RESUMO
OBJECTIVE: Erectile dysfunction (ED) and benign prostatic hyperplasia (BPH) commonly affect older men. There is limited epidemiology information on coexisting ED and BPH. This study assessed self-reported prevalence of ED with or without a diagnosis of BPH (ED/DxBPH versus ED only) in US men. METHODS: Men ≥40 years old, who reported experiencing ED in the past 6 months with or without a diagnosis of BPH, were identified from the nationally representative 2011 US National Health and Wellness Survey (NHWS) - a cross-sectional, self-administered online survey. Unpaired t-tests were used to compare characteristics between ED-only and ED/DxBPH populations. RESULTS: The prevalence of ED only and ED/DxBPH was 24.6% and 4.9% (mean ages of 60 and 68 years, respectively). About two-thirds of those with ED only and ED/DxBPH reported speaking to their physician about ED. About 23% of either group reported currently using ED medication and 11.7% of men with ED only were prescribed ED medication by a urologist, compared to 31.1% with ED/DxBPH. Approximately 51.7% of men with ED/DxBPH were taking BPH medication. Overall, 37.3% of men with ED only and 74.6% with ED/DxBPH reported moderate-to-severe urinary symptoms on the American Urological Association-Symptom Index (AUA-SI ≥8). CONCLUSION: While self-reported ED is common, few men with ED in the US population report being diagnosed with BPH. The majority of ED only and ED/DxBPH men reported speaking to a physician about ED; however, few reported currently taking ED medication. A majority of men with ED/DxBPH reported an AUA-SI score ≥8, but only half reported taking BPH medications. Thus, although men are experiencing erectile or urinary symptoms, many remain untreated. A limitation of this study is that symptoms and diagnosis were self-reported and may not reflect how these conditions are diagnosed in a healthcare setting; however, patient self-report provides a unique perspective on the burden associated with these conditions.
Assuntos
Disfunção Erétil/complicações , Disfunção Erétil/epidemiologia , Hiperplasia Prostática/complicações , Hiperplasia Prostática/epidemiologia , Adulto , Idoso , Coleta de Dados , Disfunção Erétil/tratamento farmacológico , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Hiperplasia Prostática/tratamento farmacológico , Estados Unidos/epidemiologiaRESUMO
Tumor blood vessels are thought to contain genetically normal and stable endothelial cells (ECs), unlike tumor cells, which typically display genetic instability. Yet, chromosomal aberration in human tumor-associated ECs (hTECs) in carcinoma has not yet been investigated. Here we isolated TECs from 20 human renal cell carcinomas and analyzed their cytogenetic abnormalities. The degree of aneuploidy was analyzed by fluorescence in situ hybridization using chromosome 7 and chromosome 8 DNA probes in isolated hTECs. In human renal cell carcinomas, 22-58% (median, 33%) of uncultured hTECs were aneuploid, whereas normal ECs were diploid. The mechanisms governing TEC aneuploidy were then studied using mouse TECs (mTECs) isolated from xenografts of human epithelial tumors. To investigate the contribution of progenitor cells to aneuploidy in mTECs, CD133(+) and CD133(-) mTECs were compared for aneuploidy. CD133(+) mTECs showed aneuploidy more frequently than CD133(-) mTECs. This is the first report showing cytogenetic abnormality of hTECs in carcinoma, contrary to traditional belief. Cytogenetic alterations in tumor vessels of carcinoma therefore can occur and may play a significant role in modifying tumor- stromal interactions.
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Carcinoma de Células Renais/irrigação sanguínea , Carcinoma de Células Renais/genética , Células Endoteliais/patologia , Neoplasias Renais/irrigação sanguínea , Neoplasias Renais/genética , Neovascularização Patológica/genética , Antígeno AC133 , Antígenos CD/biossíntese , Separação Celular , Proteínas Cromossômicas não Histona/biossíntese , Proteínas Cromossômicas não Histona/genética , Aberrações Cromossômicas , Citometria de Fluxo , Glicoproteínas/biossíntese , Humanos , Imuno-Histoquímica , Hibridização in Situ Fluorescente , Peptídeos , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
Different steps of embryonic pancreas and liver development require inductive signals from endothelial cells. During liver development, interactions between newly specified hepatic endoderm cells and nascent endothelial cells are crucial for the endoderm's subsequent growth and morphogenesis into a liver bud. Reconstitution of endothelial cell stimulation of hepatic cell growth with embryonic tissue explants demonstrated that endothelial signalling occurs independent of the blood supply. During pancreas development, midgut endoderm interactions with aortic endothelial cells induce Ptf1a, a crucial pancreatic determinant. Endothelial cells also have a later effect on pancreas development, by promoting survival of the dorsal mesenchyme, which in turn produces factors supporting pancreatic endoderm. A major goal of our laboratory is to determine the endothelial-derived molecules involved in these inductive events. Our data show that cultured endothelial cells induce Ptf1a in dorsal endoderm explants lacking an endogenous vasculature. We are purifying endothelial cell line product(s) responsible for this effect. We are also identifying endothelial-responsive regulatory elements in genes such as Ptf1a by genetic mapping and chromatin-based assays. These latter approaches will allow us to track endothelial-responsive signal pathways from DNA targets within progenitor cells. The diversity of organogenic steps dependent upon endothelial cell signalling suggests that cross-regulation of tissue development with its vasculature is a general phenomenon.
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Células Endoteliais/citologia , Fígado/embriologia , Pâncreas/embriologia , Animais , Vasos Sanguíneos/citologia , Vasos Sanguíneos/embriologia , Proliferação de Células , Fígado/citologia , Camundongos , Pâncreas/irrigação sanguínea , Pâncreas/citologia , Transdução de Sinais , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/deficiênciaRESUMO
BACKGROUND/PURPOSE: This study was aimed at determining whether cartilaginous grafts engineered from mesenchymal cells normally present in the amniotic fluid could be used in fetal tracheal repair. METHODS: Ovine mesenchymal amniocytes were expanded in culture, labeled with green fluorescent protein, and seeded onto biodegradable scaffold tubes maintained in chondrogenic medium. After chondrogenic differentiation of the constructs was confirmed, they were used to repair either partial or full circumferential tracheal defects in allogeneic fetal lambs (n = 7). Newborns were evaluated for signs of airway compromise. Implants were harvested over a 10-day period postnatally for multiple analyses. RESULTS: All 5 lambs that survived to term were able to breathe spontaneously at birth, 4 (80%) of them without stridor. However, variable degrees of stridor developed over time in all but one animal. Mild-to-moderate tracheal stenosis was present in all specimens. Histologically, grafts contained green fluorescent protein-positive cells, were lined with pseudostratified columnar epithelium, and remodeled into a predominantly fibrous cartilage pattern. Implants showed no significant changes in glycosaminoglycans, collagen, and elastin content at harvest. CONCLUSIONS: Engineered cartilaginous grafts derived from mesenchymal amniocytes may become a viable alternative for tracheal repair. The amniotic fluid can be a practical cell source for engineered tracheal reconstruction.
Assuntos
Líquido Amniótico/citologia , Cartilagem/transplante , Transplante de Células , Feto/cirurgia , Mesoderma/citologia , Engenharia Tecidual , Traqueia/cirurgia , Animais , OvinosRESUMO
BACKGROUND/PURPOSE: Sclerotherapy for vascular malformations is often limited by luminal recanalization. This study examined whether an injectable tissue-engineered construct could prevent this complication in a rabbit model of venous sclerotherapy. METHODS: Ethanol sclerotherapy of a temporarily occluded jugular vein segment was performed in 46 rabbits, which were then divided into 3 groups. Group I (n = 16) had no further manipulations. In groups II (n = 15) and III (n = 15), 0.5 mL collagen hydrogel was injected intraluminally, respectively, devoid of and seeded with autologous fibroblasts. At 1, 4, and 20 to 24 weeks postoperatively, vein segments were examined for patency and resected for histological evaluation. Statistical analysis was by Fisher's Exact test. RESULTS: All vein segments were occluded at 1 and 4 weeks in all groups, despite histological evidence of progressive endothelial ingrowth. However, at 20 to 24 weeks, angiography demonstrated restoration of vessel patency in groups I (3/6) and II (3/5), but not in group III (0/6; P = .043), in which histology confirmed an obliterated lumen for all vessels. CONCLUSION: An injectable, fibroblast-based, engineered construct prevents midterm to long-term recanalization in a leporine model of vascular sclerotherapy. This novel therapeutic approach may prevent recurrence of vascular malformations after sclerotherapy, thus reducing the need for repeated procedures and morbid operative resections.
Assuntos
Malformações Arteriovenosas/terapia , Inflamação/prevenção & controle , Veias Jugulares/anormalidades , Soluções Esclerosantes , Escleroterapia/métodos , Animais , Modelos Animais de Doenças , Etanol/uso terapêutico , Fibroblastos/transplante , Humanos , Hidrogel de Polietilenoglicol-Dimetacrilato/administração & dosagem , Injeções Intravenosas , Veias Jugulares/anatomia & histologia , Coelhos , Engenharia Tecidual , Transplante AutólogoRESUMO
Here we report for the first time that loss of CDK2 activity, by translational inhibition and through CDK2 inhibition by p21(Cip1/Waf1), may be responsible for endothelial senescence. We show that expression of dominant-negative p53 extends human umbilical vein endothelial cell (HUVEC) lifespan past senescence. HUVEC expressing telomerase can completely bypass senescence and become immortal (i-HUVEC). Surprisingly, early passage i-HUVEC, like senescent HUVEC, express high levels of the CDK inhibitors p16(INK4a) and p21(Cip1/Waf1). Expression of p16(INK4a) can persist for over 280 population doublings, while p21(Cip1/Waf1) expression was eventually lost in five of six i-HUVEC lines. Senescent HUVEC contain undetectable CDK2 activity, which results from a dramatic reduction of CDK2 protein levels and inhibition of remaining CDK2 by p21(Cip1/Waf1). The decreased CDK2 levels in senescent HUVEC are not due to decreased transcription or protein stability; rather, CDK2 translation declines during senescence. Bypass of endothelial senescence by telomerase entails the restoration of CDK2 translation and activity. These results suggest that p16(INK4a) does not play a role in endothelial senescence. Rather, CDK2 translational down-regulation may be a key regulatory event in replicative senescence of endothelial cells. Understanding the mechanisms regulating endothelial senescence will be critical in determining the role of endothelial senescence in tumor growth.
Assuntos
Quinases relacionadas a CDC2 e CDC28/metabolismo , Senescência Celular , Regulação para Baixo , Western Blotting , Quinases relacionadas a CDC2 e CDC28/análise , Quinases relacionadas a CDC2 e CDC28/genética , Técnicas de Cultura de Células , Ciclo Celular , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Linhagem Celular Transformada , Células Cultivadas , Células Clonais , Quinase 2 Dependente de Ciclina , Inibidor p16 de Quinase Dependente de Ciclina/antagonistas & inibidores , Inibidor de Quinase Dependente de Ciclina p21 , Endotélio Vascular/citologia , Vetores Genéticos , Proteínas de Fluorescência Verde/metabolismo , Humanos , Cinética , Mitose , Modelos Biológicos , Testes de Precipitina , Retroviridae/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Telomerase/metabolismo , Veias Umbilicais/citologiaRESUMO
BACKGROUND/PURPOSE: Treatment of vascular malformations with sclerotherapy is often complicated by reexpansion secondary to endothelial recanalization. This study examined the use of an autologous fibroblast construct to enhance intraluminal scar formation after sclerotherapy. METHODS: New Zealand rabbits (n = 15) underwent ethanol sclerotherapy of a segment of the facial vein. After intraluminal saline flush, animals were equally divided into 3 groups. In group I, no further manipulations were performed. In groups II and III, collagen hydrogel was injected into the sclerosed vein, respectively, without and seeded with autologous green fluorescent protein-labeled fibroblasts. One week postoperatively, the vein segments were examined for patency and resected for histology. RESULTS: The sclerosed vein segments remained occluded in all animals. Histological examination of luminal thrombi demonstrated numerous viable fibroblasts in group III, whereas there were none in the control specimens from groups I and II. The presence of the injected autologous green fluorescent protein-labeled fibroblasts within thrombi of group III was confirmed by immunohistochemistry. CONCLUSIONS: An injectable tissue-engineered construct enhances sclerotherapy of the jugular vein in a leporine model by reliably delivering fibroblasts that populate the resultant thrombus. Further analysis of this novel therapeutic concept as a means to augment permanent scar formation and reduce luminal recanalization is warranted.
Assuntos
Fibroblastos/transplante , Escleroterapia/métodos , Engenharia Tecidual , Veias/anormalidades , Animais , Anormalidades Cardiovasculares/terapia , Cicatriz , Face/irrigação sanguínea , Hidrogéis , CoelhosRESUMO
Vascular endothelial cells line the interior of blood vessels. As in other cell types, the proliferative lifespan of endothelial cells is limited; after a given number of replication cycles, they undergo senescence. Angiogenesis, the formation of new capillaries from pre-existing vasculature, is a process that involves endothelial cell proliferation. Angiogenesis thus has the possibility to be limited by the occurrence of senescence in the endothelial cell population. While there is evidence that endothelial cells undergo senescence in vivo, there are also data implying that endothelial senescence can be delayed or prevented in certain situations. Such a prevention of senescence would allow continued endothelial cell proliferation and continued angiogenesis in both physiological and pathological settings. This review discusses endothelial cell senescence and its bypass in vitro and in vivo.
Assuntos
Senescência Celular , Endotélio Vascular/patologia , Animais , Aterosclerose/patologia , Técnicas de Cultura de Células , Linhagem Celular Tumoral , Quinases Ciclina-Dependentes/antagonistas & inibidores , Endotélio Vascular/metabolismo , Humanos , Neoplasias/patologia , Neovascularização Patológica , Telômero/ultraestrutura , Proteína Supressora de Tumor p53/metabolismo , CicatrizaçãoRESUMO
Here we report the characterization of a series of telomerase-immortalized human umbilical vein endothelial cell lines (i-HUVEC). These cells maintain endothelial characteristics such as marker expression, dependence on basic fibroblast growth factor for proliferation, and the ability to form tube structures on Matrigel. In addition, these cells do not show signs of tumorigenic transformation because their growth is contact-inhibited, serum-dependent, and anchorage-dependent. In addition, i-HUVEC do not grow or survive when implanted subcutaneously in immunocompromised mice. Notably, the i-HUVEC lines maintain normal p53-dependent checkpoint control, inducing expression of p21(Cip1/Waf1) in response to DNA damage. These cells subsequently decrease phosphorylation of pRb and arrest in G1. Furthermore, the i-HUVEC lines maintain normal p53-independent checkpoint control, inducing expression of p27(Kip1) in response to lovastatin treatment, with a subsequent decrease in pRb phosphorylation. Lovastatin-treated i-HUVEC lines undergo a G1 arrest that can be reversed with comparable kinetics to that of low passage HUVEC. Together these data demonstrate that telomerase-immortalized endothelial cells can retain normal phenotypes and cell cycle regulation. This result could have significant implications in the study of angiogenic processes such as tumor growth, wound healing, and the vascularization of engineered tissue.
Assuntos
Células Endoteliais/citologia , Células Endoteliais/enzimologia , Fase G1/fisiologia , Genes cdc/fisiologia , Telomerase/biossíntese , Animais , Proteínas de Ciclo Celular/fisiologia , Extratos Celulares/química , Linhagem Celular , Linhagem Celular Transformada , Proliferação de Células/efeitos dos fármacos , Transformação Celular Neoplásica/metabolismo , Células Endoteliais/transplante , Endotélio Vascular/enzimologia , Humanos , Rim/embriologia , Rim/enzimologia , Camundongos , Camundongos SCID , Fenótipo , Proteína Supressora de Tumor p53/fisiologia , Veias Umbilicais/enzimologiaRESUMO
[(THF)3Sm(SePh)2Zn(SePh)2]n decomposes to give a variety of products, including [(THF)8Sm4Se(SePh)8](2+)[Zn8Se(SePh)16](2-), an ionic cluster that can also be prepared in more than 60% yield by stoichiometric addition of Se to a mixture of Sm(SePh)3 and Zn(SePh)2. The isostructural Nd compound [(THF)8Nd4Se(SePh)8](2+)[Zn8Se(SePh)16](2-) was also prepared by the stoichiometric route to establish the viability of this cluster type with redox-inactive Ln. In addition, the salt [Yb(THF)6](3+)[Fe4Se4(SePh)4](3-) was isolated and structurally characterized. These ionic cluster materials illustrate the difficulties associated with doping Ln ions into covalent metal chalcogenido matrixes.
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Aqueous humor is a clear fluid, primarily a blood filtrate, which circulates through the anterior chamber of the eye and bathes the cornea. We explored the possibility that components in the aqueous humor play a direct part in maintaining the avascular environment of the cornea. We report here that heparan sulfate proteoglycan (HSPG) was found in bovine aqueous humor and that it directly inhibits binding of basic fibroblast growth factor and vascular endothelial growth factor to cell-surface heparan sulfate. We demonstrate that this holds true for all heparin binding proteins tested but not for epidermal growth factor, which does not bind heparin. Furthermore, we show, with mathematical modeling, that the concentration of HSPG in aqueous humor (approximately 4 microg/ml), when combined with the clearance of aqueous humor from the eye due to circulation, is sufficient to block the binding of heparin binding growth factors to corneal endothelium. This mechanism suggests a physiological process to control bioavailability of angiogenic growth factors in the cornea.
Assuntos
Humor Aquoso/química , Fatores de Crescimento Endotelial/metabolismo , Endotélio Vascular/efeitos dos fármacos , Fator 2 de Crescimento de Fibroblastos/metabolismo , Proteoglicanas de Heparan Sulfato/farmacologia , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Linfocinas/metabolismo , Animais , Ligação Competitiva/efeitos dos fármacos , Linhagem Celular , Meios de Cultivo Condicionados/química , Endotélio Vascular/citologia , Endotélio Vascular/metabolismo , Glicosaminoglicanos/metabolismo , Proteoglicanas de Heparan Sulfato/metabolismo , Modelos Biológicos , Polissacarídeo-Liases/metabolismo , Ligação Proteica , Receptores de Fatores de Crescimento de Fibroblastos/metabolismo , Fator A de Crescimento do Endotélio Vascular , Fatores de Crescimento do Endotélio VascularRESUMO
Several drugs approved for a variety of indications have been shown to exhibit antiangiogenic effects. Our study focuses on the PPARgamma ligand rosiglitazone, a compound widely used in the treatment of type 2 diabetes. We demonstrate, for the first time to our knowledge, that PPARgamma is highly expressed in tumor endothelium and is activated by rosiglitazone in cultured endothelial cells. Furthermore, we show that rosiglitazone suppresses primary tumor growth and metastasis by both direct and indirect antiangiogenic effects. Rosiglitazone inhibits bovine capillary endothelial cell but not tumor cell proliferation at low doses in vitro and decreases VEGF production by tumor cells. In our in vivo studies, rosiglitazone suppresses angiogenesis in the chick chorioallantoic membrane, in the avascular cornea, and in a variety of primary tumors. These results suggest that PPARgamma ligands may be useful in treating angiogenic diseases such as cancer by inhibiting angiogenesis.
Assuntos
Inibidores da Angiogênese/farmacologia , Antineoplásicos/farmacologia , Metástase Neoplásica/prevenção & controle , Receptores Citoplasmáticos e Nucleares/fisiologia , Tiazóis/farmacologia , Tiazolidinedionas , Fatores de Transcrição/fisiologia , Animais , Bovinos , Fator 2 de Crescimento de Fibroblastos/fisiologia , Humanos , Ligantes , Invasividade NeoplásicaRESUMO
Lanthanide metals react with PhTeTePh and elemental Te in pyridine to give (py)(y)Ln(4)(Te)(TeTe)(2)(TeTeTe(Ph)TeTe)(Te(x)TePh) (Ln = Sm (y = 9; x = 0); Tb, Ho (y = 8, x = 0.1)), and (py)(7)Tm(4)(Te)[(TeTe)(4)TePh](Te(0.6)TePh) clusters. The Sm, Tb, and Ho compounds contain a square array of Ln(III) ions all connected to a central Te(2-) ligand. Two adjacent edges of the square are bridged by ditelluride ligands, with the Ln ion that is eta(2) bound to both of these TeTe ligands also coordinating to a terminal TePh ligand. The other two edges of the square are spanned by ditellurides that both coordinate a TePh ligand that has been displaced from the Ln ion by pyridine, to give the pentaanion (mu-eta(2)-eta(2)-Te(2)Te(Ph)Te(2)).(5-) In the Tm compound, the displaced TePh interacts with all four TeTe units. The compounds are air-, light-, and temperature-sensitive. Upon thermolysis, they decompose to give solid-state TbTe(2-x), HoTe, or TmTe, with elimination of Te and TePh(2).
RESUMO
Octametallic (L)(8)Ln(8)E(6)(EPh)(12) clusters (L = Lewis base; Ln = lanthanide ion; E = S, Se; EPh = SPh, SePh) can be prepared either by the reduction of Se-C bonds with low-valent Ln or by the reaction of Ln(SePh)(3) with elemental E. Because all possible ligand sites (i.e., L, E, EPh) are reactive, the ligands can be varied systematically to further the understanding of structure/property relationships. Chalcogenolate ligands can be selectively varied, as in the reaction of (THF)(8)Sm(8)Se(6)(SePh)(12) with PhSSPh to form (THF)(8)Sm(8)Se(6)(SPh)(12). Neutral L can be altered without disrupting structure, as in the replacement of THF with pyridine to give (py)(8)Sm(8)Se(6)(SePh)(12). Even chalcogenido ligands can be chemically replaced: the reaction of (THF)(8)Sm(8)Se(6)(SPh)(12) with elemental S gives the all-sulfur cluster (THF)(8)Sm(8)S(6)(SPh)(12). All compounds were isolated and characterized by IR and UV-visible spectroscopy and by low-temperature single-crystal X-ray diffraction to confirm that the structures contain cubes of Ln(III) ions with E(2)(-) capping the faces and EPh bridging the edges of the cube. The Sm(8)Se(6)(EPh)(12) clusters are intensely colored because of a Se(2)(-) to Sm(III) charge transfer absorption, while the sulfido clusters exhibit the light yellow color characteristic of Sm(III) complexes. The light green Nd complex (py)(8)Nd(8)Se(6)(SePh)(12) was isolated from the reaction of Nd(SePh)(3) with Se to confirm that chalcogenolate displacement is general to the redox-inactive lanthanides and that the intense colors of the Sm selenido clusters are related to the redox activity of the Ln. The two pyridine complexes (py)(8)LnSe(6)(SePh)(12) (Ln = Nd, Sm) are isostructural. Crystal data (Mo Kalpha, 153(2) K) are as follows. (THF)(8)Sm(8)Se(6)(SPh)(12): triclinic space group P&onemacr;, a = 17.637(7) Å, b = 18.337(5) Å, c = 20.466(12) Å, alpha = 103.04(4) degrees, beta = 94.71(4) degrees, gamma = 94.28(3) degrees, Z = 2. (py)(8)Sm(8)Se(6)(SePh)(12): monoclinic space group C2/m, a = 18.770(2) Å, b = 28.113(4) Å, c = 16.461(3) Å, beta = 120.65(1) degrees, Z = 2. (THF)(8)Sm(8)S(6)(SePh)(12): orthorhombic space group Pcab, a = 19.803(3) Å, b = 22.446(3) Å, c = 26.072(4) Å, Z = 8.
RESUMO
The early and late lanthanides form stable complexes with the pyridinethiolate (2-S-NC(5)H(4), or SPy) ligands. The Ce compound Ce(SPy)(3) is relatively insoluble in neutral organic donor solvents such as THF or pyridine but can be solubilized by the addition of [PEt(4)][SPy] to form the orange homoleptic cerium thiolate [PEt(4)][Ce(SPy)(4)] (1). Low-temperature structural characterization of 1 showed that the complex is isostructural with the known Eu(III) derivative. Further oxidation of Ce(III) with dipyridyl disulfide does not occur. Molecular 1 is colored due to a low-energy f(1)-to-d(1) promotion. As the size of the lanthanide ion decreases, the solubility of neutral Ln(SPy)(3) appears to increase. Colorless [PEt(4)][Ln(SPy)(4)] (Ln = Ho (2), Tm (3)) can also be isolated by fractional crystallization, and the compounds are isostructural with the Ce and Eu derivatives. The neutral complexes of Ho and Tm are also slightly soluble in acetonitrile and dimethoxyethane and very soluble in pyridine. Both divalent and trivalent Yb complexes of the pyridinethiolate ligand dissolve in and crystallize from pyridine. Divalent Yb(SPy)(2) crystallizes as the pentagonal bipyramidal molecule (py)(3)Yb(SPy)(2) (4). One pyridine nitrogen and the four donor atoms of the two pyridinethiolate ligands are bound in equatorial positions, and two neutral pyridine ligands occupy the axial sites. The Yb(III) compound crystallizes readily from pyridine as molecular 8-coordinate (py)(2)Yb(SPy)(3) (5). Compounds 4 and 5 are intensely colored; 4 has a visible Yb(II)-to-pyridine charge transfer excitation that is virtually identical in energy to the analogous excitation in SmI(2)(py)(4), while 5 has a visible S-to-Yb charge transfer absorption. Crystal data (Mo Kalpha, 153(5) K) are as follows: 1, monoclinic space group P2/n, a = 15.118(6) Å, b = 16.117(4) Å, c = 26.443(7) Å, beta = 90.14(3) degrees, Z = 4; 4, monoclinic space group Cc, a = 10.588(1) Å, b = 16.810(3) Å, c = 14.833(5) Å, beta = 109.12(2) degrees, Z = 4; 5, monoclinic space group P2(1)/n, a = 9.672(2) Å, b = 16.293(4) Å, c = 19.214(3) Å, beta = 101.51(2) degrees, Z = 4.