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Biomedical subjects

G Marrone

Publications and source records attributed to G Marrone.

14 recordsLinked to original sources
PubMed1994

Cultures of human embryonic osteoblasts. A new in vitro model for biocompatibility studies.

Cell populations derived from human embryonic bone were isolated according to the ability of osteoblasts to migrate from bone onto glass fragments. Morphologic and biochemical assays showed (1) osteoblast-like appearance; (2) elevated alkaline phosphatase 1,25(OH)2D3 responsive activity associated with plasma membranes and matrix vesicles; (3) production of a thick extracellular matrix, mainly composed of Type I collagen, which mineralized in the presence of 10 mM beta-glycerophosphate; and (4) higher growth rate and viability when compared with their mature counterpart. Cultures of embryonic cells were challenged with particles of several biomaterials, and their effects on morphology, vitality, and osteogenic capacity of the cultured cells were tested. Stainless steel, titanium alloy, Co-Cr-Mo alloy (vitallium), carbon fiber-reinforced polybutylene terephtalate, ultra-high molecular weight polyethylene, ceramic, calcium phosphate, and hydroxyapatite did not exert any significant deleterious effects on the cultured human osteoblasts.

Alkaline Phosphatase↗
PubMed1993

Effect of retinoic acid on osteocalcin gene expression in human osteoblasts.

It is well known that the expression of osteocalcin, the only recognized osteoblast-specific protein, is regulated by 1 alpha-25-dihydroxyvitamin D3 through a distinct vitamin D3 receptor and a cis-acting DNA response element. In addition, recent data obtained with plasmid constructs have shown a positive interaction between retinoic acid activated receptor(s) and the osteocalcin gene promoter. Our studies, carried out on primary cultures of human osteoblasts, have demonstrated for the first time the activation of the osteocalcin gene expression by retinoic acid. Moreover, a remarkable synergistic effect between the hormonal forms of vitamin A and D3 on the synthesis of this bone-specific protein was observed.

Calcitriol↗
PubMed1993

Side effects and complications associated with third molar surgery.

A retrospective analysis of complications and side effects associated with surgery for 1000 mandibular and 500 maxillary impacted third molars was performed. The analysis included 614 patients with impacted mandibular third molars and 274 with impacted maxillary third molars who were treated in a 5-year timeframe from 1987 to 1992. The incidence of intraoperative complications and side effects of mandibular third molar surgery was 1.1% and 4% for maxillary third molar surgery whereas postoperative complications were 4.3% and 1.2%, respectively.

Adolescent↗
PubMed1992

Isolation and characterization of human embryonic osteoblasts.

Human osteoblasts were obtained by migration and proliferation of cells from embryonic membranous bone on glass fragments. Light and electron microscopy analyses revealed a typical osteoblast-like appearance with high protein synthesis activity. The cells showed high alkaline phosphatase activity that was associated with plasma membranes and matrix vesicles and was 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] responsive. In contrast to the adult osteoblasts, embryonic cells could not produce detectable levels of osteocalcin, not even in the presence of 1,25(OH)2D3. Osteoblasts grown in multilayers produced a thick extracellular matrix, mainly composed of type I collagen, that mineralized in the presence of 10 mM beta-glycerophosphate. Because of their intrinsic osteogenic capacity, embryonic osteoblasts represent a valuable model for studying the mineralization process in vitro. In addition, the embryonic origin of these cells renders them a precious experimental system for the elucidation of mechanisms at the basis of differentiation of osteoblastic lineage.

Alkaline Phosphatase↗
PubMed1991

Profound hypothermia (less than 10 degrees C) compared with deep hypothermia (15 degrees C) improves neurologic outcome in dogs after two hours' circulatory arrest induced to enable resuscitative surgery.

Deaths from uncontrollable hemorrhage might be prevented by arresting the circulation under protective hypothermia to allow resuscitative surgery to repair these injuries in a bloodless field. We have shown previously that in hemorrhagic shock, circulatory arrest of 60 minutes under deep hypothermia (tympanic membrane temperature, Ttm = 15 degrees C) was the maximum duration of arrest that allowed normal brain recovery. We hypothesize that profound cerebral hypothermia (Ttm less than 10 degrees C) could extend the duration of safe circulatory arrest. In pilot experiments, we found that the cardiopulmonary system did not tolerate arrest at a core (esophageal) temperature (Tes) of less than 10 degrees C. Twenty-two dogs underwent 30-minute hemorrhagic shock (mean arterial pressure 40 mm Hg), rapid cooling by cardiopulmonary bypass (CPB), blood washout to a hematocrit of less than 10%, and circulatory arrest of 2 hours. In deep hypothermia group 1 (n = 10), Ttm was maintained at 15 degrees C during arrest. In profound hypothermia group 2 (n = 12), during cooling with CPB, the head was immersed in ice water, which decreased Ttm to 4 degrees-7 degrees C. The Tes was 10 degrees C in all dogs during arrest. Reperfusion and rewarming were by CPB for 2 hours. Controlled ventilation was to 24 hours, intensive care to 72 hours. In the 20 dogs that followed protocol, best neurologic deficit scores (0% = normal, 100% = brain death) at 24-72 hours were 23% +/- 19% in group 1 and 12% +/- 8% in group 2 (p = 0.15). Overall performance categories and histologic damage scores were significantly better in group 2 (p = 0.04 and p less than 0.001, respectively). We conclude that profound cerebral hypothermia with CPB plus ice water immersion of the head can extend the brain's tolerance of therapeutic circulatory arrest beyond that achieved with deep hypothermia.

Animals↗
PubMed1986

Effect of simulated systemic administration of aspirin, salicylate, and indomethacin on amphibian gastric mucosa.

The effects of 20 mM aspirin (ASA), 20 mM sodium salicylate (SA), or 10(-4) M indomethacin placed in the nutrient solution (N) to stimulate systemic administration were investigated at pHN 7.3 in Ussing-chambered amphibian gastric mucosae. In histamine-stimulated tissues, the initial rise and subsequent rapid fall in potential difference, rise in resistance, and inhibition of hydrogen ion (H+) secretion induced by SAN did not occur with ASAN unless hydrolysis of ASAN produced a SAN of greater than 3 mM. In metiamide-treated tissues, 20 mM SAN caused an immediate fall in potential difference and an increase in resistance; 2 mM SAN and 20 mM ASA produced similar qualitative electrical changes, but only those induced by ASA were reversible. IndomethacinN caused no significant changes in potential difference, resistance, or H+ secretion in histamine- or metiamide-treated tissues. Despite producing highly significant reductions in generation of prostaglandin E2, and prostaglanndin F2 alpha and 6-keto prostaglandin F1 alpha, ASAN and indomethacin caused no surface ulceration. Sodium salicylate placed in the nutrient solution caused only a small reduction in prostaglandin F2 alpha, without change in the other prostaglandins, and produced extensive edema in the lamina propria, histologically. We conclude the following: (a) The inhibition of H+ secretion and electrical changes caused by SAN in histamine-treated gastric fundus are not observed with ASAN unless there is hydrolysis to [SAN] greater than 3 mM. (b) Our data strongly implicate the SAN in ASAN-containing solutions as being responsible for the electrical effects and inhibition of H+ secretion. (c) There is no correlation in vitro between inhibition of prostaglandin synthesis and the electrical or morphologic changes produced by nutrient exposure to ASA, SA, or indomethacin.

16,16-Dimethylprostaglandin E2↗
PubMed1985

In vitro protection of amphibian gastric mucosa by nutrient HCO3- against aspirin injury.

The effects of luminal aspirin [acetylsalicylic acid (ASA)] at luminal pH 4.5 and pH 3.0 on Ussing chambered amphibian gastric fundic and antral mucosae were investigated using different concentrations of HCO3- ([HCO3-]) in the nutrient solution in histamine-stimulated or metiamide-treated tissues. The severe surface cell and oxyntic gland injury seen in histamine-stimulated tissues after a 3-h exposure to 20 mM ASA at luminal pH 4.5 in HCO3- -free nutrient solution (HEPES) was prevented by including 18 mM or 48 mM HCO3- in the nutrient solution. At luminal pH 3.0, 48 mM HCO3- in the nutrient solution delayed the histologic damage to the surface epithelium and oxyntic glands caused by a 30-min exposure to 20 mM luminal ASA, but it afforded no protection to a 60-min exposure. This protection of the gastric epithelium by a high nutrient [HCO3-] did not occur in metiamide-treated tissues at luminal pH 3.0. Although the injury to antral epithelial cells exposed to 20 mM luminal ASA at luminal pH 3.0 or 4.5 was less severe than that in fundic mucosae, 48 mM HCO3- in the nutrient solution also afforded clear protection in this tissue. A high nutrient [HCO3-] prevented the sharp fall in the potential difference observed in fundus exposed to ASA at luminal pH 4.5 and delayed the fall in potential difference observed in fundic and antral mucosae exposed to ASA at luminal pH 3.0. The high nutrient [HCO3-] did not prevent the increase in resistance observed in tissues during ASA exposure at luminal pH 4.5 and 3.0. The electrical data reflect not only the damaged surface and oxyntic cells caused by ASA, but also the complex effects of ASA on active and passive ion transport. We conclude the following: (a) The mucosal injury to the fundus and antrum caused by luminal ASA is prevented by 48 mM HCO3- in the nutrient solution when luminal pH is 3.0 and by 18 mM HCO3- when luminal pH is 4.5. Absence of nutrient HCO3- accentuates the injury caused by luminal ASA. (b) The luminal pH, concentration, and time of exposure influence the depth and severity of ASA injury to the fundic and antral mucosa. (c) The electrophysiologic and morphologic changes after ASA exposure are not interrelated, due to the complex effects of ASA on the ion transport and morphology of the gastric epithelium.

Animals↗
PubMed1985

Characteristics of sudden potential drop in bullfrog gastric mucosa.

An unusual sudden potential drop (SPD) has been described by Kidder in bullfrog gastric mucosa exposed to anoxia and a serosal pH less than or equal to 7.1. We found that anoxia was not a prerequisite, since under fully oxygenated conditions the SPD occurred reliably in metiamide-treated tissues when the pH of the nutrient solution (pHN) was below 7.1. The SPD was observed also in metiamide-treated tissues exposed to 20 mM luminal or nutrient acetylsalicylic acid (ASA) with pHN = 7.3, an effect that was abolished by increased nutrient HCO3- concentration. The SPD occurred when NO3- but not isethionate or acetate replaced Cl- in the bathing media. A marked increase in potential difference in response to changing luminal Cl- concentration was observed after the SPD, uptake of Cl- from the luminal solution into the tissue increased, but transmural fluxes of Cl- decreased bidirectionally. Permeability to H+ was unaltered in the post-SPD state. An SPD never occurred in antrum under conditions causing SPD in fundus, suggesting that oxyntic cells are prerequisite. We conclude that, under conditions which cause tissue or cellular acidosis and cessation of H+ secretion, fundic mucosae respond with an anion-selective increase in apical permeability manifest as the SPD.

Animals↗
PubMedDate not supplied

Early diagnosis and follow-up by echocardiography of acquired cor triatriatum after orthotopic heart transplantation.

Acquired cor triatriatum in a heart transplant recipient, secondary to a prominent left atrial suture line and torsion of the atria, was diagnosed immediately after cardiopulmonary bypass by transesophageal echocardiography. The patient was followed with serial echocardiograms and right heart catheterizations, showing resolution of the obstruction.

Cardiac Catheterization↗
PubMedDate not supplied

Localization of proliferating cell nuclear antigen-immunoreactivity in human dental pulp and gingiva.

The proliferating cell nuclear antigen (PCNA) is regarded as an operational marker of proliferating cells. We have used PC10 monoclonal antibody to PCNA to reveal proliferation sites in human dental pulp and gingiva. Intense PCNA-immunoreactivity was observed in the basal layer of the gingiva lining epithelium and within some cells of the underlying connective tissues, including some endothelial and perivascular cells. PCNA-reactive cells were scattered throughout the pulp tissue, but were particularly numerous in the peripheral part. Since PCNA is an endogenous cell cycle-related molecule, we propose that PCNA-antibodies may represent useful for studying cell kinetics in human oral tissues in normal as well as pathological situations, such as tumours, wound healing and inflammation.

Basement Membrane↗