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H Inoue

Publications and source records attributed to H Inoue.

At least 55 records · Page 3Linked to original sources
PubMed2005

Acarbose, an alpha-glucosidase inhibitor, improves insulin resistance in fructose-fed rats.

Insulin resistance is one of the determinants of postprandial hyperglycemia. Acarbose is an alpha-glucosidase inhibitor that delays the absorption of carbohydrates from the small intestine, thereby suppressing postprandial hyperglycemia. Recently, acarbose has been found to reduce the incidence of cardiovascular disease (CVD) in patients with diabetes. These observations suggest that intervention of postprandial hyperglycemia with acarbose is a promising strategy for the prevention of CVD in diabetic patients. However, the effects of acarbose on insulin sensitivity are not fully understood. In this study, we examined whether oral administration of acarbose could improve insulin sensitivity in fructose-fed rats, a widely used insulin-resistant animal model. Although plasma glucose levels remained unchanged during the experiments, serum insulin levels were significantly increased in fructose-fed rats, which were suppressed by 4 weeks of treatment with acarbose. Acarbose treatment also increased high-density lipoprotein levels in fructose-fed rats. Furthermore, treatment of acarbose inhibited the elevation of systolic blood pressure levels in fructose-fed rats. These results indicate that oral administration of acarbose improves insulin sensitivity in fructose-fed rats. Our present study suggests that the cardioprotecive effects of acarbose could be ascribed, at least in part, to its insulin-sensitizing property.

Acarbose↗
PubMed2005

Renoprotective effects of azelnidipine, a dihydropyridine-based calcium antagonist in advanced glycation end product (AGE)-injected rats.

Diabetic nephropathy is a leading cause of end-stage renal disease in industrialized countries. Although the molecular mechanisms for the development and progression of diabetic nephropathy are not fully understood, the formation and accumulation of advanced glycation end products (AGEs) have been considered to play a major role in the pathogenesis of diabetic nephropathy. Hypertension is also an independent risk factor for the progression of diabetic nephropathy. However, functional cross-talk between AGEs and blood pressure and their involvement in diabetic nephropathy remain to be elucidated. In this study, we examined the effects of oral administration of azelnidipine, a commercially available dihydropyridine-based calcium antagonist, on renal injury in AGE-treated rats. Administration of azelnidipine inhibited the increase of systolic and diastolic blood pressure levels and urinary N-acetyl-beta-D-glucosaminidase activity in exogenously AGE-injected rats. Furthermore, azelnidipine treatment also prevented glomerulosclerosis in AGE-treated rats. These results indicate that renal damage in AGE-injected rats could be mediated, at least in part, by the elevation of blood pressure. Our present study suggests that azelnidipine would represent a valuable drug for the treatment of diabetic nephropathy by blocking the deleterious effects of AGEs.

Acetylglucosamine↗
PubMed2005

Azelnidipine, a dihydropyridine-based calcium antagonist, inhibits angiotensin II-induced oxidative stress generation and downregulation of pigment epithelium-derived factor mRNA levels in microvascular endothelial cells.

We have previously shown that azelnidipine, a long-acting dihydropyridine-based calcium antagonist (DHP), inhibited tumor necrosis factor-alpha-induced endothelial cell (EC) activation through its antioxidative properties. However whether azelnidipine could also block the angiotensin II (Ang II)-signaling in ECs remains to be elucidated. Since Ang II-type 1 receptor interaction could contribute to exacerbation of diabetic retinopathy by downregulating pigment epithelium-derived factor (PEDF) gene expression in ECs, we examined here whether azelnidipine inhibited the Ang II-induced reactive oxygen species (ROS) generation and subsequent PEDF gene suppression in microvascular ECs. Azelnidipine, but not nitrendipine, the other popular DHFP completely inhibited the Ang II-induced ROS generation in ECs. Furthermore, azelnidipine, but not nitrendipine, was found to partially restore decreased PEDF mRNA levels in Ang II-exposed ECs. The present study suggests that azelnidipine could inhibit the Ang II-induced decrease in PEDF mRNA levels in ECs through its antioxidative properties. Upregulation of PEDF by azelnidipine may become a therapeutic target for the treatment of diabetic retinopathy associated with hypertension.

Angiotensin II↗
PubMed2005

Inhibition by advanced glycation end products (AGEs) of pigment epithelium-derived factor (PEDF) gene expression in microvascular endothelial cells.

Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Recently, decreased levels of PEDF in the mammalian eye have been shown to participate in the pathogenesis of diabetic retinopathy In addition, advanced glycation end products (AGEs), senescent macroprotein derivatives that form at an accelerated rate under diabetes, have also been implicated in the development and progression of diabetic retinopathy. However the role of AGEs in decreased levels of PEDF in the eye remains to be elucidated. In this study, we examined the effects of AGEs on PEDF gene expression in microvascular endothelial cells (ECs). Various types of immunochemically distinct AGEs, which were prepared in vitro by incubating bovine serum albumin with glucose, glyceraldehyde or glycolaldehyde, significantly decreased endothelial mRNA levels of PEDF Furthermore, H2O2 dose-dependently suppressed PEDF gene expression in ECs. Our present results suggest that AGEs could down-regulate mRNA levels of PEDF in ECs, probably via oxidative stress generation. The deleterious effects of AGEs on diabetic retinopathy could be due, at least in part, to their PEDF-inhibitory properties.

Cells, Cultured↗
PubMed2005

Pigment epithelium-derived factor is a pericyte mitogen secreted by microvascular endothelial cells: possible participation of angiotensin II-elicited PEDF downregulation in diabetic retinopathy.

Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Decreased levels of PEDF in the mammalian eye have been shown to participate in proliferative diabetic retinopathy. In addition, we have recently found in in vitro experiments that PEDF protected against pericyte apoptosis, the earliest histopathological hallmark of diabetic retinopathy. These observations suggest that the loss of PEDF in the mammalian eye plays an important role in the development and progression of diabetic retinopathy. However, the functional role of endothelial cell (EC)-derived PEDF in pericyte survival and the regulation of PEDF gene expression remain to be elucidated. In this study, we examined the effects of anti-PEDF antibody (Ab) on the viable cell number of cocultured pericytes with microvascular ECs. We further studied the effects of angiotensin II (Ang II) on PEDF gene expression in ECs. Anti-PEDF Ab significantly inhibited the growth-stimulating effects of cocultured ECs on pericytes. Furthermore, Ang II significantly decreased PEDF mRNA levels in ECs, which was completely reversed by an Ang II type 1 receptor blocker, telmisartan. Our present results suggest that PEDF is an EC-derived mitogen or survival factor for retinal pericytes. Suppression by Ang II of the EC-derived PEDF may be involved in exacerbation of diabetic retinopathy in patients with hypertension.

Adult↗
PubMed2004

Clinical significance of Caveolin-1, Caveolin-2 and HER2/neu mRNA expression in human breast cancer.

Caveolin-1 and -2 (CAV1, CAV2) are closely linked genes localised to the fragile region of 7q31 (FRA7G), and loss of heterozygosity involving this region has been reported in breast cancer. Several studies have suggested that CAV1 is a negative regulator of HER2/neu signal transduction in vitro. However, the clinical significance of CAV1 in breast cancer has not yet been clarified. We examined quantitatively the mRNA levels of CAV1, CAV2 and HER2/neu in 162 cases of breast cancer using real-time PCR. Caveolin-1 and -2 protein expression was also examined by Western blotting and immunohistochemistry. We then evaluated for correlations between CAV1, CAV2 and HER2/neu gene expression and clinicopathologic factors in the 162 breast cancer cases. Results showed higher HER2/neu mRMA levels and lower CAV1 and CAV2 mRMA levels in breast cancer tissues than in corresponding normal tissues (P<0.001). Caveolin-1 and -2 protein expression levels were also suppressed in cancer tissues compared to normal tissues by Western blotting. Immunohistochemistry revealed that CAV1 and CAV2 proteins were abundantly expressed in mammary gland myoepithelial cells, but only weakly in ductalepithelial cells. Reduced CAV1 mRNA level was significantly associated with increasing tumour size (P=0.041), and negative oestrogen receptor status (P=0.021). There was also a significant association between low CAV2 mRNA level and negative progesterone receptor status (P=0.013), and between high HER2/neu mRNA level and negative hormonal receptor status (ER, P=0.029, PgR, P=0.019). While there was no relationship between HER2/neu and CAV1 mRNA levels, a significant association between CAV1 and CAV2 mRNA levels was observed (P<0.001). Our results indicated that CAV1 suppression correlated closely with that of CAV2 in breast cancer, that CAV1 level was inversely correlated with tumour size, and that CAV1 and CAV2 levels were correlated with hormonal receptor status. Therefore, CAV1 and CAV2 play an important role in tumour progression in breast cancer patients.

Biomarkers, Tumor↗
PubMed2004

Clinical significance of elongation factor-1 delta mRNA expression in oesophageal carcinoma.

Elongation factor-1 (EF-1) delta is a subunit of EF-1, which is a protein complex that participates in the elongation step of mRNA translation and has recently been considered to correlate with oncogenic transformation. However, there has been no information regarding the clinical significance of EF-1 delta mRNA expression in malignant tumours, including oesophageal carcinoma. Thus, we quantitated the expression of EF-1 delta in malignant and benign oesophageal tissues and associated these levels with clinicopathologic parameters of oesophageal carcinoma. Paired oesophageal tissue samples from cancerous and corresponding noncancerous parts were obtained from 52 patients who underwent curative oesophagectomy. Quantitative analyses of EF-1 delta expression were performed using real-time quantitative reverse transcription-polymerase chain reaction. Elongation factor-1 delta mRNA overexpression in cancerous tissues compared to normal counterparts was observed in 38 of 52 (73%) patients. The mean expression level of EF-1 delta mRNA in cancerous tissues was significantly higher than that in noncancerous tissues (P<0.01). A higher expression of EF-1 delta was significantly correlated with lymph node metastases (P<0.05) and advanced stages (P<0.05). Furthermore, the cause-specific survival of patients with a higher expression of EF-1 delta was significantly poorer than those with a lower expression (5-year cause-specific survival rates; 23 and 54%, respectively, P<0.05). The results of this study indicated that EF-1 delta mRNA expression was significantly higher in cancerous compared to noncancerous oesophageal tissues, and a higher expression of EF-1 delta mRNA was correlated with lymph node metastases, advanced disease stages and poorer prognosis for patients with oesophageal carcinoma.

Adenocarcinoma↗
PubMed2004

HDL3 induces cyclooxygenase-2 expression and prostacyclin release in human endothelial cells via a p38 MAPK/CRE-dependent pathway: effects on COX-2/PGI-synthase coupling.

OBJECTIVE: In endothelial cells, cyclooxygenase-1 (COX-1) and COX-2 both contribute to prostacyclin production. Recent findings suggest that COX-2 contributes significantly to systemic prostacyclin synthesis in humans; whether COX-2 inhibition is related to an increased cardiovascular risk is undergoing debate. HDLs have been shown to increase prostacyclin synthesis, thus in the present study we investigated the molecular mechanisms involved in this effect in endothelial cells. METHODS AND RESULTS: HDL3 (30 microg/mL) induced COX-2 expression in a time- and dose-dependent manner. COX-2 was found mainly in the perinuclear area where it co-localizes with PGI synthase. Transient transfection experiments showed that CRE is required for HDL-induced COX-2 transcription, and we demonstrated that p38 MAPK activation by HDL3 is involved in COX-2 mRNA transcription and stabilization. As a consequence of COX-2-induction by HDL3 prostacyclin production increased, incubation with a COX-2 selective inhibitor blocked this effect. Moreover, HDL3 increased caveolin-1 phosphorylation, thus promoting PGI-synthase shuttling from the membrane to the perinuclear area. CONCLUSIONS: We conclude that in endothelial cells, HDL modulates COX-2/PGI-S activity via both p38 MAPK-dependent COX-2 mRNA stability and transcription and both caveolin-1-dependent PGI-synthase shuttling and COX-2 coupling. The understanding of these mechanisms may provide new insights into the antiatherogenic role of HDL.

Caveolin 1↗
PubMed2004

An expression profile of human pancreatic islet mRNAs by Serial Analysis of Gene Expression (SAGE).

AIMS/HYPOTHESIS: The Human Genome Project seeks to identify all genes with the ultimate goal of evaluation of relative expression levels in physiology and in disease states. The purpose of the current study was the identification of the most abundant transcripts in human pancreatic islets and their relative expression levels using Serial Analysis of Gene Expression. METHODS: By cutting cDNAs into small uniform fragments (tags) and concatemerizing them into larger clones, the identity and relative abundance of genes can be estimated for a cDNA library. Approximately 49,000 SAGE tags were obtained from three human libraries: (i) ficoll gradient-purified islets (ii) islets further individually isolated by hand-picking, and (iii) pancreatic exocrine tissue. RESULTS: The relative abundance of each of the genes identified was approximated by the frequency of the tags. Gene ontology functions showed that all three libraries contained transcripts mostly encoding secreted factors. Comparison of the two islet libraries showed various degrees of contamination from the surrounding exocrine tissue (11 vs 25%). After removal of exocrine transcripts, the relative abundance of 2180 islet transcripts was determined. In addition to the most common genes (e.g. insulin, transthyretin, glucagon), a number of other abundant genes with ill-defined functions such as proSAAS or secretagogin, were also observed. CONCLUSION/INTERPRETATION: This information could serve as a resource for gene discovery, for comparison of transcript abundance between tissues, and for monitoring gene expression in the study of beta-cell dysfunction of diabetes. Since the chromosomal location of the identified genes is known, this SAGE expression data can be used in setting priorities for candidate genes that map to linkage peaks in families affected with diabetes.

Chromosomes, Human, Pair 1↗
PubMed2004

Possible contribution of adipocytokines on diabetic neuropathy.

Neuropathy is one of the typical features of chronic complications of diabetes mellitus. Recent analyses indicate that subjects with impaired glucose tolerance (IGT) already have disturbance of peripheral nerve function. To test the role of adipocytokines, that tend to be abnormal in IGT subjects, on diabetic neuropathy, we analyzed the relationship between plasma adipocytokine levels (TNFalpha, adiponectin, and leptin) and nerve conduction velocity in 105 type 2 diabetic subjects (M/F = 66/39, age = 60.8 +/- 11.8 years, BMI = 24.7 +/- 5.0kg/m2). Adipocytokines were measured by ELISA, and motor conduction velocity (MCV) and sensory conduction velocity (SCV) in median, ulnar, and tibial nerve were measured by electrical stimulation. Motor conduction velocity and SCV were corrected by age to be 1.0 as the normal value, and the average of three nerves were used to be the representative value. Relationship between corrected MCV or corrected SCV as a dependent variable and the duration of diabetes, HbA1C, BMI, TNFalpha, adiponectin, and leptin concentrations as independent variables were analyzed by multiple regression. Duration of diabetes and HbA1C were highly related with both corrected MCV (P < 0.02 and P < 0.001) and SCV (P < 0.02 and P < 0.05) by this analysis. Only corrected SCV was related significantly with TNFalpha (P < 0.05), and close to significantly with leptin (P = 0.059) concentrations. These results indicate that increased plasma glucose levels and duration of diabetes are the major factors that modulate diabetic neuropathy. However, nerve function may be affected by plasma cytokine levels like TNFalpha, and this effect was more significant on sensory nerves than motor nerves. The present results suggest that adipocytokines may play a role not only on angiopathy but also on neuropathy in diabetics.

Adipocytes↗
PubMed2004

Comparison of duodenal stent placement with surgical gastrojejunostomy for palliation in patients with duodenal obstructions caused by pancreaticobiliary malignancies.

BACKGROUND AND STUDY AIMS: Palliative treatment for duodenal stenosis with an enteral stent is effective in enhancing the quality of life of patients with duodenal obstruction. There have been no thorough comparisons of duodenal stent placement with standard surgical gastrojejunostomy. The present study evaluated the outcome of duodenal stent placement and surgical gastrojejunostomy for palliation of duodenal stenosis caused by pancreaticobiliary malignancies. PATIENTS AND METHODS: Medical records for patients who underwent palliative enteral stenting during the past 9 years were retrospectively reviewed, and the patients' clinical outcome was compared with that in patients who underwent open surgical gastrojejunostomy during the same period. Patients who underwent prophylactic gastrojejunostomy were excluded from the study. RESULTS: Twenty patients (11 men, nine women; mean age 71.8 years) with pancreaticobiliary malignancy underwent palliative enteral stenting (stent group). Nineteen patients (12 men, seven women; mean age 68.7 years) with pancreaticobiliary malignancies underwent surgical gastrojejunostomy (bypass group). In the stent group, the diagnoses were 12 pancreatic cancers, six gallbladder cancers, one bile duct cancer, and one ampullary cancer. In the bypass group, the diagnoses were 14 pancreatic cancers and five gallbladder cancers. There were no significant differences between the two groups with regard to clinical background. Both procedures were successful. There were no differences between the two groups with regard to the technical or clinical success rates, patient survival, possibility of discharge, need for parenteral nutrition, or incidence of complications. However, the time from the procedure to resumption of food intake was shorter in the stent group than in the bypass group (1 day vs. 9 days; P < 0.0001). Improvement in the performance score after the procedure was observed more frequently in the stent group (65 % vs. 26.3 %; P < 0.05). In terms of the median hospital stay from the time of the procedure to the time of initial discharge home (12 patients vs. nine patients), there was no statistical difference (15 days vs. 30 days) due to the small size of the sample. There was no procedure-related mortality in either group. CONCLUSIONS: Palliative stent placement was more beneficial than surgical gastrojejunostomy in enhancing the quality of life of patients with duodenal obstruction due to pancreaticobiliary malignancies.

Aged↗
PubMed2004

Squamous reepithelialization after circumferential endoscopic mucosal resection of superficial carcinoma arising in Barrett's esophagus.

Recent reports on the results of endoscopic ablation of Barrett's mucosa have been promising, particularly when total mucosal ablation is coupled with aggressive acid-suppression treatment using high-dose proton-pump inhibitor therapy. There is also a considerable literature on reepithelialization after ablative treatments in Barrett's esophagus. This report describes a case of multifocal superficial adenocarcinoma arising in Barrett's mucosa that was successfully treated with total circumferential endoscopic mucosal resection, with a subsequent follow-up of more than 2 years. This is the first report describing the process of squamous reepithelialization after endoscopic mucosal resection in Barrett's esophagus.

Adenocarcinoma↗
PubMed2004

Reflux esophagitis after eradication of Helicobacter pylori is associated with the degree of hiatal hernia.

BACKGROUND: Several studies have shown that reflux esophagitis (RE) occurs after eradication of Helicobacter pylori. However, endoscopic findings do not allow prediction of the development of RE after successful treatment. In this study, we evaluated the relationship between the prevalence of RE after eradication therapy and the degree of hiatal hernia. METHODS: The study comprised 148 patients who had undergone H. pylori eradication therapy over the past 5 years. The degree of RE and hiatal hernia was evaluated based on endoscopic findings. Hiatal hernia was graded according to Hill's gastroesophageal flap valve (GEFV; grades I-IV) classification. RE after eradication therapy was graded according to the Los Angeles classification system. H. pylori infection was confirmed in all patients by culture, urease test and histological examination of antral and fundic biopsy specimens. RESULTS: Among 148 patients, there were 122 patients (82.4%) with successful and 26 (17.6%) with failed eradication therapy. RE was diagnosed in 25 (20.5%) out of 122 patients with successful therapy but only in 1 (3.8%) out of 26 patients with failed therapy (P < 0.05). After successful eradication, 25 patients had mild RE (12 with grade A, 13 with grade B). Among patients of the successful eradication group (n = 122), RE was diagnosed in 2 (5.3%) out of 38 patients without hiatal hernia and in 23 (27.4%) out of 84 patients with hiatal hernia (P = 0.0051). Furthermore, RE was diagnosed in 2 (5.3%) out of 38 patients with GEFV grade I, 13 (24.1%) out of 54 with grade II, 7 (30.4%) among 23 with grade III, and 3 (42.9%) out of 7 patients with grade IV. The pH level of gastric juice after eradication therapy was lower in the group with successful eradication than in the group with failed therapy regardless of the incidence and degree of RE. CONCLUSIONS: There is a high incidence of RE after successful H. pylori eradication therapy. This incidence of RE was closely associated with the presence and degree of hiatal hernia and with the decrease in gastric juice pH. These findings suggest that the presence of hiatal hernia together with increase in gastric acidity are important determinant factors for the development of RE after successful H. pylori eradication therapy.

Endoscopy, Gastrointestinal↗
PubMed2004

Clinical significance of the overexpression of the candidate oncogene CYP24 in esophageal cancer.

BACKGROUND: By using array comparative genomic hybridization (CGH), the increased copy number of CYP24 (which encodes vitamin D 24-hydroxylase) at 20q13.2 was previously reported, leading to the identification of CYP24 as a candidate oncogene in breast cancer. CYP24 leads to abrogate growth control mediated by vitamin D. MATERIALS AND METHODS: We examined CYP24 expression as well as VDR (vitamin D receptor) gene expression in 42 esophageal cancer cases using semi-quantitative RT-PCR assay. We induced CYP24 in seven esophageal cancer cell lines using 25-hydroxyvitamin D3 [25(OH)D3] and compared cell growth rate, measured using the 3-(4, 5-dimethylthiazol-2-y)-2, 5-diphenyltetrazolium bromide (MTT) assay system. RESULTS: The overall survival rate was significantly higher in 25 cases of lower CYP24 expression than 17 cases of higher CYP24 expression (P <0.05); on the other hand, 23 cases of low VDR expression had a poorer prognosis than 19 cases of high VDR expression. Moreover, we disclosed that the inverse correlation between CYP24 and VDR expression is significant in esophageal cancer cases (P <0.05). Furthermore, the cell growth evaluated by MTT assay was greatly increased in CYP24-induced and VDR-diminished cells than non-responding cells by 25(OH)D3 activity (P <0.01). CONCLUSIONS: Overexpression of the candidate oncogene CYP24 is inversely correlated to vitamin D receptor expression, and may play an important role in determination of the malignant potential of esophageal cancer.

Adult↗
PubMed2004

Clinical significance of bone marrow micrometastases in esophageal cancer.

Using the reverse transcriptase-polymerase chain reaction (RT-PCR), we investigated the clinical significance of bone marrow micrometastases in patients with esophageal cancer. Bone marrow samples from 57 patients with esophageal cancer, who underwent esophagotomy, were investigated by specific RT-PCR for carcinoembryonic antigens (CEA). A total of 40 out of 57 patients (70.1%) were positive for CEA mRNA in the bone marrow. Among curatively resected cases, 34 of 50 patients (68.0%) were positive for CEA. Ten of 13 T1 patients (76.9%) were positive for CEA. Although the CEA-positive rate was high, there was no significant correlation between CEA positivity and any clinical characteristics. Among the 40 CEA-positive patients, 50% have shown recurrence so far. Detection of cancer cells in the bone marrow by RT-PCR may not always correspond to the malignant potential or other characteristics of the tumor. CEA-positive 'micrometastases' might actually represent isolated circulating tumor cells without much biological significance.

Adult↗
PubMed2004

Increased cancer risk in heavy drinkers with the alcohol dehydrogenase 1C*1 allele, possibly due to salivary acetaldehyde.

BACKGROUND: Chronic ethanol consumption is associated with an increased risk of upper aerodigestive tract cancer. As acetaldehyde seems to be a carcinogenic factor associated with chronic alcohol consumption, alcoholics with the alcohol dehydrogenase (ADH) 1C*1 allele seem to be particularly at risk as this allele encodes for a rapidly ethanol metabolising enzyme leading to increased acetaldehyde levels. Recent epidemiological studies resulted in contradictory results and therefore we have investigated ADH1C genotypes in heavy alcohol consumers only. METHODS: We analysed the ADH1C genotype in 107 heavy drinkers with upper aerodigestive tract cancer and in 103 age matched alcoholic controls without cancer who consumed similar amounts of alcohol. Genotyping of the ADH1C locus was performed using polymerase chain reaction based on restriction fragment length polymorphism methods on leucocyte DNA. In addition, ethanol was administered orally (0.3 g/kg body weight) to 21 healthy volunteers with the ADH1C*1,1, ADH1C*1,2, and ADH1C*2,2 genotypes, and 12 volunteers with various ADH genotypes consumed ethanol ad libitum (mean 211 (29) g). Subsequently, salivary acetaldehyde concentrations were measured by gas chromatography or high performance liquid chromatography. RESULTS: The allele frequency of the ADH1C*1 allele was found to be significantly increased in heavy drinkers with upper aerodigestive tract cancer compared with age matched alcoholic controls without cancer (61.7% v 49.0%; p = 0.011). The unadjusted and adjusted odds ratios for all cancer cases versus all alcoholic controls were 1.67 and 1.69, respectively. Healthy volunteers homozygous for the ADH1C*1 allele had higher salivary acetaldehyde concentrations following alcohol ingestion than volunteers heterozygous for ADH1C (p = 0.056) or homozygous for ADH1C*2 (p = 0.011). CONCLUSIONS: These data demonstrate that heavy drinkers homozygous for the ADH1C*1 allele have a predisposition to develop upper aerodigestive tract cancer, possibly due to elevated salivary acetaldehyde levels following alcohol consumption.

Acetaldehyde↗
PubMed2004

A new scoring system for Perthes' disease based on combined lateral and posterior pillar classifications.

We have devised a combined pillar score (CPS) system, based on the lateral pillar (LP) and the posterior pillar (PP) classifications, together with the age at onset of Perthes' disease, and examined its correlation with prognosis. The correlation coefficient of the Catterall classification, LP, PP, and CPS systems with the Stulberg system was 0.39, 0.52, 0.50, and 0.70, respectively. Overall 21 of the 22 hips (95.4%) with a CPS of 0 to 1 point had a good outcome and 12 of the 13 hips (92.3%) with a CPS of 3 points or more had a fair or poor outcome. None with a CPS of 2 points, had a poor outcome. The study shows that an accurate prediction of the prognosis is not possible with the LP classification alone for patients classified as belonging to group B (LP height 50% to 100% of contralateral height). The CPS system does allow accurate prediction of outcome.

Age of Onset↗