Biomedical subjects

A Dogan

Publications and source records attributed to A Dogan.

At least 55 records · Page 3Linked to original sources

PubMed2001

Cytotoxicity of provisional crown and bridge restoration materials: an in vitro study.

There are numerous materials used to provide temporary coverage for teeth while permanent restorations are being fabricated. The biocompatibility of these materials is important for the protection of teeth and gingiva, but there is little information on this subject. This study aimed to examine possible time-dependent toxic effects of provisional crown and bridge restoration materials, manipulated intraorally or extraorally, on epithelia cells. A total of 20 discs, 4 sample discs from each product having dimensions of 4 mm diameter and 2 mm thickness, were prepared. After sterilization, toxicity of these discs was evaluated in the Madin Darby Bovine Kidney (MDBK) cell line. Morphological cell changes were observed microscopically at the 3rd, 6th, 12th, and 24th hours by the filter diffusion test method. After the 3rd hour, Artglass and Structur produced cytotoxic symptoms. Temdent had the least toxic effects at the end of the 12th hour. However, after the 24th hour, the toxic values were similar for all materials. The results of this study show that although the toxicity response of chemically and light curing materials had changed in different time periods, all of them had the same toxic effects at the end of the 24th hour.

Animals↗

PubMed2001

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain.

Traumatic injury to rat brain induced by controlled cortical impact (CCI) results in chronic neuronal death in the hippocampus. In the normal brain, glutamate transporters actively clear the glutamate released synaptically to prevent receptor overactivation and excitotoxicity. Glutamate transporter 1 (GLT-1) is the most abundant and active glutamate transporter, which mediates the bulk of glutamate uptake. CCI injury significantly decreased GLT-1 mRNA (by 49-66%, P < 0.05) and protein (by 29-44%, P < 0.05) levels in the ipsilateral hippocampus, compared with either the respective contralateral hippocampus or the sham-operated control, 24-72 h after the injury. CCI injury in rats infused with GLT-1 antisense oligodeoxynucleotides (ODNs) exacerbated the hippocampal neuronal death and mortality, compared with the GLT-1 sense/random ODN-infused controls. At 7 days after the injury, hippocampal neuronal numbers were significantly lower in the CA1 (reduced by 32%, P < 0.05), CA2 (by 45%, P < 0.01), CA3 (by 68%, P < 0.01) and dentate gyrus (by 31%, P < 0.05) in GLT-1 antisense ODN-infused rats, compared with the GLT-1 sense/random ODN-infused controls. This study suggested a role for GLT-1 dysfunction in promoting the hippocampal neuronal death after traumatic brain injury.

ATP-Binding Cassette Transporters↗

PubMed2000

BCL10 gene mutation in lymphoma.

BCL10 is directly involved in t(1;14)(p22;q32) of mucosa-associated lymphoid tissue (MALT) lymphoma. Wild-type BCL10 promoted apoptosis and suppressed malignant transformation in vitro, whereas truncated mutants lost the pro-apoptotic activity and exhibited gain of function enhancement of transformation. We studied 220 lymphomas for genomic BCL10 mutation by polymerase chain reaction-single-strand conformational polymorphism and DNA sequencing. Nineteen mutations were found in 13 lymphoma specimens, as follows: 8 of 120 (6.7%) mucosa-associated lymphoid tissue (MALT) lymphomas, 4 of 42 (9.5%) follicular lymphomas, and 1 of 23 (4.3%) diffuse large B-cell lymphomas. No mutations were found in 14 mantle cell lymphomas or 21 T-cell lymphomas. High-grade MALT lymphoma tended to show a slightly higher mutation frequency (2 of 25, 8%) than low-grade MALT tumor (6 of 95, 6.3%). Among low-grade gastric MALT lymphoma, mutations were found in 3 of 11 tumors that did not respond to Helicobacter pylori eradication therapy, but none were found in 22 tumors that regressed completely after H pylori eradication. All 14 potentially pathogenic mutations were distributed in the carboxyl terminal domain of BCL10. Deletion accounted for 10 of these mutations; 10 of 14 mutations caused truncated forms of BCL10. Western blot analysis of a mutant case confirmed the presence of truncated BCL10 products of anticipated size. Our results suggest that BCL10 mutation may play a pathogenic role in B-cell lymphoma development, particularly in aggressive and antibiotic unresponsive MALT lymphomas, and may further implicate the biologic importance of the carboxyl terminal of the molecule. (Blood. 2000;95:3885-3890)

Adaptor Proteins, Signal Transducing↗

PubMed2000

Studies on the protonation constants and solvation of alpha-amino acids in dioxan-water mixtures.

To gain more information about the effect of solvent on alpha-amino acids, the stoichiometric protonation constants of 10 alpha-amino acids (glycine, DL-alanine, DL-valine, L-leucine, L-isoleucine, DL-phenylalanine, L-serine, L-threonine, L-asparagine, and L-glutamine) in different dioxan-water mixtures have been determined potentiometrically using a combined pH electrode system calibrated in concentration units of hydrogen ion at 25 degrees C with an ionic strength of 0.10 M. For all amino acids studied, it was observed that the log K(1) values relating to the protonation equilibria of the anionic form are almost unaltered by the change in solvent composition. However, the log K(2) values corresponding to the formation equilibria of cationic form increase with the increase in dioxan content. The variation of these constants is discussed on the basis of specific solute-solvent interactions and structural changes of amino acids from water to dioxan-water media. The zwitterionic to neutral form ratio of these acids in dioxan-water mixtures is also discussed.

Amino Acids↗

PubMed2000

Clone-specific PCR reveals wide dissemination of gastric MALT lymphoma to the gastric mucosa.

The development of low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma is closely associated with Helicobacter pylori infection. Despite its indolent clinical course and prolonged localization to the site of origin, the lymphoma frequently presents with multifocal lesions. However, the true extent of tumour involvement in the gastric mucosa is unclear, since reactive appearing lymphocytic infiltrates are always present and could contain tumour cells that are not readily identifiable on cytological grounds. Gastrectomy specimens of four MALT lymphoma cases were studied by microdissection and clone-specific polymerase chain reaction (CS-PCR) and of a further case with t(1;14)(p22;q32) by immunohistochemistry for BCL10 protein, which acted as a tumour marker for tumour cells carrying the translocation. CS-PCR revealed that tumour cells were commonly present in histologically non-lymphomatous lymphocytic infiltrates microdissected from areas well separated from tumour lesions. Tumour cells were also frequently found in infiltrates microdissected from the resection margins. These findings were reinforced by direct identification of tumour cells, as recognized by strong BCL10 nuclear staining, in non-lymphomatous lymphocytic infiltrates in the case with t(1;14)(p22;q32). The results show that gastric MALT lymphoma disseminates widely within the gastric mucosa without necessarily forming diagnostic lesions.

Chromosomes, Human, Pair 1↗

PubMed2000

Traumatic brain injury leads to increased expression of peripheral-type benzodiazepine receptors, neuronal death, and activation of astrocytes and microglia in rat thalamus.

In mammalian CNS, the peripheral-type benzodiazepine receptor (PTBR) is localized on the outer mitochondrial membrane within the astrocytes and microglia. PTBR transports cholesterol to the site of neurosteroid biosynthesis. Several neurodegenerative disorders were reported to be associated with increased densities of PTBR. In the present study, we evaluated the changes in the PTBR density and gene expression in the brains of rats as a function of time (6 h to 14 days) after traumatic brain injury (TBI). Sham-operated rats served as control. Between 3 and 14 days after TBI, there was a significant increased in the binding of PTBR antagonist [(3)H]PK11195 (by 106 to 185%, P < 0.01, as assessed by quantitative autoradiography and in vitro filtration binding) and PTBR mRNA expression (by 2- to 3. 4-fold, P < 0.01, as assessed by RT-PCR) in the ipsilateral thalamus. At 14 days after the injury, the neuronal number decreased significantly (by 85 to 90%, P < 0.01) in the ipsilateral thalamus. At the same time point, the ipsilateral thalamus also showed increased numbers of the glial fibrillary acidic protein positive cells (astrocytes, by approximately 3.5-fold) and the ED-1 positive cells (microglia/macrophages, by approximately 36-fold), the two cell types known to be associated with PTBR. Increased PTBR expression following TBI seems to be associated with microglia/macrophages than astrocytes as PTBR density at different periods after TBI correlated better with the number of ED-1 positive cells (r(2) = 0.95) than the GFAP positive cells (r(2) = 0.56). TBI-induced increased PTBR expression is possibly an adaptive response to cellular injury and may play a role in the pathophysiology of TBI.

Animals↗

PubMed2000

BCL10 expression in normal and neoplastic lymphoid tissue. Nuclear localization in MALT lymphoma.

BCL10 is an apoptotic regulatory molecule identified through its direct involvement in t(1;14)(p22;q32) of mucosa-associated lymphoid tissue (MALT) lymphoma. We examined BCL10 protein expression in various normal tissues and B-cell lymphomas by immunohistochemistry of formalin-fixed and paraffin-embedded tissues using mouse BCL10 monoclonal antibodies. BCL10 protein was expressed in lymphoid tissue but not in 21 various other tissues with the exception of breast. In normal B-cell follicles, the protein was expressed abundantly in the germinal center B cells, moderately in the marginal zone, but only weakly in the mantle zone B cells. Irrespective of their stage of B-cell maturation, BCL10 was predominantly expressed in the cytoplasm. In contrast, each of the four MALT lymphomas with t(1;14)(p22;q32) showed strong BCL10 expression in both the nucleus and cytoplasm. Twenty of 36 (55%) MALT lymphomas lacking the translocation exhibited BCL10 expression in both the nucleus and cytoplasm although at a much lower level, whereas the remaining 16 cases displayed only cytoplasmic BCL10. Unlike MALT lymphoma, both follicular and mantle cell lymphomas generally displayed BCL10 expression compatible to their normal cell counterparts. Our results show differential expression of BCL10 protein among various B-cell populations of the B-cell follicle, indicating its importance in B-cell maturation. The subcellular localization of BCL10 was frequently altered in MALT lymphoma in comparison with its normal cell counterparts, suggesting that ectopic BCL10 expression may be important in the development of this type of tumor.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Glial glutamate transporter GLT-1 down-regulation precedes delayed neuronal death in gerbil hippocampus following transient global cerebral ischemia.

Glial (GLT-1 and GLAST) and neuronal (EAAC1) high-affinity transporters mediate the sodium dependent glutamate reuptake in mammalian brain. Their dysfunction leads to neuronal damage by allowing glutamate to remain in the synaptic cleft for a longer duration. The purpose of the present study is to understand their contribution to the ischemic delayed neuronal death seen in gerbil hippocampus following transient global cerebral ischemia. The protein levels of these three transporters were studied by immunoblotting as a function of reperfusion time (6 h to 7 days) following a 10 min occlusion of bilateral common carotid arteries in gerbils. In the vulnerable hippocampus, there was a significant decrease in the protein levels of GLT-1 (by 36-46%, P < 0.05; between 1 and 3 days of reperfusion) and EAAC1 (by 42-68%, P < 0.05; between 1 and 7 days of reperfusion). Histopathological evaluation showed no neuronal loss up to 2 days of reperfusion but an extensive neuronal loss (by approximately 84%, P < 0.01) at 7 days of reperfusion in the hippocampal CA1 region. The time frame of GLT-1 dysfunction (1-3 days of reperfusion) precedes the initiation of delayed neuronal death (2-3 days of reperfusion). This suggests GLT-1 dysfunction as a contributing factor for the hippocampal neuronal death following transient global cerebral ischemia. Furthermore, decreased EAAC1 levels may contribute to GABAergic dysfunction and excitatory/inhibitory imbalance following transient global ischemia.

ATP-Binding Cassette Transporters↗

PubMed2000

CD10 and BCL-6 expression in paraffin sections of normal lymphoid tissue and B-cell lymphomas.

In this study the authors explored the value of immunostaining for follicular center B-cell markers, BCL-6 and CD10, in paraffin sections as a tool for the differential diagnosis of B-cell lymphomas. The cases studied comprised reactive lymphoid hyperplasia (RLH; n = 19), follicular lymphoma (FL; n = 50), low-grade mucosa-associated lymphoid tissue (MALT) lymphoma (n = 24), mantle cell lymphoma (n = 19), splenic marginal zone lymphoma (n = 13), diffuse large B-cell lymphoma (DLBCL; n = 54), Burkitt's lymphoma (BL; n = 20), nodular lymphocyte predominance Hodgkin's disease (NLPHD; n = 16), and classic Hodgkin's disease (CHD; n = 13). In RLH, CD10 and BCL-6 were expressed almost exclusively by the follicular center cells. In contrast in FL, the expression of CD10 (39/50) and BCL-6 (34/36) was seen in both follicular and interfollicular neoplastic B cells. Marginal zone/MALT lymphomas and mantle cell lymphoma were always negative. In DLBCL the expression was variable for both CD10 (21/54) and BCL-6 (39/47), with some tumors, including cases of transformed follicular lymphoma (9/10), coexpressing CD10 and BCL-6, and others expressing only BCL-6, and a small group expressing neither marker, possibly reflecting the underlying primary pathogenetic events such as the rearrangement of BCL-2 or BCL-6 genes. BL was always both CD10 and BCL-6 positive. In NLPHD the L&H cells expressed BCL-6 (11/13) but not CD10, whereas in CHD BCL-6 expression was seen in half of the cases. This study demonstrates that both CD10 and BCL-6 are reliable markers of follicular center B-cell differentiation. CD10 and BCL-6 immunostaining have an important role in differential diagnosis of FL from RLH and other low-grade B-cell lymphomas. The results also suggest that a CD10/BCL-6 expression pattern may be helpful in identifying main subsets of DLBCL. However, additional studies comparing genotype with immunophenotype are required.

Biomarkers↗

PubMed2000

Bilateral median nerve compression at the level of Struthers' ligament. Case report.

Struthers' ligament syndrome is a rare cause of median nerve entrapment. Bilateral compression of the median nerve is even more rare. It presents with pain, sensory disturbance, and/or motor function loss at the median nerve's dermatomal area. The authors present the case of a 21-year-old woman with bilateral median nerve compression caused by Struthers' ligament. She underwent surgical decompression of the nerve on both sides. To the authors' knowledge, this case is the first reported bilateral compression of the median nerve caused by Struthers' ligament. The presentation and symptomatology of Struthers' ligament syndrome must be differentiated from median nerve compression arising from other causes.

Adult↗

PubMed2000

Diagnostic modalities for carotid artery disease.

Stroke secondary to atherosclerosis is one of the most common causes of death in the United States. A major cause of thromboembolic stroke is atherosclerotic narrowing and ulceration in the region of the carotid bifurcation. The indication for carotid surgery may or may not include the presence of symptoms, but all indications include the presence of an atherosclerotic plaque that may result in embolic or occlusive disease. Because the protective results of surgery depend on accurately defining the presence of these plaques and the degree of carotid artery stenosis, it is essential to understand the diagnostic methods used in determining carotid disease and grading carotid artery stenosis. An understanding of their reliability and associated risks is essential for the proper management of patients with carotid bifurcation disease.

Carotid Artery Diseases↗

PubMed1999

Nonimmunoglobulin gene hypermutation in germinal center B cells.

Somatic hypermutation is the most critical mechanism underlying the diversification of Ig genes. Although mutation occurs specifically in B cells during the germinal center reaction, it remains a matter of debate whether the mutation machinery also targets non-Ig genes. We have studied mutations in the 5' noncoding region of the Bcl6 gene in different subtypes of lymphomas. We found frequent hypermutation in follicular lymphoma (25 of 59 = 42%) (germinal center cell origin) and mucosa-associated lymphoid tissue (MALT) lymphoma (19 of 45 = 42%) (postgerminal center), but only occasionally in mantle cell lymphoma (1 of 21 = 4.8%) (pregerminal center). Most mutations were outside the motifs potentially important for transcription, suggesting they were not important in lymphomagenesis but may, like Ig mutation, represent an inherent feature of the lymphoma precursor cells. Therefore, we investigated their normal cell counterparts microdissected from a reactive tonsil. Bcl6 mutation was found in 13 of 24 (54%) clones from the germinal centre but only in 1 of 24 (4%) clones from the naive B cells of the mantle zone. The frequency, distribution, and nature of these mutations were similar to those resulting from the Ig hypermutation process. The results show unequivocal evidence of non-Ig gene hypermutation in germinal center B cells and provide fresh insights into the process of hypermutation and lymphomagenesis.

Adult↗

PubMed1999

Protective effects of memantine against ischemia-reperfusion injury in spontaneously hypertensive rats.

Memantine, an uncompetitive NMDA open-channel blocker, has been shown to be effective in preventing neuronal damage after permanent focal cerebral ischemia. Reperfusion after a long period of ischemia may aggravate the progression of neuronal damage. Those drugs that show protective effects after permanent cerebral ischemia, therefore, might fail to do so against ischemia-reperfusion injury. In this study we evaluated the effects of memantine on brain edema formation and ischemic injury volume after transient cerebral ischemia. Male Spontaneously Hypertensive Rats (SHR) weighing 250-300 g were anesthetized with halothane and subjected to 1 hour of temporary middle cerebral artery occlusion by an intraluminal suture. 20 mg/kg of memantine or saline were injected intraperitoneally 5 min. after the induction of ischemia. Physiological parameters and regional cerebral blood flow were monitored during the surgical procedure. Brain water content and ischemic injury volume were measured with the wet dry method and 2,3,5-triphenyl tetrazolium chloride monohydrate (TTC) staining, respectively, at 24 hours after occlusion. There were no statistically significant differences between the groups regarding physiological parameters during the procedure. Memantine treatment (n=9) reduced the brain water content significantly in the cortex compared to saline treatment (n=8; 83. 1+/-0.7% vs. 84.5+/-1.5%, respectively, p<0.05). The total volume of ischemic brain injury was 300+/-49 mm(3) in the animals treated with saline (n=13). Treatment with 20 mg/kg memantine (n=14) reduced the ischemic injury volume to 233+/-61 mm(3) (P<0.01). These results demonstrate that the harmful effects of recirculation after a period of ischemia can be attenuated by the treatment of memantine, perhaps by its action at the NMDA receptors.

Animals↗

PubMed1999

Fulminant hepatic failure caused by adenovirus infection following bone marrow transplantation for Hodgkin's disease.

Adenoviruses are increasingly realised to be responsible for serious morbidity and mortality following allogeneic bone marrow transplantation. We describe a case of fulminant hepatic failure due to adenovirus serotype 2 in a 39-year-old woman who received a matched sibling allogeneic bone marrow transplant for multiply relapsed Hodgkin's disease. Isolated fulminant hepatic failure caused by this serotype of adenovirus has not previously been described.

Adenoviridae Infections↗

PubMed1999

Traumatic injury to rat brain upregulates neuronal nitric oxide synthase expression and L-[3H]nitroarginine binding.

Overstimulation of N-methyl-D-aspartate (NMDA) receptors is felt to precipitate the neuronal damage following traumatic brain injury (TBI). NMDA receptor-mediated, glutamate-induced excitotoxicity is thought to be mediated via nitric oxide (NO) formed by neuronal nitric oxide synthase (nNOS). The present study examined the mRNA and protein levels of nNOS in the ipsilateral and contralateral cortex of rats as a function of time (5 minutes to 1 week) after controlled cortical impact (CCI) brain injury. Sham-operated rats served as controls. TBI resulted in a significant increase in the levels of nNOS mRNA (1.5- to 2.8-fold, p < .05) between 2 and 4 hours after the injury. There was also a significant increase in the levels of nNOS protein (by 55% to 90%, p < .05) and binding densities of the nNOS-specific ligand L-[3H]nitroarginine (L-[3H]NOARG) (by 35% to 59%, p < .05) between 2 and 12 hours after the injury. Increased nNOS expression and function may contribute to the concomitant excitotoxic neuronal death after TBI.

Animals↗

PubMed1998

Extrathymic T cell differentiation in the human intestine early in life.

It is clear from experimental studies in mice that T cell maturation can occur outside the thymus, especially in the intestine. There is little sound evidence so far that extrathymic T cell maturation occurs to any significant extent in human gut, and, postnatally, there is abundant evidence that the gut mucosa is an immune effector organ. Here, we describe a large population of T lymphocytes in human fetal intestinal mucosa that are proliferating (Ki67+) in the absence of foreign Ag (CD3+, Ki67+ lamina propria lymphocytes (LPL) 22 +/- 1.8% and CD3+, Ki67+ intraepithelial lymphocytes (IEL) 9.1 +/- 1.4%), that express the T cell activation markers CD103, HLA-DR, and L-selectin(low), and that express mRNA transcripts for pre-TCR-alpha. There is also a substantial proportion of CD7+ LPLs that do not express CD3 (CD3-7+, 14 +/- 7% of all LPLs) in the fetal gut that may be differentiating into CD3+ cells. Rearranged TCR-beta transcripts of fetal LPLs, IELs, and paired blood lymphocytes were cloned and sequenced, and virtually no overlap of clonality was observed between blood and intestine, suggesting that gut T cells may not be derived from the blood. In addition, 30 days after engraftment of SCID mice with fetal intestine, CD3-7+ cells, proliferating T cells, and pre-TCR-alpha transcripts were abundant, and there is a threefold increase in CD3+ IELs. These data show that in the human intestine before birth a population of precursor T cells exists that may be differentiating into mature T cells in situ.

Aging↗

PubMed1998

Follicular lymphomas contain a clonally linked but phenotypically distinct neoplastic B-cell population in the interfollicular zone.

Follicular lymphomas are thought to arise from the follicle center B cells and are characterized by follicular structures that recapitulate many features of normal secondary lymphoid follicles. The neoplastic B cells of follicular lymphoma reside not only in follicles but also in the interfollicular zone in which they form a diffuse infiltrate. We have investigated the frequency, extent, and biological characteristics of this interfollicular component in 30 cases of follicular lymphoma. An interfollicular B-cell infiltrate of variable extent (minimal, moderate, or prominent) was present in all cases. Morphologically interfollicular neoplastic B cells were small centrocyte-like cells with lower grade cytology and lower proliferation fraction compared with the neoplastic follicles. The neoplastic phenotype of these cells (CD20+, light chain restricted) was confirmed in 18 cases. Clonal identity between the follicular and interfollicular components was shown in five cases using microdissection and PCR amplification of immunoglobulin heavy chain genes. Analysis of Ig heavy chain gene sequences showed identical variants of tumor subclones in both follicular and interfollicular compartments, indicating active tumor cell traffic between the two. In six cases in which frozen tissue was available, the immunophenotype of follicular and interfollicular tumor cells were compared using immunohistochemistry. Activation markers such as CD10, CD38, and CD95 and T-cell costimulatory molecules CD80 and CD86, which were expressed by neoplastic follicles, were either downregulated or absent in the interfollicular component in most of the cases. The low-grade cytological features, low proliferation fraction, and downregulation of activation markers in the interfollicular neoplastic B cells suggests that these are resting cells analogous to memory B cells of normal lymphoid tissues. The presence of such a resting tumor cell subpopulation in the majority of follicular lymphomas may partly account for the remarkable resistance to therapy of this disease.

Antigens, CD↗

PubMed1998

Fluorometric assay of nitrite and nitrate in brain tissue after traumatic brain injury and cerebral ischemia.

Nitric oxide synthase (NOS) is distributed within the brain, and nitric oxide (NO) is felt to be involved in the pathophysiology of deterioration after head injury and cerebral ischemia. This study determined the levels of the stable end products of NOS (NOx=nitrite+nitrate) after traumatic brain injury (TBI) and transient cerebral ischemia. A fluorometric assay using nitrate reductase and the NADPH regenerating system was used to quantitate NOx in ultrafiltered (10-kDa cutoff) cortical and hippocampal extracts after reduction of nitrate. In TBI rats, both the plasma and tissue showed a sharp increase in NOx levels 5 min after injury. Plasma NOx returned to control levels by 2 h after injury. Ipsilateral-cortex NOx levels returned to control levels approximately 6 h after injury and remained constant from 6-24 h. Contralateral-cortex returned near to control levels after 1 h. Hippocampus also followed a similar trend. In gerbils, there was a significant elevation in tissue NOx levels immediately after 10 min transient cerebral ischemia, which gradually returned to control levels over 24 h reperfusion. This striking burst of NO synthesis immediately after injury is clearly evident whether the injury is head trauma or ischemia, or whether the measurements were performed on tissue or plasma. It is unknown whether endothelial NOS, neuronal NOS, or both caused the elevation of the NO end products seen after the CNS insults.

2-Naphthylamine↗