PubMed Health⌕ Search

Biomedical subjects

R Pyka

Publications and source records attributed to R Pyka.

7 recordsLinked to original sources
PubMed1993

Vertebrodiatasis experimental lengthening of the juvenile goat spine.

The purpose of this study is to describe the biology of spinal lengthening (vertebrodiatasis) in a juvenile goat model. A small Orthofix dynamic fixator was affixed to 5.5 mm pedicular halfpins placed bilaterally at T12, L1, L5 and L6 in six juvenile goats. Distraction was performed across vertebral endplates between L1 and L5. Uninstrumented twins served as controls. Two pairs of animals were deleted due to anesthetic complications. Lumbar lengthening was successful in 3 animals resulting in an increase in length of up to 696% from L1 to L5 compared to the growth rate of the controls (mean 4.3 cm vs. mean .56 cm, respectively). Lengthening of the spinal cord was not associated with brain stem migration or spinal cord injury.

Animals↗
PubMed1993

Placement of a ferromagnetic intracerebral aneurysm clip in a magnetic field with a fatal outcome.

Magnetic resonance (MR) imaging may be contraindicated in patients with biomedical devices, among the most dangerous of which are intracranial aneurysm clips, owing to the possibility of torque and dislodgement. A case is presented in which a patient with a reportedly nonferromagnetic clip was placed in a magnetic field. The patient developed an acute intracerebral hemorrhage in the MR unit, with a fatal outcome. Imaging studies strongly suggested a torqued clip as the cause. Autopsy revealed a torn middle cerebral artery from clip movement, and the clip was identified as a ferromagnetic type. This is the first reported case, to the authors' knowledge, of a fatal outcome due to an intracranial aneurysm clip placed in a magnetic field.

Acute Disease↗
PubMed1986

Lymphocyte subsets and activation in prediabetes.

Peripheral blood lymphocytes were obtained from 65 individuals: 34 nondiabetic patients with islet cell autoantibodies (ICA) (prediabetic phase), 9 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM), 6 ICA-negative siblings or offsprings of IDDM patients, and 16 ICA-negative controls. The presence of lymphocyte abnormalities and/or activation was examined with dual fluorescence flow cytometry. The percentages of B cells, total T-lymphocyte, and helper T-lymphocyte (Th) and cytotoxic/suppressor T-lymphocyte (Tc/s) subsets and their ratio were not significantly different among the patient groups. No increased expression of interleukin 2 receptor on T-lymphocyte was found in newly diagnosed IDDM or prediabetic individuals. Sixteen of 49 patients had significantly increased number of T-lymphocyte expressing HLA-DR. A significant increase in the number of both Th and Tc/s subsets expressing HLA-DR was found in only 3 of 16 patients. This increase was unrelated to the patients's relative ICA titer or HLA-DR phenotype. On the other hand, the relative density of the DR antigen (RAD-DR) was significantly increased on both Th (886 +/- 120) and Tc/s (1250 +/- 273) in 13 of 38 patients compared with control patients (Th 484 +/- 129 and Tc/s 460 +/- 166). The RAD-DR on Tc/s correlated with the relative ICA titer and was greatest on DR3/4-phenotyped T-lymphocytes. In addition, significantly increased RAD-DR was found in noncontrol patients with impaired insulin release responses at 1 and 3 min to intravenous glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1976

[Detection of HBSAG in cerebrospinal fluid by means of a radioimmunoassay technique (author's transl)].

HBSAg was demonstrated radioimmunologically in cerebrospinal fluid in 7 out of 11 seropositive children with acute viral hepatitis B (1/2), fulminant viral hepatitis (0/1), chronic active hepatitis (2/4), chronic persistent hepatitis (1/1), cirrhosis (1/1), and asymptomatic carrier status (2/2). Counterelectrophoresis and complement fixation test lacked the necessary sensitivity to detect the antigen even in patients with high serum concentrations. The pass over of the cerebrospinal barrier appears to be dependent of the serum titer. Some neurologic symptoms in the early stage of acute viral hepatitis are probably connected with the appearance of HBSAg in cerebrospinal fluid. It is however unlikely that central-nervous-system dysfunctions observed in association with fulminant viral hepatitis and coma result from a direct effect of HBSAg or hepatitis B-virus. In chronic carriers the cerebrospinal fluid probably contains the antigen more frequent. The cerebrospinal fluid of HBSAg-positive patients has to be regarded as an infectious agent.

Acute Disease↗