Biomedical subjects

Christoph Bührer

Publications and source records attributed to Christoph Bührer.

42 records · Page 3Linked to original sources

PubMed2002

Rate and risk factors of hypoglycemia in large-for-gestational-age newborn infants of nondiabetic mothers.

OBJECTIVE: The purpose of this study was to investigate the rate of hypoglycemia in large-for-gestational-age infants of nondiabetic mothers in relation to maternal or neonatal risk factors. STUDY DESIGN: Hospital charts of all term large-for-gestational-age infants born between 1994 and 1998 (n = 1136) were analyzed for the rate of neonatal hypoglycemia (capillary glucose level, < or =30 mg/dL) during the first 24 hours of life. Infants of women with preexisting or gestational diabetes mellitus were excluded (n = 180). Neonatal glucose testing was performed at 1 or 2 hours of life, with subsequent measurements every 4 to 6 hours. Maternal and neonatal parameters were compared between neonates with and without hypoglycemia, including recent oral glucose tolerance test values in those women who were tested (n = 358). RESULTS: Of 956 infants, 69 infants (7.2%) were not tested for hypoglycemia. In the remaining 887 infants, hypoglycemia occurred in 142 infants (16%) within the first 24 hours of life. The incidence of hypoglycemia decreased sharply during the first few hours of life, from 9.2% within the first hour of life, to 3.5% between 2 to 5 hours (cumulative) of life, and 2.4% between 6 and 24 hours of life. Gestational age at delivery was the only neonatal parameter that differed significantly between infants with and without hypoglycemia (39.5 vs 39.3 weeks, P =.01). The antenatal 1-hour oral glucose tolerance test value was the only predictive maternal parameter (141.5 vs 163.0 mg/dL, P <.006). There was an incremental risk of hypoglycemia with increasing 1-hour oral glucose tolerance test values, with hypoglycemia rates of 2.5%, 9.3%, 22.0%, and 50.0% that were associated with maternal 1-hour glucose values of <120, 120-179, 180-239, and > or =240 mg/dL, respectively (P <.05, for all comparisons). CONCLUSION: Routine glucose testing is indicated in large-for-gestational-age newborn infants of nondiabetic mothers. The 1-hour glucose value of the maternal oral glucose tolerance test is a fairly good predictor of subsequent neonatal hypoglycemia. A single elevated 1-hour value of > or =180 mg/dL markedly increases the risk of neonatal hypoglycemia.

Adult↗

PubMed2002

Complement activation by in vivo neonatal and in vitro extracorporeal membrane oxygenation.

Complment activation during extracorporeal membrane oxygenation (ECMO) in newborns can be caused by both the underlying disease processes and by blood contact with the ECMO circuit. We investigated the relative importance of these mechanisms by measuring C3a, C5a and sC5b-9 before, during and after neonatal ECMO in six consecutive newborn patients using enzyme-linked immunoassay. In addition complement activation during in vitro ECMO with repeated flow of the same blood volume was measured using blood from healthy adult donors. C3a increased significantly in vivo after 1 h (from 1035+/-193 to 1865+/-419 microg/l) and in vitro ECMO (from 314+/-75 to 1962+/-1062 microg/l). C5a increased during ECMO without significant differences between in vivo and in vitro activation. In neonatal patients, sC5b-9 rose faster than in vitro, but the rapid increase was also significant for in vitro experiments (in vivo: from 328+/-63 to 1623+/-387 microg/l after 2 h; and in vitro: from 78+/-32 to 453+/-179 microg/l after 8 h). After this initial peak at 1-2 h, complement activation decreased gradually until 2-3 days after the initiation of ECMO. We conclude that in newborns the rapid activation of the complement system after the start of ECMO is predominantly caused by contact with artificial surfaces rather than the patient's underlying disease.

Complement Activation↗

PubMed2002

Soluble intercellular cell adhesion molecule-1 and L-selectin plasma concentrations and response to surfactant in preterm infants.

OBJECTIVE: To investigate whether plasma concentrations of soluble intercellular cell adhesion molecule (ICAM)-1 and L-selectin at 24 hrs of life are related to good or poor response to exogenous surfactant in preterm infants. DESIGN: Prospective study of markers of inflammation in circulating blood at 24 hrs of life. SETTING: Level III neonatal intensive care unit. PATIENTS: Twenty-nine preterm newborns suffering from severe respiratory distress syndrome (Fio(2) > 0.4) without signs of infection or fetal acidosis, and 17 healthy preterm newborns of similar gestational age serving as controls. INTERVENTIONS: Infants with respiratory distress were treated with natural surfactant at 0.3-5 hrs of life. A response to surfactant, defined as a decrease of Fio(2) >50% within 6 hrs after surfactant, was seen in 21 infants. MEASUREMENTS AND MAIN RESULTS: Soluble ICAM-1 and L-selectin concentrations were determined in plasma samples taken at 24 hrs of age. ICAM-1 was elevated (p <.001) in infants who responded poorly to surfactant (median, 392 ng/mL; range, 58.26-4884.24 ng/mL) compared with good responders (20.52 ng/mL, 2.32-138.58 ng/mL) or controls (21.91 ng/mL, 2.61-65.73 ng/mL), without differences between controls and good responders. L-selectin was lower (p =.004) in surfactant-treated infants (4.45 nmol/L, 2.0-10.4 ng/mL) than in controls (6.0/2.35-10.25 nmol/L) without differences between surfactant good and poor responders. However, infants requiring supplemental oxygen at 36 wks of gestational age had reduced L-selectin at 24 hrs of age (3.2/2.0-3.45 vs. 5.0/2.35-10.4 nmol/L, p =.004), whereas there was no difference in ICAM-1. CONCLUSIONS: In preterm infants with respiratory distress, a poor response to surfactant within 6 hrs of administration is associated with elevated circulating ICAM-1 concentrations at 24 hrs of age. Low plasma L-selectin at 24 hrs of age predicts prolonged requirement for supplemental oxygen.

Journal Article↗

PubMed2002

Severe spinal muscular atrophy variant associated with congenital bone fractures.

Infantile autosomal recessive spinal muscular atrophy (type I) represents a lethal disorder leading to progressive symmetric muscular atrophy of limb and trunk muscles. Ninety-six percent cases of spinal muscular atrophy type I are caused by deletions or mutations in the survival motoneuron gene (SMNI) on chromosome 5q11.2-13.3. However, a number of chromosome 5q-negative patients with additional clinical features (respiratory distress, cerebellar hypoplasia) have been designated in the literature as infantile spinal muscular atrophy plus forms. In addition, the combination of severe spinal muscular atrophy and neurogenic arthrogryposis has been described. We present clinical, molecular, and autopsy findings of a newborn boy presenting with generalized muscular atrophy in combination with congenital bone fractures and extremely thin ribs but without contractures.

Bone and Bones↗

PubMed2002

Fas (CD95/Apo-1)/Fas ligand expression in neonates with pontosubicular neuron necrosis.

Pontosubicular neuron necrosis (PSN) represents an age-specific response to severe hypoxic-ischemic injury occurring in human neonates but not in older children or adults. Histologically, PSN is characterized by acute neuronal death in the pontine nuclei and the hippocampal subiculum bearing the hallmarks of apoptosis. In animal models of hypoxic-ischemic injury, induction of neuronal apoptosis can be triggered by Fas (CD95/Apo-1), a cell surface receptor of the tumor necrosis factor-alpha superfamily, which transduces apoptotic death signals when cross-linked by its natural ligand. Here, we have investigated the expression of Fas/Fas ligand in human autopsy material consisting of 13 PSN cases and 10 age-matched cases without PSN. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, immunohistochemistry, and double labeling for Fas/Fas ligand and the astrocyte marker glial fibrillary acid protein, the microglia/macrophage specific marker KiM1P, and the neuronal marker NeuN were performed on formalin-fixed brain specimens. Although mainly neurons of both PSN and controls expressed Fas receptor, expression was significantly increased (p = 0.001) in PSN cases in which predominantly degenerating cells with signs of early apoptosis showed Fas expression. In contrast, Fas ligand expression was found mainly on astrocytes and microglial cells. There was no significant difference between cases with and without PSN. We conclude that in the developing human brain, cells expressing the Fas receptor may be susceptible to undergoing apoptosis in response to hypoxic-ischemic injury.

Adult↗

PubMedDate not supplied

Optical molecular imaging of lymph nodes using a targeted vascular contrast agent.

We develop a highly specific antibody-dye conjugate for optical imaging of peripheral lymph nodes. The contrast agent consists of the monoclonal antibody recognizing endothelial ligands for the lymphocyte homing receptor L-selectin, MECA-79, and a near-infrared (near-IR) fluorescent indotricarbocyanine dye. The targeting and biodistribution behavior of MECA-79 is studied after radio-iodination and intravenous injection into mice demonstrating specific uptake in lymph nodes and accumulation in high endothelial venules (HEV). After conjugation of MECA-79 with indotricarbocyanine dye, the fluorescence imaging properties of the MECA-79 dye conjugate are examined by intravenous injection in nude mice and laser-induced fluorescence whole-body imaging in vivo. The MECA-79 antibody-dye conjugate accumulates in peripheral lymph nodes, whereas an isotype antibody-dye conjugate does not. Specific lymph node near-IR fluorescent signals become detectable within minutes after injection, and stable imaging persists for more than 24 h. The results demonstrate that vascular targeting of endothelial expression of glyocproteins is feasible to visualize the accumulation of near-IR fluorescent MECA-79 in lymph nodes, making this technology potentially useful to characterize processes of inflammation.

Animals↗