background The influence of excess body weight on the risk of death from cancer has not been fully characterized. methods In a prospectively studied population of more than 900,000 U.S. adults (404,576 men and 495,477 women) who were free of cancer at enrollment in 1982, there were 57,145 deaths from cancer during 16 years of follow-up. We examined the relation in men and women between the body-mass index in 1982 and the risk of death from all cancers and from cancers at individual sites, while controlling for other risk factors in multivariate proportional-hazards models. We calculated the proportion of all deaths from cancer that was attributable to overweight and obesity in the U.S. population on the basis of risk estimates from the current study and national estimates of the prevalence of overweight and obesity in the U.S. adult population. results The heaviest members of this cohort (those with a body-mass index [the weight in kilograms divided by the square of the height in meters] of at least 40) had death rates from all cancers combined that were 52 percent higher (for men) and 62 percent higher (for women) than the rates in men and women of normal weight. For men, the relative risk of death was 1.52 (95 percent confidence interval, 1.13 to 2.05); for women, the relative risk was 1.62 (95 percent confidence interval, 1.40 to 1.87). In both men and women, body-mass index was also significantly associated with higher rates of death due to cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney; the same was true for death due to non-Hodgkin’s lymphoma and multiple myeloma. Significant trends of increasing risk with higher body-mass-index values were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast, uterus, cervix, and ovary in women. On the basis of associations observed in this study, we estimate that current patterns of overweight and obesity in the United States could account for 14 percent of all deaths from cancer in men and 20 percent of those in women. conclusions Increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites.

/pdf/overweight-obesity-and-mortality-from-cancer-in-a-3whc0l70ow.pdf

Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults.

https://www.cdc.gov/coronavirus/mers/downloads/Isolation2007.pdf

2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Health Care Settings.

https://in.bgu.ac.il/en/fohs/communityhealth/Family/Documents/DOCTOR-PATIENT%20COMMUNICATION%20A%20REVIEW%20OF.pdf

Doctor-patient communication: a review of the literature.

A case-control study of oral and pharyngeal cancer conducted in four areas of the United States provided information on the tobacco and alcohol use of 1114 patients and 1268 population-based controls. Because of the large study size, it could be shown that the risks of these cancers among nondrinkers increased with amount smoked, and conversely that the risks among nonsmokers increased with the level of alcohol intake. Among consumers of both products, risks of oropharyngeal cancer tended to combine more in a multiplicative than additive fashion and were increased more than 35-fold among those who consumed two or more packs of cigarettes and more than four alcoholic drinks/day. Cigarette, cigar, and pipe smoking were separately implicated, although it was shown for the first time that risk was not as high among male lifelong filter cigarette smokers. Cessation of smoking was associated with a sharply reduced risk of this cancer, with no excess detected among those having quit for 10 or more years, suggesting that smoking affects primarily a late stage in the process of oropharyngeal carcinogenesis. The risks varied by type of alcoholic beverage, being higher among those consuming hard liquor or beer than wine. The relative risk patterns were generally similar among whites and blacks, and among males and females, and showed little difference when oral and pharyngeal cancers were analyzed separately. From calculations of attributable risk, we estimate that tobacco smoking and alcohol drinking combine to account for approximately three-fourths of all oral and pharyngeal cancers in the United States.

https://cancerres.aacrjournals.org/content/canres/48/11/3282.full.pdf

Smoking and Drinking in Relation to Oral and Pharyngeal Cancer

Mammographic features are associated with breast cancer risk, but estimates of the strength of the association vary markedly between studies, and it is uncertain whether the association is modified by other risk factors. We conducted a systematic review and meta-analysis of publications on mammographic patterns in relation to breast cancer risk. Random effects models were used to combine study-specific relative risks. Aggregate data for > 14,000 cases and 226,000 noncases from 42 studies were included. Associations were consistent in studies conducted in the general population but were highly heterogeneous in symptomatic populations. They were much stronger for percentage density than for Wolfe grade or Breast Imaging Reporting and Data System classification and were 20% to 30% stronger in studies of incident than of prevalent cancer. No differences were observed by age/menopausal status at mammography or by ethnicity. For percentage density measured using prediagnostic mammograms, combined relative risks of incident breast cancer in the general population were 1.79 (95% confidence interval, 1.48-2.16), 2.11 (1.70-2.63), 2.92 (2.49-3.42), and 4.64 (3.64-5.91) for categories 5% to 24%, 25% to 49%, 50% to 74%, and > or = 75% relative to < 5%. This association remained strong after excluding cancers diagnosed in the first-year postmammography. This review explains some of the heterogeneity in associations of breast density with breast cancer risk and shows that, in well-conducted studies, this is one of the strongest risk factors for breast cancer. It also refutes the suggestion that the association is an artifact of masking bias or that it is only present in a restricted age range.

/pdf/breast-density-and-parenchymal-patterns-as-markers-of-breast-433mjyvr1f.pdf

Breast Density and Parenchymal Patterns as Markers of Breast Cancer Risk: A Meta-analysis

Treatment of hemangiomas in children.

Conflicting reports have appeared in the recent literature on a presumed association between coffee intake and \"fibrocystic breast disease.\" The hypothesis suggesting that abstention from coffee and caffeine consumption eliminates breast pain and resolves breast nodules was based on an uncontrolled clinical study. For a condition with a notorious reputation for \"waxing and waning,\" it is essential to document the stability versus instability of clinical findings, keeping the methyl xanthine consumption constant. Seventy-two women, all with palpable breast nodules, were followed over a 6-month period with monthly examinations and questionnaires on intake of coffee, tea, soft drinks, chocolate, candies, and caffeine-containing drugs. The methyl xanthine consumption remained remarkably constant throughout the observation time. The examiner was uninformed as to previous examination findings and pain reports of each woman. In 21 (15%) breasts with nodularity, the nodules had completely disappeared by the termination of the study. A total of 125 (87%) breasts of the sample manifested a change in the number of nodules or a change in position. Forty-eight of the 72 women were menopausal. For a chronic condition with so much variety of subjective sensitivity and great variability of objective clinical palpation, it is difficult to relate the amount of methyl xanthine consumption to \"fibrocystic breast disease.\

Prospective study of fibrocystic breast disease and caffeine consumption

The relationships among anserine (beta-alanyl-1-methyl-L-histidine), carnosine (beta-alanyl-L-histidine), free histidine, and histamine metabolism were examined in rats wounded by dorsal skin incision. Following wounding, rats were treated with either a histamine liberator (compound 48/80) or a histidine decarboxylase inhibitor (4-imidazolyl-3-amino-2-butanone). The liberator greatly enhanced wounded skin-breaking strength and collagen deposition at the wound site, while the histidine decarboxylase inhibitor reduced skin-breaking strength and collagen deposition. In the second experiment of this study, histamine or histidine treatment was shown to prevent trauma-induced reductions of tissue carnosine but was less effective in ameliorating tissue anserine loss. The results illustrate an interaction between imidazole dipeptides and stress and suggest that carnosine acts as a histidine reserve in relation to histamine synthesis during trauma.

Histamine synthesis, imidazole dipeptides, and wound healing

Cross-reacting tumor-associated antigens have been demonstrated to be present in the cytoplasm of melanocytes in malignant melanoma. We have utilized both the leukocyte migration inhibition and the lymphocyte stimulation assays to determine the intracellular location(s) of these antigens in both human malignant melanoma and B-16 murine melanoma. The results of both assays indicate that this antigen(s) is associated with the membranous organelles, particularly the melanin granules, and is not found in the soluble components of the cytoplasm, as suggested by other studies.

Intracellular localization of tumor-associated antigens in murine and human malignant melanoma

An inflammatory focus was produced by implantation of gauze below the hide in the flanks of six sheep with flank lymph fistulas. Physiologic and metabolic parameters were monitored in the unanesthetized animals for 7 days, after which the gauze was removed and monitoring continued for another 5 days. Animals were then killed. Lung and liver tissue was inspected and analyzed for lipid peroxide content. Data were compared with those of six controls in which gauze was not implanted. We noted a transient significant increase (on day 1 only) in wound lymph, thromboxane B2, and 6-keto-PGF1 alpha from baseline values of 190 +/- 70 and 20 +/- 10 pg/ml to 1000 +/- 240 and 420 +/- 70 pg/ml, respectively. Plasma values were also significantly increased on day 1. Body temperature increased by 1 degree C and cardiac index increased by 30% during this period, whereas oxygen consumption, VO2, was not significantly increased. The VO2 and cardiac index increased by 50% over baseline, beginning on day 5, whereas systemic vascular resistance decreased. Body temperature was not increased. These changes corresponded with an increase in wound lymph monocyte count from 0% to 15% of total. The VO2 and cardiac index remained increased after gauze removal. No bacteria were found in the wound. Postmortem analysis revealed a marked monocyte-macrophage infiltration in both lung and liver. Lung water, represented as water content over dry weight, was normal. Lung and liver lipid peroxidation, measured by the by-product malondialdehyde content, increased 300% and 90% over control values, respectively. We conclude that a local, nonbacteria-induced wound inflammation increases VO2, with the increase not corresponding to increase in body temperature. Distant organ changes, namely, changes in lung and liver, were also evident 5 days after gauze removal.

Hal G. Bingham

Papers

Treatment of hemangiomas in children.

Prospective study of fibrocystic breast disease and caffeine consumption

Histamine synthesis, imidazole dipeptides, and wound healing

Intracellular localization of tumor-associated antigens in murine and human malignant melanoma

Tissue inflammation without bacteria produces increased oxygen consumption and distant organ lipid peroxidation