Introduction and hypothesis
The objective was to characterize postoperative bowel symptoms in women undergoing vaginal prolapse reconstructive surgery randomized to preoperative bowel preparation vs ...a regular diet.
Methods
Subjects (
N
= 121) completed two bowel diaries: a 7-day bowel diary immediately before surgery and a 14-day diary postoperatively. Self-reported bowel diary data and symptoms included the time to first bowel movement (BM), daily number of BMs, Bristol Stool Form Scale score, pain, and urgency associated with BM, episodes of fecal incontinence, and use of laxatives. Antiemetic use was abstracted from medical records. Outcomes of groups were compared using Chi-squared/Fisher’s exact test or Student’s
t
test as appropriate.
Results
Mean time to first postoperative BM was similar in the bowel preparation (
n
= 60) and control groups (
n
= 61), 81.2 ± 28.9 vs 78.6 ± 28.2 h,
p
= 0.85. With the first BM, there were no significant differences between bowel preparation and control groups regarding pain (17.2 vs 27.9 %,
p
= 0.17), fecal urgency with defecation (56.9 vs 52.5 %,
p
= 0.63), fecal incontinence (14.0 vs 15.0 %,
p
= 0.88) and >1 use of laxatives (93.3 vs 96.7 %
p
= 0.44) respectively. Antiemetic use was similar in both groups (48.3 vs 55.7 % respectively,
p
= 0.42).
Conclusions
There were no differences in the return of bowel function and other bowel symptoms postoperatively between the randomized groups. Lack of bowel preparation does not have an impact on the risk of painful defecation postoperatively. This information may be used to inform patients regarding expectations for bowel function after vaginal reconstructive surgery.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Rationale, aims and objectives
Frequent follow‐up is recommended for the more than 3 million breast cancer survivors living in the USA. Given the multidisciplinary nature of breast cancer treatment, ...follow‐up may be provided by medical oncologists, radiation oncologists, surgeons and primary care providers. This creates the potential for significant redundancy as well as gaps in care. The objective was to examine patterns of breast cancer follow‐up provided by different types of oncologists and develop a statistical means of quantifying visit distribution over time.
Methods
We identified stage I–III breast cancer patients who underwent breast conservation from 2000 to 2006 (n = 12 139) within the SEER‐Medicare linked database. Provider type was defined using Medicare specialty provider codes and AMA Masterfile. The coefficient of variation (CV) for time between oncologist follow‐up visits was calculated. Ordinal logistic regression assessed factors associated with CV.
Results
Substantial variation in CV was observed. Sixty‐seven per cent of patients with low CV (high visit regularity) received follow‐up from a single oncologist type, versus 8% with high CV (low visit regularity). The number of oncologist types participating in follow‐up had the greatest association with high CV (odds ratio 7.4 6.7–8.3 and 15.4 13.6–17.6 for two and three oncologist types).
Conclusions
Using a novel means of quantifying follow‐up visit regularity, we determined that breast cancer patients with dispersed follow‐up with more than one oncologist have more disordered care. The CV could be used in electronic medical records to identify cancer survivors with more disordered.
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DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by autoantibody production and organ damage. Lupus nephritis (LN) is one of the most severe manifestations of SLE. ...Multiple studies reported associations between renal diseases and variants in the non-muscle myosin heavy chain 9 (MYH9) and the neighboring apolipoprotein L 1 (APOL1) genes. We evaluated 167 variants spanning MYH9 for association with LN in a multiethnic sample. The two previously identified risk variants in APOL1 were also tested for association with LN in European-Americans (EAs) (N = 579) and African-Americans (AAs) (N = 407). Multiple peaks of association exceeding a Bonferroni corrected P-value of P < 2.03 × 10(-3) were observed between LN and MYH9 in EAs (N = 4620), with the most pronounced association at rs2157257 (P = 4.7 × 10(-4), odds ratio (OR) = 1.205). A modest effect with MYH9 was also detected in Gullah (rs8136069, P = 0.0019, OR = 2.304). No association between LN and MYH9 was found in AAs, Asians, Amerindians or Hispanics. This study provides the first investigation of MYH9 in LN in non-Africans and of APOL1 in LN in any population, and presents novel insight into the potential role of MYH9 in LN in EAs.
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DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UILJ, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Genetic risk factors are important contributors to the development of colorectal cancer. Following the definition of a linkage signal at 9q22-31, we fine mapped this region in an independent ...collection of colon cancer families. We used a custom array of single-nucleotide polymorphisms (SNP) densely spaced across the candidate region, performing both single-SNP and moving-window association analyses to identify a colon neoplasia risk haplotype. Through this approach, we isolated the association effect to a five-SNP haplotype centered at 98.15 Mb on chromosome 9q. This haplotype is in strong linkage disequilibrium with the haplotype block containing HABP4 and may be a surrogate for the effect of this CD30 Ki-1 antigen. It is also in close proximity to GALNT12, also recently shown to be altered in colon tumors. We used a predictive modeling algorithm to show the contribution of this risk haplotype and surrounding candidate genes in distinguishing between colon cancer cases and healthy controls. The ability to replicate this finding, the strength of the haplotype association (odds ratio, 3.68), and the accuracy of our prediction model (approximately 60%) all strongly support the presence of a locus for familial colon cancer on chromosome 9q.
Abstract
The purpose of this study was to analyze the integrity of the adult human mandibular angle. The left hemimandibles of 24 human cadavers were selected and divided into three groups based upon ...remaining dental status. The height of the left mandibular body was measured. Hemimandibles were mounted in acrylic bone cement at the mandibular condyle. The left mounted hemimandibles were secured into an Instron 5565 mechanical unit and the occlusal plane was sequentially loaded until fracture of the mandibular bone occurred. Minimum, maximum, mean, and standard deviations for compressive force as well as displacement of the occlusal plane were derived and compared for descriptive statistics. The correlations between the gender, mandibular body height, and maximal load were examined. The mean mandibular heights among males and females were 22.44 mm and 17.53 mm, respectively. Results portrayed a significant correlation between gender and mandibular height. The mean maximal loads among males and females were 1,174.17 and 828.14 N, respectively. Results portrayed a statistically significant difference between males and females regarding maximum load as well as the height of the mandible (
p
= 0.0103 and
p
= 0.0067, respectively). No statistically significant association between maximum load and dental status (presence/absence of molar teeth) was found (
p
> 0.05). The maximal load of human mandibular angle was found to be higher than that of the heavily investigated polyurethane synthetic mandible replica. The average height of the mandibular body in males was found to be greater than that of females. Mandibular body height showed a direct correlation to maximal load of the hemimandibular angle. In maxillofacial research, biomechanical evaluations of mandibular angle fractures and plating techniques with human cadaveric bone should be considered alongside or in place of conventional synthetic polyurethane mandibles.
Genetic Epidemiology of Obesity and Cancer Gray-McGuire, Courtney; Adrianto, Indra; Nguyen, Thuan ...
Cancer and Energy Balance, Epidemiology and Overview,
2010, 20100312, Volume:
2
Book Chapter
To understand the genetic epidemiology of obesity and cancer means to consider the genetics of not only these two complex diseases but also the many risk factors associated with them and the ...molecular mechanisms likely to contribute to their underlying etiology. It is therefore the purpose of this chapter to highlight the following: genetic mapping studies that have been done to isolate genes related to obesity, genetic studies aimed to identify genes for obesity risk factors, and, finally, a discussion of the genes shared across or among the studies of obesity and/or its risk factors and the various cancers. This is by no means an exhaustive discussion as these are each complex traits with complex molecular mechanisms. It is, however, intended to be an overview of the genes likely to be involved in the cascade of pathways linking obesity and cancer.
It is well known that obesity continues to be a leading public health concern not only in the United States but now worldwide. From 1980 to 2002, the prevalence of obesity doubled in adults aged over 20 and overweight prevalence tripled in children and adolescents aged 6–9 years. The estimates of overweight and obesity in 2003–2004 showed that 17.1% of US children and adolescents were overweight and 32.2% of adults were obese 143.
The increasing rates of obesity among children are especially alarming and suggest continuing increases in the rates of obesity-related cancers. Since being overweight in childhood predicts obesity in adulthood 208, obesity occurring in childhood may operate as a ‘cumulative’ exposure that influences cancer risk in later life. Obese children may be subject to potentially long periods of hormonal exposures that operate during adolescence to influence propensity to neoplastic diseases. In females, childhood obesity may also affect the levels of sex hormone at adolescence. A prospective study of 55-year follow-up on 508 adolescents at 13–18 years from Harvard Growth Study showed that overweight adolescent boys had a nine-fold increased risk of colorectal cancer mortality 161. Associations between adolescent weight and cancer persisted even after adjusting for adult BMI.
A 50-year follow-up of >2,000 British children showed an overall 9% increase in cancer incidence per standard deviation increase in BMI, with effects three times larger for smoking-related cancers. There is also evidence from an Israeli case–control study which indicated that being in the upper quartile of BMI at age 18 years was associated with a 42% increase for ovarian cancer 24. However, the mechanisms underlying the association between childhood obesity and cancer are not well understood, particularly in conjunction with genetic data. In one case–control study of 40 obese and 40 non-obese prepubertal children, the obese group showed higher levels of IGF-1, insulin, and lower sex-binding hormone than that of the non-obese group 182. This suggests that high levels of growth factors and altered sex hormone profiles are present in obese children and the exposures to an adverse metabolic milieu may begin early in life.
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FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ