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Biomedical subjects

A Ertan

Publications and source records attributed to A Ertan.

At least 19 recordsLinked to original sources
PubMed2005

Comparison of additional intraocular pressure-lowering effects of latanoprost vs brimonidine in primary open-angle glaucoma patients with intraocular pressure uncontrolled by timolol-dorzolamide combination.

PURPOSE: To compare the additive intraocular pressure (IOP)-lowering effects of latanoprost 0.005% and brimonidine 0.2% in primary open-angle glaucoma (POAG) patients uncontrolled on fixed combination of timolol 0.5% and dorzolamide 2% (TDC) alone. METHODS: In all, 80 eyes of 80 POAG patients with IOP inadequately controlled by TDC were randomly assigned to receive either latanoprost 0.005% or brimonidine 0.2%. IOP measurements were recorded at 1000 (peak effect) and 1600 (trough effect) on day 0 (baseline) and at 1 and 3 months. At each stage and time point, the mean IOP reductions from baseline were evaluated for both groups, and success rates (minimum 15% reduction) were determined. RESULTS: At baseline, the mean peak/trough IOPs with TDC were 20.2/21.6 and 19.9/21.4 mmHg in latanoprost and brimonidine groups, respectively. Latanoprost+TDC reduced the mean peak/trough IOP by 4.4/3.4 and 5.2/3.5 mmHg at 1 and 3 months. The corresponding values for brimonidine+TDC were 3.9/2.9 and 4.6/2.9 mmHg. Each of these results represented a significant reduction from baseline (P<0.001 for all); however, the groups' peak/trough reductions from baseline did not differ at any time point (P>0.05 for all). With the latanoprost+TDC combination, the peak/trough success rates at 1 and 3 months were 76.3%/42.1% and 77.1%/40%. The corresponding values with the brimonidine+TDC combination were 71.8%/41% and 77.7%/41.7%. There were no significant differences in the groups' success rates at any time point (P>0.05 for all). CONCLUSION: Addition of latanoprost 0.005% or brimonidine 0.2% to TDC reduces peak/trough IOPs significantly and the effects of these combinations are comparable.

Adult↗
PubMed2003

Detection of oxidative DNA damage in oesophageal biopsies of patients with reflux symptoms and normal pH monitoring.

BACKGROUND: Gastro-oesophageal reflux has been shown to induce oxidative DNA damage. AIM: To determine whether oxidative DNA damage, detected in oesophageal biopsies by simple immunohistochemical staining, correlates with gastro-oesophageal reflux disease as determined by pH monitoring. METHODS: The study included 47 patients with reflux symptoms who had oesophageal biopsy and 24-h pH monitoring studies performed within 3 months of each other with no variation in treatment in the time between the two procedures. Sections of formalin-fixed and paraffin-embedded oesophageal biopsies were stained for 8-hydroxy-2'-deoxyguanosine using the standard immunoperoxidase method. Positive nuclear immunoreactivity was considered to indicate oxidative DNA damage. RESULTS: Seven (33%) of the 21 cases with normal 24-h pH monitoring results were negative for oxidative DNA damage, compared with only two (8%) of the 26 cases with abnormal 24-h pH results (P=0.058, two-sided Fisher's exact test). Five of the patients with normal 24-h pH results had oesophageal biopsies performed within 24 h of the monitoring procedure and, of these, four (80%) were positive for oxidative DNA damage, including a case in which both biopsy and 24-h pH monitoring were performed on the same day whilst the patient was on proton pump inhibitor therapy. All cases with normal 24-h pH results and positive oxidative DNA damage showed features of reflux on routine morphological evaluation. CONCLUSIONS: Oxidative DNA damage can occur in the absence of acid reflux and despite adequate antisecretory therapy. This may indicate that other agents, such as bile, can induce oxidative DNA damage in an acid-suppressed environment. The significant discordance between oxidative DNA damage and 24-h pH results makes the determination of oxidative DNA damage a poor surrogate marker for 24-h pH monitoring.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2002

Incidence and survival trends of esophageal carcinoma in the United States: racial and gender differences by histological type.

BACKGROUND: The incidence of esophageal adenocarcinoma in White males has been reported to be increasing. The aims of this study were to determine: 1) the incidence trends of esophageal carcinoma in the United States with an emphasis on histologic type, sex, and ethnicity, 2) whether the reported increase in stage IV tumors can be confirmed, and 3) survival trends and factors affecting survival. METHODS: Data from the SEER program of the National Cancer Institute with submission dates 1973-98 were used. Data on Hispanics were available for analysis only for the years 1992-98. Statistical analysis was performed utilizing SEER*Stat and SAS statistical software packages. RESULTS: The incidence of adenocarcinoma in White males is still rising (7.8%/year, P < 0.0001); however, the same trend was observed for White females (6.48%/year; P < 0.0001). Hispanic males (3.91 %/year; P < 0.02), and Hispanic females (9.4%/ year; P < 0.04). The incidence of squamous cell carcinoma has been steadily declining in White males and females and in Black females since 1973, with the incidence showing a dramatic and significant decline in Black males beginning in 1992 (8.53%/year; P = 0.0009). Stage 4 carcinoma is declining in incidence. Survival of patients with esophageal carcinomas has been improving. In a Cox multivariate model, independent prognostic factors in esophageal carcinoma included tumor stage, tumor type, gender, race, age at diagnosis, and year of diagnosis. CONCLUSIONS: 1) The incidence of adenocarcinoma continues to rise in White males and females, but also in Hispanics, while squamous cell carcinoma is declining; 2) the incidence of stage 4 carcinomas has been declining, and 3) survival has been steadily improving, independently of all other risk factors.

Adenocarcinoma↗
PubMed2001

Effect of different acid treatments on a porcelain surface.

The objective of this study was to determine the effect of selected surface treatments on the surface texture of a feldspathic porcelain. The three different etchant treatments were, acidulated phosphate fluoride (APF) applied for 10 min and hydrofluoric acid (HF) applied for 1 and 4 min. After acid treatment, half of the specimens from each group were cleansed with water and others were subjected to ultrasonic cleaning and then dried. Half of the specimens cleansed with two different methods were treated with silane. Scanning electron microscopy (SEM) and energy dispersive spectroscopy (EDS) were used to characterize the effects of such treatments. Etching with APF displays shallow patterns. Etching for 1 min with HF displays deep channels, pores and precipitates on the surface and as the etching time increased these channels were replaced by larger channels. EDS analyses show that the crystalline precipitates on the etched surfaces, which were not readily soluble in water, were the reaction products of Na, K, Ca, Al, etc. HF displayed a more roughened surface than the APF gel. However, the precipitates remain on the surface after acid application, they can only be removed by ultrasonic cleaning and cannot be removed by rinsing.

Acid Etching, Dental↗
PubMed2000

Fas ligand expression in esophageal carcinomas and their lymph node metastases.

BACKGROUND: Although esophageal adenocarcinomas (EADCA) have been shown to have substantially reduced or absent Fas expression, the status of Fas ligand (FasL) in these tumors, especially adenocarcinomas, is largely unknown. METHODS: Using immunohistochemistry, the authors investigated FasL expression in sections of formalin fixed, paraffin embedded tissue from 13 EADCA. They also studied sections of 15 esophageal squamous cell carcinomas (ESCCA) and of lymph node metastases from 7 EADCA and 4 ESCCA. The percentage of FasL positive cells in each tumor was recorded. FasL expression in EADCA was compared with that in ESCCA and with lymph node status. Statistical analysis was performed using the Fisher exact test. RESULTS: No specific staining pattern was seen in adenocarcinomas. In ESCCA, FasL was often located in the cells at the periphery of tumor nests. All (100%) of EADCA showed FasL expression in greater than 25% of the cancer cells, and all were associated with lymph node metastasis. Fifty-three percent of ESCCA showed FasL expression in greater than 25% of the cancer cells and 33% had lymph node metastasis. Expression of FasL in greater than 25% of tumor cells was associated with a significantly higher incidence of lymph node metastasis (P=0.0001). All lymph node metastases from esophageal carcinomas showed FasL immunoreactivity in greater than 50% of the metastatic tumor cells. CONCLUSIONS: FasL expression in greater than 25% of cancer cells correlates with a high incidence of lymph node metastasis in esophageal carcinomas. All cancer metastases in lymph nodes express FasL in >50% of the cells. These findings indicate that FasL plays an important role in the immune evasion and metastasis of esophageal carcinomas.

Adenocarcinoma↗
PubMed2000

Barrett's esophagus.

Barrett's esophagus occurs more frequently than previously anticipated. Detection of Barrett's esophagus is by endoscopic biopsy in which normal squamous epithelium of the esophagus is replaced by a specialized columnar epithelium of any length. Patients with more than five years of gastroesophageal reflux symptoms, particularly those 50 years of age or older, should have upper endoscopy to detect Barrett's esophagus. With recognition of Barrett's esophagus as a premalignant lesion, the crucial issue is surveillance for detection of dysplasia. Although the natural history of dysplasia is incompletely defined, it is clear that patients with dysplasia have a higher risk for adenocarcinoma than those without dysplasia. Dysplasia is not the ideal marker for selecting patients at high risk for adenocarcinoma, however; recent studies have shown that p53 protein accumulation appears to be earlier and more specific/sensitive marker of malignant potential in Barrett's esophagus. Management of Barrett's esophagus often involves a multidisciplinary evaluation and its current status is reviewed.

Barrett Esophagus↗
PubMed2000

Decreased expression of Fas (CD95/APO1) associated with goblet cell metaplasia in Barrett's esophagus.

Fas ligand (FasL) has been shown to induce apoptosis in cells expressing its receptor Fas. We have recently shown that Fas ligand is overexpressed in all cases of Barrett's metaplasia (BM) with dysplasia and esophageal adenocarcinomas, and in a few cases of BM negative with dysplasia. The aim of this work was to determine the status of Fas expression in BM with and without dysplasia or carcinoma. Formalin-fixed and paraffin-embedded tissue sections from esophageal biopsies and esophagectomy specimens with BM, with and without dysplasia and carcinoma, were immunostained for Fas and FasL using the immunoperoxidase technique. The percentage of positive cells in each case was evaluated and compared with the degree of dysplasia. When Fas expression was assessed in glands with goblet cell metaplasia, Fas immunoreactivity was either undetected or present in less than 10% of the cells in 85% of the cases, and only 1 (4%) of the 28 cases examined showed Fas immunoreactivity in more than 25% of the cells. When we compared Fas expression in goblet cell-containing glands with glands of gastric cardia phenotype, we found that in the 26 cases of BM with or without dysplasia Fas was completely undetectable in goblet cell-containing glands in 15 (58%) of the cases but was undetectable in only 3 (12%) of the glands with gastric cardia phenotype (P = .002). Fas is usually undetectable or is expressed at a low level in BM with or without dysplasia or carcinoma. Fas expression in goblet cell-containing glands is less frequent than in glands with gastric cardia phenotype in the same specimens. BM with dysplasia or carcinoma overexpress FasL, so decreased Fas expression may protect BM with dysplasia and carcinoma from self-destruction while allowing them to evade immune surveillance.

Adenocarcinoma↗
PubMed2000

Long-term results after endoscopic pancreatic stent placement without pancreatic papillotomy in acute recurrent pancreatitis due to pancreas divisum.

BACKGROUND: There is no consensus regarding the appropriate endoscopic treatment for acute recurrent pancreatitis associated with pancreas divisum. Endoscopic papillotomy of the minor papilla appears to yield improvement in most cases, but optimal depth and height have not been defined. METHODS: Endoscopic pancreatic stent placement after minor papilla dilation was performed in 25 patients with pancreas divisum and acute recurrent pancreatitis. Five patients drank alcohol daily; no other cause of pancreatitis was detected. After adequate dilation, a transpapillary pancreatic stent (5F to 7F, 5 to 7 cm) was inserted over a guidewire into the dorsal duct. The stent was replaced twice, after 2- to 3-month intervals. RESULTS: While stents were in place, no further episodes of pancreatitis occurred in 23 patients. However, dorsal duct changes of unknown clinical significance were seen in 21 cases. At mean follow-up of 24 months (range 3 to 70 months) after stent removal, 19 (76%) remained symptom free. Pancreatitis recurred in 6 patients during the follow-up after final stent removal; no further pancreatitis occurred in 2 of 3 who underwent repeat stent insertion. Complications in the series were minimal. CONCLUSION: Endoscopic pancreatic stent placement after minor papilla and dorsal duct dilation, without endoscopic papillotomy, provided safe and effective endoscopic treatment in patients with pancreas divisum and acute recurrent pancreatitis.

Acute Disease↗
PubMed1997

p53 Protein accumulation is a specific marker of malignant potential in Barrett's metaplasia.

Our aim was to determine the sensitivity and specificity of p53 accumulation as a marker of malignant potential in Barrett's metaplasia (BM). One hundred eighty biopsies from 61 patients with BM were evaluated for p53 accumulation by immunohistochemistry. Of 25 patients with LGD, 9 had p53-positive biopsies, and of these 5 (56%) developed HGD/CA, whereas 16 had p53-negative biopsies and none (0%) developed HGD/CA after similar follow-up times (P = 0.0108). As a marker of malignant potential in BM, p53 accumulation has a sensitivity of 100%, specificity of 93%, and a predictive value of a positive test of 0.56, compared to sensitivity of 100%, specificity of 64%, and predictive value of a positive test of 0.2 for a histologic diagnosis of LGD. We conclude that: (1) p53 accumulation is more specific and has better predictive value for subsequent development of HGD/CA than histologic diagnosis of LGD. (2) Patients with LGD and p53-positive biopsies are more likely to develop HGD/CA; therefore, they should be followed up more closely than those with LGD and p53-negative biopsies.

Barrett Esophagus↗
PubMed1997

Human erythrocyte glucose transporter (Glut1) is immunohistochemically detected as a late event during malignant progression in Barrett's metaplasia.

We have previously demonstrated that the human erythrocyte glucose transporter (Glut1) is expressed in adenocarcinoma arising in Barrett's metaplasia (BM). We have also shown that Glut1 is expressed as a late event during colorectal carcinogenesis. The aim of this work was to determine the chronology of Glut1 expression during the neoplastic progression in Barrett's metaplasia. Formalin-fixed, paraffin-embedded tissue sections of 251 biopsies from 97 patients with BM were immunostained with the anti-Glut1 antibody MYM, after microwave-aided antigen retrieval, using the standard avidin-biotin complex immunoperoxidase technique. Dysplasia was graded as negative (ND), low grade (LGD)/indefinite or high grade (HGD). None of the 181 biopsies with ND (0%) or 51 biopsies with LGD (0%) showed Glut1 immunoreactivity. More importantly, although 0 of 6 biopsies with HGD (0%) expressed Glut1, 9 of 13 biopsies with adenocarcinoma (69%) were Glut1 positive (P = 0.0108, Fisher's exact test). Our results indicate that Glut1 is expressed as a late event during the neoplastic progression in BM. Prospective studies are needed to determine the clinical utility of Glut1 immunoreactivity as a marker of carcinoma in patients with BM.

Adenocarcinoma↗
PubMed1996

Synthesis and pharmacology of the enantiomers of UH301: opposing interactions with 5-HT1A receptors.

The (S)-enantiomer of 5-fluoro-8-hydroxy-2-(dipropylamino) tetralin [(S)-2a; (S)-UH301] was the first reported 5-HT1A receptor antagonist. We now give a full account on the synthetic effort leading to the preparation of the racemate and the enantiomers of 2a. The crystal and molecular structure of 2a. HBr has been determined by X-ray diffraction and the absolute configuration has been deduced using statistical tests of the crystallographic R values. The unit cell is tetragonal (P4(1)2(1)2) with a = b = 13.2235(2), c = 39.560(1) A and contains two crystallographically independent molecules in each asymmetric unit. The two solid state conformers differ in the conformation of the N-propyl groups. The pharmacological characterization of the enantiomers was done by use of in vivo biochemical and behavioural assays in rats. The (R)-enantiomer of 2a is a 5-HT1A receptor agonist of low potency while (S)-2a does not exhibit any agonist properties at 5-HT1A receptors. As a consequence of the opposing effects of the enantiomers, the racemate, rac-2a, does not produce any clear-cut effects in rats. The reduced efficacy of (S)-2a as compared to the well known 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino) tetralin (1;8-OH-DPAT) may be due to the fluoro-substituent induced negative potential of the aromatic ring.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Alpha 1-antitrypsin deficiency and chronic pancreatitis.

Alpha 1-antitrypsin deficiency is a genetic disorder commonly associated with pulmonary and hepatic injury. Low serum levels of this glycoprotein result in an imbalance between circulating protease and protease inhibitors, which is thought to play a role in the development of emphysema. In recent studies, a protease-to-protease inhibitor imbalance in patients with alpha 1-antitrypsin deficiency was thought to be a mechanism contributing to the development of chronic pancreatitis. The heterozygous phenotype and low levels of this glycoprotein have been reported to occur more frequently in patients with chronic pancreatitis than in healthy controls. We report a patient with Pi-SS phenotype alpha 1-antitrypsin deficiency and chronic pancreatitis complicated by recurrent pancreatic pseudocysts and chronic abdominal pain. Our case supports the association between chronic pancreatitis and alpha 1-antitrypsin deficiency. Furthermore, this case provides support for the use of pancreatic stent drainage in the management of intractable abdominal pain in patients with chronic pancreatitis and a dominant stricture.

Abdominal Pain↗
PubMed1995

Effect of PACAP on gastric acid secretion in rats.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a new VIP-like brain-gut peptide. Its effects on the motility and secretory functions of the gastrointestinal system have been shown in previous studies. In this study we investigated the effect of intravenous PACAP on gastric acid secretion in conscious pylorus-ligated rats and in gastric fistula rats. PACAP showed significant inhibitory effects on pentagastrin- and histamine-stimulated gastric acid secretion, but no effect on basal or carbachol-stimulated secretion in pylorus-ligated rats. It did show dose-related inhibitory effects both on basal gastric acid secretion and on secretion stimulated by pentagastrin, histamine, or carbachol in gastric fistula rats. PACAP did not alter serum gastrin levels. Inhibition of prostaglandin synthesis with indomethacin and immunoneutralization of somatostatin with anti-somatostatin serum did not prevent the inhibitory effect of PACAP on gastric acid secretion in pylorus-ligated rats. We conclude that PACAP most likely has a direct effect on parietal cells and that this effect may be mediated, at least partially, by inhibition of the action of histamine on parietal cells.

Adenylyl Cyclases↗
PubMed1995

Esophageal adenocarcinoma associated with Barrett's esophagus: long-term management with laser ablation.

We report the use of neodymium:yttrium-aluminum-garnet (Nd:YAG) laser ablation to treat high-grade dysplasia and intramucosal esophageal adenocarcinoma associated with Barrett's esophagus in a patient who refused surgery. Throughout laser therapy, the patient received omeprazole 40 mg/day. After 1 1/2 yr, five laser treatments totaling 22,055 J given over a period of 13 months achieved squamous reepithelialization and absence of malignant transformation in the first area in which carcinoma was diagnosed. Squamous reepithelialization was maintained 1 yr later, confirming recent reports that photoablation plus omeprazole can achieve regression of Barrett's esophagus. During the last year of follow-up, a second contiguous area discovered to contain carcinoma was treated three times by photoablation, with a total of 13,164 J; biopsy showed only low-grade dysplasia in this area after two laser treatments totaling 8,108 J. No complications were seen during or after any of the laser sessions, and the patient remained asymptomatic 2 1/2 yr after the first photoablation and 3 yr after presentation.

Adenocarcinoma↗
PubMed1993

Galanin: structure-dependent effect on pancreatic amylase secretion and jejunal strip contraction.

Rat and porcine galanin and their fragments inhibited cholecystokinin-8 (CCK-8)-stimulated amylase secretion with the following activities: rat galanin-(1-29) = porcine galanin-(1-29) = galanin-(1-15) = rat galanin-(3-29) > rat galanin-(2-29) = porcine galanin-(2-29) > galanin-(1-10). Fragments of rat galanin-(9-29) and N alpha-acetyl-galanin-(9-29) were able to inhibit CCK-8-stimulated pancreatic amylase secretion but only at higher dose levels. Porcine galanin-(15-29) and rat galanin-(21-29) were unable to produce significant inhibition. Rat and porcine galanin-(1-29), galanin-(1-15) and rat N alpha-acetyl-galanin-(9-29) also inhibited basal pancreatic amylase secretion. In the rat jejunal strip contraction model, rat galanin-(1-29) and porcine galanin-(1-29) have similar potencies. Galanin-(1-15) and galanin-(1-10) stimulate rat jejunal strip contraction with decreasing potencies. Elimination of Gly1 from the N-terminus of both rat and porcine galanin had no significant effect either on pancreatic amylase secretion or on jejunal strip contraction. The rat galanin-(3-29) and (9-29) are not active in the stimulation of rat jejunal strip contraction. Acetylation of porcine galanin-(9-29) created a peptide that was a powerful stimulator of rat jejunal strip contraction. The present data indicate that N-terminal rat galanin amino acid residues are crucial for rat jejunal strip contraction but are not required for inhibition of pancreatic amylase. These results suggest that the galanin amino acid sequence contains several specific domains, which can be recognized by specific galanin receptor subsets.

Amino Acid Sequence↗