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Biomedical subjects

L Birnbaum

Publications and source records attributed to L Birnbaum.

17 recordsLinked to original sources
PubMed2006

Effect of blood donation on maximal oxygen consumption.

AIM: This study determined the effect of donating one unit of blood on various physiological parameters associated with a VO2(max) test. METHODS: Ten healthy, male subjects (23+/-4 years, 178+/-7.6 cm, 74.4+/-12.3 kg) completed a VO2(max) test 24 h before donating one unit of blood (~500 mL) and 24 h after donating blood. The Bruce protocol was used to determine the subjects' VO2(max). Physiological responses were measured at the end of the VO2(max) test. A repeated measures ANOVA was used to determine if there were significant (P<0.05) differences in the subjects' physiological responses between the VO2(max) before and after blood donation. RESULTS: Significant differences were found in VO2(max) (mean+/-SD, 3.18+/-0.74 vs 2.87+/-0.53 L.min(-1)), cardiac output (Q, 25+/-5 vs 22.5+/-3.3 L.min(-1)), stroke volume (SV, 134+/-37 vs 121+/-22 mL.beat(-1)), delivery of oxygen (DO(2), 5+/-.87 vs 3.97+/-.68 L.min(-1)), and hemoglobin concentration (Hb, 153+/-12 vs 135+/-16 gm.L(-1)). No significant changes were observed for heart rate (HR); arteriovenous oxygen difference (a-vO(2) diff), systolic blood pressure (SBP), and diastolic blood pressure (DBP). CONCLUSIONS: These findings indicate that donating one unit of blood decreased VO2(max) due to the decrease in Q, which resulted from the decrease in SV since HR was unchanged. The lower VO2(max) along with the decrease in DO(2) would be expected to have a negative effect on athletic performance.

Adult↗
PubMed2005

Overlapping stent-supported coil embolization of wide-neck basilar tip aneurysm: technical case reports.

We report two cases in which wide-neck basilar aneurysms were treated with overlapping stent-supported coil embolization. This overlapping technique ensures complete stent interface with the aneurysm neck and likely improves long-term outcomes. We demonstrated the feasibility of this novel technique and suggest its application for other bifurcation aneurysms requiring stent-supported coil embolization.

Adult↗
PubMed1998

Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife.

An expert meeting was organized by the World Health Organization (WHO) and held in Stockholm on 15-18 June 1997. The objective of this meeting was to derive consensus toxic equivalency factors (TEFs) for polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) and dioxinlike polychlorinated biphenyls (PCBs) for both human, fish, and wildlife risk assessment. Based on existing literature data, TEFs were (re)evaluated and either revised (mammals) or established (fish and birds). A few mammalian WHO-TEFs were revised, including 1,2,3,7,8-pentachlorinated DD, octachlorinated DD, octachlorinated DF, and PCB 77. These mammalian TEFs are also considered applicable for humans and wild mammalian species. Furthermore, it was concluded that there was insufficient in vivo evidence to continue the use of TEFs for some di-ortho PCBs, as suggested earlier by Ahlborg et al. [Chemosphere 28:1049-1067 (1994)]. In addition, TEFs for fish and birds were determined. The WHO working group attempted to harmonize TEFs across different taxa to the extent possible. However, total synchronization of TEFs was not feasible, as there were orders of a magnitude difference in TEFs between taxa for some compounds. In this respect, the absent or very low response of fish to mono-ortho PCBs is most noticeable compared to mammals and birds. Uncertainties that could compromise the TEF concept were also reviewed, including nonadditive interactions, differences in shape of the dose-response curve, and species responsiveness. In spite of these uncertainties, it was concluded that the TEF concept is still the most plausible and feasible approach for risk assessment of halogenated aromatic hydrocarbons with dioxinlike properties.

Animals↗
PubMed1996

Promotion of endometriosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats and mice: time-dose dependence and species comparison.

In the disease of endometriosis, endometrial tissue grows outside the uterus, usually in the peritoneal cavity. Rodent models of endometriosis allow a way to reproduce the disease, evaluate effects of chemicals, and study mechanisms. Twenty-one days prior to induction surgery which produces endometriosis, female Sprague-Dawley rats and B6C3F1 mice were pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at 0, 3 or 10 micrograms TCDD/kg. Animals were treated again at the time of surgery and at 3, 6, and 9 weeks following surgery. Evaluations were made at 3, 6, 9, and 12 weeks postsurgery. TCDD produced a dose-dependent increase in endometriotic site diameter when all time points were pooled within each dose in rats and a dramatic increase in site diameter in mice at 9 and 12 weeks. In rats but not mice, ovarian weight was decreased at 9 and 12 weeks, the occurrence of persistent vaginal estrus was increased at these times, and histological evaluation of the ovaries revealed ovulatory arrest at 12 weeks. In both species, thymic antrophy, indicating immune dysfunction, and hepatomegaly were observed as consequences of TCDD exposure. Body weight was reduced in rats but not in mice. Histological evaluations of endometriotic sites revealed fibrosis in control rats, necrotic and inflammatory changes in the sites from TCDD-treated rats, and predominantly fibrotic changes in sites from TCDD-treated mice. Differences observed between the rat and the mouse with respect to (a) the magnitude of the effect on endometrial site diameter (rats < mice), (b) measured effects on ovarian function (rats > mice) that may be based on the partial antiestrogenicity of TCDD, and (c) evidence that mice and rats differ in their immune response to TCDD suggest that the mechanisms mediating TCDD's action to promote endometriosis are complex and may be different in rats and mice. The mouse may be a better model for future studies necessary to elucidate these mechanisms.

Animals↗
PubMed1995

Induction of cytochrome P450 isoenzymes after toxicokinetic interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin and 2,2',4,4',5,5'-hexachlorobiphenyl in the liver of the mouse.

One group of male C57BL/6J mice received a single oral dose of 1 nmol 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg. Six other groups received single oral doses of 100, 300, or 1000 mumol 2,2',4,4',5,5'-hexachlorobiphenyl (HxCB)/kg, alone or in combination with 1 nmol/kg TCDD. Liver deposition of both compounds was studied at Day 3 after dosage. Hepatic CYP1A1 and CYP1A2 protein levels and related 7-ethoxyresorufin-O-deethylation (EROD) and acetanilide 4-hydroxylation (ACOH) activities were also studied. A significant increase in the hepatic deposition of TCDD was observed in all three mixed dose groups but TCDD did not influence hepatic HxCB deposition. TCDD did increase both CYP1A1 and CYP1A2 protein levels. In the HxCB-treated groups, CYP1A2 levels were also increased in a dose-dependent way but CYP1A1 levels were not increased. CYP1A2 activities (ACOH), but not protein levels, in the TCDD groups cotreated with HxCB were higher than those in the group treated with TCDD alone. CYP1A1-dependent EROD activity and CYP1A2-dependent ACOH activity were induced in all treated dose groups. It is concluded that the present results do not confirm a direct role of CYP1A2 induction in the increase of hepatic TCDD levels by HxCB cotreatment in the mixed HxCB/TCDD dose groups. However, in this aspect, the discrepancy between CYP1A2 activities and protein levels remains to be explained.

Animals↗
PubMed1995

The effects of 2,2',4,4',5,5'-hexachlorobiphenyl cotreatment on the disposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice.

Two groups of C57BL/6J mice received a single oral dose of 1 nmol/kg 2,3,7,8-[3H]tetrachlorodibenzo-p-dioxin (TCDD) alone or in combination with 300 mumol/kg 2,2',4,4',5,5'-hexachlorobiphenyl (HxCB). The disposition of TCDD in liver, fat, skin, spleen, lung and blood was studied at days 3, 7, 13 and 34 after dosage. HxCB cotreatment increased hepatic TCDD levels and, consequently, significant increases of the liver/fat distribution ratio were observed. HxCB cotreatment did not significantly affect TCDD levels in fat or other tissues. The elimination rates of TCDD were not influenced by HxCB cotreatment in any of the tissues. It is concluded that HxCB cotreatment alters the body distribution of TCDD in mice but does not influence the elimination rate of TCDD.

Adipose Tissue↗
PubMed1994

Relative sensitivities of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced Cyp1a-1 and Cyp1a-2 gene expression and immunotoxicity in female B6C3F1 mice.

Improvements in risk assessment require better linkage of exposure to response by the determination of target tissue dose. The relative sensitivity of several responses in female B6C3F1 mice was compared on the basis of administered and target tissue dose spanning 3 orders of magnitude. Twenty-four hours after administration, [3H]TCDD was detected in the heart, spleen, kidney, uterus, thymus, lung, and liver, and the highest concentrations were noted in the liver, uterus, and lung. At doses from 5 to 25 ng/kg, hepatic [3H]TCDD levels associated with the cytosolic and nuclear subcellular fractions increased from 12 to 62% of the total liver levels and then decreased at higher doses. At the two lowest doses used in the enzyme induction study, 5 and 10 ng/kg, the levels of specifically bound nuclear Ah receptor complex liganded with [3H]TCDD were 2.3 and 2.5 fmol/mg protein. Slightly higher levels of nuclear Ah receptor complex were observed at doses between 25 and 100 ng/kg (i.e., 3.6 to 4.2 fmol/mg protein) and a steep dose-dependent increase in nuclear Ah receptor levels was noted at doses of 500, 1000, and 5000 ng/kg (8.0, 39.3, and 92.8 fmol/mg protein, respectively). The dose-dependent effects of [3H]TCDD on hepatic Cyp1a-1 and Cyp1a-2 mRNA levels, ethoxyresorufin O-deethylase (EROD) activity, and the splenic antibody plaque-forming cell (PFC) response to sheep red blood cells were also determined; the latter response was determined 9 days after administration of TCDD. Statistically significant induction of hepatic Cyp1a-1 was observed at lower doses (25 ng/kg) than any other marker, followed by induction of EROD and PFCs expressed per spleen or per 10(6) cells which was observed at 100 ng TCDD/kg and at higher doses. Cyp1a-2 was elevated significantly relative to control at doses > or = 1000 ng/kg. The ED50 value for PFCs/10(6) cells was the lowest of the variables analyzed and was not statistically significantly different from control (91 +/- 92 ng/kg). A 50% increase in Cyp1a-2 and Cyp1a-1 mRNA levels was observed at doses of 736 +/- 132 and 1630 +/- 431 ng/kg, respectively. Due to variability in response in PFCs/spleen and the submaximal induction of EROD activity, ED50 values could not be calculated for these responses. The analyses indicate that the immunosuppressive response (when normalized for the number of spleen cells) may be depressed by administered doses as low as 90 ng TCDD/kg body weight. A 50% increase in Cyp1a-1 or Cyp1a-2 was observed at higher administered doses (1630 or 736 ng/kg, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Toxicity equivalency factors for PCBs?

In December 1990 the U.S. Environmental Protection Agency sponsored a workshop to discuss the applicability of an interim "toxicity equivalency factor" (TEF) approach to assessing risks posed by exposures to complex mixtures of polychlorinated biphenyls (PCBs). The group concluded that application of the TEF approach to PCBs would be less straightforward than it was in the case of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs/CDFs). It appears that "dioxin"-like properties of some PCB congeners are amenable to a TEF treatment that is compatible with that used for CDDs/CDFs. Such a scheme also seems to have utility in assessing risks to wildlife. Other non-"dioxin"-like toxic endpoints (e.g., neurotoxicity) appear to have a different structure-activity-related mechanism-of-action that requires a separate TEF scheme. The workshop identified data gaps in toxicology and analytical chemistry that hinder adoption of proposed TEF schemes for PCBs at this time.

Benzofurans↗
PubMed1981

Reconstruction of the aesthetically pleasing breast.

Techniques are outlined to assist in obtaining a superior result in difficult breast reconstruction problems. The use of multiple adjustments, broad-based implants, and dermal contouring for nipple-areola reconstruction are discussed.

Adult↗
PubMed1979

Use of dermal grafts to cover implants in breast reconstructions.

The use of dermal grafts for the reinforcement of the cover over implants in breast reconstructions after radical mastectomy is illustrated in several cases. By carefully selecting the patients, we feel that this relatively minor procedure may replace the use of local of distant flaps in a good many breast reconstructions.

Adult↗
PubMed1978

Breast reconstruction following radical mastectomy, using custom designed implants.

Procedures are described for total breast reconstruction in patients who have undergone radical and modified radical mastectomies. The reconstruction includes restoration of the contour of the breast, including the nipple-areola complex and filling the defect from loss of the pectoral muscles. The reconstructions have been done in 37 patients with good results, and several are illustrated.

Adult↗
PubMedDate not supplied

Addition of conjugated linoleic acid to a herbal anticellulite pill.

This study investigated the effect of a herbal anticellulite pill on visible cellulite in the thighs. Sixty female volunteers took a herbal anticellulite pill or a herbal anticellulite pill plus supplements of conjugated linoleic acid for 60 days. The combination treatment had a beneficial effect in as many as 75% of the women. The appearance of the skin improved significantly, and thigh circumference was reduced by an average of 0.88 inch. Further investigation in a larger, longer placebo-controlled trial is warranted.

Adipose Tissue↗