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Background: Excess alcohol consumption adversely affects one-carbon metabolism and increases the risk of liver disease and liver cancer. Conversely, higher folate levels have been inversely associated with liver damage. The current study investigated the effects of alcohol and one-carbon metabolite intake on liver cancer incidence and liver disease mortality within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study., Methods: Cox proportional hazards modeling was used to calculate hazard ratios and 95% confidence intervals (CIs) in a population of 27,086 Finnish males with 194 incident liver cancers and 213 liver disease deaths. In a nested case-control subset (95 liver cancers, 103 controls), logistic regression was used to calculate odds ratios and 95% CIs for serum one-carbon metabolites in relation to liver cancer risk., Results: Daily alcohol consumption of more than 20.44 g was associated with an increased risk of both liver cancer incidence (Hazard Ratio (HR) 1.52, 95%CI 1.06-2.18) and liver disease mortality (HR 6.68, 95%CI 4.16-10.71). These risks were unaffected by one-carbon metabolite intake. Similarly, in the case-control study, none of the serum one-carbon metabolites were associated with liver cancer., Conclusions: The current study provided no convincing evidence for a protective association of one-carbon metabolite intake or serum level on the risk of liver cancer or liver disease mortality.

Background: Excessive alcohol consumption is a well-established risk factor for liver disease and hepatocellular carcinoma (HCC). Previous studies have found that increased alcohol consumption can lead to lower absorption of folate. Conversely, higher folate intake has been inversely associated with liver damage and HCC. In the current study, we investigate the effect of alcohol consumption and folate intake on HCC incidence and liver disease mortality in the NIH-American Association of Retired Persons Diet and Health Study., Methods: The study population included 494,743 participants who reported at baseline their dietary intake for the previous year. Alcohol and folate were analyzed with hazards ratios (HR) and 95% confidence intervals (CI) using multivariate Cox proportional hazards regression models adjusted for age, sex, race, education, smoking, body mass index, and diabetes. HCC incidence (n = 435) was determined through 2006 via linkage with cancer registries, and liver disease mortality (n = 789) was determined through 2008 via linkage to the U.S. Social Security Administration Death Master File and the National Death Index Plus by the National Center for Health Statistics., Results: Consumption of more than three drinks per day was positively associated with both HCC incidence (HR: 1.92; 95%CI: 1.42-2.60) and liver disease mortality (HR: 5.84; 95%CI: 4.81-7.10), whereas folate intake was associated with neither outcome. Folate, however, modified the relationship between alcohol and HCC incidence (Pinteraction = 0.03), but had no effect on the relationship between alcohol and liver disease mortality (Pinteraction = 0.54)., Conclusions: These results suggest that higher folate intake may ameliorate the effect of alcohol consumption on the development of HCC., Impact: Folate intake may be beneficial in the prevention of alcohol-associated HCC.

Dichlorodiphenyltrichloroethane (p,p'-DDT), an organochlorine pesticide known to have deleterious health effects in humans, has been linked to hepatocellular carcinoma (HCC) in rodents. A recent study has reported that p,p'-DDT and its most persistent metabolite, dichlorodiphenyldichloroethylene (p,p'-DDE), may also be associated with HCC in humans. To examine whether there is an association between p,p'-DDT and/or p,p'-DDE in a population at high-risk of developing HCC, a nested case-control study was conducted within the 83,794 person Haimen City Cohort in China. Sera and questionnaire data were collected from all participants between 1992 and 1993. This study included 473 persons who developed HCC and 492 who did not, frequency matched on sex, age and area of residence. p,p'-DDT and p,p'-DDE levels were determined by mass spectrometry. Hepatitis B viral infection status (based on hepatitis B virus surface antigen; HBsAg) was also determined. p,p'-DDT and/or p,p'-DDE serum levels were significantly associated with sex, area of residence, occupation, alcohol consumption and cigarette smoking. Adjusting for age, sex, area of residence, HBsAg, family history of HCC, history of acute hepatitis, smoking, alcohol, occupation (farmer vs. other) and levels of p,p'-DDT or p,p'-DDE, odds ratios (OR) and 95% confidence intervals (CI) were calculated via unconditional logistic regression. Overall, the highest quintile of p,p'-DDT was associated with an increased risk of HCC, OR = 2.96 95% CI; 1.19-7.40. There were no statistically significant associations with p,p'-DDE. Overall, these results suggest that recent exposure to p,p'-DDT may increase risk of HCC., (Copyright © 2012 UICC.)

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief and Authors. The authors recently discovered two programming errors that affected the results in their article on the epidemiology of esophageal and stomach cancers in human immunodeficiency virus infected people. As a result of these errors, the standardized incidence ratios (SIRs) were too high. The corrected SIRs are all lower than the authors reported, and the corrected SIR for stomach cancer is no longer significantly elevated. These errors affect Tables 2-5 in the paper. Because the new findings alter the conclusions, the editors and authors have jointly made the decision to retract the paper. The authors would like to express their sincere regret at the errors in their initial report and any inconvenience or confusion that they created. The corrected results may be obtained by contacting the corresponding author, Dr. Eric A. Engels, by email at engelse@exchange.nih.gov., (Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Background: Liver cancer incidence rates in the United States have increased for several decades for reasons that are not entirely clear. Regardless of aetiology, cirrhosis is a strong risk factor for liver cancer. As mortality from cirrhosis has been declining in recent decades, it is possible that the risk of liver cancer among persons with cirrhosis has been affected., Methods: Data from the US Veterans Affairs medical records database were analysed after adjustment for attained age, race, number of hospital visits, obesity, diabetes, and chronic obstructive pulmonary disease. Hazard ratio (HR) and 95% confidence interval (95% CI) were calculated using Cox proportional hazards modelling. Survival analyses were conducted using age as the time metric and incidence of cirrhosis as a time-dependent covariate., Results: Among 103 257 men with incident cirrhosis, 788 liver cancers developed. The HR of liver cancer was highest among men with viral-related cirrhosis (HR=37.59, 95% CI: 22.57-62.61), lowest among men with alcohol-related cirrhosis (HR=8.20, 95% CI: 7.55-8.91) and intermediate among men with idiopathic cirrhosis (HR=10.45, 95% CI: 8.52-12.81), when compared with those without cirrhosis. Regardless of cirrhosis type, white men had higher HRs than black men. The HR of developing liver cancer increased from 6.40 (95% CI: 4.40-9.33) in 1969-1973 to 34.71 (95% CI: 23.10-52.16) in 1992-1996 for those with cirrhosis compared with those without., Conclusion: In conclusion, the significantly increased HR of developing liver cancer among men with cirrhosis compared with men without cirrhosis in the United States may be contributing to the increasing incidence of liver cancer.

Fumonisin B1 (FB1), a mycotoxin that contaminates corn in certain climates, has been demonstrated to cause hepatocellular cancer (HCC) in animal models. Whether a relationship between FB1 and HCC exists in humans is not known. To examine the hypothesis, we conducted case-control studies nested within two large cohorts in China; the Haimen City Cohort and the General Population Study of the Nutritional Intervention Trials cohort in Linxian. In the Haimen City Cohort, nail FB1 levels were determined in 271 HCC cases and 280 controls. In the General Population Nutritional Intervention Trial, nail FB1 levels were determined in 72 HCC cases and 147 controls. In each population, odds ratios and 95% confidence intervals (95%CI) from logistic regression models estimated the association between measurable FB1 and HCC, adjusting for hepatitis B virus infection and other factors. A meta-analysis that included both populations was also conducted. The analysis revealed no statistically significant association between FB1 and HCC in either Haimen City (OR=1.10, 95%CI=0.64-1.89) or in Linxian (OR=1.47, 95%CI=0.70-3.07). Similarly, the pooled meta-analysis showed no statistically significant association between FB1 exposure and HCC (OR=1.22, 95%CI=0.79-1.89). These findings, although somewhat preliminary, do not support an associated between FB1 and HCC., (Published by Elsevier Ltd.)

Background: To establish optimal cutoff values for serologic diagnosis of fundic atrophy in a high-risk area for oesophageal squamous cell carcinoma and gastric cancer with high prevalence of Helicobacter pylori (H. pylori) in Northern Iran, we performed an endoscopy-room-based validation study., Methods: We measured serum pepsinogens I (PGI) and II (PGII), gastrin 17 (G-17), and antibodies against whole H. pylori, or cytotoxin-associated gene A (CagA) antigen among 309 consecutive patients in two major endoscopy clinics in northeastern Iran. Updated Sydney System was used as histology gold standard. Areas under curves (AUCs), optimal cutoff and predictive values were calculated for serum biomarkers against the histology., Results: 309 persons were recruited (mean age: 63.5 years old, 59.5% female). 84.5% were H. pylori positive and 77.5% were CagA positive. 21 fundic atrophy and 101 nonatrophic pangastritis were diagnosed. The best cutoff values in fundic atrophy assessment were calculated at PGI<56 µg/l (sensitivity: 61.9%, specificity: 94.8%) and PGI/PGII ratio<5 (sensitivity: 75.0%, specificity: 91.0%). A serum G-17<2.6 pmol/l or G-17>40 pmol/l was 81% sensitive and 73.3% specific for diagnosing fundic atrophy. At cutoff concentration of 11.8 µg/l, PGII showed 84.2% sensitivity and 45.4% specificity to distinguish nonatrophic pangastritis. Exclusion of nonatrophic pangastritis enhanced diagnostic ability of PGI/PGII ratio (from AUC = 0.66 to 0.90) but did not affect AUC of PGI. After restricting study samples to those with PGII<11.8, the sensitivity of using PGI<56 to define fundic atrophy increased to 83.3% (95%CI 51.6-97.9) and its specificity decreased to 88.8% (95%CI 80.8-94.3)., Conclusions: Among endoscopy clinic patients, PGII is a sensitive marker for extension of nonatrophic gastritis toward the corpus. PGI is a stable biomarker in assessment of fundic atrophy and has similar accuracy to PGI/PGII ratio among populations with prevalent nonatrophic pangastritis.

Pre-speech in 35 children with clefts of the lip and palate or palate only were analyzed for place and manner of articulation. Transcriptions were made from tape recorded babbling sequences. Two children without clefts were used as reference. All of the children with clefts were treated according to a regimen of early surgical repair of the velum cleft and delayed closure of the cleft in the hard palate. The frequency of selected phonetic features was calculated. Correlations between phonetic/perceptual and functional and morphological factors were tested. Supraglottal articulation dominated among all the children indicating a sufficient velopharyngeal mechanism. The results also showed correlations between cleft type and place of articulation. Anteriorly placed sounds (i.e., bilabial, dental, and alveolar sounds) occurred frequently among the children with cleft palate only and in the noncleft children. In children with cleft lip and palate, posteriorly placed articulations predominated. It was postulated that early intervention may have a positive effect on articulatory development.

The speech of 31 consecutive patients with isolated cleft palate was evaluated when they were between 10 and 14 years of age. All the children had Wardill-Kilner push-back repairs at a mean age of 7.9 months. Several speech variables were assessed by two trained listeners. In addition, an overall evaluation of the quality of the patients' speech was made by the listeners and by the patients themselves. The patients had some remaining speech problems, mainly hypernasality which was moderate or severe in 7 (23%). The prevalence of compensatory articulations was low, however (n = 4, 13%), and most patients thought that their own speech was normal or relatively normal.

Maxillary morphology and dental occlusion were studied from infancy to age 10 years in 32 patients born with isolated cleft palate. Wardill-Kilner push back repair of the palate had been done at a mean age of 7.5 months. Measurements obtained from casts of the jaws showed that the average maxillary dimensions before as well as after operation were less than those reported for children without clefts. The mean reduction was similar whether the cleft reached into the hard palate or affected the soft palate only. Preoperative anterior maxillary arch width in particular, and also distance from scar line to selected teeth seemed to influence postoperative development of the maxillary dental arch in individual patients.

During the period 1958-1985, 230 patients with cleft palate were operated on in the Department of Plastic Surgery, University of Göteborg, Sweden. A modified push-back technique according to Wardill and Kilner was used. The children were operated on at a mean age of 13 months. They were divided into two groups, the first in which the cleft affected the velum only (n = 121) and the other in which it also affected the hard palate (n = 109). Postoperative dehiscences and fistulas occurred in 19 (8%) patients, of which 16 (15%) belonged to the group in which the cleft affected the hard palate. Only three (2%) of the 121 patients with a cleft in the soft palate only developed dehiscences. The total number of patients who had to be reoperated on because of dehiscences were 10 (4%) and palatopharyngeal flaps had to be performed in 25 patients (11%) because of speech problems.

The purpose of the study was to evaluate the result in adults of Class I malocclusion cases who had all their first premolars extracted as the sole treatment of space deficiency in the mixed or early permanent dentition. The mean age at premolar removal was 10 1/2 years. Forty-two out of 44 cases were re-examined at a mean age of 30 years and 4 months. Observations of dental occlusion and oral health were compared to observations of control samples. The average malocclusion in the adults, as judged by a score method, was similar to that reported for an appliance-treated sample. Marked spontaneous arch alignment and residual space closure with age was seen in most cases. Despite earlier tooth removal, on average crowding developed to about the same degree as that of an non-extraction normal occlusion sample. No detrimental effects were seen with regard to overjet or overbite. Neither did the figures for lower incisor position at the follow-up examination differ from that of the normal occlusion sample. Although tipping of adjacent teeth towards the extraction site was frequent, especially in the mandible, no effect on marginal bone height was evident as judged by comparison with a non-extraction control sample. The results reveal a significant capacity for spontaneous improvements with age in dental arch morphology and relationship in extraction cases, provided that specific features have been looked for in case selection.

The wide therapeutic use of hormones enhances the importance of detailed knowledge of the effects on skull growth. Thyroxine is known to regulate maturation of cell populations and long bone growth, but the influence on craniofacial bone remodelling is still obscure. One side effect of substitution therapy with thyroxine in children is premature closure of cranial sutures. The aim of the present study was to describe longitudinally the effect of different serum levels of thyroxine on craniofacial growth. In young rats injected with 20 micrograms/kg b.w. l-thyroxine for 28 days a change was found in craniofacial morphology measured by a cephalometric technique. A decrease in length of the viscerocranium was evident after 14 days, and occurred in connection with raised serum levels of thyroxine. In contrast, cranial base growth was increased between day 14 and 28 and also a catch-up growth in the viscerocranium was observed during this period. This observed change occurred after the induced peak in levels of thyroxine in serum had subsided. The inhibited forward directed growth of the viscerocranium was consistent with the fact that the skull in the thyroxine group developed a klinorhycial form in contrast to the normal orthocranialization. Thus, the craniofacial growth pattern was influenced by variations in the serum level of thyroxine. The effects of thyroxine on skull growth sites observed are consistent with reported effects of low dose of thyroxine on long bone growth.