Search PubMed⌕ Search

Biomedical subjects

A Yildiz

Publications and source records attributed to A Yildiz.

95 records · Page 6Linked to original sources

Immunofluorescence demonstrates the distribution of actin, myosin and intermediate filaments in cultured neuroblastoma cells.

Monolayers of cultured neuroblastoma cells were examined for immunofluorescent reactivity with antibodies directed against actin, myosin or intermediate filaments. In well spread cells, antibody to intermediate filaments stained an intricate cytoplasmic network which extended as filament bundles into cell processes; in poorly spread or rounded cells, the antibody stained thick juxtanuclear filament bundles. By contrast, antibodies to actin or myosin reacted with microspikes and with axonal growth cones. The different topographical distribution of actin, myosin and intermediate filaments suggests that while actin and myosin may have roles in axon elongation, intermediate filaments may function as an internal cytoskeleton as well as in axoplasmic transport. The different distribution of intermediate filaments in well spread compared with rounded cells suggests that the cell makes its filaments prior to axon development and that the filaments subsequently unwind and migrate into the cell processes to form the axon skeleton.

Actins↗

Cytoplasmic intermediate filaments in cultured glial cells.

Monolayer cultures of rat glial cells derived from 12 to 14 day fetal spinal cords and rat C6 glioma cells were examined for immunofluorescent reactivity with human or rabbit autoantibodies to intermediate filaments and with rabbit antibody to GFAP. The embryonic glial cells and C6 glima cells reacted identically with both. Protoplasmic astrocytes gave immunofluorescent staining of an intricate network of cytoplasmic filaments while fibrous astrocytes and C6 glioma cells gave diffuse cytoplasmic staining of the cell body and cell processes. Cells, pretreated with colchicine or vinblastine, showed staining of thick coils of peri-nuclear, circum-nuclear, or juxtanuclear filaments. The observations suggest that intermediate filaments in glial cells contain unique antigenic determinants as well as antigenic determinants shared with intermediate filaments in other cell types,

Animals↗

QT dispersion and signal-averaged electrocardiogram in hemodialysis and CAPD patients.

OBJECTIVE: The aim of this study was to compare QT dispersion (QTd) and signal-averaged electrocardiogram (SA-ECG) parameters that may predict risk of malignant arrhythmias in patients on hemodialysis (HD), on continuous ambulatory peritoneal dialysis (CAPD), and in controls. SETTING: Controlled cross-sectional study in a tertiary-care setting. PATIENTS: 28 HD (M/F 18/10; mean age 32 +/- 9 years), 29 CAPD (M/F 17/12; mean age 34 +/- 10 years), and 29 healthy controls (M/F 17/12; mean age 32 +/- 8 years) were included. INTERVENTIONS: On ECG, minimum (QTmin) and maximum (QTmax) QT duration and their difference (QTd) were measured. In SA-ECG, duration of filtered QRS, HFLA signals less than 40 microV, and RMS voltage (40 ms) were also measured. RESULTS: Higher serum Ca2+ and lower K+ levels were found in CAPD compared to HD. All QT parameters were increased in HD and CAPD compared to controls. QT dispersion was significantly prolonged in HD compared to CAPD. In HD, QTd was correlated with left ventricular (LV) mass index (r = 0.53, p = 0.004), but not in CAPD (r = -0.09, p = 0.63). QT dispersion was significantly prolonged in patients with LV hypertrophy compared to patients without hypertrophy on HD (68 +/- 18 ms vs 49 +/- 18 ms, p = 0.008). In the analysis of SA-ECG, 3 of the 28 (11%) HD and 2 of the 29 (7%) CAPD patients had abnormal late potentials. Patients on HD and CAPD had significantly higher filtered-QRS duration compared to controls (105 +/- 15 ms and 104 +/- 12 ms vs 95 +/- 5 ms, respectively, p = 0.04). Patients with LV hypertrophy had higher filtered-QRS duration compared to patients without hypertrophy (109 +/- 12 ms vs 95 +/- 8 ms, p < 0.001). CONCLUSION: Dialysis patients had prolonged QTd and increased filtered-QRS duration in SA-ECG compared to controls. Patients on HD had longer QTd than patients on CAPD. QTd has been correlated to LV mass index in HD, but not in CAPD. This difference might be due to the effect of different dialysis modalities on electrolytes, especially the higher serum Ca2+ levels.

Adult↗

Cardiac and intestinal amyloidosis in a renal transplant recipient with familial Mediterranean fever.

In Turkey, familial Mediterranean fever (FMF) is an important cause of nephrotic syndrome and endstage renal disease due to renal deposition of AA type amyloid. We report a case of living-related donor renal transplant recipient with FMF and renal AA type amyloidosis, who died of progressive heart failure due to cardiac involvement. The patient also had intractable diarrhea caused by biopsy-proven intestinal amyloidosis. The patient was on 1 mg/day colchicine. Although he was attack-free throughout the post-transplant period, intestinal and clinically significant cardiac amyloidosis, which implied the presence of sustained inflammation and continuing amyloid deposition, appeared three years after renal transplantation. Cardiac deposition of AA amyloid may cause clinically significant heart disease, leading to cardiovascular mortality after renal transplantation for end-stage renal disease in FMF patients.

Adult↗

Successful therapy combined with surgery for severe post-transplant nocardiosis.

We report a case of a 35-year-old man with nocardiosis infection involving soft tissue and the central nervous system who had received a cadaveric donor kidney. The patient was admitted with fever, malaise and right shoulder pain. Soft tissue abscess was seen on ultrasound examination. It was presumed due to gram (+) microorganisms, so 4 g day (IV) ampicillin/sulbactam was started empirically once the abscess was drained. Nocardia asteroides was found in the pus specimen. On the second day in hospital, severe headache, ataxia and signs of meningeal irritation appeared. The cranial CT showed two intracranial abscesses in the frontal lobe and cerebellum. We assumed Nocardia asteroides was the infective agent for the cerebral abscesses, so antibiotic therapy was switched to trimethoprim-sulphamethox-asole (3x160/800 mg/d). Nausea and vomiting occurred on the fifth day of therapy, improving after drainage from the frontal abscess. However, these complaints recurred five days later. CT showed cerebellar abscess had become bigger. The patient's complaints improved after the second surgical drainage. N. asteroides was again grown in the aspiration fluids of both cerebral abscesses. Complete regression of the abscesses was seen in the CT after two months. Co-trimoxazole was continued for six months then withdrawn. Graft dysfunction was not observed. Early medical and surgical interventions may be life-saving in this potentially lethal disease.

Adult↗