News Article | December 2, 2016
The International Association of HealthCare Professionals is pleased to welcome Robert Roy Recker, MD, FACE, MACP, Endocrinologist, to their prestigious organization with his upcoming publication in The Leading Physicians of the World. He is a highly trained and qualified endocrinologist with an extensive expertise in all facets of his work. Dr. Robert Roy Recker has been in practice for more than 53 years and is currently serving as a Professor of Medicine and Endocrinologist at Alegent Creighton Clinic in Omaha, Nebraska. Additionally, he is affiliated with Creighton University Medical Center. Dr. Recker graduated with his Medical Degree in 1963 from the Creighton University School of Medicine in Omaha, Nebraska where he is now currently working. Following his graduation, Dr. Recker completed his internship at Wilford Hall USAF Hospital, prior to completing his residency and then fellowship at Creighton University School of Medicine and Affiliated Hospital. Dr. Recker holds board certification by the American Board of Internal Medicine, is nationally renowned as an expert in endocrinology, diabetes and metabolism, and is renowned as one of America’s foremost experts on osteoporosis and postmenopausal osteoporosis. He is the Director of the Osteoporosis Research Center, and Associate Editor of BONE journal. Dr. Recker has had many articles published in this area, and has earned the coveted title of Fellow of the American College of Endocrinology, and Master of the American College of Physicians. Dr. Recker attributes his great success to his research skills as well as his desire to make a difference. When he is not working, Dr. Recker enjoys skiing and sailing. Learn more about Dr. Recker by reading his upcoming publication in The Leading Physicians of the World. FindaTopDoc.com is a hub for all things medicine, featuring detailed descriptions of medical professionals across all areas of expertise, and information on thousands of healthcare topics. Each month, millions of patients use FindaTopDoc to find a doctor nearby and instantly book an appointment online or create a review. FindaTopDoc.com features each doctor’s full professional biography highlighting their achievements, experience, patient reviews and areas of expertise. A leading provider of valuable health information that helps empower patient and doctor alike, FindaTopDoc enables readers to live a happier and healthier life. For more information about FindaTopDoc, visit http://www.findatopdoc.com
Zhang Y.,PLA Fourth Military Medical University |
Wang J.-H.,Affiliated Hospital |
Lu Q.,PLA Fourth Military Medical University |
Wang Y.-J.,PLA Fourth Military Medical University
Oncology Reports | Year: 2012
In non-small cell lung cancer (NSCLC) certain molecular characteristics, which are related to molecular alterations have been investigated. These are responsible for both the initiation and maintenance of the malignancy in lung cancer. The aim of this study was to evaluate the influence of Bag3 (Bcl-2 associated athanogene 3) in the regulation of apoptosis on NSCLC. Bag3 and Hsp70 expression were examined by immunohistochemistry to confirm their potential roles in the prevalence of NSCLC. We also established human normal bronchial epithelial cells and HOP-62 cell line as the model to analyze cell apoptosis and the expression of Hsp70, Bcl-X L and Bcl-2, which were affected by Bag3. In this study, we found that Bag3 and Hsp70 are highly expressed in few tissues and cell lines of NSCLC. Bag3 inhibits apoptosis in human normal bronchial epithelial cell lines and sustain the survival of NSCLC cells. Bag3, Hsp70, Bcl-X L and Bcl-2 are up-regulated in NSCLC cell lines. At the same time, the silencing of Bag3 results in diminishing protein levels of Bcl-X L and Bcl-2. The results of immunoprecipitation identified that Bag3 could interact with Hsp70, Bcl-X L and Bcl-2 NSCLC cells directly or indirectly. We conclude that NSCLC cells were protected from apoptosis through increasing Bag3 expression and consequently promoted the expression of Bcl-X L and Bcl-2.
Zhang B.,Dalian Medical University |
Zhang X.,Dalian Medical University |
Tang B.,Shandong Cancer Hospital |
Zheng P.,Affiliated Hospital |
And 2 more authors.
Breast Cancer Research and Treatment | Year: 2012
Endocrine therapy is an important therapeutic approach for the treatment of oestrogen receptor (ER)- positive breast cancer. However, a number of these endocrine therapies can fail when the tumour loses its ER expression during treatment. To date, few studies have explored the potential clinical significance of traditional Chinese medicine in inducing the reversal of resistance to endocrine therapy in breast cancers. We used the ERαnegative MCF7 breast cancer cell line to create a tamoxifen (TAM)-resistant cell line, MCF7/TAM cells. After treating MCF7/TAM cells with ELE to induce the re-expression of ERα, we investigated the role and molecular mechanisms by which elemene (ELE) promotes the reversal of resistance to endocrine therapy. We discovered that treatment with 10 lg/ml ELE restored the sensitivity of MCF7/TAM cells to TAM. RT-PCR analysis revealed that ELE treatment upregulated ERα mRNA levels in MCF7/TAM cells, and immunohistochemistry confirmed the upregulation of ERα expression. Western blot analysis revealed that ELE treatment decreased the protein expression levels of Ras, MEK1/2 and p-ERK1/2 in MCF7/TAM cells. The loss of ERα expression was the primary reason for TAM resistance in MCF7 cells. The ELE-induced reversal of TAM resistance was mediated by the upregulation of ERα mRNA and the re-expression of ERα through the MAPK pathway. © Springer Science+Business Media New York 2012.
Wang L.,Fudan University |
Qiu X.-M.,Fudan University |
Hao Q.,Fudan University |
Li D.-J.,Fudan University |
Li D.-J.,Affiliated Hospital
Cell Death and Disease | Year: 2013
Bu-Shen-Ning-Xin Decoction (BSNXD) administration has alleviated the early pathologic damage of atherosclerosis by inhibiting the adhesion molecule expression and upregulating the estrogen receptor (ER) b expression in endothelial cells, and increasing the serum nitric oxide (NO) level without any effect on serum lipid status, endometrium and fat deposition in liver in ovariectomized rabbits. The BSNXD-derived serum increases ER b expression in the human umbilical vein endothelial cells (HUVECs), and decreases malondialdehyde (MDA) production, and upregulates eNOS expression then increases NO synthesis through ERβ-dependent pathway. NO not only suppresses the LPS-induced NF-kb transcription in HUVECs, but also decreases apoptosis of endothelial cells. The BSNXD-derived serum decreases monocyte chemoattractant protein-1 production, and suppresses cell adhesion molecules (ICAM-1, VCAM-1 and E-selectin) expression in HUVECs injured by oxidized low-density lipoproteins (ox-LDL), and these effects can be abolished by ERβ antagonist (R,RTHC) and NO synthase inhibitor (L-NAME). The BSNXD-derived serum-treated HUVECs supernatant reduces CCR2, LFA-1 and VLA-4 expression in monocytes cell line U937 cells, which in turn inhibits adherence of U937 to injured endothelial cells. NO synthesis increases, and MDA production decreases through ERβ-mediated pathway that suppresses apoptosis and NF-kb activity in endothelial cells that downregulates adhesion molecules expression on endothelial cells via ERβ/NO/NF-kb pathway, and in turn leukocyte adhesion, which suggests BSNXD potential value in prophylaxis atherosclerosis. © 2013 Macmillan Publishers Limited.
Huang T.,Affiliated Hospital |
Chen Z.,Affiliated Hospital |
Fang L.,Jinling Hospital of Nanjing
Oncology Reports | Year: 2013
Epithelial-mesenchymal transition (EMT) is considered a critical event in cancer cell invasion and metastasis. Emerging evidence has shown that curcumin may prevent or delay the progression of cancer, an effect that may be partially due to its ability to disrupt EMT, yet this has not yet been demonstrated. In this study, we used lipopolysaccharide (LPS) to trigger EMT in MCF-7 and MDA-MB-231 breast cancer cell lines and showed that curcumin inhibited LPS-induced morphological changes, decreased the expression of LPS-induced markers of EMT such as vimentin, and increased the expression of E-cadherin, resulting in the inhibition of in vitro cell motility and invasiveness. We discovered that these actions were mediated through the inactivation of NF-?B-Snail signaling pathways. Our results indicate that curcumin plays an important role in the inhibition of LPS-induced EMT in breast cancer cells through the downregulation of NF-?B-Snail activity. These data provide a new perspective of the anti-invasive mechanism of curcumin, indicating that the effect is partly due to its ability to attack the EMT process.
Zhao Z.-K.,Affiliated Hospital
Chinese Journal of Pathology | Year: 2010
Objective To study the therapeutic efficacy of siRNA fragments silencing p75 neurotrophin receptor ( p75 NTR ), which may be a key regulator of glioma cell apoptosis and invasion. Methods The siRNA sequence fragments targeting p75 NTR were designed and transferred into human glioma cell line U251. RT-PCR and immuocytochemistry method were used to explore the expression of p75 NTR mRNA and protein. Cell adhesion assay was employed to detect cellular adhesion ability, and son agar clone formation assay was adopted to identify oncogenicity ,and a U251 glioma model was established in nude mice. The intracranial tumor volume was detected by MRI. The expression of p75 NTR, NGF and cyclin D2 were identified using immunohistochemistry. Cell apoptosis was detected by apoptosis kit in situ. Results The siRNA fragments targeting p75 NTR were capable of decreasing mRNA and protein expression of p75 NTR in U251 glioma cell line. Both the cellular adhesion ability and oncogenicity were weakly relevant The p75 NTR expression level was negatively correlated with cyclin D2 and apoptosis, and positively correlated with NGF expression. The siRNA sequence fragments targeting p75 NTR were effective in decreasing the gross volume of tumor; prolonged the survival time of mice, and the edge of tumor was much sharper than that of the control group. Conclusions The gene silencing technique by siRNA targeting p75 NTR is capable of decreasing tumor invasion and cell proliferation as well ais inducing cell apoptosis. It is expected to be a new choice for glioma gene therapy.
Zhu J.J.,Affiliated Hospital
Zhonghua nan ke xue = National journal of andrology | Year: 2012
To investigate the influence of temperature on the expressions of c-kit and PI3K in spermatogonia cultured in vitro at 32 degrees C and 37 degrees C, and provide basic scientific data for the mechanism of spermatogenic impairment due to body temperature (37 degrees C). Isolated spermatogenic cells were cultured in vitro at 32 degrees C and 37 degrees C, and their adherence, proliferation and morphologic changes were observed and recorded under the inverted phase contrast microscope. At 8 days, the spermatogonia were separated by Percoll density gradient centrifugation and the differential adhesion method. The expressions of c-kit and PI3K mRNA and proteins in the separated cells were detected by real time polymerase chain reaction and Western blot, respectively. The c-kit gene was sequenced to identify the occurrence of mutations. Adherence, division and proliferation of the cells were observed in both the 32 degrees C and 37 degrees C groups. The expressions of c-kit and PI3K mRNA and proteins in the spermatogonia were significantly higher in the 32 degrees C group than in the 37 degrees C group (P < 0.05). The 32 degrees C group showed no mutation of c-kit in exon 9, 11 and 13; the 37 degrees C group exhibited no mutation in exon 11 and 13, but possible insertion or deletion mutations in exon 9. Culturing in vitro at 37 degrees C could inhibit the expression of proliferation- and differentiation-related genes in spermatogenic cells and lead to the mutation of the c-kit gene.
Wang Y.,Affiliated Hospital
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] | Year: 2012
To explore the correlation between single nucleotide polymorphisms (SNPs) of interleukin-28B (IL-28B) gene and the susceptibility to primary hepatocellular carcinoma (HCC). A total of 300 histologically confirmed HCC cases (from November 2001 to April 2010) and 310 healthy controls with no history of chronic hepatitis B or hepatocellular carcinoma (2009-2010) were selected from a hospital in Guilin and a hospital in Beijing for this case-control study.139 HCC patients in the case group had complete clinical tracking data. All the subjects were Han Chinese, with no age or gender restrictions.2 ml peripheral blood samples were drawn from each subject with informed consent. SNP of rs12972991, rs4803223, rs8099917 and rs12979860 four loci in IL-28B gene were analyzed by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF). The frequencies of C allele at rs12972991, G allele at rs8099917 and G allele at rs4803223 were 6.7% (40/598), 7.9% (47/598) and 10.0% (59/588) respectively in case group; all higher than the corresponding frequencies in control group, separately 2.9% (18/618), 4.1% (25/616) and 3.6% (21/608). The differences were statistically significant (χ2=9.542, 7.858, 20.736, P values all<0.05). The above alleles could increase the risk of HCC, and the OR (95%CI) values were separately 1.67 (1.13-2.46), 1.49 (1.08-2.06) and 2.91 (1.79-4.72). The genotype frequencies of AC+CC at rs12972991, GT+GG at rs8099917, GA+GG at rs4803223 were 13.0% (39/299), 14.7% (44/299) and 19.0% (56/296) respectively in case group; while the frequencies were lower in control group, separately 5.8% (18/309), 8.1% (25/308) and 6.6% (20/304). The differences were statistically significant (χ2=9.319, 6.557, 20.948, P values all<0.05). These genotypes may increase the risk of HCC, and the adjusted OR (95%CI) values were 2.24 (1.31-3.83), 1.81 (1.14-2.88) and 2.90 (1.78-4.70), respectively. The stratified analysis of the clinical data indicated that the frequency of genotype GA+GG at rs4803223 was 50.0% (13/26) in patients of tumor thrombosis in portal vein (TTPV), higher than the frequency of genotype AA (21.1%, 23/109). The difference was statistically significant (χ2=8.965, P=0.003). The results suggested that IL-28B gene polymorphisms was correlated to the susceptibility to HCC in Chinese Han ethnic population. Among them, GA + GG genotype at rs4803223 could increase the risk of TTPV in HCC patients.
Wei L.Q.,Affiliated Hospital
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences | Year: 2011
To investigate the effects of atorvastatin on matrix metalloproteinase-9 (MMP-9) and the tissue inhibitor-1 of matrix metalloproteinase (TIMP-1) levels in bronchoalveolar lavage fluid (BALF) and serum of rats with experimental pulmonary fibrosis. Pulmonary fibrosis was induced by intratracheal administration of bleomycin in 30 female rats, which were further divided into two groups: Group M (without treatment) and Group A (treated with atorvastatin 10 mg/kg); control group (n = 5, Group C) was intratracheally administrated with same volume of saline. Five animals were sacrificed at 2 weeks (M2 and A2), 4 weeks (M4 and A4) and 6 weeks (M6 and A6) after model establishment, respectively. Lung tissue samples were harvested and prepared for HE and Masson's trichrome staining. Concentrations of MMP-9 and TIMP-1 in BALF and serum were measured by ELISA. The severity of inflammation and pulmonary fibrosis was significantly reduced in Group A than that in Group M, especially at week 6. No significant difference was noted in the serum concentrations of MMP-9 and TIMP-1 among the Group M, A and Group C. The BALF concentrations of MMP-9 in Group M2 and M6 were significantly higher than those in Group C (P < 0.01 and 0.05), whereas those in the atorvastatin groups (A2, A4 and A6) were lower than those in M2, M4 and M6. Although the MMP-9 was still higher in Groups A2 and A4 than in the Group C, there was no significant difference in MMP-9 between Group A6 and Group C. TIMP-1 levels in BALF were significantly higher in M4 and M6 than Group C (P < 0.01 and 0.05), there were no significant differences between Group M2 and Group C. The TIMP-1 levels in BALF of atorvastatin groups were significantly lower than those of model groups and control group (P < 0.01 and 0.05), which resulted in a significantly increased ratio of MMP-9 to TIMP-1 in the atorvastatin groups. Atorvastatin inhibits the synthesis and release of MMP-9 and TIMP-1 in the lung tissue of rats with bleomycin-induced pulmonary fibrosis, and has no significant effect on circulating MMP-9 and TIMP-1, which may be associated with the attenuation of experimental pulmonary fibrosis in rats.
Qin Y.,Affiliated Hospital
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2013
To investigate the levels of FasL mRNA in peripheral blood mononualear cells (PBMCs), serum soluble Fas ligand (sFasL) and their regulatory effect on T lymphocyte subsets in patients with severe acute pancreatitis (SAP). Forty-eight patients with pancreatitis were randomly divided into two groups: 20 cases with SAP and 28 cases with mild acute pancreatitis (MAP). Twenty-eight healthy volunteers were selected as control group. The expression of FasL mRNA in PBMCs was detected by real-time quantitative PCR(qRT-PCR), and serum sFasL was measured by ELISA. T lymphocyte subsets in peripheral blood were detected by flow cytometry. Compared with control group and MAP group, FasL mRNA of PBMCs and serum sFasL increased significantly in SAP group (P<0.05), a little increase in MAP group, and there was no significant difference between MAP group and control group (P>0.05). The CD4(+) T cell ratio, CD4(+)/CD8(+) ratio decreased significantly in SAP group (P<0.05) vs control group and MAP group), and they were found negatively related to FasL mRNA, serum sFasL level. The SAP patients showed the significantly increased FasL mRNA of PBMCs and serum sFasL and decreased CD4(+) T-cell ratio, CD4(+)/CD8(+) ratio. FasL may mediate the apoptosis of T lymphocytes.