Biomedical subjects
Suat Simsek
Publications and source records attributed to Suat Simsek.
Paradoxical reaction on treatment with 131I.
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Microvascular disease in type 1 diabetes alters brain activation: a functional magnetic resonance imaging study.
Individuals with type 1 diabetes have mild performance deficits on a range of neuropsychological tests compared with nondiabetic control subjects. The mechanisms underlying this cognitive deterioration are still poorly understood, but chronic hyperglycemia is now emerging as a potential determinant, possibly through microvascular changes in the brain. In 24 type 1 diabetic patients, we tested at euglycemia and at acute hypoglycemia whether the presence of proliferative diabetic retinopathy, as a marker of microvascular disease, adversely affects the ability of the brain to respond to standardized hypoglycemia, using functional magnetic resonance imaging with a cognitive task. Patients with retinopathy, compared with patients without, showed less deactivation (hence, an increased response) in the anterior cingulate and the orbital frontal gyrus during hypoglycemia compared with euglycemia (P < 0.05). Task performance and reaction time were not significantly different for either group. We conclude that microvascular damage in the brain of patients with retinopathy caused this increased brain response to compensate for functional loss.
Severe atherosclerosis of the radial artery in a free radial forearm flap precluding its use.
The free radial forearm flap is the most frequently used free flap for head and neck reconstructions. Survival of free flaps is dependent on adequate blood supply. A 69-year old woman was scheduled for excision of a T3N0M0 oropharyngeal carcinoma, neck dissections and reconstruction with a free vascularized radial forearm flap. During the operation it appeared that the entire radial artery was almost completely obstructed by atherosclerotic plaques precluding microvascular anastomosis. Despite systemic risk factors certain artery types are more prone to develop clinically manifest atherosclerosis. There are no reports on the pathology of the radial artery in free flap reconstructions. In head and neck cancer patients severe atherosclerosis of the radial artery is very rare, but if present makes free radial forearm flap reconstruction impossible. Therefore, in patients with risk factors for peripheral vascular disease screening for radial artery stenosis should be considered.
Genetic analysis of patients with leukocyte adhesion deficiency: genomic sequencing reveals otherwise undetectable mutations.
OBJECTIVE: The aim of this study was to analyze mutations in DNA from patients with leukocyte adhesion deficiency (LAD), an immunodeficiency caused by absence of the beta(2) subunit (CD18) of the leukocyte integrins LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), p150,95 (CD11c/CD18), and CR4 (CD11d/CD18). METHODS: We developed genomic DNA PCR sequencing to detect mutations not only in exons but also in introns. RESULTS: Eight LAD patients were analyzed, of which five had homozygous mutations, i.e., a 0.8-kb deletion, a branchpoint mutation in intron 5 causing mRNA missplicing, a nonsense mutation, and two missense mutations. Four of these mutations are novel. We cotransfected the two mutant CD18 proteins with normal CD11a, b, or c in COS cells. This resulted in absence of all three beta(2) integrins on the surface of cells transfected with CD18(252Arg). However, CD18(593Cys) supported some LFA-1 and p150,95 formation in COS cells. The other three patients were compound heterozygotes in which only one allele had previously been characterized, because the other alleles were undetectable at the cDNA level. We identified the unknown mutations as a novel two-nucleotide deletion, a nonsense mutation, and a single nucleotide deletion. CONCLUSION: Our method allows identification of mutations in CD18 from genomic DNA. This opens the possibility of early prenatal diagnosis of LAD and reliable carrier detection.