Trend differences in men and women in rural and urban U.S. settings.

BACKGROUND: Smoking prevalence is declining at a slower rate in rural than urban settings in the United States (U.S.), and known predictors of smoking do not readily account for this trend difference. Given that socioeconomic and psychosocial determinants of health disparities accumulate in rural settings and that life-course disadvantages are often greater in women than men, we examined whether smoking trends are different for rural and urban men and women. METHOD: We used yearly cross-sectional data (n = 303,311) from the U.S. National Survey on Drug Use and Health (NSDUH) from 2007 through 2014 to compare cigarette smoking trends in men and women across rural and urban areas. Current smoking status was modelled using logistic regression controlling for confounding risk factors. RESULTS: Regression derived graphs predicting unadjusted prevalence estimates and 95% confidence bands revealed that whereas the smoking trends of rural men, urban men, and urban women significantly declined from 2007 to 2014, the trend for rural women was flat. Controlling for demographic, socioeconomic and psychosocial predictors of smoking did not explain rural women's significantly different trend from those of the other three groups. CONCLUSION: Rural women lag behind rural men, urban men and urban women in decreasing smoking, a health disparity finding that supports the need for tobacco control and regulatory policies and interventions that are more effective in reducing smoking among rural women.

A growing geographic disparity: Rural and urban cigarette smoking trends in the United States.

Rural areas of the United States have a higher smoking prevalence than urban areas. However, no recent studies have rigorously examined potential changes in this disparity over time or whether the disparity can be explained by demographic or psychosocial characteristics associated with smoking. The present study used yearly cross sectional data from the National Survey on Drug Use and Health from 2007 through 2014 to examine cigarette smoking trends in rural versus urban areas of the United States. The analytic sample included 303,311 respondents. Two regression models were built to examine (a) unadjusted rural and urban trends in prevalence of current smoking and (b) whether differences remained after adjusting for demographic and psychosocial characteristics. Results of the unadjusted model showed disparate and diverging cigarette use trends during the 8-year time period. The adjusted model also showed diverging trends, initially with no or small differences that became more pronounced across the 8-year period. We conclude that differences reported in earlier studies may be explained by differences in rural versus urban demographic and psychosocial risk factors, while more recent and growing disparities appear to be related to other factors. These emergent differences may be attributable to policy-level tobacco control and regulatory factors that disproportionately benefit urban areas such as enforcement of regulations around the sale and marketing of tobacco products and treatment availability. Strong federal policies and targeted or tailored interventions may be important to expanding tobacco control and regulatory benefits to vulnerable populations including rural Americans.

Leptomeningeal melanocytosis in an adult male without large congenital nevi: a rare and atypical case of neurocutaneous melanosis.

Leptomeningeal melanocytosis is a primary melanocytic lesion of the central nervous system that is characterized by diffuse melanocytic infiltration of the leptomeninges. It is seen almost exclusively in children with large congenital nevi and together the findings form a dermatologic syndrome known as neurocutaneous melanosis. We report a rare and atypical case of a 31-year-old adult male with no evident congenital melanocytic lesions who presented with neurologic symptoms and was found to have leptomeningeal melanocytosis. The brain biopsy demonstrated a conspicuous but benign-appearing melanocytic infiltrate that was discordant with the severity of the patient's symptoms. Ultimately, the patient was suspected to represent a case of former fruste neurocutaneous melanosis. Herein the relevant clinical and histopathologic features are discussed along with a brief review of the literature.

Rat and human explant metabolism, binding studies, and DNA adduct analysis of benzo(a)pyrene and its 6-nitro derivative.

Human colon and bronchus tissue explants were incubated with either [3H]benzo(a)pyrene ([3H]BP) or [3H]-6-nitrobenzo(a)pyrene ([3H]-6-NBP). The total percentage of metabolism of BP and 6-NBP was, respectively, 8-59% and 18-41% in bronchus and 11-23% and 36-50% in colon. A product tentatively identified as 3-hydroxy-6-NBP was isolated from the 6-NBP incubation medium. BP and 6-NBP when incubated at equivalent concentrations were found to bind covalently to the DNA of human bronchi from 15 cases at means of 42 and 50.9 pmol/10 mg DNA, respectively, and to the DNA of human colon from 6 cases at means of 66.5 and 35 pmol/10 mg DNA, respectively. The range among individuals was within one order of magnitude. High pressure liquid chromatography (HPLC) of enzymic hydrolysates of human bronchus explant DNA revealed one adduct from the BP-incubated bronchus which cochromatographed with (+/-)-7,8-dihydroxy-9,10-epoxy-7,8,9, 10-tetrahydrobenzo(a)pyrene-deoxyguanosine and a possible two adducts from the 6-NBP-incubated bronchus which eluted earlier than did the BP adduct. DNA obtained from the lung or liver of rats given 2.0-mg/kg doses of either [3H]BP or [3H]-6-NBP by i.p. injection was also enzymically hydrolyzed and analyzed on HPLC. Three DNA adducts were observed in liver and two were observed in lung DNA hydrolysates from rats given injections of [3H]BP. One adduct from each organ cochromatographed with (+/-)-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene- deoxyguanosine; however, the major adduct in each case eluted earlier. Only one adduct was detected in liver and lung DNA hydrolysates from rats given [3H]-6-NBP, and this had the same retention time as did the major adduct isolated from human bronchus that had been incubated previously with [3H]-6-NBP. Salmonella typhimurium TA98 was incubated with [3H]-6-NBP and Aroclor-induced rat liver S9. Enzymically hydrolyzed DNA analyzed by HPLC revealed three adducts, two of which cochromatographed with the two DNA adducts isolated from human bronchus DNA adduct which had the same retention time as did the major liver and lung DNA adduct from rats given i.p. injections of [3H]-6-NBP. In each case the major adduct from DNA hydrolysates of rat liver and lung, human bronchus, and S. typhimurium, all treated with [3H]-6-NBP, cochromatographed with the major DNA adduct isolated from liver and lung DNA of rats given [3H]BP.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired immunodeficiency syndrome-related primary intraocular lymphoma.

A 37-year-old man with acquired immunodeficiency syndrome and cytomegalovirus retinitis developed primary intraocular and central nervous system lymphoma. Intraocular involvement was documented before death with vitrectomy. Autopsy demonstrated the presence of cytomegalovirus retinitis in the right eye and lymphoma in both eyes and the brain. We believe this is the first report of autopsy-confirmed primary intraocular lymphoma in a patient with the acquired immunodeficiency syndrome.

Optic chiasm, optic nerve, and retinal involvement secondary to varicella-zoster virus.

Immunocompromised patients are known to be at risk for varicella-zoster virus reactivation, often in atypical manners. We describe a 30-year-old man with simultaneous involvement of the retina, optic chiasm, and optic nerve with varicella-zoster virus who had a bitemporal visual field defect.

Perineural spread of rhinocerebral mucormycosis.

An unusual pathway of local spread of rhinocerebral mucormycosis is presented with MR and pathologic correlation. Perineural extension, proved with pathology, followed the trigeminal nerve to the pons. Enhancement of the nerve was seen on MR.

Development and reproducibility of a brief food frequency questionnaire for assessing the fat, fiber, and fruit and vegetable intakes of rural adolescents.

OBJECTIVE: To describe the systematic development and reproducibility of a food frequency questionnaire (FFQ) designed to meet the specific research requirements of the Goals for Health cancer prevention intervention program for rural middle school children. DESIGN: A 4-step process was used to develop a brief FFQ for scoring intakes of total fat, fiber, and fruits and vegetables. The resulting questionnaire consisted of 25 food frequency items and 10 supplemental questions. Reproducibility of the questionnaire was determined by comparing responses at the beginning and end of a 4-month interval. SUBJECTS: Study subjects were sixth- and seventh-grade students attending middle schools in rural areas of Virginia and upstate New York. Seventh-grade students participated in the pilot study, and sixth-grade students participated in the reproducibility study. The final version of the FFQ was completed twice by 539 sixth graders. After exclusions for missing and unreliable data, the usable sample size was 415. Boys were somewhat more likely than girls to be excluded for missing data. African-American students comprised 32% of the population. STATISTICAL ANALYSES PERFORMED: Each food frequency item was associated with 3 scores--a fat score, a fiber score, and a combined score for the number of servings of fruits and vegetables. Means and standard deviations were determined for nutrient variables, differences between repeat administrations were tested for significance by paired t test, and Pearson correlation coefficients were calculated for nutrients and for individual food items. RESULTS: Correlation coefficients for nutrient scores were 0.58 for fat, 0.49 for fiber, and 0.51 for fruits and vegetables. For individual food items, correlations ranged from 0.24 to 0.59 (mean=0.41). APPLICATIONS/CONCLUSIONS: Using a systematic approach to developing a study-specific FFQ for rural adolescents is feasible. Further, the reproducibility of the Goals for Health questionnaire was demonstrated for the 3 nutrient scores it was designed to measure. This developmental approach may be readily adapted to other populations, study designs, and nutrients of interest. The validity of the questionnaire remains to be tested.

The effect of acetyl-CoA supplementation on the mutagenicity of benzidines in the Ames assay.

The conventional Ames assay metabolising system was confirmed to be deficient in its ability to N-acetylate. This may render the test less sensitive to compounds which normally have an acetylation step during their in vivo activation to carcinogens. The addition of acetyl-coenzyme A to the S9 mix in the Ames assay increased the mutagenicity of benzidine in Salmonella typhimurium strains TA98 and TA1538 4-5-fold. This was consistent with the observation that benzidine is N-acetylated prior to DNA binding in vivo in rat liver. Two 3,3'-disubstituted benzidines, o-tolidine and o-dianisidine, were also tested. A smaller increase in o-tolidine mutagenicity, compared to that observed with benzidine, occurred with the addition of acetyl-coenzyme A. However, the production of acetylated metabolites from o-tolidine was only 37% of that from benzidine. The mutagenicity of o-dianisidine was unaffected by acetyl-coenzyme A. Acetylation of o-dianisidine was only 16% of that observed with benzidine, and the N-acetyl derivatives of o-dianisidine showed lower mutagenicity than the parent amine. The differing responses of benzidine, o-tolidine and o-dianisidine to addition of acetyl-coenzyme A suggests it may not be possible to simply infer the metabolism of 3,3'-disubstituted benzidines to DNA binding species from data on benzidine itself.

Effect of storage at 4 degrees on prepared Salmonella/microsome test plates.

Salmonella/microsome soft-agar overlay ('Ames' test) plates were prepared using the previously published 'York' method. Plates treated with either added 3-methylcholanthrene (3MC) or 3,3'-dichlorobenzidine (DCB) and Aroclor-induced rat-liver S9 were stored at 4 degrees after preparation and removed at time intervals thereafter for incubation at 37 degrees. The number of 3MC-induced mutants in TA100 fell within 24 h of storage by 50% but then remained at this level until 96 h. Storage for a total of 336 h still showed some residual mono-oxygenase activity. On the other hand the ability to convert DCB to a mutagen for TA98 appeared to increase with storage, reaching a peak by 96 h. After this time the number of induced mutants fell until by 336 h the numbers were approximately equal to those plates which had not been stored in the cold.

Chest wall metastasis from recurrent meningioma.

Meningiomas are generally considered benign lesions. A minority, however, are capable of metastasis. The ones most likely to do so are commonly recurrent or frankly malignant in nature. The optimal management of such metastases is unclear. This is the first reported case of meningioma presenting as an isolated metastasis to the chest wall. This case involves a 64-year-old woman without significant medical or family history who underwent resection of a meningioma of the right cerebral hemisphere. She was treated 10 years later for recurrence by stereotactic radiosurgery. Three years after that, the patient's family noticed a mass on the left chest wall. A CT scan revealed destruction of the ninth rib laterally and subpleural extension. The patient subsequently underwent resection of full-thickness chest wall for a presumed soft-tissue sarcoma. Further pathologic evaluation including electron microscopy and immunohistochemistry revealed metastatic meningioma. The patient received adjuvant radiation to the chest wall and is currently free of disease at the chest wall one year after surgery. This case illustrates the difficulty in establishing an accurate diagnosis of metastatic meningioma. Consequently in selected patients with a history of the disease the diagnosis of metastatic meningioma must at least be considered. Resection of an isolated metastasis in this setting appears warranted.

Effects of neutering on bodyweight, metabolic rate and glucose tolerance of domestic cats.

Few controlled studies have been made of the possible mechanisms and physiological consequences of weight gain after cats have been neutered. In this study, six male and six female cats were gonadectomised and compared with five entire male and six entire female cats, before they were neutered and one and three months later. The neutered males gained significantly more weight (mean [SEM] per cent) than the entire males (30.2 [5.2] v 11.8 [2.3]) and the entire females gained 40.0 (7.3) v 16.1 (3.3) per cent, (P < 0.05). The castrated males gained more weight as fat than the sexually intact males (22.0 [3.3] v 8.8 [4.5] per cent, P < 0.05). There was a significant increase (P < 0.05) in daily food intake after neutering. Spayed females underwent a significant decrease in fasting metabolic rate (83.7 [5.5] v 67.2 [2.3] kcal/kg bodyweight0.75/day P < 0.05). Gonadectomy had minimal effects on serum thyroid hormone concentrations, the resting or fasting metabolic rates in males, or on indices of glucose tolerance.

Effects of weight gain and loss on metabolic rate, glucose tolerance, and serum lipids in domestic cats.

Weight gain is a common problem in domestic cats, but little is known about its metabolic effects. The purpose of this study was to determine the effects of diet-induced weight gain and subsequent weight loss on metabolic rate, body composition, and glucose tolerance. Gain of approximately 20 per cent body weight (divided approximately equally between fat and fat-free mass) over three months resulted in insulin resistance in females, indicated by increases in basal insulin concentration (68.2+/-7.9 to 119+/-16.5 pmol litre(-1), P<0.05), insulin peak response to glucose (241.1+/-31.6 to 315.0+/-23.0 pmol litre(-1), P<0.05), and deltaI/deltaG (14.2+/-2.6 to 18.1+/-1.3 pmol mmol(-1), P<0.05) compared with pre-gain values. The same numerical trend was noted in male cats, however, changes were not significant (P>0.05). Alterations in serum lipids included significant (P<0.05) elevations in triglyceride concentrations in male cats and decreased beta-lipoprotein concentrations in both genders. Weight loss over three months normalised basal insulin, insulin response to glucose, and serum triglyceride concentrations, and resulted in significant (P<0.05) decreases in serum concentrations of beta- and prebeta-lipoproteins, cholesterol, and triiodothyronine. Diet-induced weight gain of three months' duration, followed by three months' maintenance of increased body weight did not affect fasting or resting metabolic rate. Development and severity of impaired glucose tolerance, insulin resistance, and other changes may be affected by duration and possibly severity of weight gain.

Bioelectrical impedance and zoometry for body composition analysis in domestic cats.

Zoometric measurements and bioelectrical impedance analysis were evaluated as methods of body composition determination in healthy cats. Zoometric and impedance measurements were taken on 22 anesthetized adult cats of various ages, genders, breeds, and body weights. The cats were then euthanatized. The bodies were processed through a tissue homogenizer and free-catch specimens were taken, freeze-dried, and analyzed for total body water, protein, fat, potassium, and ash content. Stepwise regression analysis was implemented to identify statistically significant relationships between the chemically determined dependent variables (total body water, protein, potassium, fat-free mass, fat mass, and percent body fat) and the zoometric measurements, with or without bioelectrical impedance analysis. Statistical analysis revealed high correlations between the dependent variables and the corresponding predicted values of those variables. Body weight alone was a poor predictor of body composition in these cats. On the basis of these findings, we suggest that zoometric and bioelectrical impedance measurements may serve as practical, noninvasive, simple, and accurate methods for estimating body composition in domestic cats.

The mutagenicity and DNA base sequence changes induced by 1-nitroso- and 1-nitropyrene in the cI gene of lambda prophage.

The mutagenicity of 1-nitropyrene and its reduced metabolite 1-nitrosopyrene was determined in the lambda cI gene of an Escherichia coli uvr- lysogen. 1-Nitropyrene induced a mutation frequency of 3.8 x 10(-6), which was approximately 2-fold higher than the background mutation frequency, whereas an equimolar dose of 1-nitrosopyrene induced a much higher mutation frequency of 1.4 x 10(-4). Previous studies have established that both compounds form the same premutagenic lesion, viz. N-(deoxyguanosin-8-yl)-1-aminopyrene in bacterial DNA. In order to determine how this initial premutational lesion is converted to a stable heritable mutation, DNA sequences were determined for 30 mutations induced by 1-nitrosopyrene that mapped between bp 1 and 352 in the lambda cI gene of E.coli lysogens. We show here that these mutations are mainly frameshifts involving the addition or deletion of a single GC or CG base pair. A small proportion of mutations were base substitutions which were equally divided between transitions and transversions. These also occurred primarily at GC or CG sites.

Sudden death in epilepsy due to an isolated subependymal giant cell astrocytoma of the septum pellucidum.

We report a case of sudden unexpected death in an individual with epilepsy. Autopsy revealed a subependymal giant cell astrocytoma of the septum pellucidum, but there were no other lesions of tuberous sclerosis. We discuss sudden death in epilepsy, deaths related to primary brain tumors, the pathology of subependymal giant cell astrocytoma, and whether or not such a tumor can exist outside the setting of tuberous sclerosis. We also discuss the implications such findings may have on surviving family members, as well as the important role of the forensic pathologist in such cases.

Topical 5-fluorouracil in treating epithelial neoplasia of the conjunctiva and cornea.

PURPOSES: To evaluate the efficacy of topical 5-fluorouracil (5-FU) in treating conjunctival and corneal epithelial neoplasia. METHODS: Three patients underwent surgical excision of bulky disease followed by topical 1% 5-FU in artificial tear base for 2 to 3 weeks or until epithelial separation occurred. An additional three patients underwent treatment with topical 1% 5-FU alone. RESULTS: Minimum follow-up was 6 months. In one patient with conjunctival in situ carcinoma and no detectable normal conjunctiva, who had normal findings on conjunctival histologic examination after application of topical 5-FU, a focus of invasive disease requiring orbital exenteration. One patient had a favorable response to 5-FU therapy but required a repeat excision for control of bulky disease. Four patients have remained disease-free for 10, 13, 18, and 30 months after topical 5-FU therapy. CONCLUSION: With its potential selective toxicity on dysplastic epithelium, topical 5-FU shows promise as an adjunctive treatment for managing conjunctival and corneal epithelial neoplasia.

Macromolecular binding of [3H]6-nitrobenzo[a]pyrene in male rats.

Generally labelled [3H]6-nitrobenzo[a]pyrene (6NBP) when administered to male rats by i.p. injection was widely distributed throughout the body. After a single injection of 4.2 mg/kg the highest concentration was found in the liver (5% at 2 h) followed by the spleen greater than kidney greater than lung. Maximal covalent binding to macromolecules occurred between 8 and 24 h depending upon the organ; the order of binding/mg macromolecule was RNA greater than DNA greater than protein for all organs studied. In the liver maximal binding was found 8 h after 6NBP administration at which time there were 45 +/- 7 pmol 6NBP/mg bound to DNA and 114 +/- 40 pmol/mg to RNA following a dose of 4.2 mg/kg. These levels fall to 14 +/- 4 and 12 +/- 6 pmol/mg, respectively, after 168 h, the longest time point so far studied. At a lower dose of 1.4 mg/kg the values for DNA at 8 h were 14 +/- 2 pmol/mg and at 168 h 3 +/- 2 pmol/mg while for RNA the corresponding values were 29 +/- 8 and 15 +/- 3 pmol/mg. After gastric intubation at a dose of 4.2 mg/kg there was no difference in liver macromolecular binding at 24 h between conventional and germ-free animals. Enzymic digestion of liver DNA from [3H]6NBP injected animals and reversed-phase h.p.l.c. of the digests showed two peaks of radioactivity. The percentage of total radioactivity in each peak varied from preparation to preparation suggesting that one peak may be a degradation product of the other although experimental variability cannot be ruled out. The implications of these findings in relation to the potential carcinogenicity of 6NBP are discussed.

Studies on the detoxication of microsomally-activated aflatoxin B1 by glutathione and glutathione transferases in vitro.

Aflatoxin B1 (AFB1)-8,9-oxide, the proposed ultimate carcinogen is conjugated enzymically with glutathione (GSH) to give 8-(S-glutathionyl)-9-hydroxy-8,9-dihydro AFB1 (AFB1-SG). The GSH conjugate isolated from rat bile was shown, on the basis of 1H n.m.r. to be identical to AFB1-SG. Of the seven soluble rat liver GSH transferases tested, namely GSH transferases 1-1, 1-2, 2-2, 3-3, 3-4, 4-4 and 5-5 (see reference 1 for the new system of nomenclature), only the first three were active with microsomally generated AFB1-8,9-oxide, their rates of conjugation being 1.1, 0.61 and 0.64 nmol/min/mg enzyme, respectively. AFB1-SG is a thioacetal, but it was not formed from the incubation of the hemiacetal, AFB1-8,9-dihydrodiol, with GSH or GSH plus GSH transferase 1-1 plus 1-2. The covalent binding of in vitro microsomally activated AFB1 to DNA and the formation of AFB1-SG were linearly related to AFB1 concentration in the range of 0.2-2 micrograms/ml. DNA binding was decreased by 38% by the competing formation of AFB1-SG throughout this range of concentrations. These results are in accord with the observation of Scott Appleton et al. (Cancer Res., 42, 3659-3662) that, in the rat in vivo, there is no evident threshold for the binding of AFB1 to DNA. These findings are also consistent with the further observation, reported in this paper that GSH and GSH transferases have no effect on the mutagenicity of microsomally activated AFB1 to Salmonella typhimurium TA 100.