Pancreaticojejunostomy for chronic pancreatitis.

The treatment of chronic pancreatitis commonly yields disappointing results. Patients with chronic pancreatitis and a dilated pancreatic duct can be treated by longitudinal pancreaticojejunostomy. In order to evaluate the procedure, 20 patients undergoing pancreaticojejunostomy were followed for a median time of more than 5 years. Their clinical characteristics and outcomes have been compared with a group of 43 patients with chronic pancreatitis and small pancreatic ducts. There were no differences between the two groups in the major epidemiological parameters, except that calcification in the gland was more frequently noted in those with large ducts. The operation of longitudinal pancreaticojejunostomy could be accomplished with an acceptable morbidity. There was one death in the postoperative period. Seventy-six per cent of patients were found to have benefited clinically at five years, compared with 48% of those with small duct disease. This difference was statistically significant. Patients who benefited were defined by four factors; they were carrying out their usual occupation at the time of surgery, they were not narcotic dependent at the time of surgery, they had a pancreatic duct width greater than 7 mm and, they had totally abstained from alcohol from before the operation to the time of follow-up. Longitudinal pancreaticojejunostomy probably remains the best surgical treatment for suitable patients with chronic pancreatitis. The operation should only be performed when the pancreatic duct is greater than 7 mm in width. In such patients the operation produces considerable improvement of pain with minimal metabolic disturbance.     

Genomic rearrangements in mouse C3H/10T1/2 cells transformed by X-rays, UV-C, and 3-methylcholanthrene, detected by a DNA fingerprint assay.

Genomic rearrangements occurring in C3H/10T1/2 cells transformed by X-rays were examined with a DNA fingerprint assay. Four multilocus and multiallele probes were employed (M, X, H10, and H16) that detect different families of minisatellite sequences dispersed throughout the genome. Genomic rearrangements were detectable only with probe M. This specificity may be explained by a genomic instability owing to a specific sequence or structure of DNA recognized by probe M. Genomic rearrangements were detected in 5 of 12 type III foci transformed by 600 cGy of X-rays and in all clones isolated from a previously transformed clone exposed to a second dose of 600 cGy and recloned. The latter data suggest that the stage of transformation and the occurrence of genomic rearrangement induced by X-rays may be related. An intensity shift or a complete deletion of band 2 was common to these X-ray-induced clones, as well as to clones transformed by UV-C (1 of 5) or 3-methylcholanthrene (4 of 6). This band did not hybridize to probes for the retinoblastoma gene RB or for p53. We hypothesize that the loss of band 2 may reflect a significant genetic change in the transformation of 10T1/2 cells, perhaps representing the inactivation of a tumor suppressor gene other than RB or p53. Additional rearrangements occurred in X-ray-transformed clones; these rearrangements were not observed with the other carcinogens. Aside from the changes in band 2, however, no specific pattern of genomic rearrangement was associated with X-ray transformation, and the presence or absence of rearrangements did not correlate with tumorigenicity in syngeneic nonimmunosuppressed C3H mice.     

Metastatic renal carcinoma: rare cause of outflow obstruction (a case report).

A case of bladder tumour arising as a metastasis of renal carcinoma and presenting as obstruction to urinary outflow is described. The possible mechanism of spread to bladder is also suggested.     

Nurse Migration: A Canadian Case Study

Objective. To synthesize information about nurse migration in and out of Canada and analyze its role as a policy lever to address the Canadian nursing shortage.
Principal Findings. Canada is both a source and a destination country for international nurse migration with an estimated net loss of nurses. The United States is the major beneficiary of Canadian nurse emigration resulting from the reduction of full-time jobs for nurses in Canada due to health system reforms. Canada faces a significant projected shortage of nurses that is too large to be ameliorated by ethical international nurse recruitment and immigration.
Conclusions. The current and projected shortage of nurses in Canada is a product of health care cost containment policies that failed to take into account long-term consequences for nurse workforce adequacy. An aging nurse workforce, exacerbated by layoffs of younger nurses with less seniority, and increasing demand for nurses contribute to a projection of nurse shortage that is too great to be solved ethically through international nurse recruitment. National policies to increase domestic nurse production and retention are recommended in addition to international collaboration among developed countries to move toward greater national nurse workforce self sufficiency.     

Longitudinal predictors of continued tobacco use among patients diagnosed with cancer

Even though continued smoking by cancer patients adversely affects survival and quality of life, about one third of patients who smoked prior to their diagnosis continue to smoke after their diagnosis. The implementation of smoking cessation treatments for cancer patients has been slowed by the lack of data on correlates of tobacco use in this population. Thus, this longitudinal study assessed demographic, medical, addiction, and psychological predictors of tobacco use among 74 head, neck, and lung cancer patients. Multivariable binary logistic regression analyses, with outcome categorized as smoker or nonsmoker, indicated that the likelihoodthat patients would be a smoker was associated with lower levels of perceived risk and a higher level of quitting cons. Multivariable nominal logistic regression, with outcome classified as continuous smoker, continuous quitter, relapser, or follow-up quitter, indicated that: (a) patients categorized as continuous smokers reported significantly lower quitting self-efficacy than follow-up quitters and continuous quitters, (b) relapsers reported a significantly lower level of quitting self-efficacy than either follow-up quitters or continuous quitters, and (c) continuous smokers exhibited a significantly lower level of risk perceptions than continuous abstainers. These findings can be useful for the development and evaluation of treatments to promote smoking cessation among cancer patients. Support for this study was provided by National Institutes of Health Grants CA57708, CA06927, CA88610, CA95678, and CA76644.     

Brain growth among fetuses exposed to cocaine in utero: asymmetrical growth retardation

Fetal growth retardation may be associated with maternal cocaine use during pregnancy. The pattern of fetal growth retardation was analyzed in infants born to 80 women who used cocaine, but not alcohol, during pregnancy, and in two comparison groups: 100 infants born to mothers who used neither alcohol nor cocaine during pregnancy and 67 infants whose mothers used alcohol but not cocaine during pregnancy. There were statistically significant differences in head size between the unexposed and cocaine-exposed infants (P less than .001). Notably, head circumference was reduced proportionately more than birth weight in cocaine-exposed infants, a pattern similar to that observed in alcohol-exposed infants. Alcohol- and cocaine-exposed infants were not statistically different in head circumference. We conclude that brain growth of cocaine-exposed infants is similar to that reported for alcohol-exposed infants, and that cocaine-exposed infants may be characterized as having asymmetrical growth retardation.     

A system for assaying homologous recombination at the endogenous human thymidine kinase gene.

A system for assaying human interchromosomal recombination in vitro was developed, using a cell line containing two different mutant thymidine kinase genes (TK) on chromosomes 17. Heteroalleles were generated in the TK+/+ parent B-lymphoblast cell line WIL-2 by repeated exposure to the alkylating nitrogen mustard ICR-191, which preferentially causes +1 or -1 frameshifts. Resulting TK-/- mutants were selected in medium containing the toxic thymidine analog trifluorothymidine. Mutations were characterized by exon-specific polymerase chain reaction amplification and direct sequencing. In two lines, heterozygous frameshifts were located in exons 4 and 7 of the TK gene separated by approximately 8 kilobases. These lines undergo spontaneous reversion to TK+ at a frequency of less than 10(-7), and revertants can be selected in cytidine/hypoxanthine/aminopterin/thymidine medium. The nature and location of these heteroallelic mutations make large deletions, rearrangements, nondisjunction, and reduplication unlikely mechanisms for reversion to TK+. The mode of reversion to TK+ was specifically assessed by DNA sequencing, use of single-strand conformation polymorphisms, and analysis of various restriction fragment length polymorphisms (RFLPs) linked to the TK gene on chromosome 17. Our data suggest that a proportion of revertants has undergone recombination and gene conversion at the TK locus, with concomitant loss of frameshifts and allele loss at linked RFLPs. Models are presented for the origin of two recombinants.     

Enhancement of benzo[a]pyrene-induced sister chromatid exchanges in lymphocytes from cigarette smokers occupationally exposed to asbestos

The frequencies of base-line and benzo[a]pyrene [(BP) CAS 50-38-8]-induced sister chromatid exchanges (SCE) were measured in peripheral blood lymphocytes from 22 male asbestos-exposed workers and 10 nonexposed workers of comparable age. A clear association between cigarette smoking and asbestos exposure in the sensitivity of lymphocytes to BP was observed. Among asbestos-exposed workers, lymphocytes from those who smoked cigarettes were significantly more susceptible to the induction of SCE by in vitro exposure to BP (P = .01) than were lymphocytes from nonsmokers. Active smoking elevated the base-line SCE frequency in both asbestos-exposed and nonexposed workers (P = .001), and an interaction between smoking and asbestos in the production of base-line SCE was suggested (P = .07). Asbestos exposure alone was not associated with an enhanced susceptibility to the induction of SCE by BP or with an elevation of base-line SCE. Increased age was associated with an increase in SCE inducibility by BP (P = .01), and a history of smoking was marginally associated with SCE inducibility by BP (P = .07). These findings support the hypothesis that an increased susceptibility of asbestos-exposed individuals to polyaromatic hydrocarbon-induced cancer results from an enhanced sensitivity to the induction of genetic damage rather than to an asbestos-induced differential cellular metabolic capacity.