Biomedical subjects
Publications and source records attributed to C Heller.
Isolated ischemia of the cervical spinal cord is an uncommon but increasingly recognized complication of vertebral artery dissection (VAD). The authors report a young patient with congenital afibrinogenemia, who developed VAD with extensive unilateral spinal cord infarction, probably caused by local compression of spinal radicular feeders at their origin by vertebral artery hematoma.
BACKGROUND: Traumatic stroke usually occurs after dissection of large extracranial or intracranial vessels, leading to disseminated cerebral embolism. Stretching and distorting forces in cerebral intraparenchymal end arteries can cause intimal lesions followed by an occluding thrombus. OBJECTIVE: To investigate the importance of traumatic endothelial lesions in intraparenchymal end arteries after minor head injuries. METHODS: The cases of eight children are reported. They were aged between two and seven years (mean 6.2 years), and they developed significant neurological deficits at 15 minutes to 72 hours (mean 16.3 hours) after minor head injuries. RESULTS: The the patients all had hemiparesis combined with other signs, including central facial paralysis, dysphasia, dysphagia, and extrapyramidal signs. Computed tomography or magnetic resonance imaging showed cerebral infarctions affecting branches of the middle cerebral artery (n = 3), anterior cerebral artery (n = 1), posterior cerebral artery (n = 1), and basilar artery (n = 3). These lesions affected the basal ganglia, the internal capsule, and the brain stem. Neither heart disease nor dissections of large vessels were present. Two children had prothrombotic risk factors (an increase in lipoprotein (a) and a factor V Leiden mutation). The follow up period was between three months and 13 years (mean 3.9 years). Outcome was classified according to the Glasgow outcome scale as moderate disability (n = 4), severe disability (n = 2), non-disabling sequelae (n = 1), and total recovery (n = 1). CONCLUSIONS: Minor head injuries can be cause and co-factor in the aetiology of stroke. The frequency of this may be underestimated, and detailed medical history of the days before stroke manifestation may identify more traumatic events, especially in the group of so called "idiopathic" strokes.
During the last decade, capillary electrophoresis (CE) of DNA has undergone rapid development. This improvement was especially important for DNA sequencing, where CE has now become a standard method facilitating to decipher several genomes within a very short time. Here, we give a review of the fundamentals of DNA separation in CE and the major factors influencing the performance.
BACKGROUND AND PURPOSE: We sought to compare different antithrombotic secondary treatments (mainly medium-dose aspirin with low-dose low-molecular-weight heparin [LMWH]) in pediatric patients with a first ischemic stroke onset with regard to the risk of stroke recurrence. METHODS: The population comprised 135 consecutively recruited children aged >/=6 months to </=18 years with a first episode of ischemic stroke (idiopathic, n=79; cardiac, n=15; vascular, n=30; infectious, n=11). The stroke patients enrolled received prophylactic antithrombotic therapy (aspirin, n=49; LMWH, n=86) in a nonrandomized fashion and were prospectively followed up for a median (range) of 36 (8 to 48) months. The study end point was recurrent stroke. RESULTS: Recurrent ischemic stroke was diagnosed at a median (range) of 5 (2 to 13) months after the first stroke onset in 13 of the 135 children (9.6%) receiving antithrombotic therapy. In the majority of cases (84.6%) the same vascular territory was involved. No significant difference was found with respect to the antithrombotic medication used (P=0.76, Fisher's exact test). No major drug-related side effects were observed. CONCLUSIONS: This prospective multicenter follow-up study has provided evidence that low-dose LMWH is not superior to aspirin and vice versa in preventing recurrent stroke in white pediatric stroke patients. However, further adequately sized randomized trials are required to obtain reliable information on safety and efficacy with respect to the antithrombotic medications used.
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Explore the source record for details and available documents.
This work is a continuation of earlier studies on the influence of polymer concentration and polymer composition on the capillary electrophoretic separation of DNA. The focus is on the capillary dimensions and the electric field strength as factors influencing the resolution. The aim was to establish optimum conditions for the separation of single-stranded DNA in capillaries and derive strategies for the construction of micromachined separation devices.
The factor V (FV) G1691A mutation, the prothrombin (PT) G20210A variant, the methylenetetrahydrofolate reductase (MTHFR) T677T genotype, together with fasting homocysteine (HCY) concentration, lipoprotein (Lp)(a), anti-thrombin (AT), protein C (PC), protein S (PS) and anti-cardiolipin antibodies were investigated in 65 consecutively recruited infants (neonate to < 12 months) with renal venous thrombosis (RVT; n = 31), portal vein thrombosis (PVT; n = 24) or hepatic vein thrombosis (HVT n = 10), and 100 age- and sex-matched healthy controls. FV G1691A was found in 14 babies (heterozygous: RVT n = 9, PVT n = 4; homozygous HVT n = 1) and five controls, the MTHFR TT677 genotype together with increased HCY in four infants with thrombosis (RVT n = 2; PVT n = 1; HVT n = 1) compared with one control, and the PT G20210A variant was present in one control only. PC type I deficiency was diagnosed in three patients (RVT n = 2; PVT n = 1) and AT deficiency in two patients (RVT n = 1; PVT n = 1). Three neonates with spontaneous thrombosis showed FV G1691A combined with Lp(a) and the FV G1691A was combined with the PT G20210A genotype in two infants. Additional triggering factors were reported in 27 patients (41.5%). The overall odds ratios (ORs) and 95% confidence intervals (CIs) with respect to the different thrombosis locations were: RVT (OR/CI: 10.9/3.85-31.1; P < 0.0001), PVT (5.47/1.7-17.6; P < 0.0007) and HVT (3.3/0.58-18.7; P = 0.18). The data presented here suggest that genetic prothrombotic risk factors also play an important role in abdominal venous thrombosis during infancy.
BACKGROUND AND PURPOSE: The present multicenter case-control study was prospectively designed to assess the extent to which single and combined clotting factor abnormalities influence the onset of symptomatic ischemic stroke in full-term neonates. METHODS: Lipoprotein (Lp)(a); the factor V (FV) G1691A mutation; the prothrombin (PT) G20210A variant; the methylenetetrahydrofolate reductase (MTHFR) T677T genotype; antithrombin; protein C; protein S; and anticardiolipin antibodies (ACAs) were investigated in 91 consecutively recruited neonatal stroke patients and 182 age- and sex-matched healthy controls. RESULTS: Sixty-two of 91 stroke patients (68.1%) had at least 1 prothrombotic risk factor compared with 44 control subjects (24.2%) (odds ratio [OR]/95% confidence interval [CI], 6.70/3.84 to 11.67). An increased Lp(a) level (>30 mg/dL) was found in 20 patients and 10 controls (OR/95% CI, 4.84/2. 16 to 10.86); FV G1691A was present in 17 patients and 10 controls (OR/95% CI, 3.95/1.72 to 9.0); the PT G20210A variant was detected in 4 patients and 4 controls (OR/95% CI, 2.04/0.49 to 8.3); the MTHFR TT677 genotype was found in 15 patients and 20 controls (OR/95% CI, 1.59/0.77 to 3.29); and protein C type I deficiency was found in 6 neonates. Neither antithrombin deficiency nor protein S deficiency was found in the neonatal patients studied. Acquired IgG ACAs were found in 3 cases. Additional triggering factors, ie, asphyxia, septicemia, maternal diabetes, and perinatally acquired renal venous thrombosis, were reported in 54.0% of patients. CONCLUSIONS: Besides acquired triggering factors, the data presented here suggest that genetic prothrombotic risk factors play a role in symptomatic neonatal stroke.
We describe the construction and performance of a fully automated multicapillary electrophoresis system for the analysis of fluorescently labeled biomolecules. A special detection system allows the simultaneous spectral analysis of all 96 capillaries. The main features are true parallel detection without any moving parts, high robustness, and full compatibility to existing protocols. The device can process up to 40 microtiter plates (96 and 384 well) without human interference, which means up to 15,000 samples before it has to be reloaded.
We have studied the separation of single-stranded and double-stranded DNA in a matrix of entangled, linear poly-N,N-dimethylacrylamide. Our results give better insight into the mechanisms involved during separations in polymer solutions. The dependence of different parameters on DNA size, electric field, pore size and the polymer chain length are evaluated and compared to theoretical predictions. Striking differences between experimental data and predicted scaling laws are found. Our data should help to optimize DNA separation in capillary electrophoresis and to improve existing models for DNA separation in porous matrices.
The electrophoretic separation of single-stranded and double-stranded DNA has been examined, using a matrix of linear poly-N,N-dimethylacrylamide (pDMA). The dependence of peak spacing, peak width and resolution on important parameters such as polymer concentration, polymer chain length and electric field strength, has been studied. This work complements our systematic study on electrophoretic mobility under different conditions (C. Heller, Electrophoresis 1999, 20, 1962-1977), and will help to further optimize and improve high performance DNA separation in capillary electrophoresis with entangled polymer solutions.
UNLABELLED: Many studies have shown a high percentage of venous thromboses in children to be associated with haematological disorders. However, studies assessing the influence of haemostaseological disorders on paediatric stroke are rare. We compared 26 children with cerebral infarction (median age 2 months, range 0-16.2 years) and 17 with venous thrombosis (median age 4.5 years, range 0-17 years) with regard to prothrombotic risk factors. Prothrombotic disorders were found in 8 out of 26 patients with cerebral infarction (FV Leiden mutation: n = 4; protein C deficiency: n = 1; FV Leiden mutation + protein C deficiency: n = 2; prothrombin mutation G20210A: n = 1) and in 13 out of 17 with venous thrombosis (FV Leiden mutation n = 3; protein C deficiency n = 5; elevated HRGP + PAI: n = 1, combined deficiency of AT, protein C and plasminogen: n = 1; F XII deficiency: n = 1; lupus anticoagulans n = 1; FV Leiden + F XII deficiency + lupus anticoagulans + PAI: n = 1). Comparison of these prevalences with those of 150 healthy paediatric controls showed in children with FV Leiden mutation and/or protein C deficiency an increased risk of cerebral infarction (patients vs. controls: 26.9% vs. 6%; OR 5.77; 95%-CI 1.92-17.3; P = 0.0031) as well as of venous thrombosis (53% vs. 5.3% 19.9; 95%-CI 6-65.6; P < 0.0001). This result is in contrast with reports on thrombophilia in cerebral infarction in adult patients. CONCLUSION: Our results indicate that FV Leiden mutation and protein C deficiency may contribute to the multifactorial aetiology of stroke in early childhood.
We compare diverging evolution of a two-component (gas+stars) galactic disk embedded in a "live" halo with that of an identical pure stellar disk. Our modeling supports the conjecture that the growth of central concentration in galaxies dissolves the main family of regular orbits in the stellar bar and assists in the formation of a galactic bulge.