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At least 145 records · Page 8Linked to original sources
PubMed1999

Developmental toxicity of diethanolamine applied cutaneously to CD rats and New Zealand White rabbits.

Diethanolamine (DEA) was administered cutaneously to pregnant CD rats and New Zealand White rabbits during the periods of major organogenesis, Gestation Days 6-15 for rats and 6-18 for rabbits. Doses employed were 0, 150, 500, and 1500 mg/kg/day for rats and 0, 35, 100, and 350 mg/kg/day for rabbits. Rat dams exhibited reduced body weight at 1500 mg/kg/day, skin irritation and increased kidney weights at 500 and 1500 mg/kg/day, and a slight microcytic anemia with abnormal red blood cell morphology at all dose levels. Rat fetuses had increased incidences of six skeletal variations at 1500 mg/kg/day. Lower doses were without effect on the fetuses. Rabbit dams administered 350 mg/kg/day exhibited various skin lesions, reduced food consumption, and color changes in the kidneys but no hematological changes. Body weight gain was reduced at >/=100 mg/kg/day. There was no evidence of maternal toxicity at 35 mg/kg/day and no evidence of developmental toxicity in rabbits at any dose level. Developmental toxicity was observed only in the rat and only at doses causing significant maternal toxicity, including hematological effects. Due to a dose discrepancy, the no observable effect level (NOEL) for DEA developmental toxicity in rats was adjusted to 380 mg/kg/day. In rabbits, the embryonal/fetal NOEL was 350 mg/kg/day.

Abnormalities, Drug-Induced↗
PubMed1980

Effects of the principal hydroxy-metabolites of benzene on microtubule polymerization.

The principal hydroxy-metabolites of benzene - phenol, catechol and hydroquinone - possess characteristics and produce toxicity similar to those reported for certain inhibitors of microtubule polymerization. In this study we examined the effects of phenol, catechol and hydroquinone on purified microtubule polymerization and the decay of tubulin-colchicine binding activity. Hydroquinone, but not catechol or phenol, inhibited microtubule polymerization and accelerated the decay of tubulin-colchicine binding activity. The latter effect was shown to be dependent on the concentration of GTP. Hydroquinone did not directly complex with GTP or ATP but bound to the high molecular weight fraction of tubulin. concentration ratios of hydroquinone to tubulin resulting in altered activity were low, suggesting a specific interaction, presumably at the tubulin-GTP binding site. The acceleration of tubulin-colchicine binding activity decay was completely prevented under anaerobic conditions, indicative of an oxidative mechanism. These studies suggest that hydroquinone, which auto-oxidizes, may interfere with microtubule function, nucleotide binding or both and that this mechanism may be involved in eliciting the wide range of cytoskeletal-related abnormalities observed in cells exposed to benzene in vivo or its metabolites in vitro.

Animals↗
PubMed1983

Coronary bypass surgery in juvenile onset diabetes.

Atherosclerotic cardiovascular disease is the major cause of death in insulin-dependent diabetics of juvenile onset (JODM). This report summarizes our experience in coronary artery bypass surgery performed between 1971 and 1980 on 13 JODM patients. Preoperatively, 12 of 13 patients had NYHA class IV symptoms with 78% of patients having either left main or multivessel coronary artery disease. With a mean follow-up of 4 years, 12 of 13 patients are alive and 8 of 12 are either NYHA class I or II. We conclude that in a select subset of JODM, bypass surgery can be performed with a low operative morbidity and mortality and results in long-term symptomatic improvement.

Adolescent↗
PubMed1980

Surgical management of chest wall tumors.

A new technique for reconstruction of the chest wall providing immediate chest wall stability was employed in six patients who required extensive chest wall resection for a variety of neoplasms. Despite preoperative impairment of pulmonary function, early extubation was possible in all patients. Pulmonary function was well preserved on follow-up examination.

Adenocarcinoma↗
PubMed1982

Esophagectomy without thoracotomy for carcinoma of the esophagus.

During the past 2.5 years, 13 patients underwent esophagectomy for carcinoma of the esophagus without the use of a thoracotomy. During the same period, 81 operations on the esophagus or cardia were performed, 73 of which were esophagogastrectomies. Two patients died, for a hospital mortality rate of 2.7 percent. Of the 13 patients, there were 7 women and 6 men with an average age of 59.7 years. The lesion was located in the cervical esophagus in two, the upper thoracic esophagus in eight and the lower esophagus in three. One patient died on the 12th postoperative day, for a hospital mortality rate of 7.7 percent. Satisfactory relief of dysphagia was accomplished in all surviving patients, five of whom have died from the disease, for an average survival of 13.1 months. Seven are currently alive, with the longest period of survival 20.5 months. Esophagectomy without thoracotomy can be carried out with low mortality and morbidity rates. It is most applicable to patients with early lesions, particularly those in the cervical esophagus and the upper thoracic esophagus.

Adenocarcinoma↗
PubMed1992

Thoracic surgery and the war against smoking: Richard H. Overholt, MD.

Richard H. Overholt was born at the beginning of the twentieth century when thoracic surgery hardly existed. During the first 20 years of his life progress in the field was slow. The next 20 years, which coincided with Overholt's surgical training and his early years as a thoracic surgeon, saw a rapid and almost explosive growth. Overholt's contributions were legion. They included the world's first successful right pneumonectomy, advancements in surgical treatment of tuberculosis, development of segmental resection, and introduction of the prone operative position. He was a bold and creative pioneer thoracic surgeon with consumate technical skills. Sixty years ago, when Overholt started his career as a thoracic surgeon, the hazards of smoking were not appreciated, the habit was fashionable, and consumption of tobacco was rapidly rising. In the early 1930s Overholt was among the very few physicians who recognized the perils of smoking and initiated a long but initially unrewarding antismoking crusade. By the early 1950s evidence about the ill effects of tobacco use began to accumulate. Organized medicine, voluntary health groups, and governmental agencies joined in a concerted effort to educate and to contain smoking. During the ensuing 30 years the antismoking movement achieved ever-increasing success. Today, it is widely recognized that smoking is a major health hazard and tobacco consumption is on the decline. Richard Overholt issued the first warning signals about the perils of tobacco and served as an indefatigable leader of the antismoking crusade throughout his professional career.

History, 20th Century↗
PubMed1992

A new idea.

Explore the source record for details and available documents.

Hemodilution↗
PubMed1986

Substrate-selective induction of rabbit hepatic UDP-glucuronyltransferases by ethanol and other xenobiotics.

Male New Zealand white rabbits were treated with various inducers of hepatic metabolism enzymes to characterize the induction of UDP-glucuronyltransferase (UDP-GT) enzymes. Rabbits were pretreated with phenobarbital, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), 3-methylcholanthrene, beta-naphthoflavone, Aroclor 1254, ethanol, trans-stilbene oxide, pregnenolone-16 alpha-carbonitrile, or clofibric acid. Hepatic microsomes from treated and control animals were incubated with the GT1-type substrates, p-nitrophenol and 1-naphthol; the GT2-type substrate, morphine; and the steroid substrate, estrone. Compared to the rat, the rabbit was particularly resistant to UDP-GT induction. Ethanol was the most potent inducer for both GT1 and GT2 activities, but it failed to induce steroid (estrone, estradiol, and testosterone) UDP-GT activities. Ethanol pretreatment increased oxazepam-GT but it decreased bilirubin-GT activity. 3-Methylcholanthrene (3MC) and beta-naphthoflavone (BNF) are the prototypic GT1 inducers in the rat, but 3MC caused no induction of GT1 activity and BNF caused induction of both GT1 and GT2 activities in the rabbit. None of the xenobiotic pretreatments increased the hepatic microsomal glucuronidation of estrone. These results demonstrate that the induction of UDP-GT activities, and the use of this phenomenon to classify UDP-GT forms, is somewhat species-specific and cannot necessarily be extrapolated from rats to other species. In addition, the substrate selectivity of ethanol-induced microsomal UDP-GT was established.

Animals↗
PubMed1986

Functions of mononuclear phagocytes in mice exposed to diethylstilbestrol: a model of aberrant macrophage development.

Administration of the synthetic estrogen diethylstilbestrol (DES) lowers the systemic resistance of mice to challenge with either tumor cells or the facultative intracellular parasite Listeria monocytogenes. To assess the potential role of impaired mononuclear phagocyte system (MPS) function in this depression of host resistance, we addressed the question of systemic perturbations of the MPS induced by administration of DES. A panel of objective quantitative markers which have been previously shown to identify and characterize macrophages in the several stages of development of activation was employed. DES perturbed the resident population of peritoneal macrophages by increasing their number approximately twofold and by enhancing their competence for phagocytosis, cytostasis of tumor cells, and secretion of plasminogen activator. When we examined the competence of the MPS in DES-treated mice to respond to challenge with activating stimuli, we found that DES systemically suppressed the development of macrophages, in response to either pyran copolymer or BCG, to develop tumoricidal function and to gain competence for secretion of reactive oxygen intermediates such as H2O2. Since these data suggested that DES inhibited the development of macrophages from a precursor stage (i.e., responsive macrophages) to activated macrophages in vivo, we tested this possibility directly by applying known activating signals in vitro to responsive macrophages. Responsive macrophages from DES-treated mice did not become activated in response to the application of two known potent activating signals (i.e., MAF + LPS). Taken together, the data indicate that DES systemically perturbs the MPS and does so by enhancing development of the early stages of maturation and suppressing subsequent development.

Animals↗
PubMed1989

The carbon budget in the outer solar nebula.

Detailed models of the internal structures of Pluto and Charon, assuming rock and water ice as the only constituents, indicate that the mean silicate mass fraction of this two-body system is on the order of 0.7; thus the Pluto/Charon system is significantly "rockier" than the satellites of the giant planets (silicate mass fraction approximately 0.55). This compositional contrast reflects different formation mechanisms: it is likely that Pluto and Charon formed directly from the solar nebula, while the circumplanetary nebulae that produced the giant planet satellites were derived from envelopes that surrounded the forming giant planets (envelopes in which icy planetesimals dissolved more readily than rocky planetesimals). Simple cosmic abundance calculations, and the assumption that the Pluto/Charon system formed directly from solar nebula condensates, strongly suggest that the majority of the carbon in the outer solar nebula was in the form of carbon monoxide; these results are consistent with (1) inheritance from the dense molecular clouds in the interstellar medium (where CH4/CO < 10(-2) in the gas phase) and/or (2) of the Lewis and Prinn kinetic inhibition model of solar nebula chemistry. Theoretical predictions of the C/H enhancements in the atmospheres of the giant planets, when compared to the actual observed enhancements, suggest that 10%, or slightly more, of the carbon in the outer solar nebula was in the form of condensed materials (although the amount of condensed C may have dropped slightly with increasing heliocentric distance). Strict compositional limits computed for the Pluto/Charon system using the densities of CH4 and CO ices indicate that these pure ices are at best minor components in the interiors of these bodies, and imply that CH4 and CO ices were not the dominant C-bearing solids in the outer nebula. Clathrate-hydrates could not have appropriated enough CH4 or CO to be the major form of condensed carbon, although such clathrates may be necessary to explain the presence of methane on Pluto after its formation from a CO-rich nebula. Laboratory studies of carbonaceous chondrites, and spacecraft observations of Comet Halley, strongly suggest that of the remaining possibilities, organic material, rather than elemental carbon, is the most likely candidate for the dominant C-bearing solid in the outer solar nebula. We conclude that the majority of the carbon in the outer solar nebula was in gaseous CO; 10% to a few tens of percent of the C was in condensed organic materials; and at least a trace amount of carbon was in methane gas.

Carbon↗
PubMed1990

Deuterium enrichment in the primitive ices of the protosolar nebula.

We have estimated the D/H ratio that may have been present in the primitive ices in the protosolar nebula. Using observations of the CH3D/CH4 ratio in the outer planets, we developed two simple but limiting models which constrain the amount of dilution that deuterated volatiles which were contributed to the planetary atmospheres by evaporated primordial ices may have undergone by mixing with the original hydrogen envelopes. The models suggest that the D/H ratio in these ices was probably somewhere between a few times 10(-4) and 10(-3). These planetary-atmosphere-derived results are compared with other solar system bodies thought to contain primitive material and with D/H ratios observed in interstellar polyatomic molecules.

Atmosphere↗
PubMed1995

Accuracy assessment of methods for determining hip movement in seated cycling.

The goal of this research was to examine the accuracy of three methods used to indicate the hip joint center (HJC) in seated steady-state cycling. Two of the methods have been used in previous studies of cycling biomechanics and included tracking a marker placed over the superior aspect of the greater trochanter, a location that estimates the center of rotation of the hip joint, and assuming that the hip is fixed. The third method was new and utilized an anthropometric relationship to determine the hip joint location from a marker placed over the anterior-superior iliac spine. To perform a comparative analysis of errors inherent in the three methods, a standard method which located the true hip joint center was developed. The standard method involved establishing a pelvis-fixed coordinate system using a triad of video markers attached to an intracortical pin. Three-dimensional motion analysis quantified the true hip joint center position coordinates. To provide data for the comparative analysis, the intracortical pin was anchored to a single subject who pedaled at nine cadence-workrate combinations while data for all four methods were simultaneously recorded. At all cadence-workrate combinations the new method was more accurate than the trochanter method with movement errors lower by a factor of 2 in the vertical direction and a factor of 3 in the horizontal direction. Relative to the errors introduced by the fixed hip assumption, the new method was also generally more accurate by at least a factor of 2 in the horizontal direction and had comparable accuracy in the vertical direction. For computed kinetic quantities, the new method most accurately indicated hip joint force power but the fixed hip method most accurately indicated the work produced by the hip joint force over the crank cycle.

Bicycling↗