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T Ozcelik

Publications and source records attributed to T Ozcelik.

16 recordsLinked to original sources
PubMed2006

Tumor lysis syndrome as a contributory factor to the development of reversible posterior leukoencephalopathy.

INTRODUCTION: Reversible posterior leukoencephalopathy syndrome (RPLS) is a recently described clinical and radiological entity comprising headache, seizures, altered level of consciousness and visual disturbances in association with transient posterior cerebral white-matter abnormalities. METHOD: We report a young woman with Burkitt's lymphoma who developed RPLS after combined chemotherapy administered during the tumor lysis syndrome. RESULTS: The symptoms in this patient fitted well with those of RPLS; they included abrupt alterations in mental status, seizures, headache, visual changes and characteristic neuroradiological findings. She was given further combination chemotherapy without any neurological complications, at which time she had already recovered from both RPLS and tumor lysis syndrome. CONCLUSION: Although many etiological factors have been reported in the development of RPLS, the underlying mechanism is not yet well understood. With prompt and appropriate management, RPLS is usually reversible, and chemotherapy can be continued after complete recovery from RPLS. We suggest that tumor lysis syndrome should be considered as a contributory factor to the development of RPLS in patients for whom treatment with combined chemotherapy for hematological malignancies is planned.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

Bacillus spp. among hospitalized patients with haematological malignancies: clinical features, epidemics and outcomes.

Between April 2000 and May 2005, 350 bacteraemic episodes occurred among patients treated in our haematology unit. Two hundred and twenty-eight of these episodes were caused by Gram-positive pathogens, most commonly coagulase-negative staphylococci and Staphylococcus aureus. One hundred and twenty-two episodes were due to Gram-negative pathogens, with a predominance of Escherichia coli, Acinetobacter baumannii and Pseudomonas aeruginosa. Bacillus bacteraemias constituted 12 of these episodes occurring in 12 patients, and accounted for 3.4% of all bacteraemic episodes. Of the 12 strains evaluated, seven were Bacillus licheniformis, three were Bacillus cereus and two were Bacillus pumilus. Seven episodes presented with bloodstream infection, three with pneumonia, one with severe abdominal pain and deterioration of liver function, and one with a catheter-related bloodstream infection. B. licheniformis was isolated from five patients who had been hospitalized at the same time. This outbreak was related to non-sterile cotton wool used during skin disinfection. B. cereus and B. licheniformis isolates were susceptible to cefepime, carbapenems, aminoglycosides and vancomycin, but B. pumilus isolates were resistant to all antibiotics except for quinolones and vancomycin. Two deaths were observed. In conclusion, Bacillus spp. may cause serious infections, diagnostic and therapeutic dilemmas, and high morbidity and mortality in patients with haematological malignancies. Both B. cereus and B. licheniformis may be among the 'new' Gram-positive pathogens to cause serious infection in patients with neutropenia.

Acinetobacter baumannii↗
PubMed2006

Narrowband UVB phototherapy for small plaque parapsoriasis.

BACKGROUND: Narrowband UVB (NB-UVB) phototherapy has been shown to be effective for the treatment of various dermatoses. OBJECTIVE: To analyze the effects of NB-UVB phototherapy for small plaque parapsoriasis (SPP). METHODS: The response of 45 patients (24 females, 21 males, age range 20-58 years) with histologically confirmed SPP were assessed. NB-UVB therapy was given 3-4 times weekly. The initial treatment dose was 70% of the minimal erythema dose. The doses were increased gradually with a standard increment of 20/10/0. Clinical response was determined as follows: complete response (CR), at least 90% clearing of skin lesions; partial response (PR), at least 50% but less than 90% clearing and no response (NR), less than 50% clearing. The follow-up period was 6-24 months after the treatment. RESULTS: NB-UVB treatment led to CR in 33 of 45 patients (73.3%) with a mean cumulative dose of 14.3 J/cm(2) (range 3.2-24.1 J/cm(2)) after a mean number of 29 exposures (range 16-51 sessions); PR in 12 of 45 (26.6%) with a cumulative dose of 15.6 J/cm(2) (range 10.4-23.3 J/cm(2)) after a mean number of 29.4 exposures (range 25-50 sessions). Nineteen patients with CR had skin phototype II, 13 had type III and 1 had type I. Among the patients with PR, 7 had skin phototype II and 5 had type III. Postinflammatory hyperpigmentation was observed in 51% of the patients. Relapses occurred in six patients within a mean time of 7.5 months (2-12 months). CONCLUSION: NB-UVB phototherapy has several advantages over treatment with broadband UVB and PUVA. NB-UVB therapy for patients with SPP is an effective, safe and practical alternative treatment modality. Further larger studies with longer follow-up periods are necessary to determine the proper clinical response and long-term complications of NB-UVB therapy in this disease.

Adult↗
PubMed2001

Survey of factor V leiden and prothrombin gene mutations in systemic lupus erythematosus.

The two most common hereditary risk factors for thrombosis are factor V Leiden mutation and a prothrombin gene mutation. There is indeed a thrombotic tendency in patients with systemic lupus erythematosis (SLE) and it is not always associated with antiphospholipid antibodies. We aimed to determine the relationship between both factor V Leiden and prothrombin gene mutations and SLE. Using polymerase chain reaction (PCR) the factor V Leiden and prothrombin gene mutations were evaluated in 55 patients (20 children and 35 adults) with SLE. Although seven patients were found to have factor V Leiden mutation in the heterozygous state, two had the heterozygous G-->A (20210) prothrombin gene mutation. Although one had these two mutations concurrently, these two patients did not have thrombosis. The factor V Leiden mutation frequency (12.7%) was higher than that of our general population (7.1%). On the other hand, seven of the patients with SLE had a thrombotic event. Although of these seven, four (57%) had factor V Leiden mutation, three (43%) had no mutation. Of 48 patients with no thrombotic history, only three had the factor V mutation (6.25%). The prevalence of the factor V Leiden mutation in SLE patients with and without thrombosis was significantly different by Fisher's exact test (p<0.05). The risk of venous thrombosis in patients with factor V Leiden increased threefold compared to that in those without factor V Leiden mutation (odds ratio 20.1; CI 2.99-133.6). Although factor V Leiden mutation seems to play a role in the development of venous thrombosis in SLE, the development of thrombosis in SLE is multifactorial.

Adolescent↗
PubMed2001

Frequent demonstration of human herpesvirus 8 (HHV-8) in bone marrow biopsy samples from Turkish patients with multiple myeloma (MM).

In order to investigate the frequency of HHV-8 in MM patients from another geographic location, we obtained fresh bone marrow (BM) biopsies from Turkish patients with MM (n = 21), monoclonal gammopathy of undetermined significance (MGUS) (n = 2), plasmacytoma (n = 1) with BM plasma cell infiltration, various hematological disorders (n = 6), and five healthy Turkish controls. The frequency of HHV-8 was analyzed by polymerase chain reaction (PCR) in two independent laboratories in the USA and in Turkey. Using fresh BM biopsies, 17/21 MM patients were positive for HHV-8 whereas all five healthy controls, and six patients with other hematological disorders were negative. Two patients with MGUS, and one patient with a solitary plasmacytoma were also negative. The data from the two laboratories were completely concordant. Also using primer pairs for v IRF and v IL-8R confirmed the results observed with the KS330233 primers. Furthermore, sequence analysis demonstrated a C3 strain pattern in the ORF26 region which was also found in MM patients from the US. Thus, HHV-8 is present in the majority of Turkish MM patients, and the absence of the virus in healthy controls further supports its role in the pathogenesis of MM.

Biopsy↗
PubMed1997

Audiological findings in kernicteric patients.

Audiological findings in kernicteric patients. Thirty patients followed up because of kernicterus sequelae and 15 normal children serving as control group were examined to determine their hearing status and evoked response audiometry (ERA) results. Seventeen out of the 30 patients (57%) had high frequency sensorineural hearing loss. Sixteen of them had bilateral hearing loss. Ten had no response or prolonged bilateral latencies. The results showed that high neonatal serum bilirubin levels affect the hearing adversely.

Adolescent↗
PubMed1996

Auditory nerve-brainstem responses in cystic fibrosis patients.

We conducted a study in 30 children with cystic fibrosis (CF) to determine if their hearing had been affected. Their ages ranged between 2 to 17 years and they were studied by means of complete audiologic evaluation and brainstem evoked response audiometry (BERA). Twenty of them had received some ototoxic drugs for variable periods. The results showed that there was no significant correlation between CF and BERA findings. The findings indicated that, except a few middle ear problems such as serous otitis media, CF did not affect hearing status of the CF children per se.

Adolescent↗
PubMed1995

An unusual presentation: primary tuberculosis of the middle ear cleft.

Tuberculosis rarely affects the middle ear cleft; therefore, except for those working in close association with respiratory physicians, the disease is a curiosity and not often considered in the differential diagnosis of otorrhea. The diagnosis is thus made too late, with resulting complications such as irreversible hearing loss and facial nerve paralysis. A case report and review of the literature are presented, emphasizing that tuberculosis should be considered in the differential diagnosis of chronic ear infection.

Child↗
PubMed1993

Human dystroglycan: skeletal muscle cDNA, genomic structure, origin of tissue specific isoforms and chromosomal localization.

Dystroglycan is a novel laminin binding component of the dystrophin-glycoprotein complex which provides a linkage between the subsarcolemmal cytoskeleton and the extracellular matrix. Here we report the cDNA and genomic structure of human dystroglycan. The human dystroglycan is encoded by a single gene (DAG1) mapped to chromosome 3 band p21. The coding sequence is organized into two exons, separated by a large intron. The predicted amino acid sequence of human and rabbit dystroglycan are 93% identical with predicted glycosylation sites being conserved. Human dystroglycan is expressed in a variety of fetal and adult tissues. Our data suggest that muscle and non-muscle isoforms of dystroglycan differ by carbohydrate moieties but not protein sequence. Therefore, we hypothesize that variable glycosylation of the conserved protein core might modulate laminin binding. The relationship of dystroglycan to human diseases is discussed.

Amino Acid Sequence↗
PubMed1992

Trembler mouse carries a point mutation in a myelin gene.

The autosomal dominant trembler mutation (Tr), maps to mouse chromosome 11 (ref. 2) and manifests as a Schwann-cell defect characterized by severe hypomyelination and continuing Schwann-cell proliferation throughout life. Affected animals move clumsily and develop tremor and transient seizures at a young age. We have recently described a potentially growth-regulating myelin protein, peripheral myelin protein-22 (PMP-22; refs 7, 8), which is expressed by Schwann cells and found in peripheral myelin. We now report the assignment of the gene for PMP-22 to mouse chromosome 11. Cloning and sequencing of PMP-22 complementary DNAs from inbred Tr mice reveals a point mutation that substitutes an aspartic acid residue for a glycine in a putative membrane-associated domain of the PMP-22 protein. Our results identify the PMP-22 gene as a likely candidate for the mouse trembler locus and will encourage the search for mutations in the corresponding human gene in pedigrees with hypertrophic neuropathies such as Charcot-Marie-Tooth and Dejerine-Sottas diseases (hereditary motor and sensory neuropathies I and III).

Amino Acid Sequence↗
PubMed1992

Phenotypic, cytogenetic, and molecular studies of three patients with constitutional deletions of chromosome 5 in the region of the gene for familial adenomatous polyposis.

We have studied three patients, one with extensive polyposis of the colon, who have constitutional interstitial deletions of the long arm of chromosome 5. High-resolution banding studies indicated that the deletion in the patient with polyposis spans the region 5q21-q22, which includes APC, a gene involved in familial adenomatous polyposis and sporadic colon cancer. Molecular analysis with probes for sequences flanking APC confirmed this conclusion. The deletions in the other two patients, who are too young to have developed polyposis, had breakpoints within this region, precluding the use of cytogenetic analysis alone in making definitive predictions about their risks. Molecular studies resolved the uncertainty; in situ and quantitative Southern hybridizations of four probes for polymorphic segments revealed that one of the patients has a deletion of MCC, a gene which is approximately 150 kb proximal to APC, and two flanking markers. He is at increased risk for polyposis, while the other patient is not. The physical descriptions of these patients, in conjunction with cases in the literature, begin to allow delineation of two distinct 5q-syndromes. These studies also provide precise physical mapping data for D5S71, D5S81, D5S84, and MCC on 5q.

Abnormalities, Multiple↗
PubMed1991

Structural and functional conservation of synaptotagmin (p65) in Drosophila and humans.

Synaptotagmin (p65) is an abundant synaptic vesicle protein that contains two copies of a sequence that is homologous to the regulatory region of protein kinase C. Full length cDNAs encoding human and Drosophila synaptotagmins were characterized to study its structural and functional conservation in evolution. The deduced amino acid sequences for human and rat synaptotagmins show 97% identity, whereas Drosophila and rat synaptotagmins are only 57% identical but exhibit a selective conservation of the two internal repeats that are homologous to the regulatory region of protein kinase C (78% invariant residues in all three species). The two internal repeats of synaptotagmin are only slightly more homologous to each other than to protein kinase C, and the differences between the repeats are conserved in evolution, suggesting that they might not be functionally equivalent. The cytoplasmic domains of human and Drosophila synaptotagmins produced as recombinant proteins in Escherichia coli specifically bound phosphatidylserine similar to rat synaptotagmin. They also hemagglutinated trypsinized erythrocytes at nanomolar concentrations. Hemagglutination was inhibited both by negatively charged phospholipids and by a recombinant fragment from rat synaptotagmin that contained only a single copy of the two internal repeats. Together these results demonstrate that synaptotagmin is highly conserved in evolution compatible with a function in the trafficking of synaptic vesicles at the active zone. The similarity of the phospholipid binding properties of the cytoplasmic domains of rat, human, and Drosophila synaptotagmins and the selective conservation of the sequences that are homologous to protein kinase C suggest that these are instrumental in phospholipid binding. The human gene for synaptotagmin was mapped by Southern blot analysis of DNA from somatic cell hybrids to chromosome 12 region cen-q21, and the Drosophila gene by in situ hybridization to 23B.

Amino Acid Sequence↗
PubMed1991

Rett syndrome: exclusion mapping following the hypothesis of germinal mosaicism for new X-linked mutations.

The hypothesis of germinal mosaicism in the unaffected mother of two half-sisters affected with Rett syndrome is postulated to explain the unusual recurrence of this genetic disorder affecting only females (1/10,000); it might be caused by new X-linked mutations with lethality in male fetuses. The analysis of 34 X-linked restriction fragment length polymorphisms (RFLPs) in these two affected females and in their unaffected mother and half-brother, together with the reconstruction of phase for 15 informative RFLPs in somatic cell hybrids retaining a single X chromosome from each female, has made it possible to exclude some regions of the X chromosome as possible sites of the mutation(s) causing Rett syndrome.

Cell Line↗