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Biomedical subjects

Serhan Sakarya

Publications and source records attributed to Serhan Sakarya.

12 recordsLinked to original sources
PubMed2005

Hepatitis A and B seropositivity among medical students.

OBJECTIVE: Health science students are commonly exposed to some infectious agents, including hepatitis A virus (HAV) and hepatitis B virus (HBV), which may cause substantial morbidity and even deaths. The identification of prevalence and risk factors is essential for implementing efficacious preventive measures. A serological survey was performed among medical students of Adnan Menderes University Medical Faculty to determine the prevalence of antibodies against HAV and HBV, and, as a secondary objective, to determine risk factors for acquisition of these infections. METHODS: Nearly all students were included in the study. All participants completed a structured questionnaire that assessed demographic and socio-economic characteristics. Anti-HAV IgG, anti-HBc IgG, HbsAg and anti-HBs were tested using commercially available Elisa kits. RESULTS: A total of 247 students, 146 (59.1%) male and 101 (40.9%) female, were included in the study. The prevalence of anti-HAV IgG was detected as 64%. Number of siblings and place of residence were detected as independent factors affecting the anti-HAV seropositivity. The prevalence of anti-HBc IgG was detected as 7.3%. Among the students positive for anti-HBc IgG, 5 (2%) students were HBsAg positive and the other 13 (5.3%) were anti-HBs positive. HBV infection in household members, risky sexual behaviour and vaccination were independent factors affecting the prevalence of anti-HBc IgG positivity. CONCLUSIONS: The high susceptibility of medical students and their increased risk of clinical HAV and HBV infection identify a need for primary prevention through the administration of vaccination in this group in western Turkey.

Adolescent↗
PubMed2004

Mobilization of neutrophil sialidase activity desialylates the pulmonary vascular endothelial surface and increases resting neutrophil adhesion to and migration across the endothelium.

The amount of sialic acid on the surface of the neutrophil (PMN) influences its ability to interact with other cells. PMN activation with various stimuli mobilizes intracellular sialidase to the plasma membrane, where it cleaves sialic acid from cell surfaces. Because enhanced PMN adherence, spreading, deformability, and motility each are associated with surface desialylation and are critical to PMN diapedesis, we studied the role of sialic acid on PMN adhesion to and migration across pulmonary vascular endothelial cell (EC) monolayers in vitro. Neuraminidase treatment of either PMN or EC increased adhesion and migration in a dose-dependent manner. Neuraminidase treatment of both PMNs and ECs increased PMN adhesion to EC more than treatment of either PMNs or ECs alone. Moreover, neuraminidase treatment of ECs did not change surface expression of adhesion molecules or release of IL-8 and IL-6. Inhibition of endogenous sialidase by either cross-protective antineuraminidase antibodies (45.5% inhibition) or competitive inhibition with pseudo-substrate (41.2% inhibition) decreased PMN adhesion to ECs; the inhibitable sialidase activity appeared to be associated with activated PMNs. Finally, EC monolayers preincubated with activated PMNs became hyperadhesive for subsequently added resting PMNs, and this hyperadhesive state was mediated through endogenous PMN sialidase activity. Blocking anti-E-selectin, anti-CD54 and anti-CD18 antibodies decreased PMN adhesion to tumor necrosis factor-activated ECs but not to PMN-treated ECs. These data implicate desialylation as a novel mechanism through which PMN-EC adhesion can be regulated independent of de novo protein synthesis or altered adhesion molecule expression. The ability of activated PMNs, through endogenous sialidase activity, to render the EC surface hyperadherent for unstimulated PMNs may provide for rapid amplification of the PMN-mediated host response.

Animals↗
PubMed2004

Elimination of intraluminal colonization by antibiotic lock in catheters.

Antibiotic lock (AL) technique for catheter related infection encompasses the filling of a catheter lumen with high concentrations of antibiotics for hours. The goal of AL therapy is to decontaminate the intraluminal surface of the catheter. However the duration of antibiotic therapy is not established. An in vitro model was designed to establish the time needed to eliminate intraluminal microbial colonization and to evaluate the efficacy of vancomycin in comparison with teicoplanin by using laboratory AL model. Human plasma was instilled into the catheters to allow deposition of fibrin and other products on the catheter wall. After 48 hours, the catheters were drained and inoculated with bacteria in tryptic soy broth. The catheters were then drained and filled with either (a) vancomycin saline solution (VSS) lock (b) teicoplanin saline solution (TSS) lock or (c) saline solution (SS) as the control and then incubated for 12 hours. After 12 hours incubation all the catheter were drained and filled with human plasma. Instillation of human plasma and AL was alternated every 12 hours to simulate clinical conditions. For each day three catheters, locked with VSS, TSS and SS were cultured for colony count. Microbial counts were expressed as total colony-forming units per longitudinal centimeters of catheter surface. A significant decrease in intraluminal catheter colonization started as early as day 1. At the end of 7th day catheters treated with VSS and TSS lock were completely sterile. The decrease of intraluminal colonization was similar in catheters treated with VSS and TSS lock. Also the decrease of intraluminal colonization were similar in catheter colonized with slime forming S. epidermidis and nonslime-forming S. epidermidis.

Anti-Bacterial Agents↗
PubMed2004

Effect of preventive applications on prevalence of hepatitis B virus and hepatitis C virus infections in West Turkey.

OBJECTIVE: Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are community health problems in developing countries and the most common causative agents of chronic hepatitis, cirrhosis and hepatocellular carcinoma. This study investigates the prevalence and the effect of preventive applications on prevalence of HBV and HCV infections in blood donors. METHODS: Blood donors enrolled to the University and State Hospital Blood Banks in Aydin region of Turkey through the years 1993 to 2002 were retrospectively analyzed. Blood donors were investigated in 2 groups, Group I (1993-1997) and Group II (1998-2002) to compare the prevalence difference in 10-years period. Serum hepatitis B antigen (HbsAg) and anti-HCV were tested by commercially available enzyme-linked immunosorbent assay kits and anti-HCV positive results were confirmed by recombinant immune blot assays HCV test. RESULTS: The prevalence of HBV and HCV infections was determined as 1.5% and 0.19% over the period 1993-2002. Although, the prevalence of HBV infection declined significantly in Group II (1.17%) in comparison with Group I (2.27%) (p<0.0001), there was no significant difference in both groups regarding HCV infection (p=0.238). CONCLUSION: Preventive applications against blood transfusion related diseases succeed to decrease HBV infection significantly in West Turkey. Vaccination seems to be the most effective method to prevent hepatitis infection.

Adult↗
PubMed2003

Escherichia coli bind to urinary bladder epithelium through nonspecific sialic acid mediated adherence.

The first step in the bacterial colonization and infection of uropathogenic Escherichia coli is adherence to uroepithelium. Over 80% of all urinary tract infections are caused by E. coli. Uropathogenic E. coli express several adherence factors including type 1 and P fimbriae, which mediate attachment to the uroepithelium through specific binding to different glycoconjugate receptors. We showed that P and type 1 fimbriae are not the sole adhesins on uropathogenic E. coli and sialic acid also mediates nonspecific bacterial adherence of uropathogenic E. coli and urinary bladder epithelium.

Animals↗
PubMed2003

Protein tyrosine phosphatase activity regulates endothelial cell-cell interactions, the paracellular pathway, and capillary tube stability.

Protein tyrosine phosphorylation is tightly regulated through the actions of both protein tyrosine kinases and protein tyrosine phosphatases. In this study, we demonstrate that protein tyrosine phosphatase inhibition promotes tyrosine phosphorylation of endothelial cell-cell adherens junction proteins, opens an endothelial paracellular pathway, and increases both transendothelial albumin flux and neutrophil migration. Tyrosine phosphatase inhibition with sodium orthovanadate or phenylarsine oxide induced dose- and time-dependent increases in [14C]bovine serum albumin flux across postconfluent bovine pulmonary artery endothelial cell monolayers. These increases in albumin flux were coincident with actin reorganization and intercellular gap formation in both postconfluent monolayers and preformed endothelial cell capillary tubes. Vanadate (25 microM) increased tyrosine phosphorylation of endothelial cell proteins 12-fold within 1 h. Tyrosine phosphorylated proteins were immunolocalized to the intercellular boundaries, and several were identified as the endothelial cell-cell adherens junction proteins, vascular-endothelial cadherin, and beta-, gamma-, and p120-catenin as well as platelet endothelial cell adhesion molecule-1. Of note, these tyrosine phosphorylation events were not associated with disassembly of the adherens junction complex or its uncoupling from the actin cytoskeleton. The dose and time requirements for vanadate-induced increases in phosphorylation were comparable with those defined for increments in transendothelial [14C]albumin flux and neutrophil migration, and pretreatment with the tyrosine kinase inhibitor herbimycin A protected against these effects. These data suggest that protein tyrosine phosphatases and their substrates, which localize to the endothelial cell-cell boundaries, regulate adherens junctional integrity, the movement of macromolecules and cells through the endothelial paracellular pathway, and capillary tube stability.

Adherens Junctions↗
PubMed2003

Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis.

BACKGROUND/AIMS: The role of nitric oxide (NO) in bacterial translocation (BT) associated with acute pancreatitis is controversial. We investigated the effects of the NO synthase substrate, L-arginine, and the NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on BT in caerulein-induced acute pancreatitis in rats. METHODS: Acute pancreatitis was induced by subcutaneous injections of caerulein (12 microg/kg) at 6-hour intervals for 2 days. Subcutaneous injections of L-arginine (100 mg/kg) or L-NAME (10 mg/kg) were administeredonce daily for 2 days. At 48 h, pancreatic injury and BT to the mesenteric lymph nodes (MLN), liver, and peritoneum were assessed. RESULTS: Compared with controls, rats that received caerulein injections alone had increased BT to the MLN and pancreatic inflammatory changes. L-Arginine significantly reduced the inflammation and BT caused by caerulein. L-NAME did not significantly alter pancreatic inflammation. Although caerulein + L-NAME-treated rats had increased BT to the peritoneum, MLN, and liver compared with controls, rates of BT did not significantly differ between caerulein alone- and caerulein + L-NAME-treated rats. CONCLUSION: In acute edematous pancreatitis, BT is increased and is regulated by NO. NO substrates limit BT and pancreatic inflammation associated with acute pancreatitis, probably by their bactericidal actions and ability to improve pancreatic blood flow.

Acute Disease↗
PubMed2003

Anthrax--an overview.

Anthrax, a disease of mammals (including humans), is caused by a spore-forming Gram-positive bacilli called Bacillus anthracis. Anthrax is one of the oldest threats to humanity, and remains endemic in animals in many parts of the world. The incidence of anthrax has decreased in developed countries, but it remains a considerable health problem in developing countries. The disease is transmitted to humans by contact with sick animals or their products, such as wool, skin, meat etc. Capsular polypeptide and anthrax toxin are the principal virulence factors of B. anthracis. Anthrax toxin consists of three proteins called protective antigen, edema factor, and lethal factor, each of which is nontoxic but acts synergistically. Human anthrax has three major clinical forms: cutaneous, inhalational, and gastrointestinal. The diagnosis is easily established in cutaneous cases, characterized by black eschar. Severe intoxication and collapse during the course of bronchopneumonia or hemorrhagic enteritis should prompt suspicion of anthrax. Treatment with antibiotics is mandatory. If untreated, anthrax in all forms can lead to septicemia and death. Recently, considerable attention has been focused on the potential for B. anthracis to be used in acts of biological terrorism. The ease of laboratory production and its dissemination via aerosol led to its adoption by terrorists, as shown by recent events in the USA. A good knowledge of anthrax, its epidemiology, pathogenesis, clinical forms and potential as a biological weapon is essential for timely prevention and treatment. This review summarizes the current knowledge on anthrax.

Animals↗
PubMed2002

Recruitment of murine neutrophils in vivo through endogenous sialidase activity.

Upon activation with various noncytokine stimuli, polymorphonuclear leukocytes (PMNs) mobilize intracellular sialidase to the plasma membrane, where the sialidase releases sialic acid from the cell surface. This desialylation enhances PMN adherence, spreading, deformability, and motility, functions critical to diapedesis. We now have examined the role of sialidase activity in PMN adhesion to and migration across the endothelium in vivo. A polyclonal antibody prepared against Clostridium perfringens neuraminidase 1) detected surface expression of sialidase on human PMNs stimulated with IL-8 in vitro and on murine PMNs stimulated in vivo, but not on that of unstimulated cells, 2) recognized proteins in human PMN lysates and granule preparations that were not detected by preimmune antibody, 3) inhibited bacterial neuraminidase and human PMN sialidase activities in vitro, and 4) inhibited both pulmonary leukostasis in mice systemically infused with cobra venom factor and intrapulmonary transendothelial migration of PMNs into the bronchoalveolar compartment of mice intranasally challenged with interleukin-8. We conclude that the chemokine interleukin-8, like other PMN agonists, induces the translocation of sialidase to the PMN surface and that surface expression of this sialidase is a prerequisite to PMN recruitment in vivo. The ability of antibodies raised against a prokaryotic neuraminidase to recognize eukaryotic sialidase extends the concept of the neuraminidase superfamily to mammalian enzymes. Inhibition of mobilized endogenous sialidase may provide a novel strategy for limiting the inflammatory response.

Animals↗
PubMed2002

Lexipafant inhibits postsurgical adhesion formation.

BACKGROUND: PAF and its antagonists have been studied in the pathophysiology of various inflammatory conditions. This study investigates the effects of a platelet activating factor antagonist, lexipafant, on peritoneal adhesion formation and wound healing. MATERIALS AND METHODS: Forty-eight Wistar albino rats (300-350 g) were divided into four equal groups; adhesion-induced lexipafant (AL), adhesion-induced saline (AS), sham-operated lexipafant (SL), and sham-operated saline (SS). All rats underwent a midline laparotomy under sterile conditions. The anterior wall of the left uterine horn was scraped to cause hemorrhages in adhesion-induced groups. Following peritoneal injections of either saline or lexipafant, the incisions were closed in layers. On the 14th day, the rats were killed and adhesions were scored from 0 (none) to 4 (dense). Tissue samples from the adhesions and the left horn of uterus were examined biochemically for hydroxyproline content, and serum IL-6 levels were determined. RESULTS: The adhesion formation score was significantly increased in the AS group compared to the SL and AL groups (P < 0.001). The IL-6 levels of the AS group were higher than those of the other groups (P < 0.05). There was no significant difference in hydroxyproline content between groups (P > 0.05). CONCLUSIONS: Lexipafant plays a role in the prevention of adhesion formation without affecting wound healing.

Animals↗
PubMedDate not supplied

Neuraminidase produces dose-dependent decrease of slime production and adherence of slime-forming, coagulase-negative staphylococci.

BACKGROUND: Slime is one of the important structures of certain bacterial strains involved in nonspecific adherence. This study was conducted to determine the role of neuraminidase on slime formation and adherence of slime-forming coagulase-negative staphylococci to inert surface. METHODS: Quantitative biofilm and qualitative bacterial adherence assays were performed with increasing concentrations of neuraminidase extracted from Clostridium perfringens-treated bacteria in polystyrene plates and polypropylene tubes. RESULTS: Slime production of slime-forming, coagulase-negative staphylococci was significantly decreased dose dependently at > or =100 mU/mL (p <0.001). Bacterial adherence to smooth surface was impeded at > or =100 mU/mL of neuraminidase treatment and adherence results were comparable with slime production assay results. CONCLUSIONS: Sialic acid may be a constituent molecule of slime and involved in bacterial adherence to inert surface. These results represent new insight into the mechanism of slime production and adherence of slime-forming, coagulase-negative staphylococci to inert surface.

Animals↗