less market competitiveness for commercial operations with model I. Meanwhile, the logistic costs of model II could be reduced to approximately US $34,514 annually.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s13205-017-0914-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5559389PMC
October 2017

Alpha1-ACT Functions as a Tumour Suppressor in Hepatocellular Carcinoma by Inhibiting the PI3K/AKT/mTOR Signalling Pathway via Activation of PTEN.

Cell Physiol Biochem 2017 26;41(6):2289-2306. Epub 2017 Apr 26.

Background & Aims: To investigate the expression and prognostic value of α1-ACT (Alpha1-antichymotrypsin) in patients with HCC (hepatocellular carcinoma) and identify the mechanism by which α1-ACT inhibits proliferation and promotes apoptosis of HCC.

Methods: We first measured α1-ACT expression levels and determined their relationship with the clinicopathological characteristics and prognosis of patients with HCC.We then established stable HCC cell lines with both α1-ACT overexpression and knockdown and performed a functional analysis in vitro.We first examined the relationship between α1-ACT and the PTEN/PI3K/AKT/mTOR pathway using Western blotting. Then, we determined whether α1-ACT can directly bind to PTEN using co-immunoprecipitation. Finally, we measured α1-ACT expression to evaluate its correlation with the PI3K/AKT/mTOR pathway-related apoptosis proteins in a xenograft tumour mouse model using immunohistochemistry.

Results: The α1-ACT expression level was significantly lower in the HCC tissues than in the paratumour tissues and was negatively positively correlated with the level of Ki67, AFP, the AJCC stage, tumour size and tumour invasion. The overexpression of α1-ACT can inhibit cell proliferation and increase cell apoptosis by activating PI3K/AKT/mTOR-mediated apoptosis via binding to PTEN and activating it in vitro. Additionally, the overexpression of α1-ACT can also increase the proportion of cells in the G0/G1 stage by increasing cyclin p21 expression and inhibiting the migration and invasion abilities of HCC cells by regulating MMP2 and MMP9. The xenotransplantation studies with nude mice also showed that overexpression of α1-ACT inhibited tumourigenesis and knockdown of α1-ACT had the opposite effect.

Conclusions: Our study demonstrates that α1-ACT suppresses liver cancer development and metastasis via targeting the PTEN/PI3K/AKT/mTOR signalling pathway, which may be a potential target for therapeutic intervention in HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000475648DOI Listing
July 2017

Prognostic value of marital status on stage at diagnosis in hepatocellular carcinoma.

Sci Rep 2017 01 31;7:41695. Epub 2017 Jan 31.

Liver Transplantation Center of the First Affiliated Hospital and State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu Province, P.R. China.

Marital status have been found as an independent prognostic factor for survival and spousal support could provide a survival advantage in various cancer types. However, the specific effect of marital status on survival in hepatocellular carcinoma (HCC) has not been explored in detail. In this study, we used the Surveillance, Epidemiology and End Results program to identify iagnosed with HCC between 1988 and 2007. Kaplan-Meier methods and multivariable Cox regression models were used to analyze long-term cancer-specific survival (CSS) outcomes and risk factors stratified by marital status. There were significant differences among these different marital status subgroups with regard to 5-year CSS rates (P < 0.001). Married HCC patients had a better 5 year CSS rate than those unmarried patients, and widowed patients were more likely to die of their cancer. A stratified analysis showed that widowed patients always had the lowest CSS rate across different cancer stage, age and gender subgroups. Even after adjusting for known confounders, unmarried patients were at greater risk of cancer-specific mortality. Social support aimed at this population could improve the likelihood of achieving cure.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/srep41695DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282486PMC
January 2017

Down-Regulation of LncRNA DGCR5 Correlates with Poor Prognosis in Hepatocellular Carcinoma.

Cell Physiol Biochem 2016 30;40(3-4):707-715. Epub 2016 Nov 30.

Key Laboratory on Living Donor Liver Transplantation, Ministry of Health, Department of Liver surgery, Collaborative Innovation Center For Cancer Personalized Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China.

Background/aims: Long non-coding RNAs (lncRNAs) have been reported to play pivotal roles in multiple tumors and can act as tumor biomarkers. In this study, we explored the association of the expression of an lncRNA, DGCR5 with clinicopathological features and prognosis in HCC.

Methods: Expression levels of DGCR5 were detected by quantitative real-time PCR (qRT-PCR) and the clinical data was obtained, including basic information, data of clinicopathology and cancer specific survival rate. Receiver operating characteristic (ROC) curve, Kaplan-Meier methods and multivariable Cox regression models were used to analyze predictive efficiency, long-term survival outcomes and risk factors.

Results: DGCR5 was found down-regulated in HCC tissues (P<0.001) and serum (P = 0.0035) and low expression of DGCR5 was correlated with a poor cancer specific survival (CSS) (P = 0.0019), as the overall 5-year CSS rates were 10.3% (low expression group) and 36.6% (high expression group), respectively. A stratified analysis demonstrated that low DGCR5 expression was an independent negative prognostic factor for HCC. In addition, the area under the ROC curve was 0.782 with a sensitivity of 0.633 and a specificity of 0.833.

Conclusions: Our results suggest that DGCR5 may be a participator in HCC and can serve as potential biomarker for the diagnosis and prognosis in HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000452582DOI Listing
February 2017

Effects of Treatment of Treadmill Combined with Electro-Acupuncture on Tibia Bone Mass and Substance PExpression of Rabbits with Sciatic Nerve Injury.

PLoS One 2016 23;11(11):e0164652. Epub 2016 Nov 23.

Program in Physical Therapy, Washington University School of Medicine, St. Louis, Missouri, United States of America.

The peripheral nervous system may play an important role in normal bone maintenance and remodeling. Substance P (SP) is a neuropeptide associated with bone loss and formation that may mediate the effects of the nervous system. The purpose of this study is to determine if treadmill running combined with electro-acupuncture at Jiaji acupoints (Jiaji-EA) affects tibial bone mass and SP expression in rabbits with sciatic nerve injury. Twenty-four juvenile male New Zealand white rabbits were randomly assigned to one of 4 groups: sham injury control (sham), sciatic never crush control (SNCr), treadmill running (treadmill), and Jiaji-EA combined with treadmill running (ET group). The SNCr, treadmill, and ET groups all had an induced sciatic never crush injury of approximately 2mm. Control groups received no intervention; the treadmill and ET groups were trained by treadmill; the ET group also received Jiaji-EA. After the 4 weeks of treatment, toe-spreading index (TSI), BMD, bone strength, and SP expression in the tibia were significantly lower in the nerve injury groups (SNCr, treadmill, and ET) compared to the sham groups (p<0.05). Treatment (treadmill and ET groups) increased all measures compared to the SNCr group (p<0.05). Further, TSI, BMD, bone strength, and SP expression in the ET group were higher than the treadmill group (p<0.05). Our results indicate that treadmill therapy combined with electro-acupuncture at Jiaji acupoints prevents bone loss in rabbit tibias after sciatic nerve injury. This may occur in two ways: indirectly in association with axon regeneration and directly via loading on the bone mediated through increased SP expression. This study provides important evidence for the clinical treatment of bone loss after peripheral nerve injury.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0164652PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5120789PMC
June 2017

Clinical outcome following DIAM implantation for symptomatic lumbar internal disk disruption: a 3-year retrospective analysis.

J Pain Res 2016 31;9:917-924. Epub 2016 Oct 31.

Department of Neurosurgery, E-Da Hospital; Department of Neurosurgery, E-Da Cancer Hospital, College of Medicine, I-Shou University, Kaohsiung, Taiwan.

Background/objective: Internal disk disruption (IDD), an early event of lumbar disk degeneration, is the most common cause of low back pain. Since increased intradiskal pressure (IDP) is associated with symptoms and progression of disk degeneration, unloading a painful disk with an interspinous process device (IPD) is a rational treatment option. The goal of this study was to evaluate the effectiveness of dynamic stabilization with an IPD in the treatment of symptomatic IDD of the lumbar spine.

Patients And Methods: Patients with symptomatic IDD were treated with implantation of an IPD, the device for intervertebral assisted motion (DIAM). Diagnosis of IDD was based on typical MRI finding of posterior annular high-intensity zone and positive provocative test on discography. IDP was analyzed intraoperatively. Axial back and leg pain was evaluated with visual analog scale, functional status with Oswestry Disability Index, and final clinical outcomes with Odom criteria. Data from 34 patients followed up for at least 3 years were collected.

Results: DIAM implantation significantly reduced IDP (n=11, <0.0001). All 34 patients reported symptom relief. Thirty-one patients (91%) remained symptom free until the last followups. Three patients (9%) experienced recurrence of pain, of which the causes were unrelated to the IDD or surgery. Disk status at the DIAM-implanted segments remained stable. Segmental flexion/extension mobility was preserved in 27 of 30 patients with preoperative mobility. No proximal or distal adjacent segment degeneration was observed. The final clinical outcomes were excellent/good in 31 and fair/poor in three patients.

Conclusion: For patients with symptomatic IDD, dynamic stabilization with DIAM provides pain relief and functional improvement. The implantation maintains disk status and prevents progression of disk degeneration, without compromising segmental flexion/extension mobility or causing adjacent segment degeneration.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/JPR.S115847DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5096761PMC
October 2016

Modulation of respiratory output by cervical epidural stimulation in the anesthetized mouse.

J Appl Physiol (1985) 2016 12 7;121(6):1272-1281. Epub 2016 Oct 7.

Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California;

Respiration is produced and controlled by well-characterized brain stem nuclei, but the contributions of spinal circuits to respiratory control and modulation remain under investigation. Many respiratory studies are conducted in in vitro preparations (e.g., brain stem slice) obtained from neonatal rodents. While informative, these studies do not fully recapitulate the complex afferent and efferent neural circuits that are likely to be involved in eupnea (i.e., quiet breathing). To begin to investigate spinal contributions to respiration, we electrically stimulated the cervical spinal cord during unassisted respiration in anesthetized, intact mice. Specifically, we used epidermal electrical stimulation at 20 Hz and varied current intensity to map changes in respiration. Stimulating at 1.5 mA at cervical level 3 (C3) consistently caused a significant increase in respiratory frequency compared with prestimulation baseline and when compared with sham stimulations. The increase in respiratory frequency persisted for several minutes after epidural stimulation ceased. There was no change in tidal volume, and the estimated minute ventilation was increased as a consequence of the increase in respiratory frequency. Sigh frequency also increased during epidural stimulation at C3. Neither the increase in respiratory frequency nor the increase in sighing were observed after stimulation at other dorsal cervical levels. These findings suggest that the spinal circuits involved in the modulation of eupnea and sighing may be preferentially activated by specific endogenous inputs. Moreover, the cervical spinal cord may play a role in respiratory modulation that affects both eupneic respiration and sigh production in intact, adult mice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1152/japplphysiol.00473.2016DOI Listing
December 2016

Associated Links Among Smoking, Chronic Obstructive Pulmonary Disease, and Small Cell Lung Cancer: A Pooled Analysis in the International Lung Cancer Consortium.

EBioMedicine 2015 Nov;2(11):1677-85

Background: The high relapse and mortality rate of small-cell lung cancer (SCLC) fuels the need for epidemiologic study to aid in its prevention.

Methods: We included 24 studies from the ILCCO collaboration. Random-effects panel logistic regression and cubic spline regression were used to estimate the effects of smoking behaviors on SCLC risk and explore their non-linearity. Further, we explored whether the risk of smoking on SCLC was mediated through COPD.

Findings: Significant dose-response relationships of SCLC risk were observed for all quantitative smoking variables. Smoking pack-years were associated with a sharper increase of SCLC risk for pack-years ranged 0 to approximately 50. The former smokers with longer cessation showed a 43%quit_for_5-9 years to 89%quit_for_≥ 20 years declined SCLC risk vs. subjects who had quit smoking < 5 years. Compared with non-COPD subjects, smoking behaviors showed a significantly higher effect on SCLC risk among COPD subjects, and further, COPD patients showed a 1.86-fold higher risk of SCLC. Furthermore, smoking behaviors on SCLC risk were significantly mediated through COPD which accounted for 0.70% to 7.55% of total effects.

Interpretation: This is the largest pooling study that provides improved understanding of smoking on SCLC, and further demonstrates a causal pathway through COPD that warrants further experimental study.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ebiom.2015.09.031DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740296PMC
November 2015

Utilization of a Cloud-Based Diabetes Management Program for Insulin Initiation and Titration Enables Collaborative Decision Making Between Healthcare Providers and Patients.

Diabetes Technol Ther 2016 Feb 8;18(2):59-67. Epub 2015 Dec 8.

4 MIT Media Lab , Cambridge, Massachusetts.

Background: Overseeing proper insulin initiation and titration remains a challenging task in diabetes care. Recent advances in mobile technology have enabled new models of collaborative care between patients and healthcare providers (HCPs). We hypothesized that the adoption of such technology could help individuals starting basal insulin achieve better glycemic control compared with standard clinical practice.

Materials And Methods: This was a 12 ± 2-week randomized controlled study with 40 individuals with type 2 diabetes who were starting basal insulin due to poor glycemic control. The control group (n = 20) received standard face-to-face care and phone follow-up as needed in a tertiary center, whereas the intervention group (n = 20) received care through the cloud-based diabetes management program where regular communications about glycemic control and insulin doses were conducted via patient self-tracking tools, shared decision-making interfaces, secure text messages, and virtual visits (audio, video, and shared screen control) instead of office visits.

Results: By intention-to-treat analysis, the intervention group achieved a greater hemoglobin A1c decline compared with the control group (3.2 ± 1.5% vs. 2.0% ± 2.0%; P = 0.048). The Diabetes Treatment Satisfaction Questionnaire showed a significant improvement in the intervention group compared with the control group (an increase of 10.1 ± 11.7 vs. 2.1 ± 6.5 points; P = 0.01). HCPs spent less time with patients in the intervention group compared with those in the control group (65.9 min per subject vs. 81.6 min per subject). However, the intervention group required additional training time to use the mobile device.

Conclusions: Mobile health technology could be an effective tool in sharing data, enhancing communication, and improving glycemic control while enabling collaborative decision making in diabetes care.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/dia.2015.0160DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753582PMC
February 2016