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Biomedical subjects

E Arias

Publications and source records attributed to E Arias.

At least 19 recordsLinked to original sources
PubMed2001

Deaths: final data for 1999.

OBJECTIVES: This report presents final 1999 data on U.S. deaths and death rates according to demographic and medical characteristics. Trends and patterns in general mortality, life expectancy, and infant and maternal mortality are also described. A previous report presented preliminary mortality data for 1999. METHODS: In 1999 a total of 2,391,399 deaths were reported in the United States. This report presents tabulations of information reported on the death certificates completed by funeral directors, attending physicians, medical examiners, and coroners. Original records are filed in the State registration offices. Statistical information is compiled into a national data base through the Vital Statistics Cooperative Program of the National Center for Health Statistics (NCHS), Centers for Disease Control and Prevention. For the first time in a final mortality data report, age-adjusted death rates are based upon the year 2000 population and causes of death are processed in accordance with the Tenth Revision of the International Classification of Diseases (ICD-10). RESULTS: The 1999 age-adjusted death rate for the United States was 881.9 deaths per 100,000 standard population, a 0.7 percent increase from the 1998 rate, and life expectancy at birth remained the same at 76.7 years. For all causes of death, age-specific death rates rose for those 45-54 years, 75-84 years, and 85 years and over and declined for a number of age groups including those 5-14 years, 55-64 years, and 65-74 years. Aortic aneurysm and dissection made its debut in the list of leading causes of death and atherosclerosis exited from the list. Heart disease and cancer continued to be the leading and second leading causes of death. The age-adjusted death rate for firearm injuries decreased for the sixth consecutive year, declining 6.2 percent between 1998 and 1999. The infant mortality rate, 7.1 infant deaths per 1,000 live births, was not statistically different from the rate in 1998. CONCLUSIONS: Generally, mortality continued long-term trends. Life expectancy in 1999 was unchanged from 1998 despite a slight increase in the age-adjusted death rate from the record low achieved in 1998. Although statistically unchanged from 1998, the trend in infant mortality has been of a steady but slowing decline. Some mortality measures for women and persons 85 years and over worsened between 1998 and 1999.

Adolescent↗
PubMed2001

Analysis of pesticide residues in wine by solid-phase extraction and gas chromatography with electron capture and nitrogen-phosphorus detection.

A feasible and reproducible method for multiresidue analysis of several common pesticides, of different polarities, in wine samples is proposed. The method combines a solid-phase extraction on polymeric cartridges eluted with ethyl acetate and a gas chromatographic determination using electron capture and nitrogen-phosphorus detection. To avoid the matrix effect, previous washing of the cartridges with a mixture of water-2-propanol (90:10) and further clean-up of the extract on Florisil cartridges, together with a calibration using spiked extracts, are recommended.

Chromatography, Gas↗
PubMed1999

Airway hyperresponsiveness to ultrasonically nebulized distilled water in subjects with tetraplegia.

The majority of otherwise healthy subjects with chronic cervical spinal cord injury (SCI) demonstrate airway hyperresponsiveness to aerosolized methacholine or histamine. The present study was performed to determine whether ultrasonically nebulized distilled water (UNDW) induces airway hyperresponsiveness and to further elucidate potential mechanisms in this population. Fifteen subjects with SCI, nine with tetraplegia (C4-7) and six with paraplegia (T9-L1), were initially exposed to UNDW for 30 s; spirometry was performed immediately and again 2 min after exposure. The challenge continued by progressively increasing exposure time until the forced expiratory volume in 1 s decreased 20% or more from baseline (PD20) or the maximal exposure time was reached. Five subjects responding to UNDW returned for a second challenge 30 min after inhalation of aerosolized ipratropium bromide (2.5 ml of a 0.6% solution). Eight of nine subjects with tetraplegia had significant bronchoconstrictor responses to UNDW (geometric mean PD20 = 7.76 +/- 7.67 ml), whereas none with paraplegia demonstrated a response (geometric mean PD20 = 24 ml). Five of the subjects with tetraplegia who initially responded to distilled water (geometric mean PD20 = 5.99 +/- 4.47 ml) were not responsive after pretreatment with ipratropium bromide (geometric mean PD20 = 24 ml). Findings that subjects with tetraplegia are hyperreactive to UNDW, a physicochemical agent, combined with previous observations of hyperreactivity to methacholine and histamine, suggest that overall airway hyperresponsiveness in these individuals is a nonspecific phenomenon similar to that observed in patients with asthma. The ability of ipratropium bromide to completely block UNDW-induced bronchoconstriction suggests that, in part, airway hyperresponsiveness in subjects with tetraplegia represents unopposed parasympathetic activity.

Adult↗
PubMed1998

Inhibitory effect of propranolol on lipid synthesis in gonadectomized male hamster flank organs.

BACKGROUND: This paper describes the inhibitory effect produced by propranolol pre-treatment on lipid synthesis in flank organs from intact, gonadectomized, and isoproterenol-treated male hamsters. Furthermore, the effect induced by the same treatments on gland sebum composition is reported. METHODS: Different groups of male hamsters were injected daily with propranolol, isoproterenol or propranolol plus isoproterenol. Treatment-effect was evaluated determining the in vitro incorporation of radioactive acetate into lipids in hamster flank organs from intact and castrated animals. Additionally, radiolabeled lipids were isolated and identified using TLC and autoradiography as methods. RESULTS: Results demonstrate that castration significantly decreases lipid synthesis in male hamster flank organs. In addition, propranolol treatment inhibits such synthesis in glands from intact, gonadectomized, and isoproterenol-treated animals. However, isoproterenol treatment was ineffective when compared to intact or gonadectomized control vehicle-treated animals. Lipid classes isolated and identified lipids either in castrated or in drug-treated animals were phospholipids, cholesterol, monoglycerides, fatty acids, waxes and cholesterol esters. CONCLUSIONS: Results indicate an inhibitory effect induced on lipid synthesis by beta-adrenergic receptor antagonists; however, beta-adrenergic agonists drugs do not stimulate it. Data suggest a permissive role of adrenergic hormones on lipid synthesis in intact and in gonadectomized animals. Furthermore, castration decreased the synthesis, suggesting that a tight coupling between beta-adrenergic receptors and androgen receptors may be a prerequisite for lipogenesis in this tissue. Pre-treatment does not modify sebum composition in gonadectomized animal glands. These data support the evidence that activation of beta-adrenergic receptors could be an independent factor in the lipid composition regulation process.

Animals↗
PubMed1994

Evaluation of the tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, in liver of Fischer 344 rats.

The tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, was tested in a two-stage protocol of hepatocarcinogenesis in male and female Fischer 344 rats. Propranolol is a lipophilic non-selective beta-blocker mainly eliminated via the liver; atenolol is a hydrophilic beta 1-selective blocking agent, mainly eliminated via the kidney. Animals were initiated with a single dose of diethylnitrosamine (DEN, 200 mg/kg, i.p.) and, after 17 days of recovery, were continuously treated with propranolol (75-100 mg/kg) or atenolol (300 mg/kg) by gavage for up to 21 months. Rats given phenobarbital (0.05% in the diet) were used as positive controls. After 2, 4 and 8 months of promotion, preneoplastic lesions were quantified by staining sections of liver for gamma-glutamyltranspeptidase (GGT). In non-initiated rats, neither propranolol nor atenolol influenced the development of spontaneous preneoplastic or neoplastic liver lesions. The results obtained in DEN-initiated rats given propranolol cannot be unequivocally interpreted. In the male, propranolol seemed to be ineffective. In the female, there was weak enhancement of DEN-induced GGT foci at 4 and 8 months and of neoplastic lesions thereafter. However, there was great interindividual variability in focus and tumor yields. Unfortunately, due to the high incidence of liver tumors in rats given DEN alone and the small number of propranolol-treated rats that survived until the end of the experiment, no definite conclusion can be drawn about the modifying potential of this beta-blocker on liver carcinogenesis. There was no evidence of liver tumor promotion in DEN-initiated rats of either sex given atenolol.

Animals↗
PubMed1992

Sister chromatid exchanges in chick embryos after treatment with the phenoxy herbicide MCPA.

The phenoxyherbicide and peroxisome proliferator 2-methyl-4-chlorophenoxyacetic acid (MCPA) was tested for its ability to induce sister-chromatid exchanges (SCE) in chick embryos. Erbitox E30 (a commercial formulation containing 28% MCPA sodium potassium salt as active ingredient) was injected into the air chamber in concentrations of MCPA of 0, 0.35, 0.7, 1.4, 2.8, or 5.6 mg/egg on day 0 of incubation. Pure MCPA sodium salt was tested at 2.8 mg/egg. Neutral red at 0.25 mg/egg was the mutagenic reference compound (positive control group). Eggs were then incubated for 4 days. MCPA induced a slight but significant increase in SCE frequency (about 1.3 times base line) at 2.8 mg/egg. The dose of 5.6 mg/egg was toxic. No difference in genetic activity between the commercial formulation and the pure compound was found. A cell cycle delaying effect of MCPA was evident at all the dose levels tested. The mitotic index remained unchanged.

2-Methyl-4-chlorophenoxyacetic Acid↗
PubMed1989

Teratological evaluation of the phenoxyacid herbicide MCPA in the regenerating forelimb of the adult newt.

The effects of a commercial formulation of the phenoxyacid herbicide 2-methyl-4-chlorophenoxyacetic acid sodium salt (MCPA) on the regenerating forelimb of the adult crested newt were studied. The animals were exposed percutaneously to 0, 200, 400, or 800 ppm of MCPA for 4 days a week throughout the regeneration period and were sacrificed 11 weeks after amputation. The concentrations tested did not cause histologically detectable toxic lesions of the examined organs. Exposure to MCPA resulted in a significant retardation of the morphogenetic process as evidenced by skeletal examination. At the highest concentration tested, a significant growth delay was also evident during the regeneration period. No significant differences in the frequency of skeletal malformations were observed between control and treated newts, although the frequency was higher in the latter.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1989

Changes in catalase, glutathione peroxidase and glutathione-S-transferase activities in the liver of newts exposed to 2-methyl-4-chlorophenoxyacetic acid (MCPA).

Activities of catalase, glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) were measured in livers of the crested newt (Urodele Amphibian) after 16 days of percutaneous exposure to the herbicide Agroxone 3, a commercial formulation of 2-methyl-4-chlorophenoxyacetic acid (MCPA) containing 25% MCPA as sodium salt and 75% wetting and dispersing ingredients. Animals of both sexes were exposed to 800 p.p.m. of the active ingredient. There was a three-fold increase in catalase and a clear enhancement of GSH-Px in the MCPA-exposed animals of both sexes. A sex-dependent effect of MCPA was observed on GST activity, which increased significantly in female newts only. Similar liver enzyme changes were observed in female newts, and not in males, given the hypolipidaemic drug clofibrate (13 mg/animal/day, by gavage, for 8 days), which is structurally related to phenoxyherbicides. These findings indicate that the crested newt is sensitive to the hepatic effects of the peroxisome proliferators.

2-Methyl-4-chlorophenoxyacetic Acid↗
PubMed1988

Evaluation of the carcinogenic risk of the phenoxyherbicide MCPA to an urodele amphibian.

To evaluate the carcinogenic potential of the phenoxyherbicide 2-methyl-4-chlorophenoxy-acetic acid (MCPA) in the crested newt, Triturus cristatus carnifex, a long-term study has been carried out exposing the animals by the percutaneous route. Two hundred adult newts were divided into one control and three experimental groups of 20 females and 30 males each. The control group was kept in tap water and the experimental groups were kept for 4 days a week in an aqueous solution of Agroxone 3, a commercial formulation of MCPA, at concentrations equivalent to 100, 200, and 400 ppm of the active ingredient. Treatment was continued for 1 year, after which all the animals were kept under observation for approximately another year. Surviving female newts were killed 22-24 months after the beginning of experimentation, whereas the male newts were killed after 28 months, at the end of 18 weeks of exposure to the tumour promoter 12-O-tetradecanoylphorbol-13-acetate. Under experimental conditions, there was no carcinogenic activity of MCPA. Putative preneoplastic nodules of the liver and tumor-like lesions of the lower jaw were occasionally observed among the animals that survived more than 22 months after the beginning of experimentation. However, no significant differences in frequency between control and experimental groups were found.

2-Methyl-4-chlorophenoxyacetic Acid↗
PubMed1988

Sister-chromatid exchanges and chromosomal aberrations in chick embryos after treatment with the fungicide maneb.

The genotoxic potential of a commercial formulation of the fungicide maneb (Maneb 80, containing 80% manganese ethylenebisdithiocarbamate as active ingredient) in chick embryos was evaluated, using as genetic end-points the frequency of sister-chromatid exchanges (SCE) and of chromosomal aberrations. Unincubated eggs were dipped in 0, 0.5, 1.5, 4.5, 13.5 or 27 g/l maneb aqueous solutions for 30 sec. Eggs were then incubated for 4 days. Maneb significantly increased SCE values at 13.5 g/l and at 27 g/l (means 1.33 and 1.74) over the control value (mean 0.87). The concentration of 27 g/l, which corresponds to 10.8 times the recommended maximum application level for use in the field, also resulted in a high mortality rate. No clastogenic effects following exposure to maneb were observed.

Animals↗
PubMed1988

Toxicity and distribution of 2-methyl-4-chlorophenoxyacetic acid (MCPA) in developing chick embryos.

The toxicity of the herbicide Erbitox E30, a commercial formulation of 2-methyl-4-chlorophenoxyacetic acid (MCPA) containing 28% MCPA as sodium-potassium salt and 72% of unknown ingredients, was tested on chick embryos. Sterile aqueous solutions of MCPA were injected into the air chamber at doses of 0, 1.5, 3.0, 6.0, 9.0, or 10.5 mg/egg on day 0 or on day 4 of incubation. The mortality rate for the embryos treated on day 0 of incubation was high in the first 5 days, low from 5-12 days and again increased by 15 days. The 15-day LD50 was 4.4 mg/egg (95% C.I. 3.7-5.3 mg/egg). HPLC analysis of albumen and yolk showed that concentrations of MCPA in the albumen were detectable at 5 min, highest at 7 days and markedly diminished by 14 days of incubation; a significantly lower concentration of MCPA was found in the yolk throughout the incubation period, except at 14 days when the yolk concentration was 4 times higher than the albumen concentration. At 15 days of incubation, MCPA was evenly distributed in the tissues of the embryo. MCPA was more toxic to 4-day embryos; concentrations above 6.0 mg/egg were lethal to all embryos within the first week of incubation. The 15-day LD50 for treatment on day 4 of incubation was 2.8 mg/egg (95% C.I. 2.5-3.2 mg/egg). The liver was affected by treatment with MCPA, being green in treated embryos. However, histological examination revealed few changes in the liver parenchyma.

2-Methyl-4-chlorophenoxyacetic Acid↗
PubMed1987

Teratogenic effects of the fungicide maneb on chick embryos.

The teratogenicity of a commercial formulation of the fungicide maneb (Maneb 80, containing 80% manganese ethylenebisdithiocarbamate and 20% inert ingredients) in chick embryos was evaluated. Unincubated eggs (157-207 per treatment group) were immersed in 0.5, 1.5, 4.5, or 13.5 g/liter maneb aqueous solutions for 30 sec. Two control groups were used: one group of 200 eggs was immersed in tap water and a second group of 205 eggs was immersed in a solution of the inert ingredients (sodium lignin sulfonate and n-butylnaphthalene sulfonate) at the concentration present in the 13.5 g/liter maneb solution. Eggs were then incubated for 19 days. A single treatment with maneb was teratogenic at all concentrations tested, producing mainly unilateral lower limb deformities. No adverse effects on development were noticed after exposure to the inert ingredients.

Animals↗