Dietary boron does not affect tooth strength,micro-hardness,and density,but affects tooth mineral composition and alveolar bone mineral density in rabbits fed a high-energy diet

The objective of this study was to determine whether dietary boron (B) affects the strength, density and mineral composition of teeth and mineral density of alveolar bone in rabbits with apparent obesity induced by a high-energy diet. Sixty female, 8-month-old, New Zealand rabbits were randomly assigned for 7 months into five groups as follows: (1) control 1, fed alfalfa hay only (5.91 MJ/kg and 57.5 mg B/kg); (2) control 2, high energy diet (11.76 MJ and 3.88 mg B/kg); (3) B10, high energy diet + 10 mg B gavage/kg body weight/96 h; (4) B30, high energy diet + 30 mg B gavage/kg body weight/96 h; (5) B50, high energy diet + 50 mg B gavage/kg body weight/96 h. Maxillary incisor teeth of the rabbits were evaluated for compression strength, mineral composition, and micro-hardness. Enamel, dentin, cementum and pulp tissue were examined histologically. Mineral densities of the incisor teeth and surrounding alveolar bone were determined by using micro-CT. When compared to controls, the different boron treatments did not significantly affect compression strength, and micro-hardness of the teeth, although the B content of teeth increased in a dose-dependent manner. Compared to control 1, B50 teeth had decreased phosphorus (P) concentrations. Histological examination revealed that teeth structure (shape and thickness of the enamel, dentin, cementum and pulp) was similar in the B-treated and control rabbits. Micro CT evaluation revealed greater alveolar bone mineral density in B10 and B30 groups than in controls. Alveolar bone density of the B50 group was not different than the controls. Although the B treatments did not affect teeth structure, strength, mineral density and micro-hardness, increasing B intake altered the mineral composition of teeth, and, in moderate amounts, had beneficial effects on surrounding alveolar bone.     

Vasoactive intestinal polypeptide-like immunoreactivity in the bovine heart: high degree of coexistence with neuropeptide Y-like immunoreactivity

Summary Recent studies have accomplished the establishment of a collagenous fiber-fringe matrix upon dental root surfaces in vitro. The present study was undertaken to follow the development of such a matrix in vitro and to test the possible effects of root surface treatments upon this matrix. Periodontal ligament cells, 0.1 to 0.2-mm thick dental root discs, and alveolar bone cells were derived after extraction from four partially erupted third molars and the accompanying interradicular bony septa of 1 male patient. Autologous serum was obtained by venipuncture. Cultures were initiated by delivering a 1-ml suspension of 50000 tritiated thymidine-labeled periodontal ligament cells and 50000 alveolar bone cells onto each of 42 culture sets. The following day, demineralized or non-demineralized root discs treated with autologous serum, fibronectin or complete medium were placed in pairs, separated by a 0.1–1.0 mm gap, upon the initial cell layer. Representative cultures were terminated after 2, 3, 4, 5 and 6 weeks, and processed for light- and electron microscopy, morphometric analysis and autoradiography. An outstanding feature of the early cultures (2, 3 and 4 weeks) was a patchwise, random distribution of matrix making a precise developmental study impossible, although collagen fibrils were produced within the first 2 weeks. Some 3-week cultures already demonstrated a mature fiber-fringe characterized electron-microscopically as oriented, densely packed collagen fibrils closely abutting the cementum-lined root discs. The treatments (including autologous serum) used in this study had no appreciable morphologic or morphometric effect upon the fiber-fringe formed. Because none of the cultures in the present or past studies have demonstrated a true cementoid matrix, this model may not be suitable for the in-vitro study of cementum formation.     

Role of alveolar macrophages in endotoxin-induced neutrophilic alveolitis in rats

Although bacterial endotoxins have potent effects on blood monocytes and tissue macrophages, the role of alveolar macrophages in regulating intrapulmonary neutrophil traffic following endotoxemia has not been studied previously. We have previously reported that a single intraperitoneal injection of endotoxin from Escherichia coli serotype 055B5 causes acute lung inflammation by neutrophils (PMN) in rats. The factors which influence the migration of PMN in the lung in this model are unknown. To determine whether macrophage-derived products could play a role in directing migration, we enumerated neutrophils in histologic sections and employed electron microscopy to document the location of neutrophils in the lung in vivo following endotoxin. We also cultured the alveolar macrophages recovered by lung lavage to measure the effect of their culture supernatants on neutrophil migration in vitro. In the first 6 hr following endotoxin, and also 24 hr later, there was an increase in the number of PMN enumerated in the lung parenchyma by light microscopy. Electron microscopy showed the location of the neutrophils to be exclusively intravascular at 6 hr. By contrast, neutrophils were observed in both interstitial and bronchoalveolar spaces at 24 hr, confirming that transvascular migration was active at that time. The pulmonary macrophages which were recovered by lung lavage from groups of rats sacrificed at 4 and at 15 hr following the administration of endotoxin were assayed for the release into culture media of migration-stimulatory activity for neutrophils. Macrophages from animals sacrificed 4 hr following endotoxin released less migration-stimulating activity into media than macrophages from controls. These macrophages could be stimulated to release migration-stimulating activity into culture media at levels comparable to macrophages from controls by the addition of opsonized Zymosan to the culture media. By contrast, macrophages from animals sacrificed 15 hr after endotoxin spontaneously released more migration-stimulating activity for neutrophils than did macrophages from controls. Thus, in this model, a specific increase in the synthesis or release by alveolar macrophages of factors which stimulate the migration of neutrophils in vitro coincided with a transition from intravascular to extravascular alveolar inflammation by neutrophils in vivo. These observations are consistent with the hypothesis that pulmonary alveolar macrophages may contribute to the regulation of alveolar inflammation following endotoxemia by releasing factors which influence the migration of neutrophils.     

Lung alveolar cell cytosomes: A consideration of their significance

Summary An ultrastructural comparison of mammalian, reptilian, and amphibian lung alveolar cells, and avian lung atrial cells reveals that morphologically similar cytoplasmic bodies (cytosomes) occur in these cells. The cytosomes, which appear generally as osmiophilic, lamellae-containing, membrane-bound, round bodies 0.3 to 0.5 in diameter, are also similar to bodies occurring in epithelial cells of both physoclistous and physostomatous swimbladders of fishes. Because the function of both lung alveolar and swimbladder epithelial cells is gas-handling, the possibility is raised that the morphologically similar lamellae-containing bodies of these vertebrate cells are functionally identical. One function, suggested by other investigators, is that, in mammalian lungs, these bodies supply a surface-tension lowering material (surfactant). Because several assumptions concerning this proposed function remain unproved, an alternative proposal is speculatively explored. The suggestion is offered that cytosomes contain an antioxidant needed to protect alveolar and swimbladder cells against the toxic effects of the relatively high concentration of oxygen to which these cells are exposed.Supported by a research grant from the American Cancer Society, Oregon Division, Inc.     

Induction of accessory cell function of human alveolar macrophages by inhalation of human natural interleukin-2

 Accessory function allows antigen-presenting cells to produce sufficient secondary signals for optimum T cell proliferation and interleukin-2 (IL-2) production. Alveolar macrophages are inferior accessory cells compared to monocytes (PBM). We report here that the accessory index (AI) of alveolar macrophages and PBM of patients with lung metastases of solid tumors treated with inhalations of human natural IL-2 (hnIL-2) increased following its administration (P<0.005). The accessory index was significantly elevated from baseline values after 2 weeks of inhalation of 300 000 IU hnIL-2/day (8.2±10.2 compared to 1.1±1; P<0.001). The inhalation of 150 000 IU also induced increases in the index (AI = 2.3±1.9), however, without reaching statistical significance. In addition at 300 000 IU IL-2/day a significant increase in the accessory index was observed for PBM (4±2.5; P<0.05). The indices of PBM and alveolar macrophages prior to inhalation showed a significant negative correlation with the age of the patients (r _s =  – 0.5; r _s =  – 0.8, respectively; P<0.03 for all comparisons). Our data demonstrate that the inhalational application of hnIL-2 enhances the accessory function of alveolar macrophages and, to lesser extent, the accessory index of PBM, indicating the occurrence of pharmacological immunostimulation. Received: 16 August 1995 / Accepted: 4 January 1996     

Toxicity to alveolar macrophages in rats following parenteral injection of mercuric chloride

Alveolar macrophages collected by pulmonary lavage from male Fisher-344 rats at intervals (24–72 h) after HgCl₂ injection (1–5 mg/kg, sc) were analyzed by several techniques. Within 24–72 h, the macrophages showed morphological signs of activation (hypertrophy and ruffled plasma membrane). Lipid peroxidation (increased malondialdehyde concentration) was not detected until 48 h. Dose- and time-related effects of HgCl₂ on malondialdehyde concentration and time-related effects of HgCl₂ on malondialdehyde concentration and mercury content of alveolar macrophages were observed 24–72 h postinjection. Diminished cell viability occurred only at 72 h after the highest dosage of HgCl₂. This study demonstrates that the alveolar macrophage was a cellular target for mercury toxicity following parenteral exposure to HgCl₂.     

Effect of canine surfactant protein (SP-A) on the respiratory burst of phagocytic cells

Cells obtained from bronchoalveolar lavage, or neutrophils of peripheral blood of dog, were incubated with the canine surfactant-associated protein A (SP-A). A significant decrease of the production of Superoxide anion was observed after subsequent stimulation with phorbol-12-myristate-13-acetate (PMA) as measured by the lucigenin-dependent chemiluminesence (CL). Several other proteins used for control experiments did not decrease lucigenin-dependent CL, indicating a specific effect of SP-A on phagocytes. Treatment of SP-A with collagenase prior to incubation with neutrophils destroyed the depleting effect on oxygen radical production of PMA-stimulated cells. We propose that SP-A acts as a regulatory factor of the respitatory burst of alveolar macrophages and neutrophils in the lungs. The inhibitory effect of SP-A is down-regulated by collagenase released from stimulated alveolar macrophages.     

Theoretical basis of single breath gas absorption tests

Absorption of gas from alveoli is examined in a simplified model of the respiratory system during a stylized single breath consisting of constant inspiratory flow, constant expiratory flow, and breathholding. The equations describing gas behavior are general since they are based upon conservation of mass. The equations simplify considerably when gases that are not soluble in pulmonary tissue and/or blood are utilized. In a three-compartment model, diffusing capacity of the lung for carbon monoxide (D _CO ) will be underestimated except when both uneven distribution of lung volume andD _CO are present; under most circumstances, the standard clinical 10-s method [9] is at least as accurate as any other. When pulmonary capillary blood flow is calculated by the one point method [2] in a one-compartment lung, it is underestimated; in the three-compartment model, it is underestimated except when both uneven distribution of . and lung volume are present. The multiple single breath method [2] accurately measuresD _CO and . Measurement of pulmonary tissue volume is improved by correcting the value of the intercept of acetylene absorption to the time when carbon monoxide apparently began rather than utilizing the beginning of inspiration.Nomenclature D _CO diffusing capacity of the lung for CO (ml CO, STPD/min/mm Hg) - pulmonary capillary blood flow rate (L/min) - V _t pulmonary tissue volume (L) - V _A alveolar compartment volume (L) - V _Ao alveolar compartment volume at conclusion of inspiratory flow (L) - inspiratory flow rate (L/sec) - expiratory flow rate (L/sec) - Bunsen coefficient of pulmonary tissue for test gas (ml test gas/ml tissue/atm) - Bunsen coefficient of pulmonary tissue for test gas (ml test gas/ml blood/atm) - F _A fractional pressure of test gas in the alveolar compartment (atm)     

Electron microscopic studies of the lung of the frog

Summary Scanning and transmission electron microscopy were used to study the inner architecture of the frog lung. In some specimens the alveolar surface mucus layer was removed to permit the examination of underlying features. The inner surface of the frog's lung is covered by a layer of microvilli belonging to only one type of epithelial cells. The boundaries of these epithelial cells are demarcated by small ridges. Different degrees of lung expansion cause variations of the surface topography. The morphology of certain surface features is examined in detail. Several methods of drying the specimens are compared.The author wishes to thank Dr. I. E. Richter, Institut für allgemeine und experimentelle Pathologie der Bundeswehr, Mainz, for the opportunity to do these investigations and for helpful discussions.