Topotecan-induced celluitis-like fixed drug eruption.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Aydin.
Explore the source record for details and available documents.
AIMS: The objective of this study was to subtype Arcobacter butzleri isolates using RAPD-PCR. METHODS AND RESULTS: Thirty-five A. butzleri isolates obtained from chicken carcasses were examined. PCR-mediated DNA fingerprinting technique with primers of the variable sequence motifs was used to detect polymorphism within the isolates. Eleven distinct DNA profiles were obtained as follows: Of the 35 strains, 10 as profile 4; seven as profile 1; five as profile 3; three as profiles 2 and 9; two as profile 10; one as profiles 5, 6, 7, 8 and 11. CONCLUSIONS: Chicken carcasses sold in markets were found to be contaminated with several different strains of A. butzleri. RAPD-PCR technique was found to be a useful technique for distinguishing A. butzleri isolates. SIGNIFICANCE AND IMPACT OF THE STUDY: The presence of several different A. butzleri strains on chicken carcasses may indicate multiple sources of contamination. The epidemiological role of A. butzleri in human and animal diseases should be investigated further.
Granulocyte-colony stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) are being administered to patients with neutropenia. However, little is known about the endogenous levels of both factors in these patients. We measured the endogenous G-CSF levels in patients with chemotherapy-induced neutropenia (n=15, study group A), in patients who had not received chemotherapy with neutropenia caused by a number of primary diseases (n=14, study group B) and in healthy volunteers (n=15, control group). Both the study groups and the control group did not show any clinical or laboratory findings of infection. The G-CSF levels were elevated in patients following chemotherapy and in patients who had neutropenia without chemotherapy, but the mean G-CSF levels in patients with chemotherapy-induced neutropenia were significantly higher than in patients with primary diseases. The levels of endogenous G-CSF were also higher in both neutropenic groups, compared to the control group. In conclusion, endogenous G-CSF levels in chemotherapy-induced neutropenia were significantly higher than non-chemotherapy related neutropenia and controls. This may be explained as G-CSF synthesizing bone marrow stromal cells may be more affected in primary disease related neutropenia than in chemotherapy induced neutropenia.
PURPOSE: To determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of twice-weekly gemcitabine (TW-G) when administered in conjunction with fixed dose amifostine (A) during external radiotherapy (RT) in patients with advanced pancreatic cancer. METHODS AND MATERIALS: Ten patients with previously untreated, locally advanced, or asymptomatic-metastatic pancreatic adenocarcinoma were enrolled in this study. RT was delivered by using the standard four-field technique (1.8 Gy daily fractions, 45 Gy followed by a boost of 5.4 Gy, in 5-1/2 weeks). The starting dose of TW-G was 60 mg/m(2) (i.v., 30-min infusion), which is equal to the upper limit of previously reported MTD of TW-G when given without A during RT. A was given just before the TW-G, at a fixed dose of 340 mg/m(2) (i.v., rapid infusion). TW-G doses were escalated by 30-mg/m(2) increments in successive cohorts of 3 to 6 additional patients until DLT was observed. Toxicities were graded using the Radiation Therapy Oncology Group and National Cancer Institute Common Toxicity Criteria, version 2.0. RESULTS: In general, therapy was well tolerated in patients treated at the first two dose levels of 60 mg/m(2) and 90 mg/m(2). The DLT of TW-G given in conjunction with A during RT were neutropenia, thrombocytopenia, and nausea/vomiting at the dose level of 120 mg/m(2). Of the 10 patients eligible for a median follow-up of 10 months, 5 remain alive; 1 complete responder, 3 partial responders, and 1 with stable disease. CONCLUSION: A dose of TW-G at a level of 90 mg/m(2) produced tolerable toxicity and it may possess significant activity when delivered in conjunction with 340 mg/m(2) dose of A during RT of the upper abdomen. Due to the higher MTD of TW-G seen in our study, we consider that the A supplementation may optimize the therapeutic index of TW-G-based chemoradiotherapy protocols in patients with pancreatic carcinoma.
AIMS: The objectives of this study were to determine the presence of thermophilic Campylobacter spp. in free range domestic geese, and to characterize isolated strains using phenotyping criteria and SDS-PAGE of whole-cell proteins. METHODS AND RESULTS: Forty cloacal swabs from two different flocks of domestic geese were examined. All Camp. jejuni strains isolated from geese were biotyped using the Lior biotyping scheme. Twelve Camp. jejuni isolates were also tested for their susceptibility to 17 different antibacterial agents by a disc diffusion METHOD: Fourteen of the isolates were also subjected to SDS-PAGE. All of the geese examined were found to harbour Camp. jejuni. Six geese carried more than one species of Campylobacter. All strains examined were susceptible to various antibiotics but resistant to penicillin G and cephalothin. Eleven strains (92%) were resistant to sodium cefuroxime, and eight (67%) were resistant to cloxacillin, ampicillin and colistin sulphate. Three strains (25%) were resistant to tetracycline, and one strain was resistant to sulfamethoxazole/trimethoprim and kanamycin. Nine strains were subtyped as Camp. jejuni subsp. jejuni biotype II and the remaining ones as biotype I. There were 96% and 100% similarities between all the strains examined by SDS-PAGE. CONCLUSION: This study showed that Camp. jejuni were common in the intestinal tract of domestic geese. SIGNIFICANCE AND IMPACT OF THE STUDY: Geese should be considered as potential reservoirs for human and animal campylobacteriosis. The antibiotic resistance data from this study also showed that fluoroquinolone resistance, which appears to be a problem in poultry isolates in some countries, is not yet a problem in these geese.
AIMS: The objective of this study was to determine the susceptibility of Arcobacter butzleri isolates to various antimicrobial agents used in the treatment of infectious diseases in humans and animals. METHODS AND RESULTS: Thirty-nine A. butzleri strains isolated from broiler chickens were tested for their susceptibility to 23 antimicrobial agents using a disc diffusion method. All isolates were resistant to aztreonam, cefuroxime sodium, cephalothin, orbenin, oxacillin, penicillin G and trimethoprim/sulphamethoxazol. Of the 39 isolates tested, 26 were also found resistant to amoxycillin, amoxycillin/clavulanic acid and ampicillin. One isolate was resistant to, and four showed intermediate level of resistance to, erythromycin. All isolates were susceptible to amikacin, chloramphenicol, danofloxacin, enrofloxacin, nitrofurantoin, nalidixic acid, tetracyclines and tobramycin. CONCLUSIONS: The majority of the isolates were found resistant to antibiotics commonly used for the treatment of infectious bacterial diseases in humans and animals. SIGNIFICANCE AND IMPACT OF THE STUDY: This study shows that A. butzleri strains vary in their resistance to certain kinds of antibiotics and caution should be taken when choosing a suitable antibiotic for the treatment of disease(s) caused by this organism.
BACKGROUND AND OBJECTIVE: Hepatocyte growth factor (HGF) is known to augment the effects of stem cell factor, interleukin-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), erythropoetin, and granulocyte colony-stimulating factor, all of which are involved in hematopoiesis. HGF is also known to have a role in immune responses. The aim of this study was to investigate whether HGF is involved in the development of dendritic cells (DC) from CD34+ bone marrow cells. DESIGN AND METHODS: CD34+ cells obtained from three healthy donors were incubated in various combinations of HGF, GM-CSF, and tumor necrosis factor (TNF) for 12 days. Developing cell populations were analyzed for surface markers, morphology and functional capacities by flow cytometry, light microscopy and mixed lymphocyte reaction, respectively. RESULTS: Incubation with HGF alone generated greater number of dendritic cells from CD34+ bone marrow cells than incubation with GM-CSF, or a combination of GM-CSF with TNF. HGF was also found to potentiate the effect of GM-CSF on DC and monocyte development. The effects of HGF were inhibited by the concurrent use of TNF. INTERPRETATION AND CONCLUSIONS: HGF appears to be a significant factor in the development of dendritic cells from CD34+ bone marrow cells.
Vasa vasorum are adventitial vessels that play a role in pathogenesis of atherosclerosis, aneurysm, vasculitides, and graft vascular disease. The existence of vasa vasorum in human intracranial arteries is not yet well defined. The specific aims of this study are to determine whether the human intracranial arteries have vasa vasorum, whether their existence is related to the thickness of tunica media as is in systemic vessels, and whether they are acquired in reaction to pathological conditions, such as atherosclerosis and arterial occlusion. Human intracranial internal carotid (i-ICA), vertebral (i-VA), basilar (BA) and middle cerebral arteries (MCA) from adults, children and newborns were examined. Systemic vessels of comparable medial thickness were used as controls. Immunohistochemical staining for Factor VIII and CD 31 was used to identify the endothelial cells. Human intracranial arteries in neonates, children and adults do not have vasa vasorum, although their medial thickness is comparable to their systemic counterparts with vasa vasorum. Only in adults did the proximal intracranial segments of i-ICA and i-VA reveal a few vasa vasorum-like vessels with unusually large diameter. They were more frequently seen in atherosclerosis and thrombotic but again limited to the proximal segments of i-ICA and i-VA. Completely obstructed bilateral carotid arteries in a child with sickle cell disorder revealed a rich adventitial neovascularization in the proximal intracranial part of the vessel. It is not yet known whether obstruction of the distal segments may create similar neovascularizations. Adventitial neovascularizations seen in the proximal i-ICA and i-VA may represent a focal intracranial extension of the vascular pathologies involving the extracranial segments of major cerebral arteries.
Explore the source record for details and available documents.
Endogenous cytokine release and bone marrow cellularity of cancer patients receiving chemotherapy were investigated to elucidate the effect of high dose medroxyprogesterone acetate (MPA). MPA (1000 mg/day p.o.) was started after the first cycle of chemotherapy in patients with neutropenia. Administration of MPA was stopped a week after the second cycle of chemotherapy. Blood samples and bone marrow aspirations were obtained for granulocyte macrophage-colony stimulating factor (GM-CSF) assay one week after the first and second cycles of chemotherapy. GM-CSF levels and bone marrow cellularities were compared before and after MPA treatment. Twelve of fifteen patients included in the study had a significant decrease in endogenous cytokine (GM-CSF) secretion after high dose MPA treatment. This result supports the hypothesis that decreased cytokine release leads to a decrease in myeloid progenitor cell proliferation and protects cells from the cytotoxic effects of chemotherapy. As a result of this protection, the myeloid cell population increases in bone marrow. No changes in erythrocytes and platelet counts were obtained.
The clinical case of a patient with a low-grade lymphocytic neoplasia is presented. The autopsy findings revealing the transformation of the process into a prolymphocytic dyscrasia are also illustrated. The differential diagnosis is discussed.
OBJECTIVE: To present, to our knowledge, the first case of primary central nervous system T-cell lymphoma in the setting of acquired immunodeficiency syndrome. Design.Clinical, radiological, laboratory, and pathological data from a young patient at advanced stage of acquired immunodeficiency syndrome were studied. RESULTS: A 38-year-old white man with stage CIII human immunodeficiency virus infection presented with headaches. Cerebrospinal fluid culture was positive for mycobacterium. He had facial herpes simplex virus and disseminated cytomegalovirus infections. Magnetic resonance imaging of the brain showed multiple areas of patchy or ring-shaped contrast enhancement in the periventricular zone of the right frontoparietal region. Stereotactic brain biopsy showed perivascular CD3 (pan T-cell marker)-positive lymphocytic infiltrates with partial necrosis extending into the neuropil. Not a single cell was labeled with L26, a B-cell marker. Negative and positive controls were appropriate. Special stains for cytomegalovirus, herpes simplex virus, Epstein-Barr virus, acid-fast bacilli, and fungi were negative. Gene rearrangement studies showed rearranged Tgamma and Tbeta bands. Polymerase chain reaction with a primer specific for Epstein-Barr virus genome-encoding nuclear antigen 1 region was positive. Human T-cell leukemia/lymphoma virus I work-up was negative. The patient was treated for mycobacteria. Four months later, he presented with a paravertebral neck mass. Needle biopsy showed a T-cell lymphoma with morphology similar to that in the brain. CONCLUSIONS: To our knowledge, this case represents the first example of T-cell lymphoma of the brain in a patient with advanced stage of acquired immunodeficiency syndrome. Epstein-Barr virus may play a role in T-cell lymphomagenesis. The other unique finding is the complete absence of B cells in a central nervous system lesion. The underlying mechanism eradicating the B cells is unknown.
To develop a primate model for liver-directed gene therapy, we studied several gene transfer vehicles and routes in eight rhesus monkeys (Macaca mulatta). For this purpose, we used first-generation, replication-deficient adenoviral vectors carrying the Escherichia coli lacZ gene (Ad.CMVlacZ) or a lacZ-containing plasmid (pCMV beta) with lipofectamine for transfection. The reporter gene construct was infused into either the portal vasculature, common bile duct, or saphenous vein. Adenovirus-mediated gene transfer via the portal vein resulted in expression of lacZ in over 70% of hepatocytes by days 3-7, but was accompanied by acute hepatitis. Adenovirus-mediated gene transfer via the common bile duct resulted in lacZ expression in less than 10% of hepatocytes and was accompanied by portal inflammation. The animals mounted a significant immune response, as demonstrated by adenoviral antigen-induced T-cell proliferation and production of neutralizing anti-adenovirus antibodies and antibodies to E. coli beta-galactosidase (beta-Gal). Activation of the immune response was associated with rapid decrease of the reporter gene by days 13-21. Lipofectamine-mediated gene transfer was inefficient, and no lacZ expression in the liver was detected. To limit the host immune response, 4 animals were immunosuppressed by cyclophosphamide/prednisone and then infused with the Ad.CMVlacZ via the portal vein or the saphenous vein. The monkeys showed sustained expression of lacZ for up to 35 days with no evidence of inflammation. The primates transduced via the saphenous vein showed a level of beta-Gal expression in the liver similar to that of the portal vein-infused animals. In conclusion, adenovirus-mediated gene transfer to non-human primate livers via the portal vein or saphenous vein is efficient, but it results in transient expression and is accompanied by an immune response to both vector and transgene products and acute hepatitis, whereas lipofectamine-mediated transfer is inefficient. Manipulation of the host immune response may expand potential applications of adenoviral vectors for liver-directed gene transfer.
The aim of the study was to investigate the effects of high-dose medroxyprogesterone acetate (MPA) on the tumor necrosis factor-alpha (TNF-alpha) release in patients with chemotherapy-induced neutropenia. We also evaluated the effects of high-dose MPA on hematological parameters (leukocyte, neutrophil, platelet, hemoglobin, hematocrit) and side effects of MPA. One week following the first cycle chemotherapy, 20 patients who developed neutropenia were enrolled in the study. One gram/day MPA was administered orally to the patients and was continued from one week following the first chemotherapy cycle to one week after the second chemotherapy cycle. The patients received the second chemotherapy cycle at the same dosages as the first cycle. Before MPA treatment TNF-alpha levels were lower than post-treatment levels, but the difference was not statistically significant (P > 0.05). The differences in the mean leukocyte and neutrophil counts before and after the high-dose MPA treatment were statistically significant (p < 0.05).
Forty patients with aggressive (intermediate-grade and high-grade) non-Hodgkin's lymphoma (NHL) were treated primarily with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy regimen, and then evaluated for prognostic features. Age, tumor stage, performance status, number of extranodal disease sites and serum concentrations of lactate dehydrogenase (LDH) were considered prognostic features. All the patients treated with the CHOP regimen were grouped into four risk categories, including low (L), low-intermediate (LI), high-intermediate (HI) and high (H) according to the International Prognostic Index. Twenty-one of 23 patients (91.3%) in the L plus LI risk groups and 5 of 17 patients (29.4%) in the H plus HI risk groups had complete response and the difference between these percentages was statistically significant (P<0.001). The overall survival rate (2 yr) of 23 patients in the L+LI risk group was 52.1% and of 17 patients in H+HI risk group was 11.7% and this difference was statistically significant (P<0.05). Our results indicated that the CHOP regimen is not effective in the HI+H risk groups of patients with aggressive NHL. New experimental approaches are needed for these patients.
A young male patient, who previously was presumed inoperable due to an existing hepatic mass with multiple cerebral metastases, was referred to us from an oncology clinic ith signs of transtentorial herniation. An operation was performed promptly; the right parietal mass, which was totally removed, proved to be an alveolar hydatid cyst. He refused the operation proposed for the hepatic lesion and was discharged.
Antibodies directed against epidermal growth factor receptor (EGFr) impede proliferation and induce differentiation of EGFr-positive cancers. To explore the effectiveness of anti-EGFr monoclonal antibodies on acoustic neuromas (ANs), we first sought to evaluate EGFr expression by ANs. The records of all patients with the diagnosis of AN at our institution from January 1989 to July 1994 were reviewed. Immunohistochemical analysis for EGFr was performed on formalin-fixed, paraffin-embedded archival surgical specimens. Skin, liver, and placenta were used as positive tissue controls. Purified rabbit immunoglobulin G replacing the experimental antibody acted as a negative control, and normal eighth cranial nerve was evaluated for background staining. Slides were scored as 0, +, ++, or and for percentage of positive cells by two pathologists, with Antoni A and Antoni B areas scored separately. Results demonstrate that most tumors are revealed to be EGFr positive with a mild degree of staining. Antoni A areas generally have greater staining than Antoni B regions, while normal eighth cranial nerves demonstrate minimal background staining. These results suggest that ANs express low levels of EGFr, with Antoni A areas having the highest levels. While further studies may more accurately quantitate EGFr levels in these tumors, the clinical efficacy of anti-EGFr-based therapies for ANs seems doubtful.
We report a case of radiation-induced dural fibrosarcoma in a 9.5-year-old male patient who was treated with radiation for medulloblastoma. He received a total dose of 53.2-Gy radiation, delivered at 1.6 and 1.8 Gy per fraction with a 6 MV linear accelerator using the standard cranial-spinal technique. A sequential magnetic resonance image at 15 months after the completion of radiation therapy showed a mass above the cerebral convexity that increased two-fold in size within a period of 4 months. The tumor showed characteristics of a low-grade fibrosarcoma. This case emphasizes the potential risk of early development of a second neoplasm after therapeutic radiation, especially in children, and also documents what is to our knowledge the shortest latent period between the administration of radiation therapy and the development of an intracranial fibrosarcoma that has been reported.