Electromagnetic implosion of spherical liner.
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Journal Article↗
Biomedical subjects
D Dietz
Publications and source records attributed to D Dietz.
The impact of anticipation of job loss on psychological distress and worksite blood pressure.
The impact of occupational stressful life events on psychological distress and blood pressure was examined among employees of a major New York City brokerage firm undergoing massive layoffs. One hundred thirty-nine employees of the firm, who had participated in a blood pressure screening in 1986, were rescreened during the period of layoffs within their company in 1989. About two-thirds of the 139 employees reported being "somewhat" or "very" anxious or upset in 1989 during the period of layoffs, and psychological distress was significantly elevated among those employees reporting possible or definite layoff or job change and/or difficulty in obtaining a comparable job. However, we found no increase in overall blood pressure level, and no effect of anticipation of job loss on 1989 blood pressure when controlling for 1986 blood pressure level, age, body mass index, work hours, and other demographic variables. On the other hand, employment in a department sold to another employer on the day of screening, as well as employment in a clerical job title, were both associated with significant increases in diastolic blood pressure of about 5 mm Hg.
Anxiety↗
Effects of pretreatment with inducers of hepatic mixed function oxidases on DNA repair elicited by various compounds in hepatocytes from adult and neonatal rats.
Studies were conducted to assess the effects of inducers of hepatic mixed function oxidases on DNA repair responses to 13 different genotoxic agents in hepatocytes from adult male mice. Phenobarbital pretreatment increased DNA repair elicited by diethylnitrosamine but had no effect on responses to the other compounds. Pretreatment with p,p'-dichlorodiphenyltrichlorethane, 3-methyl-cholanthrene or beta-naphthoflavone induced the DNA repair responses to a variety of activation-dependent carcinogens. DNA repair responses to the direct-acting alkylating agents methyl methanesulfonate and N-methyl-N'-nitro-N-nitrosoguanidine were not increased by any of the pretreatments, which indicated that the pretreatment-related enhancement of responses to the other compounds was due to induction of their metabolic activation. Taken together, the findings suggest that Aroclor, or other pretreatments, may increase the sensitivity of the hepatocyte DNA repair assay for detecting the genotoxicity of certain compounds; however, the potential benefit may be limited due to specific features of the assay. In contrast, Aroclor pretreatment did not produce any enhancement of in vivo DNA repair elicited by dimethylnitrosamine, diethylnitrosamine, o-aminoazotoluene, 2-acetylaminofluorene, 3-methylcholanthrene or aflatoxin B1, and thus does not appear to be useful for improving the sensitivity of the in vivo/in vitro assay. Whereas the amount of DNA repair produced by dimethylnitrosamine was not increased by classical inducers of liver microsomal enzymes, pretreatment with pyrazole greatly augmented in vitro and in vivo DNA repair responses to dimethylnitrosamine; responses to diethylnitrosamine were increased to a lesser degree by pyrazole pretreatment. The effects of lactational exposure to enzyme inducing agents on DNA repair in neonatal hepatocytes was also investigated.
2-Acetylaminofluorene↗
Effects of pretreatment with pyrazole and inducers of mixed function oxidases on DNA repair elicited by dimethylnitrosamine in rat hepatocytes in vivo and in vitro.
Experiments were performed to investigate the relationship between the rate of oxidative metabolism of dimethylnitrosamine (DMN) by rat liver microsomes (i.e., DMN demethylase activity, DMNd) and its genotoxicity in liver, as assessed by the in vitro and in vivo/in vitro rat hepatocyte primary culture/DNA repair (HPC/DR) assays. Pretreatment of rats with pyrazole (PYR) resulted in a 4-fold increase in DMNd and a 3-fold greater DNA repair response to in vivo administration of 5 mg DMN/kg body weight. Pretreatment with phenobarbital (PB), dichlorodiphenyltrichloroethane (DDT), 3-methylcholanthrene (3-MC), beta-naphthoflavone (beta-NF) or Aroclor 1254 (ARO) produced a variable degree of inhibition of DMNd and had no significant effects on the response to DMN in the in vivo/in vitro HPC/DR assay. DNA repair elicited by DMN in vitro was decreased in hepatocytes from rats pretreated with 3-MC, while PB, DDT, beta-NF and ARO pretreatments had little effect on the response. In contrast, PYR pretreatment produced a 4.5-6.7-fold increase in the in vitro DNA repair response to DMN, and extended detection of positive responses to lower concentrations. Most of the inducers had no effect on DNA repair elicited by the direct acting alkylator, methyl methanesulfonate (MMS). Thus, the pretreatment-related changes in DMN-induced DNA repair were probably due to alterations in DMNd rather than to effects on the DNA repair capacity of the hepatocytes.
Animals↗
Aroclor 1254 pretreatment effects on DNA repair in rat hepatocytes elicited by in vivo or in vitro exposure to various chemicals.
Inducers of liver mixed function oxidase (MFO) activities have profound effects on the genotoxicity of substances that undergo metabolic activation by the MFO system. The polychlorinated biphenyl mixture Aroclor 1254 is a broad-spectrum inducer of liver MFO activities that has been employed as a pretreatment to augment the metabolic activation capabilities of rat liver fractions used in a number of short-term tests for genotoxicity, including the Ames Salmonella/bacterial mutagenicity assay. The present study was designed to characterize the effects of Aroclor pretreatment of rats on the DNA repair responses elicited by various chemicals in the in vitro hepatocyte primary culture/DNA repair (HPC/DR) assay as well as the in vivo/in vitro HPC/DR assay. The amount of DNA repair produced in vitro by diethylnitrosamine (DEN), benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3-MC), 2-acetylaminofluorene (2-AAF), o-aminoazotoluene (o-AT), and aflatoxin B1 (AFB1) was significantly greater in hepatocytes derived from Aroclor-pretreated rats than in control rat hepatocytes; in vitro responses to dimethylnitrosamine (DMN), 7,12-dimethylbenzanthracene (DMBA), benzidine (BZ), and 2-naphthylamine (2-NA) were not significantly affected by Aroclor pretreatment. DNA repair elicited by the direct-acting alkylating agents methyl methanesulfonate and N-methyl-N'-nitro-N-nitrosoguanidine was also not increased by Aroclor pretreatment, which indicated that Aroclor does not exert a general stimulatory effect on the hepatocellular DNA repair capacity. Therefore, the pretreatment-related potentiation of DNA repair observed for 6 out of 12 compounds tested in vitro was considered to be due to enhanced metabolic activation. These results suggested that pretreatment with Aroclor may increase the sensitivity of the in vitro HPC/DR assay to certain compounds. In contrast, Aroclor pretreatment had little effect on the amount of hepatocellular DNA repair elicited by in vivo administration of DMN, DEN, o-AT, 2-AAF, 3-MC, or AFB1, which indicated that this pretreatment regimen may have little utility for improving the sensitivity of the in vivo/in vitro HPC/DR assay.
Animals↗
Thermoradiotherapy for superficial tumour deposits in the head and neck.
Tumour deposits in the head and neck region were treated with hyperthermia using 915 MHz external microwave applicators and radiation therapy between 1986 and 1990. The mean (+/- SE) radiation dose was 47 +/- 2 Gy (range 21-77 Gy). All but four patients had failed previous therapy. Mean tumour volume was 40 +/- 10 cm3 (range 0.3-276 cm3). Hyperthermia was administered biweekly in 80% of the patients in 6.0 +/- 0.4 sessions (range 1-10); thermometry involved 3.6 +/- 0.4 catheters (range 1-9) and 5.7 +/- 0.4 sensors (range 1-12) per tumour. Of the 50 lesions evaluable for response, 29 had a complete response (58%), and 20 had a partial response (40%). Lesions were stratified by depth. In tumours considered potentially heatable (i.e. depth < or = 3 cm and lateral dimensions at least 2 cm less than boundary of applicator), the complete response rate was 81% (26/32, 47 +/- 2 Gy, 15 +/- 3 cm3); whereas for patients with tumours deeper than 3 cm, the complete response rate was 17% (3/18, 48 +/- 3 Gy, 110 +/- 21 cm3), p = 0.0001. Among lesions < or = 3 cm depth that exhibited a complete response, six recurred (24%, 5.8 +/- 1.8 months) while 20 lesions were recurrence free at last follow-up of 11.9 +/- 1.2 months). The overall survival of patients with lesions < or = 3 cm depth was 11.5 +/- 1.3 months (range 2.4-32.3 months) while for patients with lesions > 3 cm depth survival was 6.7 +/- 0.9 months (range 2.1-18.6 months), p = 0.01. In superficial lesions with depth < or = 3 cm, multivariate logistic regression analysis indicated that the model best correlating with complete response included radiation dose (p = 0.08) and tumour volume (p = 0.08, model p = 0.004). Multivariate proportional hazard analysis indicated that the model best correlating with duration of local control included tumour depth (p = 0.03) and previous radiation therapy (p = 0.08, model p = 0.006). Twenty-two fields were treated without any skin reactions (39%), 23 evidenced erythema (40%) and eight thermal blistering (14%). Ulceration occurred in 11 treatment fields but in all but one of these cases the ulceration may have been due to tumour breakdown as there was direct invasion of the skin by tumour prior to the initiation of treatment. The maximal skin temperature was the best predictor of morbidity although the correlation was not statistically significant (p = 0.19).
Adenocarcinoma↗