Political demography: Powerful forces between disciplinary stools

Michael S. Teitelbaum 한국외국어대학교 국제지역연구센터 2014 International Area Studies Review Vol.17 No.2

The interconnections between politics and the dramatic demographic changes underway aroundthe world have been under-attended by the two research disciplines that could contribute most totheir understanding: demography and political science. Instead this area of “political demography”has largely been ceded to political activists, pundits and journalists, leading to often exaggeratedor garbled interpretation. The terrain includes issues that now rank among the most politicallysensitive and contested in many parts of the world, engaging high-level attention including that ofnumerous presidents and premiers: alleged demographically-determined shifts in the internationalbalance of power; low fertility, population aging, and the sustainability of public pension and otherage-related systems; international migration; national identity; compositional shifts in politicallysensitive social categories (ethnic/religious/racial/linguistic/national origin); and human rights. Moreover it now is apparent that many governments (and nongovernmental actors too) haveactively been pursuing varieties of “strategic demography”, in which one or more of the three keydemographic drivers (fertility, mortality, migration) have been deployed—consciously if not alwaysexplicitly—as instruments of their domestic or international strategies. The prospects for thecoming decades seem to be for more of the same, and it would well behoove political scientists anddemographers to employ their considerable knowledge and analytic techniques in ways that couldimprove public understanding and moderate the excessive claims and fears that prevail. The interconnections between politics and the dramatic demographic changes underway aroundthe world have been under-attended by the two research disciplines that could contribute most totheir understanding: demography and political science. Instead this area of “political demography”has largely been ceded to political activists, pundits and journalists, leading to often exaggeratedor garbled interpretation. The terrain includes issues that now rank among the most politicallysensitive and contested in many parts of the world, engaging high-level attention including that ofnumerous presidents and premiers: alleged demographically-determined shifts in the internationalbalance of power; low fertility, population aging, and the sustainability of public pension and otherage-related systems; international migration; national identity; compositional shifts in politicallysensitive social categories (ethnic/religious/racial/linguistic/national origin); and human rights.Moreover it now is apparent that many governments (and nongovernmental actors too) haveactively been pursuing varieties of “strategic demography”, in which one or more of the three keydemographic drivers (fertility, mortality, migration) have been deployed—consciously if not alwaysexplicitly—as instruments of their domestic or international strategies. The prospects for thecoming decades seem to be for more of the same, and it would well behoove political scientists anddemographers to employ their considerable knowledge and analytic techniques in ways that couldimprove public understanding and moderate the excessive claims and fears that prevail.

Calpain-6, a Target Molecule of Glucocorticoids, Regulates Osteoclastic Bone Resorption via Cytoskeletal Organization and Microtubule Acetylation

Hong, Jung Min,Teitelbaum, Steven L,Kim, Tae-Ho,Ross, F Patrick,Kim, Shin-Yoon,Kim, Hyun-Ju Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of bone and mineral research Vol.26 No.3

<P>Glucocorticoids (GCs) inhibit the resorptive capacity of the osteoclast by disrupting its cytoskeleton. We find that calpain-6 (Capn6), a unique, nonproteolytic member of its family, is suppressed 12-fold by dexamethasone (DEX) in the bone-degrading cell. While Capn6 abundance parallels commitment of naive bone marrow macrophages (BMMs) to the osteoclast phenotype, its excess or deletion does not affect the cell's differentiation. On the other hand, Capn6 localizes to the sealing zone, and its overexpression promotes osteoclast spreading and large actin ring formation, eventuating in stimulated bone degradation. Conversely, Capn6 knockdown impairs cytoskeletal organization and the cell's resorptive capacity. Capn6 complexes with tubulin, and its absence inhibits microtubule acetylation and stability in the osteoclast. Knockdown of Capn6 also reduces β<SUB>3</SUB>-integrin subunit protein, another essential regulator of osteoclast cytoskeletal function. Reflecting Capn6 as a target molecule of GCs, microtubule stability and acetylation, as well as the expression of β<SUB>3</SUB>-integrin protein, are similarly suppressed in DEX-treated osteoclasts. Moreover, overexpression of Capn6 rescues GC-mediated disruption of osteoclast cytoskeleton. Thus Capn6 promotes cytoskeletal organization and microtubule stability in osteoclasts, and its inhibition may mediate the resorption-arresting properties of GCs. © 2011 American Society for Bone and Mineral Research.</P>

Lovastatin Efficacy in Reducing Low-Density Lipoprotein Cholesterol Levels on High-vs Low-Fat Diets

Cobb, Margaret M.,Teitelbaum, Howard S.,Breslow, Jan L. MediMedia Korea 1991 JAMA-Korea Vol.6 No.6

Long-lived photoinduced response observed under extreme photoexcitation densities in a one-dimensional Peierls insulator

Wolfson, Johanna W.,Teitelbaum, Samuel W.,Shin, Taeho,Katayama, Ikufumi,Kawano, Taro,Takeda, Jun,Nelson, Keith A. American Physical Society 2018 Physical Review B Vol.98 No.5

Peritoneal dialysis adequacy: a paradigm shift

Chen Chang Huei,Teitelbaum Isaac 대한신장학회 2022 Kidney Research and Clinical Practice Vol.41 No.2

For the past 30 years, nephrologists have focused on a single minimal threshold of Kt/Vurea to determine the adequacy of peritoneal dialysis (PD). To date, there is no evidence that shows Kt/Vurea to be a good surrogate measure of uremic symptom control or nutritional state in patients on PD. Volume of distribution (Vurea) generally is considered equivalent to total body water (TBW). Yet, accurate determination of TBW is difficult. The most recent International Society for Peritoneal Dialysis practice recommendations on prescribing high-quality PD emphasized incorporation of multiple measures rather than the single value of Kt/Vurea. These measures include shared decision-making between the patient and the care team and assessment of health-related quality of life, burden of uremic symptoms, presence of residual kidney function, volume status, and biochemical measures including serum potassium and bicarbonate levels. In some cases, PD prescriptions can be tailored to the patient priorities and goals of care, such as in frail and pediatric patients. Overall, there has been a paradigm shift in providing high-quality care to PD patients. Instead of focusing on small solute clearance in the form of Kt/Vurea, nephrologists are encouraged to use a more comprehensive assessment of the patient as a whole.

The Src family kinase, Lyn, suppresses osteoclastogenesis in vitro and in vivo.

Kim, Hyun-Ju,Zhang, Kaihua,Zhang, Lihong,Ross, F Patrick,Teitelbaum, Steven L,Faccio, Roberta National Academy of Sciences 2009 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.106 No.7

<P>c-Src kinase is a rate-limiting activator of osteoclast (OC) function and Src inhibitors are therefore candidate antiosteoporosis drugs. By affecting alphavbeta3 and macrophage-colony stimulating factor (M-CSF)-induced signaling, c-Src is central to osteoclast activity, but not differentiation. We find Lyn, another member of Src family kinases (SFK) is, in contrast, a negative regulator of osteoclastic bone resorption. The absence of Lyn enhances receptor activator of NF-kappaB ligand (RANKL)-mediated differentiation of osteoclast precursors without affecting proliferation and survival, while its overexpression decreases osteoclast formation. In further contrast to c-Src, Lyn deficiency does not impact the activity of the mature cell. Reflecting increased osteoclast development in vitro, Lyn-/- mice undergo accelerated osteoclastogenesis and bone loss, in vivo, in response to RANKL. Mechanistically, Lyn forms a complex with receptor activator of NF-kappaB (RANK), the tyrosine phosphatase, SHP-1, and the adapter protein, Grb2-associated binder 2 (Gab2). Upon RANKL exposure, Gab2 phosphorylation, JNK, and NF-kappaB activation are enhanced in Lyn-/- osteoclasts, all critical events in osteoclast development. We therefore establish that Lyn regulates osteoclast formation and does it in a manner antithetical to that of c-Src. The most pragmatic aspect of our findings is that successful therapeutic inhibition of c-Src, in the context of the osteoclast, will require its stringent targeting.</P>

A Case of Osteomalacia: The Pivotal role of the Non-Decalcified Bone Biopsy

Ghi Su Kim,Michele A. Bergfeld,Steven L. Teitelbaum,Louis V. Avioli 대한내과학회 1988 The Korean Journal of Internal Medicine Vol.3 No.2

Src-like adaptor protein regulates osteoclast generation and survival

Kim, Hyun-Ju,Zou, Wei,Ito, Yuji,Kim, Shin-Yoon,Chappel, Jean,Ross, F. Patrick,Teitelbaum, Steven L. Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.110 No.1

<P>Src-like adaptor protein (SLAP) is a hematopoietic adaptor containing Src homology (SH)3 and SH2 motifs and a unique carboxy terminus. Unlike c-Src, SLAP lacks a tyrosine kinase domain. We investigated the role of SLAP in osteoclast development and resorptive function. Employing SLAP-deficient mice, we find lack of the adaptor enhances in vitro proliferation of osteoclast precursors in the form of bone marrow macrophages (BMMs), without altering their survival. Furthermore, osteoclastogenic markers appear more rapidly in SLAP−/− BMMs exposed to RANK ligand (RANKL). The accelerated proliferation of M-CSF-treated, SLAP-deficient precursors is associated with enhanced ERK activation. SLAP's role as a mediator of M-CSF signaling, in osteoclastic cells, is buttressed by complexing of the adaptor protein and c-Fms in lipid rafts. Unlike c-Src, SLAP does not impact resorptive function of mature osteoclasts but induces their early apoptosis. Thus, SLAP negatively regulates differentiation of osteoclasts and proliferation of their precursors. Conversely, SLAP decreases osteoclast death by inhibiting activation of caspase 3. These counterbalancing events yield indistinguishable bones of WT and SLAP−/− mice which contain equal numbers of osteoclasts in basal and stimulated conditions. J. Cell. Biochem. 110: 201–209, 2010. © 2010 Wiley-Liss, Inc.</P>

ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment

Li, Philip Kam-Tao,Szeto, Cheuk Chun,Piraino, Beth,de Arteaga, Javier,Fan, Stanley,Figueiredo, Ana E.,Fish, Douglas N.,Goffin, Eric,Kim, Yong-Lim,Salzer, William,Struijk, Dirk G.,Teitelbaum, Isaac,Joh Multimed Inc 2016 Peritoneal dialysis international Vol.36 No.5

Fyn promotes proliferation, differentiation, survival and function of osteoclast lineage cells

Kim, Hyun‐,Ju,Warren, Julia T.,Kim, Shin‐,Yoon,Chappel, Jean C.,DeSelm, Carl J.,Ross, F. Patrick,Zou, Wei,Teitelbaum, Steven L. Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.111 No.5

<P><B>Abstract</B></P><P>c‐Src and Lyn are the only Src family kinases (SFKs) with established activity in osteoclasts (OCs). c‐Src promotes function via cytoskeletal organization of the mature resorptive cell while Lyn is a negative regulator of osteoclastogenesis. We establish that Fyn, another SFK, also impacts the OC, but in a manner distinctly different than c‐Src and Lyn. Fyn deficiency principally alters cells throughout the osteoclastogenic process, resulting in diminished numbers of resorptive polykaryons. Arrested OC formation in the face of insufficient Fyn reflects reduced proliferation of precursors, in response to M‐CSF and retarded RANK ligand (RANKL)‐induced differentiation, attended by suppressed activation of the osteoclastogenic signaling molecules, c‐Jun, and NF‐κB. The anti‐apoptotic properties of RANKL are also compromised in cells deleted of Fyn, an event mediated by increased Bim expression and failed activation of Akt. The defective osteoclastogenesis of Fyn−/− OCs dampens bone resorption, in vitro. Finally, while Fyn deficiency does not regulate basal osteoclastogenesis, in vivo, it reduces that stimulated by RANKL by ∼2/3. Thus, Fyn is a pro‐resorptive SFK, which exerts its effects by prompting proliferation and differentiation while attenuating apoptosis of OC lineage cells. J. Cell. Biochem. 111: 1107–1113, 2010. © 2010 Wiley‐Liss, Inc.</P>