Biomedical subjects

K Cinar

Publications and source records attributed to K Cinar.

10 recordsLinked to original sources

PubMed2006

The diagnostic value of on-site cytopathological evaluation and cell block preparation in fine-needle aspiration cytology of liver masses.

OBJECTIVE: The aims of this study were to evaluate the typing accuracy of conventional smear (CS), cell block (CB) preparations and combined use of both procedures (CS + CB) for the diagnosis of hepatic malignancies and to determine whether immediate on-site cytopathological evaluation improves the diagnostic yield of liver fine-needle aspiration cytology (FNAC). METHODS: Ultrasound-guided FNABs were performed on 323 consecutive cases with liver masses between December 2002 and December 2004. Histologically and/or clinically correlated 167 cases were included in the study. Preliminary FNAB results, results of CS, CB, and combined use of CS and CB were compared regarding diagnostic sensitivity, specificity, and accuracy for the diagnosis of malignancy. Subtyping accuracies of different methods were also compared. RESULTS: The sensitivity of on-site cytopathological examination and CS were both 92.8%. The sensitivity of CS + CB was slightly better than that of CB (93.5% versus 84.8%). Specificity of all procedures was achieved 100%. Diagnostic accuracy of on-site cytopathological evaluation, CS, CB, and CS + CB were 93.9%, 93.9%, 87.2%, and 94.5%, respectively. A specific subtype diagnosis of malignant tumours could be rendered accurately on the basis of preliminary diagnosis in 71%, CS in 75.4%, CB in 78.3% and combined approach in 92% of cases. In terms of typing accuracy, 87.5% of HCCs, 93.2% of adenocarcinomas, 92.3% of neuroendocrine carcinomas, 100% of lymphomas and 100% of other malignant tumours were correctly subclassified in the final cytopathological diagnosis. The agreement between preliminary diagnosis and final cytopathological diagnosis was 77.2%. CONCLUSION: With use of on-site cytopathological evaluation and combined use of CS and CB, the diagnostic accuracy of liver tumours approaches 100% and also significantly improve diagnostic and subtyping accuracy of liver malignancies.

Adolescent↗

PubMed2006

Histological and histochemical characterization of the mucosa of the digestive tract in flower fish (Pseudophoxinus antalyae).

The wall of the digestive tract is composed of the tunica mucosa, tunica muscularis and tunica serosa. Lamina-submucosa separation or any glands were not observed in tunica mucosa. Goblet cells were determined to constitute a much larger reserve at digestive tract mucosa. Histochemical analysis of the intestine of flower fish (Pseudophoxinus antalyae) showed that gastrointestinal mucous content included sulphate-esters and/or carboxylic [Alcian blue (AB) 0.06+], glycogene and/or oxidable dioles [periodic acid/Schiff+ (PAS+)], neutral or acid-rich (PAS/AB pH 2.5+), sialic acid residues (KOH/PAS) and strong acid sulphated [Aldehyde fuchsin+ (AF+)] glycoproteins (GPs). Except these mucosubstances to lower densities, densely sulphate (AB pH 2.5+), O-sulphate esters (AB pH 1+) strong and weak sulphated (AB 0.3 M+), GPs were also determined.

Animals↗

PubMed2005

The distribution of external taste buds in flower fish (Pseudophoxinus antalyae).

Purpose of this study was to determine the distribution of external taste buds of flower fish (Pseudophoxinus antalyae) on different body locations (lip, lateral, ventral and dorsal areas, dorsal-pelvic-pectoral-anal fins). In this species, it was found that the density of taste buds was greater on lip epithelium than that of lateral (between pectoral-anal, anal-caudal fins), ventral (between pelvic and anal fins) and dorsal (close to the head) locations. It was observed that the shape of taste bud changed depending upon the epithelium thickness and it was found that some of these structures protruded towards to the exterior of epithelium.

Animals↗

PubMed2004

Ligand-induced expression of peroxisome proliferator-activated receptor alpha and activation of fatty acid oxidation enzymes in fatty liver.

BACKGROUND: Peroxisome proliferator-activated receptor alpha (PPARalpha) regulates lipid metabolism upon activation by ligands. Peroxisome proliferator-activated receptor alpha may play a role in the pathogenesis of fatty liver disease. The aim of this study was to assess the PPARalpha expression pattern and mitochondrial/peroxisomal enzyme activities in response to high fat diet (HFD) and clofibrate, a well known PPARalpha ligand. MATERIALS AND METHODS: Four groups of Wistar-Albino rats were included: (1) rats fed a control diet (CD) for 6 weeks, (2) rats fed CD (6 weeks) plus clofibrate (last 2 weeks), (3) rats fed HFD for 6 weeks, and (4) rats fed HFD (6 weeks) plus clofibrate (last 2 weeks). Peroxisome proliferator-activated receptor alpha expression was evaluated by immunohistochemistry. Fatty acid beta-oxidation (peroxisomal-acyl-CoA-oxidase and mitochondrial-acyl-CoA-dehydrogenase) and catalase enzyme activities, and malondialdehyde and glutathion levels were measured spectrophotometrically in liver tissues. RESULTS: All animals were fed HFD but only 2/12 animals were fed HFD plus clofibrate-developed fatty liver. Both HFD and clofibrate induced PPARalpha expression, clofibrate induction being more prominent than HFD. Clofibrate plus HFD did not further increase PPARalpha expression. Activities of peroxisomal-acyl-CoA-oxidase and mitochondrial-acyl-CoA-dehydrogenase enzymes were not induced by HFD alone. Clofibrate increased the activity of these enzymes in both CD- and HFD-fed animals. However, an increase of acyl-CoA-oxidase activity was blunted in rats fed HFD. Catalase activity and malondialdehyde levels were increased but glutathion levels were unchanged in rats fed HFD plus clofibrate. CONCLUSIONS: Clofibrate was a more potent inducer of PPARalpha expression than HFD in our rat fatty liver model. The finding of blunted peroxisomal enzyme response to clofibrate in fatty livers suggests that alterations in postreceptor events may exist and further contribute to liver steatosis. Clofibrate seems to stabilize glutathion content and this might contribute to the prevention of liver steatosis.

Acyl-CoA Dehydrogenase↗

PubMed2003

YSDD: a novel mutation in HBV DNA polymerase confers clinical resistance to lamivudine.

The emergence of drug-resistant virus in hepatitis B virus (HBV) patients treated with lamivudine is well documented. In this study, we determined the mutations occurring in the tyrosine-methionine-aspartate-aspartate (YMDD) amino acid motif of the HBV DNA polymerase gene, as well as upstream and downstream of this region, in patients with breakthrough virus during lamivudine therapy. Thirty-one Turkish patients (20 patients HBeAg positive, 11 patients HBeAg negative and anti-HBe positive) with chronic HBV infection who completed at least 104 weeks of lamivudine treatment were investigated. All patients received lamivudine, (150 mg/day), for 104 weeks, with or without 4 months of interferon (IFN) combination. HBV-specific sequences were amplified by polymerase chain reaction (PCR) from sera of patients with breakthrough virus, and the PCR products were directly analysed by sequencing. Breakthrough virus was detected in seven of the 31 patients (22.6%) between 9 and 18 months of therapy. Of the seven patients, six were HBeAg positive at baseline, and four had a double mutation consisting of rtM204V and rtL180M, while two had an rtM204I change. In one patient, two base substitutions at rt204 (ATG --> AGT; T to G and G to T) lead to a methionine to serine change (YMDD --> YSDD). This novel DNA pol mutation was detected at month 18 of lamivudine treatment. In addition, this new variant had the rtL180M mutation and a 12 base pair deletion in the pre-S1 region between nucleotides 43-54. The YSDD mutation was still present 6 months after lamivudine discontinuation. In vitro transfection studies also confirmed that the YSDD strain is resistant to lamivudine. In conclusion, the results indicate that, in addition to a Met --> Val and Met --> Ile change in YMDD, a Met --> Ser change at rt204 (YMDD --> YSDD) associated with the rtL180M change can also emerge during lamivudine treatment, which confers lamivudine resistance in vivo and in vitro, leading to virological breakthrough and ALT increases.

Adult↗

PubMed2000

Circulating IL-2 and IL-10 in chronic active hepatitis C with respect to the response to IFN treatment.

BACKGROUND: The importance of circulating immunoregulatory cytokines in response to IFN treatment and the change of in vivo production of these cytokines during interferon (IFN) treatment are not well known. We aimed to determine whether pretreatment serum levels of IL-2 and IL-10 are predictive of the response to IFN treatment and to investigate if treatment response or nonresponse has any effect on the circulating levels of these cytokines. PATIENTS AND METHODS: 37 patients (18 responders and 19 non-responders) with chronic hepatitis C virus (HCV) infection who received IFN-alpha2b for 6 months were studied. Responders were defined by complete alanine aminotransferase (ALT) normalization and loss of HCV RNA as detected by bDNA assay while patients who had elevated ALT levels and positive HCV RNA after 6 months were considered as nonresponders. RESULTS: Genotype distribution, ALT and HCV RNA levels were similar in responders and nonresponders. A significant number of patients with chronic hepatitis C (20/37 = 54%) had elevated IL-2 levels while IL-10 levels were not different from controls. No difference in baseline cytokine levels was observed between responders and non-responders. In the posttreatment serum samples some patients lost their detectable IL-2 or IL-10; some patients developed detectable cytokine levels after treatment irrespective of the treatment response. CONCLUSION: These results suggest that active liver injury in chronic hepatitis C is associated with increased circulating Th1 cytokine IL-2 but not with Th2 cytokine IL-10 and that circulating levels of these cytokines do not predict the response to IFN treatment. There is no constant and regular change in circulating levels of these cytokines under IFN treatment with respect to treatment response.

Adult↗

PubMed1999

Multimodality demonstration of primary splenic angiosarcoma.

Angiosarcomas are rare, accounting for only 1-2% of all soft tissue sarcomas. Primary abdominal angiosarcomas usually arise in the liver or spleen. We report the first color Doppler findings of a rare, low-grade splenic angiosarcoma in a 52-year-old woman.

Female↗

PubMed1999

Combination treatment of hepatic encephalopathy due to thioacetamide-induced fulminant hepatic failure in the rat with benzodiazepine and opioid receptor antagonists.

BACKGROUND/AIMS: Treatment of hepatic encephalopathy with drugs acting on the target organ of this syndrome, the brain, is unsatisfactory. Combination treatment with different neurotransmitter receptor antagonists may be a rational option to optimize treatment. METHODS: The effects of various doses of the benzodiazepine receptor antagonist Ro 15-3505 and the opioid receptor antagonist naloxone, alone or in combination, were tested on hepatic encephalopathy in rats with thioacetamide-induced hepatic failure in an open-field activity meter. Comparison of single and combination treatment was also done using a neurological test battery. In addition, we compared survival of treatment-responder rats with treatment non-responders. RESULTS: Naloxone dose dependently increased ambulatory activity and improved neurological score. Ro 15-3505 also improved ambulatory activity and neurological score; however, the improvement was less evident at higher doses. Combination treatment was not superior to single treatment. Survival was increased in treatment-responder rats. CONCLUSIONS: The failure of combination treatment with Ro 15-3505 and naloxone to further improve hepatic encephalopathy may suggest that the two neurotransmitter systems are interrelated or that hepatic encephalopathy may not be further improved by drugs acting on the brain.

Animals↗

PubMed1999

Serum cytotoxin and oxidant stress markers in N-acetylcysteine treated thioacetamide hepatotoxicity of rats.

N-acetylcysteine (NAC) is a glutathione precursor used to treat several clinical conditions where intracellular oxidant-antioxidant balance is disturbed, among which, acetaminophen induced hepatotoxicity may be counted. In this study, administering thioacetamide (TAA) as a hepatotoxic agent, a rat model of hepatotoxicity has been established, to investigate some of the immune mediated basic oxidant-antioxidant homeostatic mechanisms involved, and potential serum markers for follow-up of disease and treatment. To do this, four experimental groups receiving saline/saline, saline/NAC, saline/TAA and NAC/TAA as intraperitoneal injections, have been formed. Rat serum tumor necrosis factor-alpha (TNF-alpha), Interleukin1-beta (IL1-beta), malondialdehyde (MDA) as a measure of final oxidant damage and the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) have been assayed. Hepatocellular damage has been measured via the biochemical estimates ALT, AST and LDH as well as histopathological grading. It was found that both TNF-alpha and IL1-beta were significantly elevated in saline/TAA receivers (P<0.01) when compared to NAC/TAA receivers. Serum MDA was also increased in TAA receivers in addition to SOD (P<0.05) and GSH-Px (P<0.05). Serum nitrite levels have also been assayed to give an estimate of nitric oxide that is suggested as a counter-balancer of oxidant stress. NAC/saline receivers had the highest levels of nitrites in the serum (P<0.05). Our results indicate that part of the hepatocellular injury to rat liver, induced by TAA is mediated by oxidative stress caused by the action of cytokines imparted by the enzymatic SOD and GSH-Px and non-enzymatic gaseous nitric oxide mechanisms causing an alleviation on administration of NAC. In addition, TNF-alpha, IL1-beta, MDA, SOD, GSH-Px and nitrites are potential candidates of serum indicators for monitorization of pathophysiological stage of liver disease.

Acetylcysteine↗

PubMedDate not supplied

Circulating IL-2, IL-10 and TNF-alpha in chronic hepatitis B: their relations to HBeAg status and the activity of liver disease.

BACKGROUND/AIMS: Preferential production of immunoregulatory cytokines may play an important role in the pathogenesis of chronic hepatitis B. We aimed to determine the serum levels of IL-2, IL-10 and TNF-alpha in patients with chronic hepatitis B and to correlate these findings with the activity of liver disease, HBeAg/anti-HBe status and replication level of the virus. METHODOLOGY: Seventy-two chronic hepatitis B patients were categorized into 4 groups according to activity of liver disease and HBeAg status. Group 1 (n = 13): HBeAg and HBV DNA-positive with persistently normal ALT. Group 2 (n = 20): HBeAg and HBV DNA-positive patients with persistently elevated ALT. Group 3 (n = 19): HBeAg and HBV DNA-negative patients with persistently normal ALT. Group 4 (n = 20): HBeAg-negative patients with persistently elevated ALT and variable serum HBV DNA. IL-2, IL-10 and TNFa levels were determined in stored patient sera. RESULTS: Apart from group 1 patients, all patients groups had higher IL-2 levels compared to controls suggesting that IL-2 production is increased when liver disease becomes active in HBeAg-positive phase of HBV infection. Only group 2 patients had elevated IL-10 levels compared to controls. None of the HBeAg-negative patients had detectable TNF-alpha levels while 64% HBeAg-positive patients had elevated levels of TNF-alpha irrespective of the activity of liver disease. Except TNF-alpha, no association was found between HBV DNA status and the presence or absence of detectable cytokines in circulation. CONCLUSIONS: Our results suggest that circulating cytokine profile in chronic hepatitis B is related with the HBeAg status, replication level of the virus and the activity of liver disease.

Adolescent↗