bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lingual incisor traits in modern hominoids and an assessment of their utility for fossil hominoid taxonomy
Authors: Pilbrow Varsha 
Published: December 2005

AbstractThe morphology of the anterior dentition has received scant attention for purposes of taxonomic discrimination. Recently, however, lingual incisor morphology was used in differentiating several Miocene ape species and genera. This paper assesses the utility of this morphology for taxonomic discrimination by examining the nature and patterns of variation in lingual incisor morphology in extensive samples of modern chimpanzees, gorillas, orangutans, and gibbons. This paper documents discrete morphological traits on the lingual side of incisors. Trait frequencies are used in univariate and multivariate analyses to examine the apportionment of variation in species, subspecies, and populations. A correlation between lingual incisor traits, tooth dimensions, and sex attempts to determine if such factors affect the manifestation of traits. Finally, the findings are applied to understanding patterns of variation in the Miocene hominids. The study demonstrates that: 1) lingual incisor morphology differs substantially between the hylobatids and great apes; 2) variation in incisor traits is high within species, and most of it is found within local populations; and 3) incisor traits do not correlate significantly with incisor dimensions or sex. Species and to some extent subspecies of extant hominoids can be differentiated statistically using lingual incisor traits, but the frequency of traits such as continuous or discontinuous cingulum, or the presence or absence of pillars, differentiates them. Given this pattern of variation, I argue that it is necessary to assume and document similar patterns of variation in Miocene apes before incisor morphology is used for differentiating taxa. Am J Phys Anthropol, 2006. © 2005 Wiley‐Liss, Inc.
Population affinities of Neolithic Siberians: A snapshot from prehistoric Lake Baikal
Authors: Mooder K.P. , Schurr T.G. , Bamforth F.J. , Bazaliiski V.I. , Savel'ev N.A. 
Published: December 2005

AbstractArchaeological evidence supports the inhabitation of the Lake Baikal region since the Paleolithic. Both metric and nonmetric osteological studies suggest that Neolithic Cis‐Baikal populations are the ancestors of contemporary inhabitants of the region. To date, ancient DNA data have not been used to corroborate this biological continuity hypothesis. This study presents a temporal snapshot of the Cis‐Baikal Neolithic by examining mtDNA diversity in two cemetery populations situated on the Angara River downstream of Lake Baikal. The 800 years separating the use of the two cemeteries is thought to represent a biocultural hiatus in the Cis‐Baikal region, one that ended when a new group migrated into the area. To assess the likelihood that genetic continuity exists between these two Neolithic groups, we examined both mtDNA coding region and hypervariable region I (HVI) polymorphisms from skeletal remains excavated from both cemeteries (Lokomotiv and Ust'‐Ida). The mtDNA haplogroup distributions of the two cemetery populations differ significantly, suggesting that they were biologically distinct groups. When the biological distance between these Neolithic groups is compared with modern Siberian and other East Eurasian groups, the posthiatus group (Serovo‐Glazkovo) generally aligns with contemporary Siberians, while the prehiatus (Kitoi) individuals are significantly different from all but modern Kets and Shorians living in the Yenisey and Ob River basins to the west of Lake Baikal. These results suggest that the Lake Baikal region experienced a significant depopulation event during the sixth millennium BP, and was reoccupied by a new immigrant population some 800 years later. Am J Phys Anthropol, 2006. © 2005 Wiley‐Liss, Inc.
Human osseous intervertebral foramen width
Authors: Rühli F.J. , Müntener M. , Henneberg M. 
Published: December 2005

AbstractAlterations of the width of the human intervertebral foramen can play a pathophysiological role in low back pain. Osseous dimensions of the human intervertebral foramen are rarely recorded. Therefore, we present reference data obtained from skeletal samples of known lifestyle, population affinity, sex, and age at death. Cervical, thoracic, and lumbar vertebrae of functional transition zones of 71 macroscopically normal spines from early 19th century AD Swiss burial sites were selected. The intervertebral foramen widths (IFW) were analyzed with respect to possible lateralization and the impact of sex, individual age, and stature. Neither a significant side difference nor a correlation of IFW with individual age or stature could be found. Females show somewhat larger IFW than males, especially in the lumbar region. Data comparisons with earlier studies are limited due to methodological differences and possible interpopulational variations. Furthermore, the osseous intervertebral foramen only reveals a glimpse of the clinically relevant in vivo structure. Nevertheless, more focus on the osseous dimensions of the intervertebral foramen will provide baseline data of this important anatomical landmark. These data could also explore the peculiarities of the intervertebral foramen, such as its reverse sex dimorphism. Am J Phys Anthropol, 2006. © 2005 Wiley‐Liss, Inc.
Urban and rural differences in mortality and causes of death in historical Poland
Authors: Budnik Alicja , Liczbińska Grażyna 
Published: December 2005

AbstractThe purpose of this paper is to document and interpret urban‐rural differences in mortality in the past. To this end, we used data on mortality in Wielkopolska, Poland, in the 19th century and at the beginning of the 20th century. The data on mortality in rural areas (N = 1,173,910 deceased), small towns (N = 573,903 deceased), and Poznań, the capital of the Wielkopolska region (N = 86,352 deceased), were gathered from original Prussian statistical yearbooks (Preussische Statistik). Causes of death were also analyzed (rural areas, N = 449,576 deceased; small towns, N = 238,365 deceased; Poznań, N = 61,512 deceased). Mortality measures such as crude death rate (CDR), infant death rate (IDR), and neonatal and postneonatal death rates were calculated. Life tables were constructed for both stationary and stable population models and measures of the opportunity for natural selection calculated (Crow's index Im, potential gross reproduction rate Rpot, and biological state index Ibs). Relative frequencies of leading causes of death were computed. Stratification depending on the place of residence was evident in all mortality measures as well as in the values of the life tables and the measures of the opportunity for natural selection, but it was reverse of what is observed today in developed countries. In Poznań (a large industrial city), the mortality situation was the least favorable. It was caused by large population density, lack of water supply and sewage systems (up to 1896), and bad working conditions. The values of CDR ranged between 26.89–31.46, and IDR between 190.6–280.5. Newborn life expectancy (for a stable population model) was 31.6 years, Im = 0.79, Rpot = 0.85, and Ibs = 0.47. The most common causes of death were tuberculosis, other diseases of the respiratory and circulatory systems, dysentery and diarrhea, and cancer. These diseases were less common in rural areas, so they had the most favorable values of mortality measures (CDR between 22.87–27.32, IDR between 181.8–219.4, life expectancy of newborn e0 = 42.12, Im = 0.55, Rpot = 0.93, Ibs = 0.60). Infectious diseases (other than tuberculosis), frailty at birth, and frailty in old age were the most frequent causes of death in rural areas. Small towns (population <20,000) had a mortality intermediate between city and rural areas. Am J Phys Anthropol, 2006. © 2005 Wiley‐Liss, Inc.
Skeletal manifestations of rickets in infants and young children in a historic population from England
Authors: Mays S. , Brickley M. , Ives R. 
Published: December 2005

AbstractGross and radiographic changes characteristic of inadequate bone mineralization due to rickets are described in 21 immature skeletons from a 19th century urban population from Birmingham, England. The aims of the study are as follows: to evaluate and if possible augment existing dry‐bone criteria for the recognition of rickets in immature skeletal remains; to investigate the value of radiography for the paleopathological diagnosis of rickets; and to compare and contrast the expression of rickets in this group with that previously documented for a rural agrarian population from Wharram Percy, England. Some gross skeletal signs of rickets which were not previously well‐documented in paleopathological studies are noted. The worth of radiography for evaluating structural changes to both cortical and trabecular bone in the disease is demonstrated, and features useful for the interpretation of vitamin D deficiency are discussed. The pattern of skeletal elements affected and the severity of changes differs in the Birmingham group from that seen in the comparative rural population. It is emphasized that a variety of factors may influence the expression of rickets in paleopathological material, including rate of skeletal growth, age cohort affected, and intensity of vitamin D deficiency. Nevertheless, careful analysis, not only of the frequency of rickets but also of the degree of severity of lesions and the patterning with respect to skeletal elements affected, may enable more nuanced understanding of the biocultural context of the disease in earlier populations. Am J Phys Anthropol, 2006. © 2005 Wiley‐Liss, Inc.
Chemokine receptor CCR2 expression by systemic sclerosis fibroblasts: Evidence for autocrine regulation of myofibroblast differentiation
Authors: Carulli Maria Teresa , Ong Voon Hong , Ponticos Markella , Shiwen Xu , Abraham David John , Black Carol Mary , Denton Christopher Paul 
Published: December 2005

AbstractObjectiveTo investigate expression of the chemokine receptor CCR2 on key cell types involved in the pathogenesis of systemic sclerosis (SSc) and to assess the potential for autocrine activation of SSc dermal fibroblasts via CCL2/CCR2.MethodsChemokine receptor expression in skin biopsy tissues and explanted dermal fibroblasts from a well‐characterized cohort of SSc patients was examined using immunohistochemistry and flow cytometry techniques. Autocrine regulation of the expression of fibrotic markers in CCR2+ SSc fibroblast cell lines was assessed using specific ligand or receptor antagonists.ResultsWe identified strong CCR2 expression in skin biopsy samples of early‐stage diffuse cutaneous SSc (dcSSc), but not late‐stage dcSSc or limited cutaneous SSc. Double labeling confirmed up‐regulation of CCL2/CCR2 on myofibroblasts, pericytes, lymphocytes, macrophages, and endothelial cells. Explanted dermal fibroblasts from early dcSSc tissues expressed CCR2 and CXCR2 in 55% and 66% of cell strains, respectively. There was no expression in control fibroblasts. CCR2+ fibroblasts demonstrated a profibrotic phenotype, with overexpression of α‐smooth muscle actin (α‐SMA), connective tissue growth factor (CTGF), and CCL2. Flow cytometric analysis identified a subset of CCR2+ SSc fibroblasts expressing the myofibroblast marker α‐SMA. In these cultures, specific inhibition of CCL2 or CCR2 attenuated the overexpression of α‐SMA, but not CTGF or plasminogen activator inhibitor 1.ConclusionOur results show that CCR2 is up‐regulated in early dcSSc on cell types known to be activated in the disease, which is consistent with a key role in SSc pathogenesis. CCR2 expression on SSc fibroblasts appears to regulate the expression of CCL2 and α‐SMA. Our findings suggest potential autocrine regulation of key profibrotic properties via a CCL2/CCR2 loop in early‐stage dcSSc.
Induction of endothelial cell apoptosis by the binding of anti–endothelial cell antibodies to Hsp60 in vasculitis‐associated systemic autoimmune diseases
Authors: Jamin Christophe , Dugué Christophe , Alard Jean‐Éric , Jousse Sandrine , Saraux Alain , Guillevin Loïc , Piette Jean‐Charles , Youinou Pierre 
Published: December 2005

AbstractObjectiveAnti–endothelial cell antibodies (AECAs), which recognize a number of endothelial antigens, are seen in patients with systemic autoimmune diseases, more often in the presence of vasculitis than in its absence. Some AECAs induce apoptosis of endothelial cells (ECs), but their target antigens remain unknown. The aim of this study was to determine whether Hsp60 is a target antigen and whether AECAs induce apoptosis in ECs.MethodsTwo‐dimensional electrophoresis and conventional Western blotting techniques were used to characterize AECA targets. Hsp60 reactivity was determined by enzyme‐linked immunosorbent assay.ResultsHsp60 was shown to be targeted by a proportion of AECAs. The level of reactivity was higher in patients with systemic autoimmune disease and vasculitis than in those without vasculitis and in patients with systemic lupus erythematosus than in patients with other systemic autoimmune diseases. Hsp60 was expressed on the plasma membrane of heat‐stressed ECs, and this followed Hsp60 messenger RNA transcription, confinement of the protein to the cytoplasm, and translocation of the protein to the surface. Shedding of Hsp60 from ECs was induced by stress and resulted in the binding of soluble Hsp60 to the surface of ECs, particularly stressed ECs. Apoptosis of ECs was triggered by anti‐Hsp60–containing AECA‐positive sera and was inhibited by preincubation of the ECs with recombinant Hsp60.ConclusionOur data support the notion that Hsp60 is an important target for AECAs and that such an interaction contributes to pathogenic effects, especially in vasculitis‐associated systemic autoimmune disease.
Basic fibroblast growth factor inhibits the anabolic activity of insulin‐like growth factor 1 and osteogenic protein 1 in adult human articular chondrocytes
Authors: Loeser Richard F. , Chubinskaya Susan , Pacione Carol , Im Hee‐Jeong 
Published: December 2005

AbstractObjectiveTo determine the effects of basic fibroblast growth factor (bFGF) on the chondrocyte anabolic activity promoted by insulin‐like growth factor 1 (IGF‐1) and osteogenic protein 1 (OP‐1).MethodsHuman articular chondrocytes were cultured in alginate beads or as cartilage explants in serum‐free medium with or without IGF‐1 (100 ng/ml), OP‐1 (100 ng/ml), or bFGF (0–100 ng/ml). Cell survival, proliferation, proteoglycan synthesis, and total proteoglycan accumulation were measured after 21 days of culture in alginate beads, and proteoglycan synthesis was measured in explants.ResultsCell survival was not altered by bFGF at any dose, and chondrocyte proliferation was stimulated only at doses above 1 ng/ml. When combined with IGF‐1, 1 ng/ml of bFGF stimulated proliferation to 170% of control, but when combined with IGF‐1 and OP‐1, proliferation increased to 373% of control. Doses of bFGF of 100 ng/ml decreased total proteoglycan levels accumulated per cell by 60% compared with control and also inhibited the ability of IGF‐1 or OP‐1 to increase proteoglycan production. Likewise, sulfate incorporation in response to IGF‐1 and OP‐1 alone or together was completely inhibited by 50 ng/ml bFGF in both alginate and explant cultures.ConclusionThe anabolic activity of IGF‐1 and OP‐1, alone and in combination, is significantly inhibited by bFGF. The results suggest that excessive release of bFGF from the cartilage matrix during injury, with loading, or in arthritis could contribute to increased proliferation and reduced anabolic activity in articular cartilage.
Association of prevalent and incident knee cartilage defects with loss of tibial and patellar cartilage: A longitudinal study
Authors: Ding Changhai , Cicuttini Flavia , Scott Fiona , Boon Catrina , Jones Graeme 
Published: December 2005

AbstractObjectiveTo describe the association between prevalent and incident knee cartilage defects and loss of knee cartilage in male and female adults.MethodsA convenience sample of 325 subjects (mean age 45 years; age range 26–61 years) was evaluated at baseline and ∼2 years later. Knee cartilage volume, cartilage defect scores (0–4 scale), and joint surface area were determined using T1‐weighted fat‐suppression magnetic resonance imaging techniques. Height, weight, and radiographic evidence of osteoarthritis were measured by standard protocols.ResultsMultivariable analysis revealed that baseline cartilage defect scores at the medial tibia, lateral tibia, and patella had a dose‐response association with the annual rate of change in knee cartilage volume at the corresponding site (β = –1.3% to –1.2% per grade; P < 0.05 for all comparisons). In addition, an increase in knee cartilage defect score (change of ≥1) was associated with higher rates of knee cartilage volume loss at all sites (β = –1.9% to –1.7% per year; P < 0.01 for all comparisons). Furthermore, a decrease in the knee cartilage defect score (change of less than or equal to −1) was associated with an increase in knee cartilage volume at all sites (β = 1.0% to 2.7% per year; P < 0.05 for all comparisons).ConclusionPrevalent knee cartilage defects are predictive of compartment‐specific cartilage loss over 2 years. Both increases and decreases in knee cartilage defects are associated with changes in knee cartilage volume, which implies a potential for reversal of knee cartilage loss.
Precocious intima‐media thickening in patients with primary Sjögren's syndrome
Authors: Vaudo Gaetano , Bocci Elena Bartoloni , Shoenfeld Yehuda , Schillaci Giuseppe , Wu Ruihua , Del Papa Nicoletta , Vitali Claudio , Monache Francesco Delle , Marchesi Simona , Mannarino Elmo , Gerli Roberto 
Published: December 2005

AbstractObjectiveSystemic lupus erythematosus and rheumatoid arthritis represent independent risk factors for atherosclerosis (ATS), although this may be confounded by continuous pharmacologic treatment. Primary Sjögren's syndrome (SS) shares several features of these diseases and may therefore represent an interesting model for verifying the presence of accelerated ATS in the absence of pharmacologic interference. The present study therefore used this model to describe the presence of accelerated ATS in a group of young women.MethodsThirty‐seven untreated white women with primary SS were evaluated clinically and serologically. Carotid and femoral artery intima‐media thickness (IMT) was evaluated in the patients and in 35 age‐matched healthy women who served as controls.ResultsThe patients had a higher IMT than did the controls at both the carotid (mean ± SD 0.82 ± 0.24 mm versus 0.63 ± 0.20 mm; P ≤ 0.001) and the femoral (0.81 ± 0.26 mm versus 0.67 ± 0.23 mm; P ≤ 0.019) levels, and had a higher prevalence of carotid intima‐media thickening (49% versus 11% of controls; P ≤ 0.001). The patient subset with high carotid IMT showed an increased prevalence of leukopenia and circulating anti‐SSA antibodies; interestingly, the number of leukocytes was inversely correlated with the level of arterial IMT in patients with SS. Multivariate analysis demonstrated that anti‐SSA antibodies were independent predictors of carotid artery thickening, while leukopenia was a predictor of both carotid and femoral artery thickening.ConclusionSubclinical ATS was evident in about one‐half of the patients with SS. Its association with some features typical of connective tissue diseases, such as the presence of anti‐SSA and leukopenia, suggests that the immune dysregulation characterizing this autoimmune disorder may play a key role in inducing early ATS.
Raloxifene for postmenopausal women with systemic lupus erythematosus: A pilot randomized controlled study
Authors: Mok Chi Chiu , To Chi Hung , Mak Anselm , Ma Kwok Man 
Published: December 2005

AbstractObjectiveTo study the effects of raloxifene on disease activity and bone mineral density (BMD) in postmenopausal women with systemic lupus erythematosus (SLE).MethodsPostmenopausal women with osteopenia and inactive SLE were randomly assigned to receive either raloxifene (60 mg/day) plus elemental calcium (1,200 mg/day) or elemental calcium alone (control). Patients with a history of thromboembolism or antiphospholipid antibody positivity were excluded. BMD at various sites was serially measured, and lupus activity was serially assessed using the Safety of Estrogens in Lupus Erythematosus: National Assessment–Systemic Lupus Erythematosus Disease Activity Index (SELENA–SLEDAI).ResultsThe study group comprised 33 patients (16 assigned to receive raloxifene and 17 controls, mean ± SD age 53.8 ± 5.3 years). Age, body mass index, and baseline BMD values did not differ significantly between the 2 groups of patients. All patients were receiving low‐dose prednisolone. After 12 months, femoral neck BMD (mean ± SD −2.6 ± 1.0%; P = 0.02) and lumbar spine BMD (−3.3 ± 0.8%; P = 0.001) decreased significantly in the controls but not in the raloxifene group. No patient had a major flare of lupus, but mild/moderate flares occurred in 4 raloxifene‐treated and 6 control patients (P = 0.79). The total area under the curve of SELENA–SLEDAI scores was not significantly different between the 2 groups. A significant increase in the high‐density lipoprotein cholesterol level and a reduction in the low‐density lipoprotein cholesterol level were observed in the raloxifene group but not in controls. One patient in the raloxifene group (6%) withdrew from the study because of hot flushes. No thromboembolic events were reported.ConclusionRaloxifene was well tolerated in Chinese patients with SLE who had inactive disease and in whom hypercoagulability was not identified. Raloxifene maintained femoral neck and spinal BMD in patients receiving corticosteroids.
Identification of polyclonal and monoclonal antibodies against tissue plasminogen activator in the antiphospholipid syndrome
Authors: Lu Cai‐Sheng , Horizon Arash A. , Hwang Kwan‐Ki , FitzGerald John , Lin Wei‐Shiang , Hahn Bevra H. , Wallace Daniel J. , Metzger Allan L. , Weisman Michael H. , Chen Pojen P. 
Published: December 2005

AbstractObjectiveTo test the hypotheses that some plasmin‐reactive anticardiolipin antibodies (aCL) may bind to tissue plasminogen activator (tPA) and that some of the tPA‐reactive aCL may inhibit tPA activity.MethodsWe studied the reactivity of 8 patient‐derived monoclonal aCL with tPA and examined the presence of IgG anti‐tPA antibodies in patients with the antiphospholipid syndrome (APS). The effects of the reactive monoclonal aCL on the activity of tPA were also examined.ResultsSix patient‐derived plasmin‐reactive monoclonal aCL bound to tPA. Analysis of plasma samples revealed that 10 of 80 APS patients (12.5%) and 1 of 81 systemic lupus erythematosus patients (1.2%) had antibodies against fibrin‐associated tPA, based on a cutoff value equal to the mean + 2SD of the level in 28 normal subjects. Of the 6 tPA‐reactive monoclonal aCL, 2 of them (CL1 and CL15) inhibited tPA activity.ConclusionSome of the plasmin‐reactive aCL in APS patients may bind to tPA. Of the tPA‐reactive aCL, some (such as CL1 and CL15) may inhibit tPA activity and, thus, may be prothrombotic in the host.