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PubMed2006

Sacroiliac joint bridging: simple and reliable criteria for sexing the skeleton.

Vital to the study of past populations and an important phase in executing a forensic anthropological examination is the determination of skeleton sex. The aim of this study is to present an easy and reliable criterion for sexing the skeleton. The ilium and sacrum of 2845 skeletons were examined for new bone formation and for bridging/fusion in/across the sacroiliac joint. Sacroiliac joint bridging (SIB) was present in 12.27% of the males and 1.83% of the females. In 97% of the males bridging was extra-articular, whereas in all females bridging was intra-articular. In addition, computed tomograghy images of 81 in vivo individuals were examined for the same phenomenon. SIB was present in 34.2% of the males and 4.6% of the females. Bony spurs present on the ilium for a preliminary partial or full extra-articular bridging of the sacroiliac joint indicate a male skeleton. SIB presents an easy technique for sexing skeletons (especially in elderly individuals where the phenomenon of SIB becomes very common), as no prior knowledge, training, or equipment is required to apply the criterion.

Adolescent↗

PubMed1990

Elastic skeleton of intracranial cerebral aneurysms in rats.

In an attempt to clarify the developmental mechanism of cerebral aneurysms, we studied the elastic skeleton of experimentally induced cerebral aneurysms in rats under scanning electron microscopy after hot formic acid extraction followed by freeze-drying. We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate. The first noted change was the loss of folds protruding from the internal elastic lamina. Morphologic changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the elastic skeleton of first the intima, then the media. In large aneurysms with thick domes, we found proliferation of elastic lamellae that may reduce the risk of rupture. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of an aneurysm occurs due to disintegration of the elastic skeleton and not simply to rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of the cells that produce elastin.

Animals↗

PubMed1985

Linkage of a membrane skeleton to integral membrane glycoproteins in human platelets. Identification of one of the glycoproteins as glycoprotein Ib.

Experiments were performed to determine whether platelets contain a membrane skeleton. Platelets were labeled by a sodium periodate/sodium [3H]borohydride method and lysed with Triton X-100. Much of the filamentous actin could be sedimented at low g forces (15,600 g, 4 min), but some of the actin filaments required high-speed centrifugation for their sedimentation (100,000 g, 3 h). The latter filaments differed from those in the low-speed pellet in that they could not be depolymerized by Ca2+ and could not be sedimented at low g forces even from Triton X-100 lysates of platelets that had been activated with thrombin. Actin-binding protein sedimented with both types of filaments, but 3H-labeled membrane glycoproteins were recovered mainly with the high-speed filaments. The primary 3H-labeled glycoprotein recovered with this "membrane skeleton" was glycoprotein (GP) Ib. Approximately 70% of the platelet GP Ib was present in this skeleton. Several other minor glycoproteins, including greater than 50% of the GP Ia and small amounts of three unidentified glycoproteins of Mr greater than 200,000, were also recovered with the membrane skeleton. The Triton X-100 insolubility of GP Ib, GP Ia, a minor membrane glycoprotein of 250,000 Mr, and actin-binding protein resulted from their association with actin filaments as they were rendered Triton X-100-soluble when actin filaments were depolymerized with deoxyribonuclease I and co-isolated with actin filaments on sucrose gradients. When isolated platelet plasma membranes were extracted with Triton X-100, actin, actin-binding protein, and GP Ib were recovered as the Triton X-100 residue. These studies show that unstimulated platelets contain a membrane skeleton composed of actin filaments and actin-binding protein that is distinct from the rest of the cytoskeleton and is attached to GP Ib, GP Ia, and a minor glycoprotein of 250,000 Mr on the plasma membrane.

Actin Cytoskeleton↗

PubMed2003

Protein 4.2 is critical to CD47-membrane skeleton attachment in human red cells.

The reduction in expression of the integral membrane protein CD47 in human red blood cells (RBCs) deficient in protein 4.2 suggests that protein 4.2 may mediate a linkage of CD47 to the membrane skeleton. We compared the fractions of membrane skeleton-attached CD47, Rh-associated glycoprotein (RhAG), Rh, and band 3 in normal and protein 4.2-deficient cells using fluorescence-imaged microdeformation. We found that CD47 attachment decreases from 55% in normal cells to 25% to 35% in 4.2-deficient cells. RhAG, which has been shown to have no significant variation in expression among the cells studied, shows a significant decrease in membrane skeleton attachment in 4.2-deficient cells from 60% to 40%. Both Rh and band 3, which have also been shown to have no change in expression, show a smaller decrease from 75% attached in normal RBCs to 55% attached in 4.2-deficient cells. In normal cells, Rh phenotype influences CD47 expression but not the level of membrane skeleton attachment of CD47. In contrast, the results indicate that protein 4.2 strongly influences CD47 levels as well as the extent of membrane skeleton attachment in the RBC, whereas protein 4.2 affects membrane skeletal attachment of RhAG, Rh, and band 3 to a lesser extent.

Actins↗

PubMed1996

Alterations of maternal estrogen levels during gestation affect the skeleton of female offspring.

Estrogens have important effects on bone turnover in both humans and experimental animals models. Moreover, the decreased level of estrogen after menopause appears to be one of the key factors in determining postmenopausal osteoporosis. The presence of estrogen receptor in both osteoblasts and osteoclasts has suggested a direct role of these steroid hormones on bone tissue. Thus, this tissue is now regarded as a specific estrogen target tissue. Exposure to estrogens during various stages of development has been shown to irreversibly influence responsive target organs. We have recently shown that transient developmental neonatal exposure (days 1-5 of life) of female mice to estrogen resulted in an augmented bone density in the adult animals. The aim of the present study was to evaluate whether short-term modification of maternal estrogen levels during pregnancy would induce changes in the skeleton of the developing fetuses and to identify any long-term alterations that may occur. Pregnant mice were injected with varying doses (0.1-100 micrograms/kg maternal BW) of the synthetic estrogen diethylstilbestrol (DES) from day 9-16 of pregnancy. Offspring were weaned at 21 days of age, and effects on bone tissue of the female mice were evaluated in adulthood (6-9 months of age). Prenatal DES treatment(s) did not significantly affect BW. However, a dose-dependent increase in bone mass, both in the trabecular and cortical compartments, was observed in the prenatal DES-exposed female offspring. Furthermore, long bones of DES-exposed females were shorter than controls. Normal skeletal mineralization accompanied these changes in the bone tissue, as shown by a parallel increase in skeletal calcium content. Double tetracycline labeling performed in 6-month-old DES-exposed animals showed an increase in mineral apposition rate in adult DES-exposed mice as compared with untreated control animals, although no significant difference in the circulating estrogen levels was found in animals of this age. Experiments were then performed to evaluate whether perturbation of the estrogen surge at puberty in these diethylstilbestrol (DES)-exposed mice could reverse the observed changes. Femur length was chosen as a marker of potential estrogenic effect. Prepubertal ovariectomy of the prenatally DES-treated animals could only partially reverse the effects observed in the skeleton of the DES-treated animals. Further experiments were performed to evaluate whether these changes could have occurred in utero. CD-1 pregnant female mice were injected with DES (100 micrograms/kg maternal BW) from days 9-15 of gestation. On day 16 of gestation, fetuses were examined and stained by a standard Alizarin Red S and Alcian Blue procedure to visualize calcified and uncalcified skeletal tissue. Estrogen treatment induced an increase in the amount of calcified skeleton as compared with untreated controls and also a decrease in the length of long bones, strongly suggesting a change in both endochondral ossification and endosteal and periosteal bone formation. In summary, these data show, for the first time, that alterations in the maternal estrogenic levels during pregnancy can influence early phases of fetal bone tissue development and subsequently result in permanent changes in the skeleton. Finally, the effect of this short-term estrogen treatment can be seen in the fetal skeleton, suggesting an estrogen-imprinting effect on bone cell-programming in fetal life because treatment effects on bone cell turnover can be observed later in adult life.

Animals↗

PubMed1997

Differential effect of gender on the sizes of the bones in the axial and appendicular skeletons.

Recent observations suggest that throughout life the size of the vertebral bodies in females is smaller than that in males even after accounting for differences in body size. To confirm these reports and to determine whether similar differences exist in the appendicular skeleton, detailed measurements of the sizes of the vertebrae and the femur were obtained using computed tomography in 30 pairs of prepubertal boys and girls matched for age, height, and weight. Anthropometric parameters as well as gender influenced the cross-sectional area of the vertebrae. Heavier children had greater vertebral cross-sectional area than slender children regardless of gender, and the vertebral bodies were found to be significantly smaller in girls than in matched boys (approximately 11%), both using Student's t test (P < 0.0001) and its multivariate analog, the Hotelling's T2 test (P < 0.0001). In contrast to these findings in the axial skeleton, gender status did not influence the size of the bones in the appendicular skeleton, and neither the cross-sectional area (3.28 +/- 0.84 vs. 3.10 +/- 0.56 cm2) nor the cortical bone area (1.80 +/- 0.37 vs. 1.85 +/- 0.36 cm2) at the midshaft of the femur differed between boys and girls. These values, however, correlated strongly with all anthropometric indexes, and multiple regression analyses indicated that both measurements were primarily related to weight. The results suggest that although increases in mechanical loading associated with growth are the main determinant of the cross-sectional properties of the appendicular skeleton in children, factors other than body mass and related to gender have a significant role in the regulation of the sizes of the bones in the axial skeleton.

Body Weight↗

PubMed1993

Cell-cell interactions regulate skeleton formation in the sea urchin embryo.

In the sea urchin embryo, the primary mesenchyme cells (PMCs) make extensive contact with the ectoderm of the blastula wall. This contact is shown to influence production of the larval skeleton by the PMCs. A previous observation showed that treatment of embryos with NiCl2 can alter spicule number and skeletal pattern (Hardin et al. (1992) Development, 116, 671-685). Here, to explore the tissue sensitivity to NiCl2, experiments recombined normal or NiCl2-treated PMCs with either normal or NiCl2-treated PMC-less host embryos. We find that NiCl2 alters skeleton production by influencing the ectoderm of the blastula wall with which the PMCs interact. The ectoderm is responsible for specifying the number of spicules made by the PMCs. In addition, experiments examining skeleton production in vitro and in half- and quarter-sized embryos shows that cell interactions also influence skeleton size. PMCs grown in vitro away from interactions with the rest of the embryo, can produce larger spicules than in vivo. Thus, the epithelium of the blastula wall appears to provide spatial and scalar information that regulates skeleton production by the PMCs.

Animals↗

PubMed1996

Use of endogenous, stable lead isotopes to determine release of lead from the skeleton.

The stable lead isotope methodology can be used to study the release of lead from bone into the circulation because of its potential to distinguish circulatory lead from "older" and isotopically different skeletal lead that may have been accumulated years or decades earlier. Here we report the initial results from a larger ongoing study that evaluates the skeleton as a source of lead to the circulation in environmentally exposed human subjects. Lead concentrations and stable lead isotopic compositions were measured in blood and trabecular bone samples obtained from five patients who underwent total hip or knee joint replacement. All subjects contained low blood (1-6 micrograms/dl) and bone (0.6-7 micrograms/g dry weight) lead concentrations typical of environmentally exposed individuals. There were relatively large differences in the lead isotopic compositions between the paired blood and bone samples from each subject. These isotopic differences are attributed to differences in the lead isotopic compositions of past versus current lead exposures and to the long elimination half-life of lead in the skeleton compared to lead in the circulation. Based on these data, we determined that the skeleton contributed 40-70% of the lead in the blood of these subjects. This initial study demonstrates the utility of the stable lead isotope methodology for investigating the release of lead from the skeleton. It also shows that the skeleton can be an important endogenous source of lead exposure in environmentally exposed humans.

Aged↗

PubMed1984

Effect of pinealectomy on the plasma concentrations of prolactin, cortisol and testosterone in sheep in short and skeleton long photoperiods.

Two experiments were carried out to investigate the effects of pinealectomy on the responses of prolactin, cortisol and testosterone to skeleton long photoperiods (7 h light: 10 h darkness: 1 h light: 6 h darkness; 7L: 10D: 1L: 6D) compared with short photoperiods (8L: 16D) in lambs. The first experiment included 23 female Suffolk cross sheep aged 10 months, of which six were pinealectomized. The skeleton long photoperiod significantly increased plasma levels of prolactin but this was blocked by pinealectomy; there was a peak around dusk and a trough around dawn and at the time of the 1-h period of light. There was no effect of either photoperiod or pinealectomy on plasma levels of cortisol. Testosterone was not measured in this experiment. In the second experiment there were 12 intact males and 11 castrated males aged 3 months; six of the lambs in each group were pinealectomized. Prolactin was again greatly stimulated by skeleton long photoperiods and the effect was blocked by pinealectomy; there was a trough in plasma prolactin at dawn in all groups. In addition, castration increased prolactin levels on two of the four sampling days. Plasma cortisol concentrations were significantly lower under skeleton long photoperiods and this was also blocked by pinealectomy; there was no effect of castration. Testosterone was much higher in intact males. After 10 weeks of exposure, skeleton long photoperiods produced significantly lower concentrations than short photoperiods in the intact ram with pineal glands but not in those which were pinealectomized.

Animals↗

PubMed2000

The prepubertal years: a uniquely opportune stage of growth when the skeleton is most responsive to exercise?

The growing years may be the most opportune time in life for exercise to result in large increases in bone density, enough to reduce the risk of fracture late in life. However, it is not known if there is an 'optimal' time during growth when the skeleton is most responsive to exercise. Comparing the osteotrophic response to exercise between pre- and peripubertal children is complex because: (i) the development of the skeleton within each stage of puberty is characterised by differing temporal patterns of growth in bone size and mass; (ii) the hormonal regulation of the skeleton is unique to each stage of puberty; and (iii) it is difficult to equate the relative mechanical load placed on the prepubertal compared with the pubertal skeleton. There are sound biological bases for the hypotheses being proposed for both the pre- and peripubertal years being the time when the skeleton is most responsive to exercise; that is, exercise may enhance bone formation in a synergistic fashion in the presence of growth hormone (prepubertal years) or sex steroids (peripubertal years). The paucity of data and the complex methodology make it difficult to draw conclusions as to the most opportune time during growth when exercise may lead to the greatest osteotrophic response. The limited data available support the notion that the prepubertal years may be the most opportune time, due to increases in bone density and periosteal expansion of cortical bone.

Bone Density↗

PubMed1990

Artificial red cells. A link between the membrane skeleton and RES detectability?

Factors governing nonspecific reticuloendothelial system (RES)-detectability are largely unknown. Will a liposome that mimics the lipid composition of the outer leaflet of the erythrocyte membrane be invisible to the RES? On both experimental and theoretical grounds we believe the answer is no, in part because 1) sorption of proteins is believed to be important in determining RES uptake, 2) a membrane skeleton is apparently necessary to inhibit protein sorption into erythrocyte membranes and 3) Neohemocytes (a liposome encapsulated hemoglobin product) currently lack a membrane skeleton. Neohemocytes with erythrocyte outer leaflet lipid composition do have extended circulation half-times, but these are at least two orders of magnitude shorter than the circulation half-times of erythrocytes. How might a membrane skeleton modulate RES-detectability? Can avoidance of opsonization result in part from the properties of the membrane skeleton? If so, then how? To explore and quantify such questions we have developed a theoretical, statistical-thermodynamic model of protein binding into membranes. It predicts that the membrane area available for rapid lateral diffusion is critically important in controlling the amount of sorbed protein per unit area, and that a membrane skeleton can reduce a protein's sorption by several orders of magnitude. Based on theoretical results, we offer a speculative model for the detection of non-self lipid bilayers by the RES.

Blood Substitutes↗

PubMed1999

Response to parathyroidectomy at the axial and appendicular skeleton in renal patients.

AIM AND METHODS: We report increases in axial and appendicular bone density after parathyroidectomy in renal patients. Bone density was recorded pre-operatively and at 6 weeks, 6 months and 1 year post-operatively. We have previously reported that axial bone density increased dramatically at 6 weeks but that there were no early cohort increases at the appendicular skeleton [Stein et al. 1997]. RESULTS: We now report that at six months, bone density had continued to increase at the lumbar spine and femoral neck, with median respective 6 months increases over baseline of 1.3 (p < 0.01) and 0.7 (p < 0.01 ) Z-scores. Bone density then appeared to stabilize at the axial skeleton. At the appendicular skeleton increases were significant at the one year time point with median respective increases at the ultradistal radius and one third radius of 0.46 (p < 0.05) and 0.49 (p < 0.05) Z-scores. The different pattern of responses to parathyroidectomy between the axial and appendicular sites supports the concept that appendicular bone turnover is slower than axial bone turnover. Furthermore, at the appendicular skeleton, bone turnover appears similar between cortical and trabecular bone. CONCLUSION: In renal patients, bone density increases after parathyroidectomy at both the axial and appendicular skeleton. Axial increases are large and occur early. Appendicular increases occur at both cortical and trabecular sites but are slower than the axial changes.

Absorptiometry, Photon↗

PubMed2001

The skeleton in primary hyperparathyroidism: a review focusing on bone remodeling, structure, mass, and fracture.

The mechanisms behind the influence of PHPT on the skeleton are closely connected with bone turnover. Throughout life, the skeleton is continuously renewed by bone remodeling, a process which serves the purpose of repairing damaged bone and adapting the skeleton to changes in physical load. In this process, old bone is removed by osteoclastic resorption and new bone is laid down by osteoblastic formation. Bone mass increases with growth in the first decades of life, and around the age of 30 years the peak bone mass is reached. Thereafter, as a result of mechanisms involving bone remodeling, a net bone loss is seen: 1) A reversible bone loss because of increase in the remodeling space, i.e., the amount of bone resorped but not yet reformed during the remodeling cycle. This mechanism leads to decrease in average trabecular thickness and cortical width, and to increase in cortical porosity. 2) An irreversible bone loss caused by negative bone balance, where the amount of bone formed by the osteoblasts is exceeded by the amount of bone resorbed by the osteoclasts at the same remodeling site. Consequently, progressive thinning of trabecular elements, reduced cortical width and increased cortical porosity is seen. 3) Finally, perforation of trabecular plates by deep resorption lacunae leads to complete irreversible removal of structural bone components. Parathyroid hormone, together with vitamin D, are the principal modulators in calcium homeostasis. The main actions of PTH are executed in bone and kidneys. In the kidneys, PTH increases the tubular re-absorption of calcium, thereby tending to increase serum calcium. PTH also induces increased conversion of 25(OH)-D to 1,25(OH)2-D. This last action, enhances intestinal calcium absorption and increased skeletal calcium mobilization, which further adds to the circulating calcium pool. In bone, the "acute" regulatory actions of PTH on serum calcium are probably accompliced via activation of osteocytes and lining cells. A second mechanism of PTH in bone is the regulation of bone remodeling. The action seems to be an increased recruitment from osteoblastic precursor cells and activation of mature osteoclasts. It is supposed that these responses are predominantly mediated indirectly through actions on osteoblast-like or nonosteoblast-like stromal cells, as osteoclasts themselves to not have PTH receptors. Bone metabolism and bone mass are studied by biochemical bone markers, bone histomorphometry, and densitometry. As bone markers and bone histomorphometry give information on bone metabolism from different points of view, these methods are preferably combined. Histomorphometry gives detailed information about bone turnover on cellular level, the whole remodeling sequence is described, and the bone balance can be calculated. However, they focus on a small volume, and may, therefore, not be representative for the whole skeleton. On the other hand, studies of bone markers supply general information about turnover in the whole skeleton, but they do not give facts on the bone turnover on the cellular or tissue level and bone balance. Bone densitometry is the principal method in studying bone mass, but valuable information concerning bone structure also comes from histomorphometry. Bone remodeling is considerably increased in PHPT. Studies of bone markers show increase in both resorptive and formative markers, and the increases seem to be of equivalent size. This is in agreement with histomorphometric findings and shows that the coupling between resorption and formation is preserved. By histomorphometry on iliac crest biopsies, trabecular bone remodeling is found increased by 50%, judged by the increase in activation frequency; a measure of how often new remodeling is initiated on the trabecular bone surface. In PHPT, such remodeling activity is repeated about once every year. Reconstruction of the whole remodeling sequence does not show major deviations in lengths of the resorptive and formative periods compared to normal. Furthermore, the amount of bone removed by the osteoclasts during the resorptive phase is matched by the amount of new bone formed by the osteoblasts leading to a bone balance very close to zero. Compared with trabecular bone, the turnover rate in cortical bone is considerably lower, around 10%. Remodeling of the cortical bone takes place at the endocortical, the pericortical, and the Haversian surfaces. Endocortical bone remodeling activities are very similar to trabecular remodeling activities with good correlation between individual parameters. Periosteal remodeling activity is negligible in PHPT, as it is in the normal state. Cortical porosity, which reflects the remodeling activity on the Haversian surface, is increased by 30-65% in PHPT. (ABSTRACT TRUNCATED)

Animals↗

PubMed2001

Mechanical and functional aspects of membrane skeletons.

Membrane skeletons can be characterized as cytoskeletal structures lying parallel to the bilayer part of cellular and organelle membranes. Typical examples are spectrin network and actin-myosin cortex. We approach the problem of elucidating the function of membrane skeletons by theoretically analyzing mechanical models of the cellular behavior. Membranes of different physical and chemical properties are considered. In erythrocytes and some organelles membrane bilayers are smooth and simply underlaid or overlaid by membrane skeletons. It is argued that there the role of a membrane skeleton is, either, to keep the membrane composition laterally homogeneous as it is in the case of the erythrocyte, or, that it is involved in the processes of the lateral separation of integral membrane proteins as it is happening in the case of some intermediate steps of the vesicular membrane trafficking. In the second type of membranes the bilayer part is ruffled and folded, and there the membrane skeletons play a role in the determination of the cortical tension. Here we explore in more detail the mechanical behavior of a cell with such properties of its boundary. The shape transformations are described which occur under the influence (i) of different external forces, i.e., when an originally spherical cell is aspirated into the micropipette or when such a cell is adsorbed on a flat surface, and (ii) of different internal forces on the cell boundary exerted by the cytoskeletal elements.

Biomechanical Phenomena↗

PubMed1992

Solubility and posttranslational regulation of GP130/F11--a neuronal GPI-linked cell adhesion molecule enriched in the neuronal membrane skeleton.

GP130 (renamed contactin) has previously been identified by its detergent insolubility and retention with the actin-containing "membrane skeleton" isolated from chicken neurons and brain. The contactin sequence predicted a transmembrane and cytoplasmic domain for the molecule. Recently, F11 was shown to have an identical sequence except for the C terminus, and it was predicted to be linked to the plasma membrane by a glycosylphosphatidylinositol (GPI) group. Here we describe that GP130 can be released both from brain membranes and the detergent-insoluble membrane skeleton by a phosphoinositol-specific phospholipase C (PI-PLC) indicating that F11 and GP130/contactin are probably identical and that surprisingly the lipid anchor is partly or totally responsible for its non-ionic detergent insolubility. The "membrane skeleton" is a rich source of GPI-linked glycoproteins as judged by 1) most glycoproteins can be released by a PI-PLC and 2) most [3H]ethanolamine-labeled glycoproteins are present in, or enriched in the membrane skeleton. Thus, detergent insolubility appears to be a characteristic of GPI-anchored glycoproteins. No evidence has been obtained that GP130/F11 is released or secreted in vivo or in culture. In addition, GP130/F11 has an unusually long half-life in culture of greater than 3 days. The structure of the neuronal membrane skeleton and the potential function of GPI-anchored glycoproteins is discussed.

Animals↗

PubMed1992

Surgery for atrioventricular node reentry tachycardia. Results with surgical skeletonization of the atrioventricular node and discrete perinodal cryosurgery.

Surgical treatment options for interruption of atrioventricular node reentrant tachycardia include (1) skeletonization of the atrioventricular node by dissecting it from most of its atrial inputs and (2) discrete cryosurgery of the perinodal tissues by applying a series of sequential cryolesions to the atrial tissues immediately adjacent to the atrioventricular node. Both these techniques attempt to interrupt one of the dual atrioventricular node conduction pathways while preserving the other. This report describes 17 consecutive patients who underwent surgical treatment, 10 patients with skeletonization of the atrioventricular node and seven patients with discrete perinodal cryosurgery. There were 10 female and seven male patients and their ages ranged from 28 to 56 years (mean 38). Two of the 17 patients had Wolff-Parkinson-White syndrome and their accessory pathways were interrupted before the atrioventricular nodal reentrant tachycardia was ablated. All the procedures were performed in a normothermic beating heart while atrioventricular conduction was monitored closely. In the skeletonization technique, the right atrial septum was mobilized and the atrioventricular node exposed anterior to the tendon of the Todaro. The perinodal cryosurgical procedure was also performed through a right atriotomy and a series of sequential 3 mm cryolesions were placed around the borders of the triangle of Koch on the inferior right atrial septum. There were no operative deaths. Two patients who underwent the skeletonization operation had heart block necessitating pacemaker therapy. At postoperative electrophysiologic study, no echoes or atrioventricular nodal reentrant tachycardia were inducible in any of the 17 patients. All patients have remained free of arrhythmia recurrence and have required no antiarrhythmic therapy after a follow-up of 5 to 28 months (mean 14). In conclusion, both atrioventricular node skeletonization and perinodal cryosurgery successfully ablate atrioventricular nodal reentrant tachycardia; however, perinodal cryosurgery appears to be safer in avoiding heart block, is more easily performed, and is our procedure of choice for the management of medically refractory atrioventricular nodal reentrant tachycardia.

Adolescent↗

PubMed2005

[Myeloma in an archaeological skeleton from Hofstadir in Mývatnssveit].

Archaeological investigations have been ongoing in the cemetery at Hofstadir in Mývatnssveit since the summer of 1999. To date, the remains of two chapels as well as 78 skeletons have been excavated, dated to between the 11th and 15th century. A skeleton was excavated in the summer of 2003 which showed pathological changes indicative of a malignant disease. Palaeopathological cases of malignancies are very rare, and it is therefore important to report on each case. Skeleton HST-027 was a female, aged 45-50 years at the time of death. Standard osteological methods were used to determine the sex, age and stature. Macroscopic analysis was carried out on the skeleton and all pathological changes on each bone described. The cranium, ribs, left os coxa and all left long bones were then radiographed to aid in the diagnosis. The analysis showed lytic lesions in all the flat bones, as well as the vertebrae, ribs and the proximal end of the left femur, all changes indicative of multiple myeloma. Palaeopathologically myeloma and metastatic cancer (then usually due to breast cancer in the case of women) are often difficult to distinguish. However there is no new bone formation surrounding the lesions, which means that metastatic cancer is unlikely to be the cause. Skeleton HST-027 from Hofstadir is the first published case of malignant disease in Iceland, and one of the clearer cases of myeloma in an archaeological specimen, but to date, approximately twenty cases have been reported world-wide.

Bone Neoplasms↗

PubMed1991

[Study of the elastic skeleton of intracranial arteries in animal and human vessels and experimentally induced cerebral aneurysms].

In an attempt to clarify the elastic skeleton of cerebral arteries in animals and human, and experimentally induced cerebral aneurysms, following experiments were performed. Experiment (1): The elastic skeleton of major cerebral arteries in rats, monkeys, and one human were studied by scanning electron microscopy after hot-formic acid extraction followed by freeze-drying. For a comparative study, the thoracic aorta and femoral arteries of rats were also examined. The cerebral arteries of rats had one distinct internal elastic lamina connected with medial elastic tissue. This internal elastic lamina had fenestrations, which were 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 extracranial arteries. At the apical intimal pad, the internal elastic lamina appeared to be continuous, making a honeycomb-like structure there. These folds and fenestrations were numerous in the apical region. There were no essential differences between species. Experiment (2): Cerebral aneurysms were produced by ligating unilateral carotid artery and bilateral posterior branches of renal arteries, and feeding beta-aminoproprionitrile fumarate. The first noted change was the loss of fold-like structures protruding from the internal elastic lamina. Morphological changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the media. The internal elastic lamina disappeared after these consequences. In a large aneurysm with a thick dome, the wall contained fine proliferated elastic lamellae. The present 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. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of the aneurysm occurs due to disintegration of the elastic skeleton and not simply with rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of cells that produce elastin.

Animals↗