bluuebunny/crossref_metadata_2025_split huggingface dataset:
High frequency of chronic end‐stage liver disease and hepatocellular carcinoma in a Hispanic population
Authors: PEREZ ADRIANA , ANZALDUA MONICA , MCCORMICK JOSEPH , FISHER‐HOCH SUSAN 
Published: January 2004

AbstractBackground:  Texas has the highest mortality from hepatocellular carcinoma in the USA. Because end‐stage liver disease mortality is most marked in the Hispanic population in the Lower Rio Grande Valley, the aim of the present paper was to estimate the prevalence of end‐stage liver disease and associated factors in Brownsville.Methods:  A cross‐sectional study was carried out, abstracting medical charts in a community‐based clinic and a hospital. A matched case‐control analysis was performed. Cases had an International Classification of Disease (9th revision; ICD9) code 155.0 or 571.0–9 (primary liver cancer or chronic liver disease) recorded; age‐ and sex‐matched controls did not have these codes. A total of 176 cases and 352 controls was collected. The main outcome measure was the prevalence and risk factors for end‐stage liver disease.Results:  Conservative prevalence of end‐stage liver disease: 126/100 000 (386/100 000, male). Eleven out of 176 had hepatocellular carcinoma. Median age was 57 years; 72% male, 94% Hispanic. Among significant risk factors were history of hepatitis (odds ratio (OR): 19.3; 95% confidence interval (CI): 8.0–46.4), any history of alcohol use (OR: 6.6; 95%CI: 4–10.8) and history of illegal drug use (OR: 1.9; 95%CI: 1.2–2.9). Fifteen cases with no known risk factors were classified as cryptogenic cirrhosis. Only four cases out of 176 had been referred for liver transplant.Conclusions:  The prevalence of end‐stage liver disease in the Lower Rio Grande Valley is extremely high, with no single satisfactory explanation and with acute health disparities. Careful follow up of cryptogenic cirrhosis in this population may or may not lead to a new source of liver disease.© 2004 Blackwell Publishing Asia Pty Ltd
Prevalence of colonic polyps is not increased in patients with acromegaly: Analysis of 60 patients from India
Authors: BHANSALI ANIL , KOCHHAR RAKESH , CHAWLA YOGESH K , REDDY SOMASHEKARA , JIBAN DASH RADHARAMAN 
Published: January 2004

AbstractBackground:  There are conflicting data on the prevalence of colorectal adenomas in patients with acromegaly. It has been suggested that the risk of colorectal adenomas may be dependent on the geographic and ethnic origin of the patients.Materials:  Sixty consecutive patients with active acromegaly due to somatotropinoma underwent colonoscopy prior to definitive surgery. They included 35 men and 25 women with a mean (± SD) age of 37.4 ± 13.2 years and a lag time between symptomatology and diagnosis of acromegaly of 64.6 ± 58.0 months. The control group included 160 patients (88 men, 72 women; mean age, 38.2 ± 14.0 years) with a diagnosis of irritable bowel syndrome who were also subjected to colonoscopy. None of these patients had previous or family history of colonic neoplasm, bleeding or colonic surgery.Results:  Colonoscopic examination was complete to the cecum in 52 patients (88%), and to the splenic flexure in the remaining 12% . In the control group, it was complete to the cecum in 144 patients (90%). Four of the acromegalic patients (6.7%) and five in the control group (3.1%; P = 0.24) had hyperplastic polyps. No patient in either of the groups had adenomatous polyps or colonic adenocarcinoma. The group of acromegalic patients with and without polyps did not differ significantly in age, duration of disease, growth hormone levels or glycemic status. The number of skin tags, however, was significantly higher (P = 0.04) in the polyp group as compared to those without polyps.Conclusion:  The present study has failed to demonstrate the high prevalence rate of colonic neoplasia in patients with acromegaly as compared to reports from the Western world.© 2004 Blackwell Publishing Asia Pty Ltd
Role of L‐carnitine in the prevention of acute liver damage induced by carbon tetrachloride in rats
Authors: DEMIRDAG KUTBEDDIN , BAHCECIOGLU IBRAHIM HALIL , OZERCAN IBRAHIM HANIFI , ÖZDEN MEHMET , YILMAZ SEVAL , KALKAN AHMET 
Published: January 2004

AbstractBackground and Aim:  Lipid peroxidation is the most important mechanism in the pathogenesis of acute liver damage with carbon tetrachloride (CCl4). L‐carnitine may prevent lipid peroxidation and thus may protect against liver damage. In the present study we investigated the protective effect of L‐carnitine in experimental acute liver damage induced by CCl4.Methods:  Fifty rats were allocated to five equal groups. The first group was the control (group 1), the second group received an intraperitoneal CCl4 injection for 3 days (group 2), and the third group received a 50 mg/kg subcutaneous L‐carnitine injection for 4 days, beginning a day before CCl4 injection. The CCl4 injection was continued for 3 days in the concerned group (group 3). Group 4 was given a CCl4 injection for 7 days and group 5 received a 50 mg/kg subcutaneous L‐carnitine injection for 8 days, beginning a day before CCl4 injection. This group continued to receive a CCl4 injection for 7 days. Rats in groups 2 and 3 were killed on the fifth day. Rats in groups 1, 4 and 5 were killed on the ninth day. Plasma and liver tissue malondialdehyde (MDA) levels, glutathione peroxidase (GSH‐Px) activity and liver enzyme levels were studied. Histopathological investigations were conducted.Results:  Liver tissue MDA levels decreased significantly in group 3 compared to group 2 (P < 0.001). Liver tissue MDA levels in group 5 decreased significantly in comparison to those of group 4 (P < 0.001). Liver tissue GSH‐Px activity in group 5 was significantly lower than that in group 4 (P < 0.05). There were no significant differences between groups 3 and 4 regarding GSH‐Px activity (P > 0.05). Steatosis, inflammation and necrosis in group 3 were significantly reduced when compared to group 2 (P < 0.01). Fibrosis development was not identified in groups 2 and 3. Steatosis in group 5 was significantly lower than that in group 4 (P < 0.05) and there were no significant differences between groups 4 and 5 with regards to inflammation and necrosis (P > 0.05). Mild fibrosis development was identified in groups 4 and 5 but the difference between the groups was not significant.Conclusion:  It appears that L‐carnitine has a protective effect in the early stage of experimental acute liver damage induced by CCl4. As the toxic effect or damage continues, its effect lessens.© 2004 Blackwell Publishing Asia Pty Ltd
Signalling pathways involved in retinal endothelial cell proliferation induced by advanced glycation end products: inhibitory effect of gliclazide
Authors: Mamputu J.‐C. , Renier G. 
Published: January 2004

Aim:  We have previously demonstrated that advanced glycation end products (AGEs) stimulate bovine retinal endothelial cell (BREC) proliferation through induction of vascular endothelial growth factor (VEGF) production by these cells. We have also shown that gliclazide, a sulfonylurea which decreases oxidative stress, inhibits this effect. The aim of the present study was to characterize the signalling pathways involved in AGE‐induced BREC proliferation and VEGF production and mediating the inhibitory effect of gliclazide on these biological events.Methods:  BRECs were treated or not treated with AGEs in the presence or absence of gliclazide, antioxidants, protein kinase C (PKC), mitogen‐activated protein kinase (MAPK) or nuclear factor‐κB (NF‐κB) inhibitors. BREC proliferation was assessed by measuring [3H]‐thymidine incorporation into DNA. Activation of PKC, MAPK and NF‐κB signal transduction pathways and determination of VEGF expression were assessed by Western blot analysis using specific antibodies. MAPK activity was also determined by an in vitro kinase assay.Results:  Treatment of BRECs with AGEs significantly increased cell proliferation and VEGF expression. AGEs induced PKC‐β translocation, extracellular signal‐regulated protein kinase 1/2 and NF‐κB activation in these cells. Pharmacological inhibition of these signalling pathways abolished AGE effects on cell proliferation and VEGF expression. Exposure of BRECs to gliclazide or antioxidants such as vitamin E or N‐acetyl‐l‐cysteine resulted in a significant decrease in AGE‐induced activation of PKC‐, MAPK‐ and NF‐κB‐signalling pathways.Conclusions:  Our results demonstrate the involvement of PKC, MAPK and NF‐κB in AGE‐induced BREC proliferation and VEGF expression. Gliclazide inhibits BREC proliferation by interfering with these intracellular signal transduction pathways.
A placebo‐controlled crossover study comparing the effects of nateglinide and glibenclamide on postprandial hyperglycaemia and hyperinsulinaemia in patients with type 2 diabetes
Authors: Barnett A. H. , Anderson D. M. , Shelley S. , Morgan R. , Owens D. R. 
Published: January 2004

Aim:  This was a randomized, double blind, three period crossover study. The objective was to compare glucose, insulin and C‐peptide 24 h profiles in patients with type 2 diabetes mellitus after dosing with nateglinide (given preprandially before three test meals), glibenclamide (administered once before breakfast) or placebo (given before three test meals).Methods:  Fourteen patients underwent screening followed within 3 weeks by three treatment periods of 1 day, each separated by 7 days. Dosing followed a six‐sequence balanced, two 3 × 3‐replicated Latin square.Results:  Mean peak serum insulin levels were lower after nateglinide (115 mU/l) than after glibenclamide (145 mU/l.h; p = 0.017) but higher than after placebo (79 mU/l; p = 0.001). However, peak insulin levels were reached earlier after nateglinide [mean time to peak (tmax) 1.7 h] compared to glibenclamide (mean tmax 2.1 h, p = 0.06). Total insulin exposure over the day was higher after glibenclamide compared with that following nateglinide (1216 vs. 1067 mU/l.h; p = 0.009). Similar findings were seen with serum C‐peptide. Despite this, mean peak plasma glucose concentrations were lower following nateglinide (11.4 mmol/l from a baseline of 8.3 mmol/l) compared with glibenclamide (13.2 mmol/l from a baseline of 8.5 mmol/l; p = 0.001) and placebo (14.0 mmol/l from a baseline of 8.0 mmol/L; p < 0.001).Conclusions:  Nateglinide improves early prandial measures of insulin and glucose response to a standard meal, more so than glibenclamide, in people with type 2 diabetes.
The effect of high‐fat and high‐fructose diets on glucose tolerance and plasma lipid and leptin levels in rats
Authors: Huang B.‐W. , Chiang M.‐T. , Yao H.‐T. , Chiang W. 
Published: January 2004

Aim:  High‐fat and high‐fructose diets are usually used to induce animal model diabetes mellitus. The purposes of this research were to compare the abnormalities of glucose metabolism caused by high‐fructose diet and a high‐fat diet and the effects of the high‐fructose diet and high‐fat diet on plasma leptin.Methods:  In this research, 24 Sprague–Dawley rats were used as the experimental animals, which were divided into three groups: chow diet (control group), high‐fructose diet (60% fructose w/w) and high‐fat diet (20% lard w/w). They were fed for a period of 8 weeks, during which an oral glucose tolerance test was conducted in the seventh week, and after completion of the eighth week, the abdominal adipose tissue and liver of the rats were excised and weighed, and the plasma cholesterol, triglyceride, insulin and leptin concentrations were assayed.Results:  The high‐fat diet group presented a fasting blood glucose concentration that was higher than that of the control group. Furthermore, after 2 h of glucose challenge, the rats in the high‐fat and high‐fructose diet groups all presented higher plasma glucose concentrations than did the control group. The high‐fat diet group showed higher body weight, higher relative liver weight, a higher plasma cholesterol concentration and higher amylase activity than did the other groups, whereas the high‐fructose diet group showed higher fasting insulin and triglyceride concentrations. As for adipose tissue, the high‐fat diet group presented an amount that was higher than that of the high‐fructose and control groups, but the plasma leptin concentration of the high‐fructose group was higher than that of the control group.Conclusions:  It can be concluded from the above‐mentioned experimental results that a high‐fructose diet can cause hyperinsulinaemia, while a high‐fat diet can result in impaired pancreatic function of insulin secretion and glucose intolerance, indicating that high‐fructose diet and a high‐fat diet may exert divergent effects on glucose metabolism in rats.
The metabolic syndrome as a link between smoking and cardiovascular disease
Authors: Dzien A. , Dzien‐Bischinger C. , Hoppichler F. , Lechleitner M. 
Published: January 2004

Objective:  Smoking is associated with a significant increase in the cardiovascular risk. The possible relationship of smoking with insulin resistance might further enhance the cardiovascular risk of the patients and is therefore of great clinical interest.Design, Setting and Subjects:  We have retrospectively evaluated data of 3804 non‐diabetic men attending a medical outdoor clinic. Clinical [body mass index (BMI), percentage of body fat, waist‐to‐hip ratio] and laboratory results were compared between smokers (n = 124) and non‐smokers (n = 1915) without cardiovascular disease, as well as between smokers (n = 759) and non‐smokers (n = 1006) with cardiovascular disease.Results:  Smokers without clinically manifest cardiovascular disease revealed significantly higher fasting glucose (5.8 ± 0.6 mmol/l) and triglyceride levels (1.8 ± 0.9 mmol/l) than non‐smokers (fasting glucose: 5.1 ± 0.7 mmol/l, p < 0.010; triglycerides: 1.5 ± 0.8 mmol/l, p < 0.030). The adverse metabolic profile of smokers was even more pronounced in patients with cardiovascular disease. An age‐matched analysis of smokers could demonstrate that cardiovascular patients revealed higher BMI values (27.3 ± 2.4 kg/m2) and a higher percentage of body fat (25.5 ± 5.5%) than those without cardiovascular disease (BMI: 25.7 ± 2.2 kg/m2, p < 0.010; percentage of body fat: 23.0 ± 5.5%, p < 0.030).Conclusion:  In men with and without clinically manifest cardiovasular disease, smoking was associated with a metabolic profile indicating a higher degree of insulin resistance.
The effects of oral anti‐hyperglycaemic medications on serum lipid profiles in patients with type 2 diabetes
Authors: Buse J. B. , Tan M. H. , Prince M. J. , Erickson P. P. 
Published: January 2004

Aim:  Patients with type 2 diabetes often have dyslipidaemia, putting them at risk of cardiovascular disease, and are frequently treated with oral anti‐hyperglycaemic medications (OAMs). This review compares the effects of OAMs on serum lipids [total cholesterol (TC), low‐density lipoprotein cholesterol (LDL‐C), high‐density lipoprotein cholesterol (HDL‐C), triglycerides (TGs) and free fatty acids (FFAs)] in patients with type 2 diabetes.Methods:  medline was searched for entries indexed from January 1966 to November 2002; search terms included the names of OAMs and serum lipids, limited to English language and human subjects. We selected clinical studies in type 2 diabetes of OAM monotherapy that included serum lipid data, treated all patients in a treatment group with the same drug, used therapeutic OAM doses not higher than the maximum recommended in the USA, compared therapy with baseline or placebo and specified statistical tests used. One unblinded investigator selected studies for inclusion. Data reported include number of patients, study length, OAM dose, serum lipid data at baseline and endpoint, p‐values and statistical tests.Results:  Data on the serum lipid effects of sulphonylureas, repaglinide, nateglinide and miglitol were inconclusive. Acarbose increased HDL‐C and decreased LDL‐C and voglibose reduced TC. Metformin at higher doses reduced TC; data on its effects on other lipids were inconclusive. Rosiglitazone increased LDL‐C, HDL‐C and TC and reduced FFAs but had no effect on TGs. Pioglitazone increased HDL‐C and reduced TGs and FFAs but did not affect LDL‐C or TC.Conclusions:  Lipid changes as a result of improved glycaemic control are not uniform findings associated with anti‐diabetic therapy. Only metformin, acarbose, voglibose, rosiglitazone and pioglitazone had significant effects on the lipid profile. These effects should be considered when selecting OAMs for patients with type 2 diabetes.
Prevention of weight gain in type 2 diabetes requiring insulin treatment
Authors: De Boer H. , Jansen M. , Koerts J. , Verschoor L. 
Published: January 2004

Background: Patients with type 2 diabetes who are failing on oral agents will generally gain a large amount of body fat when switched to insulin treatment. This adverse effect may be related to chronic hyperinsulinism induced by long‐acting insulin compounds.Aim: To test the concept that regain of glycaemic control can be achieved without causing weight gain, using a regimen free of long‐acting insulin.Methods: In a 3‐month open‐label pilot study including 25 patients with moderate overweight and secondary failure, we investigated whether nocturnal glycaemic control could be achieved with glimepiride administered at 20:00 hours. The starting dose was 1–2 mg, with subsequent titration up to a maximum of 6 mg. Rapid‐acting insulin analogues were used three times daily to regain postprandial glucose control.Results: Glycaemic control at 3 months was established with glimepiride in a dose of 4.4 ± 0.3 mg/day (mean ± standard error of the mean), and a total daily insulin dose of 24.1 ± 2.6 IU. Fasting glucose levels decreased from 12.7 ± 0.6 mmol/l to 8.1 ± 0.3 mmol/l (p < 0.001), and target levels were reached in 14 of 25 patients (56%). Mean HbA1c decreased from 10.5 ± 0.4 to 7.7 ± 0.2% (p < 0.001). Symptomatic nocturnal hypoglycaemia was not reported. Body weight did not change (85.7 ± 3.6 kg vs. 85.7 ± 3.3 kg, p = 0.99).Conclusion: The data suggest that this new approach may be useful in about 50% of type 2 diabetes patients presenting with failure on maximal oral treatment.
Time‐specific intraocular pressure curves in Rhesus macaques (Macaca mulatta) with laser‐induced ocular hypertension
Authors: Ollivier F. J. , Brooks D. E. , Kallberg M. E. , Sapp H. L. , Komáromy A. M. , Stevens G. R. , Dawson W. W. , Sherwood M. B. , Lambrou G. N. 
Published: January 2004

AbstractObjective To detect and categorize time‐specific variations in daytime intraocular pressure (IOP) found in Rhesus monkeys with laser‐induced ocular hypertension.Procedures Ten male monkeys with argon laser‐induced ocular hypertension in one eye were anesthetized with ketamine hydrochloride, and the IOP measured in both eyes at 7 a.m., 7.30 a.m., and then hourly until 1 p.m. with a Tonopen™ XL applanation tonometer. Intraocular pressure time profiles for both eyes in each animal were developed. The means ± SD of the IOPs for both eyes were calculated for the whole 6‐h study period, and the values compared statistically. The difference between the lasered eye mean IOP standard deviation and the normal eye mean IOP standard deviation for each animal during the 6‐h follow‐up was also calculated and compared.Results Mean IOP (± SD) in the glaucoma and normal eyes for the 10 animals during the 6‐h study was 32.6 ± 2.5 and 14.9 ± 2.5 mmHg, respectively. The IOP was significantly higher in the experimental eye than in the normal eye (P = 0.0008). The mean IOP in the lasered eye did not significantly change during the study period, whereas a slight but significant increase in IOP of the normal eye over the study period was recorded (P = 0.003). The variance in IOP in the hypertensive eyes was considerably greater than that in the untreated control eyes. From 7 a.m. to 1 p.m. the IOP declined in five eyes and increased in the other five eyes with laser‐induced ocular hypertension.Conclusions The time‐specific IOP variation pattern in the daytime in the laser treated eyes is significantly greater than the variation in the normotensive eyes. This shows that in order to detect statistical differences between IOP variations induced by an IOP‐reducing drug, and the exaggerated spontaneous IOP variations present in the laser‐induced hypertensive eye, sufficient animals should be included in any study. Understanding the time‐specific IOP variation present in a group of monkeys with laser‐induced ocular hypertension is essential prior to using the model for the evaluation of IOP‐reducing drugs.
Prevalence of canine cataract: preliminary results of a cross‐sectional study
Authors: Williams D. L. , Heath M. F. , Wallis C. 
Published: January 2004

AbstractObjective  In this study 2000 dogs were examined ophthalmoscopically to determine presence of cataract.Materials and methods  The dogs examined were predominantly from veterinary hospital populations but also from the Waltham Center For Pet Nutrition, rehoming charities and breeding kennels. Prevalence of cataract was thus determined for different age groups (year cohorts). The age at which prevalence of cataract was 50% (C50) was determined indirectly from a fitted prevalence curve.Results  The mean ± standard deviation of C50 for all dogs in the study was 9.4 ± 3.3 years. All dogs over 13.5 years were affected by some degree of lens opacity. C50 was determined for animals of different genders and different breeds. For dogs of six breeds sufficient data were available for calculation of breed‐specific C50. In these dogs C50 was positively correlated with longevity with a least squares correlation coefficient of 0.74.Conclusion  The study yields novel findings regarding the prevalence and incidence of cataract in the dog and forms the basis for considerable further work on the epidemiology and pathophysiology of age‐related cataract in the dog.
Comparative morphology of the tapetum lucidum (among selected species)
Authors: Ollivier F. J. , Samuelson D. A. , Brooks D. E. , Lewis P. A. , Kallberg M. E. , Komáromy A. M. 
Published: January 2004

AbstractObjectives  The phenomenon of ‘eye‐shine’ is seen in a variety of animal species, and is generally thought to be related to the presence of an intraocular reflecting structure, the tapetum lucidum. The tapetum lucidum is a biologic reflector system that is a common feature in the eyes of vertebrates. It normally functions to provide the light‐sensitive retinal cells with a second opportunity for photon‐photoreceptor stimulation, thereby enhancing visual sensitivity at low light levels. The tapetum lucidum is presented here according to a classification based on the location, as well as the composition, of this reflective layer. Finally, the physical and chemical properties, as well as the origins of the different tapeta lucida, are discussed and compared.Methods  The anatomic and biochemical aspects of the tapetum lucidum in various vertebrates are examined. Morphologic observations were made from paraffin and plastic embedded specimens. Specimens were treated with traditional stains and observed by light and transmission electron microscopy.Results  Some species (primates, squirrels, birds, red kangaroo and pig) do not have this structure and they usually are diurnal animals. In vertebrates, the tapetum lucidum exhibits diverse structure, organization and composition. Therefore, the retinal tapetum (teleosts, crocodilians, marsupials, fruit bat), the choroidal guanine tapetum (elasmobranchs), the choroidal tapetum cellulosum (carnivores, rodents, cetacea), and the choroidal tapetum fibrosum (cow, sheep, goat, horse) are described.Conclusions  The tapetum lucidum represents a remarkable example of neural cell and tissue specialization as an adaptation to a dim light environment and, despite these differences, all tapetal variants act to increase retinal sensitivity by reflecting light back through the photoreceptor layer. These variations regarding both its location and structure, as well as the choice of reflective material, may represent selective visual adaptations associated with their feeding behavior, in response to the use of specific wavelengths and amount of reflectance required.