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PubMed1999

Ultrastructural changes of erythrocyte membrane skeletons in chorea-acanthocytosis and McLeod syndrome revealed by the quick-freezing and deep-etching method.

The shapes of acanthocytic erythrocytes have been thought to be related to changes of the organization of the membrane components. In this study, acanthocytes from a patient with chorea-acanthocytosis and a patient with McLeod syndrome were examined. These acanthocytes had a greater tendency to form spikes than normal erythrocytes in an incubation culture system, indicating their weakness against membrane tension. The membrane skeletons of erythrocytes from both patients were examined by our erythrocyte-splitting method followed by the quick-freezing and deep-etching method. The ultrastructural organization of the membrane skeletons was heterogeneous even in individual erythrocytes, indicating regional changes in the compactness of their meshworks. In the process of erythrocyte splitting, some erythrocyte membranes became reversed and protruded into the cytoplasmic side. In these regions, there were fewer filamentous structures. The focal membrane skeletal changes, which are probably one of the factors that induce the phenotype of an acanthocytic erythrocyte, were demonstrated for the first time by this method.

Acanthocytes↗

PubMed1979

Mechanical structure and function of the craniofacial skeleton of the domestic dog.

Masticatory habit is a major factor determining the morphology of the craniofacial skeleton. The craniofacial skeleton essentially comprises a series of bony stress-bearing bridges forming a structural framework. The structural framework of the skull of dog has been described as a rigid trestle-like structure; it can be illustrated by mechanically removing nonresistant areas of bone. It is then found that a framework is produced which is partially rigid (cranium) and partly flexible (rostrum). It is postulated that the flexibility of the rostrum acts to absorb shock and it is suggested that the primate postorbital bar is developed in response to craniofacial morphology which increases compressive bite forces.

Animals↗

PubMed1981

Transplacental effects of 1,25-dihydroxycholecalciferol and of 24,25-dihydroxycholecalciferol on the limb skeleton of fetuses and offspring rats.

The transplacental effects of 1,25(OH)2D3 and of 24,25(OH)2D3 on bone formation in rat fetuses and pups have been investigated. Pregnant rats treated with 1,25(OH)2D3 or with 1,25(OH)2D3 and 24,25(OH)2D3 showed hypercalcemia, while those treated with 24,25(OH)2D3 did not. Fetal weight was markedly reduced by treatment with 1,25(OH)2D3 and not with 24,25(OH)2D3 or with a combination of both metabolites. Microscopical examination of fetal long bones showed after treatment with 1,25(OH)2D3 a marked reduction in diaphysial length. Diaphyseal trabeculae were thin and disorganized. The epiphysis had a thinner layer of hypertrophic and calcified cartilage. The numbers of osteoclasts in the diaphysis and metaphysis were the same as in controls. Treatment with 24,25(OH)2D3 did not affect fetal bone length; many bone trabeculae were found in the diaphyseal cavity leaving small bone marrow spaces; the number of osteoclasts in the metaphysis and in the diaphysis was increased. All changes in the skeleton disappeared during the first week after birth. It can be suggested that high doses of 1,25(OH)2D3 inhibit bone formation and maturation of cartilage. The addition of 24,25(OH)2D3 to 1,25(OH)2D3 seemed to reduce the toxic effects of the latter on the fetal skeleton. These results point to a definite difference between the action of high doses of 1,25(OH)2D3 and 24,25(OH)2D3 on fetal bone.

24,25-Dihydroxyvitamin D 3↗

PubMed1983

Effects of retinoic acid on the development of the facial skeleton in hamsters: early changes involving cranial neural crest cells.

Treatment of gravid hamsters with 60/mg of retinoic acid on the 8th day of pregnancy resulted in facial skeleton defects in 100% of the survivors examined by alizarin staining at term. An investigation of the early stages in the development of these malformations indicated that the teratogen induced delayed and disorganized patterns of cranial neural crest cell migration as well as extensive death and damage of crest cells. The results demonstrate that retinoic acid provides a useful tool for studies in the pathogenesis of facial skeletal abnormalities in vivo. Moreover, the extensive defects seen in the teratogen-treated litters at term, together with the results of the microscopical analyses, support the hypothesis that cranial neural crest cells make an important contribution to the development of the mammalian facial skeleton.

Animals↗

PubMed1990

Study of the elastic skeleton of intracranial arteries in animal and human vessels by scanning electron microscopy.

We studied the elastic skeleton of major cerebral arteries in rats, monkeys, and one human using scanning electron microscopy after hot formic acid extraction followed by freeze-drying. For comparison, we also examined the thoracic aorta and femoral artery of rats. The cerebral arteries of rats had one distinct internal elastic lamina connected to the thin adventitia with sponge-like medial elastic tissue. This internal elastic lamina had fenestrations, which we found to be less frequent in cerebral arteries than in extracranial arteries, and fold-like protrusions into the lumen. This finding has not been recognized before. Such protrusions were more prominent in cerebral arteries than in extracerebral arteries. At the apical intimal pad, the internal elastic lamina appeared to be continuous, making a honeycomb-like structure. The folds and fenestrations were numerous at the apex. There were no essential differences among species. Our study shows that the internal elastic lamina is not a simple sheet but part of the complicated architecture of the elastic tissue of the vessel wall. These differences in the elastic skeleton, including fenestrations and fold-like structures, in various sites of different arteries may explain the development of various localized vascular diseases.

Animals↗

PubMed1982

Differential effects of endocrine dysfunction on the axial and the appendicular skeleton.

In 100 patients with various types of endocrine dysfunction, we measured bone mineral density (BMD) at the midradius (greater than 95% cortical bone) and distal radius (75% cortical and 25% trabecular bone) by single photon absorptiometry and at the lumbar spine (greater than 66% trabecular bone) using the new technique of dual photon absorptiometry. BMD in each endocrine disorder deviated in at least one site from the sex-specific age regression of 187 normal subjects. For patients with primary hyperparathyroidism, hypercortisolism, and hyperthyroidism this deviation was negative (suggesting bone loss), whereas for patients with secondary hyperparathyroidism due to chronic renal failure, acromegaly, and postsurgical hypoparathyroidism it was positive (suggesting bone gain). When all six states of endocrine dysfunction were compared concomitantly by multivariate analysis of variance, the profile of the changes in BMD differed significantly (P less than 0.001), indicating a nonuniform response of bone to the various hormonal alterations. When values for BMD at each of the three scanning sites were compared the midradius and distal radius did not differ significantly; either of the radius measurements, however, differed significantly (P less than 0.001) from the lumbar spine. Thus, the BMD of the axial skeleton cannot be reliably predicted from measurements made in the appendicular skeleton. We conclude that the effects of endocrine dysfunction on bone density are complex and are both disease and site specific.

Absorptiometry, Photon↗

PubMed1986

Rates of bone loss in the appendicular and axial skeletons of women. Evidence of substantial vertebral bone loss before menopause.

We made longitudinal measurements of bone mineral density (BMD) in 139 normal women (ages 20-88 yr) at midradius (99% cortical bone) and lumbar spine (approximately 70% trabecular bone) by single- and dual-photon absorptiometry. BMD was measured 2-6 (median, 3) times over an interval of 0.8-3.4 yr (median, 2.1 yr). For midradius, BMD did not change (+0.48%/yr, NS) before menopause but decreased (-1.01%/yr, P less than 0.001) after menopause. For lumbar spine, there was significant bone loss both before (-1.32%/yr, P less than 0.001) and after (-0.97%/yr, P = 0.006) menopause; these rates did not differ significantly from each other. Our data show that before menopause little, if any, bone is lost from the appendicular skeleton but substantial amounts are lost from the axial skeleton. Thus, factors in addition to estrogen deficiency must contribute to pathogenesis of involutional osteoporosis in women because about half of overall vertebral bone loss occurs premenopausally.

Adult↗

PubMed1999

Protein 4.1R-deficient mice are viable but have erythroid membrane skeleton abnormalities.

A diverse family of protein 4.1R isoforms is encoded by a complex gene on human chromosome 1. Although the prototypical 80-kDa 4.1R in mature erythrocytes is a key component of the erythroid membrane skeleton that regulates erythrocyte morphology and mechanical stability, little is known about 4.1R function in nucleated cells. Using gene knockout technology, we have generated mice with complete deficiency of all 4.1R protein isoforms. These 4.1R-null mice were viable, with moderate hemolytic anemia but no gross abnormalities. Erythrocytes from these mice exhibited abnormal morphology, lowered membrane stability, and reduced expression of other skeletal proteins including spectrin and ankyrin, suggesting that loss of 4. 1R compromises membrane skeleton assembly in erythroid progenitors. Platelet morphology and function were essentially normal, indicating that 4.1R deficiency may have less impact on other hematopoietic lineages. Nonerythroid 4.1R expression patterns, viewed using histochemical staining for lacZ reporter activity incorporated into the targeted gene, revealed focal expression in specific neurons in the brain and in select cells of other major organs, challenging the view that 4.1R expression is widespread among nonerythroid cells. The 4.1R knockout mice represent a valuable animal model for exploring 4.1R function in nonerythroid cells and for determining pathophysiological sequelae to 4.1R deficiency.

Animals↗

PubMed2004

Semi-skeletonized internal mammary artery grafts and sternal wound complications.

This study aimed to evaluate the risk factors for sternal wound complications in patients undergoing myocardial revascularization using bilateral semi-skeletonized internal mammary arteries. Prospectively collected data on 751 patients undergoing coronary artery surgery from September 1994 to August 2002 were analyzed. The mean age of the patients was 56 years, 633 (84%) were male, 44 (6%) were over 66 years of age, and 170 (23%) were diabetic. Forty-four (5.9%) patients developed sternal wound complications. Among these cases, sternal infection occurred in 22 (2.9%) patients, of which 15 (2.0%) had sternal infection with mediastinitis and 7 (0.9%) had sternal infection alone. Independent risk factors for any sternal wound complications were peripheral vascular disease, diet-controlled diabetes, and delayed sternal closure. The risk factors for sternal infection were diabetes, postoperative pulmonary complications, and postoperative stroke. The perioperative mortality rate was 1.5% (11 patients), including 2 patients who had sternal wound complications. The use of bilateral semi-skeletonized internal mammary artery conduits carries a comparable sternal wound complication rate as conduits harvested by other techniques.

Adult↗

PubMed1983

Pattern of uptake of americium-241 by the rat skeleton and its subsequent redistribution and retention: implications for human dosimetry and toxicology.

The distribution and retention of intravenously injected 241Am in the skeleton of the female rat has been investigated using autoradiographic and radiochemical techniques. The studies were designed to assess the dosimetric and toxicologic implications of an 241Am intake by man. They showed that in the rat approximately one third of the intravenously injected 241Am was deposited in the skeleton where it appeared to be retained with a long biological half-time. The studies also showed: 1 241Am is initially deposited onto all types of bone surface including endosteal surfaces, periosteal surfaces and those of the vascular canals within cortical bone, but seems to be preferentially deposited onto those that are resorbing, 2 Bone accretion results in the burial of surface deposits of 241Am, 3 Bone resorption causes the removal of 241Am from surfaces, 4 Resorbed 241Am is retained by phagocytic cells (probably macrophages) in the bone marrow, 5 The transfer of 241Am from the phagocytic cells in the marrow to adjacent bone surfaces seems to occur, (local recycling). 6 The possibility that some of the 241Am removed from the bone surfaces enters the blood and is redeposited in bone, (systemic recycling) cannot be dismissed. These results show that 241Am deposition and redistribution in bone shares many characteristics with other 'bone surface-seeking radionuclides' typified by 239Pu. Consequently, it is suggested that a similar model to that used to calculate annual limits of intake for 239Pu in man would be suitable for the calculation of corresponding values for the 241Am isotopes.

Americium↗

PubMed2004

Identification of RANKL in osteolytic lesions of the facial skeleton.

RANKL (receptor activator of nuclear factor kappaB ligand) promotes osteoclast differentiation, stimulates osteoclast activity, and prolongs osteoclast survival and adherence to bone. Abnormalities of the RANKL/RANK/osteoprotegerin system have been implicated in a range of diseases, including osteoporosis. To date, no work has been done in osteolytic lesions of the facial skeleton. In this study, specimens of ameloblastomas, dentigerous cysts, odontogenic keratocysts, and radicular cysts were subjected to immunohistochemical analysis for RANKL and tartrate-resistant acid phosphatase (TRAP). Immunofluorescence staining for TRAP was visualized under confocal microscopy. All specimens demonstrated distinct positive immunoreactivity to RANKL and TRAP. The TRAP-positive cells also stained with in situ hybridization for human calcitonin receptor, a definitive marker for osteoclasts. Mononuclear pre-osteoclasts were observed to migrate from blood to the connective tissue stroma and multinucleate toward the bone surface. It can be concluded that RANKL plays a role in bone resorption in osteolytic lesions of the facial skeleton.

Acid Phosphatase↗

PubMed2007

Remodeling the dentofacial skeleton: the biological basis of orthodontics and dentofacial orthopedics.

Orthodontic tooth movement is dependent upon the remodeling of the periodontal ligament and alveolar bone by mechanical means. Facial sutures are also fibrous articulations, and by remodeling these joints, one can alter the positional relationships of the bones of the facial skeleton. As might be expected from the structure and mobility of the temporomandibular joint (TMJ), this articulation is more resistant to mechanical deformation, and whether functional mandibular displacement can alter the growth of the condyle remains controversial. Clinical investigations of the effects of the Andresen activator and its variants on dentofacial growth suggest that the changes are essentially dento-alveolar. However, with the popularity of active functional appliances, such as the Herbst and twin-block based on 'jumping the bite', attention has focused on how they achieve dentofacial change. Animal experimentation enables informed decisions to be made regarding the effects of orthodontic treatment on the facial skeleton at the tissue, cellular, and molecular levels. Both rat and monkey models have been widely used, and the following conclusions can be drawn from such experimentation: (1) Facial sutures readily respond to changes in their mechanical environment; (2) anterior mandibular displacement in rat models does not increase the mitotic activity of cells within the condyle to be of clinical significance, and (3) mandibular displacement in non-human primates initiates remodeling activity within the TMJ and can alter condylar growth direction. This last conclusion may have clinical utility, particularly in an actively growing child.

Alveolar Process↗

PubMed1990

The presence of a type IV collagen skeleton associated with periductal elastosis in breast cancer.

Using serial sections of frozen and AFA-fixed tissues from 34 breast cancers, we studied the presence of basement membrane material in the areas of elastosis. Various amounts of type IV collagen but not of laminin were demonstrated in areas of periductal elastosis. In some tumors, type IV collagen accumulated beneath the basement membrane. Periductal elastosis in areas of extensive fibrosis showed focal type IV collagen immunoreactivity, indicating remnants of ducts. Interstitial elastosis corresponded with weak type IV collagen reactivity. Each tumor showed type IV collagen immunostaining of the elastotic areas, with various degrees of intensity. Negative crossreactivity of the type IV collagen antibody with elastin was verified in skin biopsies with solar elastosis. Pre-incubation of the antibody with large amounts of elastin demonstrated an identical immunoreactivity. The specificity of the antibody was confirmed by ELISA and by Western blot analysis. To explain the periductal elastosis, we propose the following hypothesis. Excessive production of basement membrane material by the epithelial cells of the ducts leads to formation of a type IV collagen skeleton. This skeleton can act as the matrix for a secondary deposition of elastic material.

Basement Membrane↗

PubMed2004

Lumbar spine fracture in a 34,100-year-old skeleton: the oldest known prehistoric spine fracture.

WE EXAMINED SPECIAL pathological changes of the lumbar spine from skeleton remains referred to as "Stetten 1," one of the earliest specimens of modern humans dating from the Early Stone Age (Upper Paleolithic). The skeleton was discovered during archaeological excavations under Riek in 1931 in the Vogelherd Cave near Stetten, close to the Lone Valley of southwestern Germany. The archaeological context is the so-called Aurignacian period (40,000-30,000 yr ago), representing the earliest cultural step of modern humans in Europe. Accelerator mass spectrometry with (14)C measurement yields a calibrated age of these remains averaging 34,100 years before the present. The L3-L4 vertebrae exhibit marginal bone fusion on the right side with a smooth surface. They show 20- to 30-degree kyphosis secondary to wedge impaction of the L4 vertebral body. The facet joints and vertebral bodies reveal small marginal osteophytes with even joint surfaces, indicating low degenerative changes. Stetten 1 is characterized by the presence of a healed lumbar spine fracture. It documents the earliest known case thus far of spine fracture among modern humans.

Adult↗

PubMed1996

Functional cooperation between the non-paralogous genes Hoxa-10 and Hoxd-11 in the developing forelimb and axial skeleton.

The Abdominal B-related Hoxa-10 gene displays similar expression patterns in the differentiating forelimbs and hindlimbs of the mouse, with preferential expression around the humeral and femoral cartilages and more diffuse expression in distal regions. We found that a targeted disruption of Hoxa-10 has almost no effect in the forelimbs, while it affects the proximal hindlimb skeleton. The alterations were located along the dorsolateral side of the femur (labium laterale), with an enlargement and distal shift of the third trochanter, a misshapen lateral knee sesamoid, a supernumerary 'ligament' connecting these structures and an occasional duplication of the femoral trochlea. Some Hoxa-10-/- mutant mice developed severe degenerative alterations of the knee articulation upon ageing. Viable Hoxa-10/Hoxd-11 double mutant mice were produced by genetic intercrosses. The compound mutation resulted in synergistic forelimb phenotypic alterations, consisting of: (i) an exacerbation of Hoxd-11-/- phenotypic traits in the carpal and digital region, e.g. more pronounced truncations of the ulna styloid, pyramidal and pisiform bones and of some metacarpal and phalangeal bones and (ii) marked alterations in a more proximal region which is nearly unaffected in Hoxd-11-/- single mutants; the entire radius and ulna were truncated and thickened, with deformations of the ulna proximal extremity. Thus, functional redundancy can occur even between non-paralogous Abdominal B-related Hox genes. The double Hoxa-10/Hoxd-11 mutation also conferred full penetrance to the sacral and caudal vertebrae transformations which are approximately 50% penetrant in Hoxd-11-/- single mutants, revealing that functional cooperation can also occur between non-paralogous Hox gene products in axial skeleton patterning.

Abnormalities, Multiple↗

PubMed1996

Specific and redundant functions of the paralogous Hoxa-9 and Hoxd-9 genes in forelimb and axial skeleton patterning.

Using gene targeting, we have produced mice with a disruption of Hoxa-9 or Hoxd-9, two paralogous Abdominal B-related genes. During embryogenesis, these genes are expressed in limb buds and along the vertebral axis with anterior expression boundaries at the level of prevertebra #20 for Hoxa-9 and #23 for Hoxd-9. Skeletal analysis revealed homeotic transformations corresponding to anteriorisations of vertebrae #21 to #25 (L1 to L5) in the lumbar region of Hoxa-9-/- mutants; vertebrae #23 to #25 (L3 to L5) in the lumbar region together with vertebrae #28, #30 and #31 (S2, S4 and Ca1) in the sacrum and tail were anteriorized in Hoxd-9-/- mutants. Thus, anteriorisation of vertebrae #23 to #25 were common to both phenotypes. Subtle forelimb (but not hindlimb) defects, corresponding to a reduction of the humerus length and malformation of its deltoid crest, were also observed in Hoxd-9-/-, but not in Hoxa-9-/-, mutant mice. By intercrosses between these two lines of mutant mice, we have produced Hoxa-9/Hoxd-9 double mutants which exhibit synergistic limb and axial malformations consisting of: (i) an increase of penetrance and expressivity of abnormalities present in the single mutants, and (ii) novel limb alterations at the level of the forelimb stylopod and additional axial skeleton transformations. These observations demonstrate that the two paralogous genes Hoxa-9 and Hoxd-9 have both specific and redundant functions in lumbosacral axial skeleton patterning and in limb morphogenesis at the stylopodal level. Taken all together, the present and previously reported results show that disruption of different Hox genes can produce similar vertebral transformations, thus supporting a combinatorial code model for specification of vertebral identity by Hox genes.

Abnormalities, Multiple↗

PubMed2002

Requirement for endoderm and FGF3 in ventral head skeleton formation.

The vertebrate head skeleton is derived in part from neural crest cells, which physically interact with head ectoderm, mesoderm and endoderm to shape the pharyngeal arches. The cellular and molecular nature of these interactions is poorly understood, and we explore here the function of endoderm in this process. By genetic ablation and reintroduction of endoderm in zebrafish, we show that it is required for the development of chondrogenic neural crest cells, including their identity, survival and differentiation into arch cartilages. Using a genetic interference approach, we further identify Fgf3 as a critical component of endodermal function that allows the development of posterior arch cartilages. Together, our results reveal for the first time that the endoderm provides differential cues along the anteroposterior axis to control ventral head skeleton development and demonstrate that this function is mediated in part by Fgf3.

Animals↗

PubMed1994

Immunolocalization of tropomodulin, tropomyosin and actin in spread human erythrocyte skeletons.

The human erythrocyte membrane skeleton consists of a network of short actin filaments cross-linked into a hexagonal network by long, flexible spectrin molecules. The lengths of the short actin filaments (33 +/- 5 nm) at the central junctions are proposed to be stabilized and limited by association with tropomyosin and the tropomyosin-binding protein, tropomodulin. Here, we use immunogold labelling followed by negative staining to specifically localize tropomodulin, tropomyosin and actin to the sites of the central junctions in spread membrane skeletons. In addition to negative staining, immunogold labelling for tropomodulin at the sites of the central junctions was also visualized by a quick-freeze, deep-etch, rotary-replication technique. These experiments confirm previous indirect evidence that the short filaments at the central junctions are indeed actin filaments and provide the first direct evidence that tropomodulin and tropomyosin are associated with the erythrocyte actin filaments in situ.

Actins↗