Robert S Weinstein

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. pmc Glucocorticoid-induced osteoporosis and osteonecrosis
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, and Central Arkansas Veterans Healthcare System at the University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, AR 72205 7199, USA
    Endocrinol Metab Clin North Am 41:595-611. 2012
  2. pmc Glucocorticoid-induced osteonecrosis
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Endocrine 41:183-90. 2012
  3. pmc Glucocorticoids, osteocytes, and skeletal fragility: the role of bone vascularity
    Robert S Weinstein
    Department of Internal Medicine and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Bone 46:564-70. 2010
  4. pmc Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, USA
    Aging Cell 9:147-61. 2010
  5. pmc Intermittent parathyroid hormone administration counteracts the adverse effects of glucocorticoids on osteoblast and osteocyte viability, bone formation, and strength in mice
    Robert S Weinstein
    University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, Arkansas 72205 7199, USA
    Endocrinology 151:2641-9. 2010
  6. pmc Osteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in mice
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Endocrinology 152:3323-31. 2011
  7. pmc Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205 7199, USA
    J Clin Invest 109:1041-8. 2002
  8. ncbi request reprint The skeletal effects of glucocorticoid excess override those of orchidectomy in mice
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 7199, USA
    Endocrinology 145:1980-7. 2004
  9. ncbi request reprint Effects of raloxifene, hormone replacement therapy, and placebo on bone turnover in postmenopausal women
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Osteoporos Int 14:814-22. 2003
  10. pmc Giant osteoclast formation and long-term oral bisphosphonate therapy
    Robert S Weinstein
    Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
    N Engl J Med 360:53-62. 2009

Research Grants

  1. GLUCOCORTICOIDS ALTER THE BIRTH AND DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 1999
  2. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2000
  3. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2001
  4. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2002
  5. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2003
  6. The Role of Osteocyte Survival in Bone Strength
    Robert Weinstein; Fiscal Year: 2004
  7. The Role of Osteocyte Survival in Bone Strength
    Robert Weinstein; Fiscal Year: 2005

Collaborators

Detail Information

Publications39

  1. pmc Glucocorticoid-induced osteoporosis and osteonecrosis
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, and Central Arkansas Veterans Healthcare System at the University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, AR 72205 7199, USA
    Endocrinol Metab Clin North Am 41:595-611. 2012
    ..This article reviews glucocorticoid-induced osteoporosis and osteonecrosis, addressing the risk factors, pathogenesis, evaluation, treatment, and uncertainties in the clinical management of these disorders...
  2. pmc Glucocorticoid-induced osteonecrosis
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Endocrine 41:183-90. 2012
    ..Current evidence indicates that bisphosphonates may rapidly reduce pain, increase ambulation, and delay joint collapse in patients with osteonecrosis...
  3. pmc Glucocorticoids, osteocytes, and skeletal fragility: the role of bone vascularity
    Robert S Weinstein
    Department of Internal Medicine and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Bone 46:564-70. 2010
    ..This review examines this connection and how it may explain the greater decline in bone strength than loss of bone mass that occurs with glucocorticoid excess...
  4. pmc Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, USA
    Aging Cell 9:147-61. 2010
    ....
  5. pmc Intermittent parathyroid hormone administration counteracts the adverse effects of glucocorticoids on osteoblast and osteocyte viability, bone formation, and strength in mice
    Robert S Weinstein
    University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, Arkansas 72205 7199, USA
    Endocrinology 151:2641-9. 2010
    ..We conclude that intermittent PTH administration directly counteracts the key pathogenetic mechanisms of glucocorticoid excess on bone, thus providing a mechanistic explanation of its efficacy against glucocorticoid-induced osteoporosis...
  6. pmc Osteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in mice
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Endocrinology 152:3323-31. 2011
    ..Based on these results, we conclude that at least part of the OPG-induced preservation of bone strength is due to the maintenance of osteocyte viability and the lacunar-canalicular network...
  7. pmc Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids
    Robert S Weinstein
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205 7199, USA
    J Clin Invest 109:1041-8. 2002
    ..Therefore, the early beneficial effects of these agents must be due, in part, to prolonging the life span of osteoblasts...
  8. ncbi request reprint The skeletal effects of glucocorticoid excess override those of orchidectomy in mice
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 7199, USA
    Endocrinology 145:1980-7. 2004
    ..These data demonstrate that hypogonadism does not occur in or contribute to glucocorticoid-induced osteoporosis and that the adverse skeletal effects of glucocorticoid excess override those of orchidectomy...
  9. ncbi request reprint Effects of raloxifene, hormone replacement therapy, and placebo on bone turnover in postmenopausal women
    Robert S Weinstein
    Center for Osteoporosis and Metabolic Bone Diseases, Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Osteoporos Int 14:814-22. 2003
    ....
  10. pmc Giant osteoclast formation and long-term oral bisphosphonate therapy
    Robert S Weinstein
    Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
    N Engl J Med 360:53-62. 2009
    ....
  11. pmc FOXOs attenuate bone formation by suppressing Wnt signaling
    Srividhya Iyer
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
    J Clin Invest 123:3409-19. 2013
    ....
  12. pmc Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
    Maria Almeida
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
    J Clin Invest 123:394-404. 2013
    ..Hence, the ERα in both osteoblast progenitors and osteoclasts functions to optimize bone mass but at distinct bone compartments and in response to different cues...
  13. pmc Non-nuclear-initiated actions of the estrogen receptor protect cortical bone mass
    Shoshana M Bartell
    Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, 4301 West Markham Street, MS 587, Little Rock, Arkansas 72205, USA
    Mol Endocrinol 27:649-56. 2013
    ..These results demonstrate that the protection of cortical bone mass by estrogens is mediated, at least in part, via a mechanism that is distinct from the classic mechanism of estrogen action on reproductive organs...
  14. pmc Estrogens attenuate oxidative stress and the differentiation and apoptosis of osteoblasts by DNA-binding-independent actions of the ERalpha
    Maria Almeida
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and Central Arkansas Veterans Health Care System, Little Rock, AR, USA
    J Bone Miner Res 25:769-81. 2010
    ....
  15. pmc The estrogen receptor-alpha in osteoclasts mediates the protective effects of estrogens on cancellous but not cortical bone
    Marta Martin-Millan
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205 7199, USA
    Mol Endocrinol 24:323-34. 2010
    ..However, additional effects of estrogens on osteoblasts, osteocytes, and perhaps other cell types are required for their protective effects on the cortical compartment, which constitutes 80% of the skeleton...
  16. pmc Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids
    Maria Almeida
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA
    J Biol Chem 282:27285-97. 2007
    ..Loss of estrogens or androgens accelerates the effects of aging on bone by decreasing defense against oxidative stress...
  17. pmc Suppression of autophagy in osteocytes mimics skeletal aging
    Melda Onal
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Biol Chem 288:17432-40. 2013
    ....
  18. pmc Decreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration
    Robert L Jilka
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, 72205, USA
    Aging Cell 9:851-67. 2010
    ..On the other hand, ordinary antioxidants cannot restore bone mass in old age because they slow remodeling and attenuate osteoblastogenesis by interfering with Wnt signaling...
  19. pmc Connexin 43 is required for the anti-apoptotic effect of bisphosphonates on osteocytes and osteoblasts in vivo
    Lilian I Plotkin
    Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, The Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
    J Bone Miner Res 23:1712-21. 2008
    ..Taken together with earlier in vitro evidence, these findings show that Cx43 is required for the anti-apoptotic effect of bisphosphonates on osteocytes and osteoblasts...
  20. ncbi request reprint Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength
    CHARLES A O'BRIEN
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
    Endocrinology 145:1835-41. 2004
    ..Furthermore, our results suggest that glucocorticoid-induced loss of bone strength results in part from increased death of osteocytes, independent of bone loss...
  21. pmc The RANKL distal control region is required for the increase in RANKL expression, but not the bone loss, associated with hyperparathyroidism or lactation in adult mice
    Melda Onal
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Mol Endocrinol 26:341-8. 2012
    ....
  22. pmc Glucocorticoids and tumor necrosis factor α increase oxidative stress and suppress Wnt protein signaling in osteoblasts
    Maria Almeida
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Health Care System, Little Rock, Arkansas 72205, USA
    J Biol Chem 286:44326-35. 2011
    ..Moreover, modulation of Akt and FoxOs by GCs and TNFα are cell-autonomous mechanisms of Wnt/β-catenin antagonism contributing to the adverse effects of GC excess and inflammatory cytokines on bone alike...
  23. ncbi request reprint IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice
    CHARLES A O'BRIEN
    Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Am J Physiol Endocrinol Metab 289:E784-93. 2005
    ..These results demonstrate that IL-6 is not required for the osteoclast formation and bone loss that accompanies continuous elevation of PTH...
  24. pmc Continuous elevation of PTH increases the number of osteoblasts via both osteoclast-dependent and -independent mechanisms
    Robert L Jilka
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Bone Miner Res 25:2427-37. 2010
    ..These results indicate that PTH stimulates osteoclast-dependent as well as osteoclast-independent (Wnt signaling) pro-osteoblastogenic pathways, both of which are required for balanced focal bone remodeling in cancellous bone...
  25. ncbi request reprint Rosiglitazone causes bone loss in mice by suppressing osteoblast differentiation and bone formation
    A Afshan Ali
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Slot 587, 4301 West Markham, Little Rock, Arkansas 72205, USA
    Endocrinology 146:1226-35. 2005
    ....
  26. pmc Matrix-embedded cells control osteoclast formation
    Jinhu Xiong
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences UAMS, Little Rock, Arkansas, USA
    Nat Med 17:1235-41. 2011
    ..These results suggest that the rate-limiting step of matrix resorption is controlled by cells embedded within the matrix itself...
  27. pmc FoxO-mediated defense against oxidative stress in osteoblasts is indispensable for skeletal homeostasis in mice
    Elena Ambrogini
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
    Cell Metab 11:136-46. 2010
    ..We conclude that FoxO-dependent oxidative defense provides a mechanism to handle the oxygen free radicals constantly generated by the aerobic metabolism of osteoblasts and is thereby indispensable for bone mass homeostasis...
  28. ncbi request reprint Osteocyte apoptosis is induced by weightlessness in mice and precedes osteoclast recruitment and bone loss
    J Ignacio Aguirre
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    J Bone Miner Res 21:605-15. 2006
    ..We report here that, conversely, reduced mechanical forces in the murine model of unloading by tail suspension increases the prevalence of osteocyte apoptosis, followed by bone resorption and loss of mineral and strength...
  29. ncbi request reprint Proteasomal degradation of Runx2 shortens parathyroid hormone-induced anti-apoptotic signaling in osteoblasts. A putative explanation for why intermittent administration is needed for bone anabolism
    Teresita Bellido
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Biol Chem 278:50259-72. 2003
    ..The self-limiting nature of PTH-induced survival signaling might explain why intermittent administration of the hormone is required for bone anabolism...
  30. pmc Targeted deletion of a distant transcriptional enhancer of the receptor activator of nuclear factor-kappaB ligand gene reduces bone remodeling and increases bone mass
    Carlo Galli
    Center for Osteoporosis and Metabolic Bone Disease, University of Arkansas for Medical Sciences, 4301 West Markham Street, MS 587, Little Rock, Arkansas 72205, USA
    Endocrinology 149:146-53. 2008
    ..These findings demonstrate that hormonal control of RANKL expression via the DCR is a critical determinant of the rate of bone remodeling...
  31. pmc Intermittent PTH stimulates periosteal bone formation by actions on post-mitotic preosteoblasts
    Robert L Jilka
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, Slot 587, University of Arkansas for Medical Sciences, 4301 W Markham, Little Rock, AR, USA
    Bone 44:275-86. 2009
    ..Targeting the latter cells is an effective mechanism for increasing osteoblast number in periosteal bone where the production of osteoblasts from replicating progenitors is slow...
  32. pmc Control of bone mass and remodeling by PTH receptor signaling in osteocytes
    CHARLES A O'BRIEN
    Division of Endocrinology, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America
    PLoS ONE 3:e2942. 2008
    ..These findings demonstrate that PTH receptor signaling in osteocytes increases bone mass and the rate of bone remodeling through LRP5-dependent and -independent mechanisms, respectively...
  33. pmc FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
    Shoshana M Bartell
    1 Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205, USA 2
    Nat Commun 5:3773. 2014
    ....
  34. pmc A novel locus on the X chromosome regulates post-maturity bone density changes in mice
    Dorota Szumska
    Department of Geriatrics, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Healthcare Service, Little Rock, AR 72205, USA
    Bone 40:758-66. 2007
    ..Hum Mol Genet 2005;14:3141-8]. A second locus, on chromosome 7, was observed in only one cross. Single-nucleotide polymorphisms (SNPs) are highly clustered near these loci, distinguishing the parental strains over only limited spans...
  35. ncbi request reprint Quantifying osteoblast and osteocyte apoptosis: challenges and rewards
    Robert L Jilka
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Bone Miner Res 22:1492-501. 2007
    ....
  36. pmc Dysapoptosis of osteoblasts and osteocytes increases cancellous bone formation but exaggerates cortical porosity with age
    Robert L Jilka
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR, USA
    J Bone Miner Res 29:103-17. 2014
    ..In addition, our findings suggest that distress signals produced by old and/or dysfunctional osteocytes are the culprits of the increased intracortical porosity in old age...
  37. pmc Osteocyte apoptosis
    Robert L Jilka
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, 4301 W Markham, Slot 587, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Bone 54:264-71. 2013
    ..The osteocyte apoptosis caused by chronic glucocorticoid administration does not increase osteoclasts; however, it does negatively impact maintenance of bone hydration, vascularity, and strength...
  38. pmc Giant osteoclasts after long-term bisphosphonate therapy: diagnostic challenges
    Nidhi Jain
    Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Nat Rev Rheumatol 5:341-6. 2009
    ..A 55-year-old woman with a 5-year history of osteoporosis treated for 4 years with an oral aminobisphosphonate presented with a recent vertebral fracture. A bone biopsy specimen revealed giant osteoclasts with more than 40 nuclear profiles...
  39. ncbi request reprint Sexual differentiation, pregnancy, calorie restriction, and aging affect the adipocyte-specific secretory protein adiponectin
    Terry P Combs
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    Diabetes 52:268-76. 2003
    ..In summary, Acrp30 levels in serum are under complex hormonal control and may play a key role in determining systemic insulin sensitivity under the respective conditions...

Research Grants7

  1. GLUCOCORTICOIDS ALTER THE BIRTH AND DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 1999
    ..abstract_text> ..
  2. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2000
    ..abstract_text> ..
  3. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2001
    ..abstract_text> ..
  4. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2002
    ..abstract_text> ..
  5. GLUCOCORTICOIDS ALTER THE BIRTH & DEATH OF OSTEOBLASTS
    Robert Weinstein; Fiscal Year: 2003
    ..abstract_text> ..
  6. The Role of Osteocyte Survival in Bone Strength
    Robert Weinstein; Fiscal Year: 2004
    ..The proposed research plan will reveal the role of osteocyte survival in bone strength and how osteocytes achieve this objective. ..
  7. The Role of Osteocyte Survival in Bone Strength
    Robert Weinstein; Fiscal Year: 2005
    ..The proposed research plan will reveal the role of osteocyte survival in bone strength and how osteocytes achieve this objective. ..