Overexpressed platelet integrin alphaIIbbeta3 in a Fechtner syndrome patient uneventfully undergoing adenotomy.
Explore the source record for details and available documents.
Adenoids↗
Biomedical subjects
C P Speer
Publications and source records attributed to C P Speer.
Pulmonary inflammation and bronchopulmonary dysplasia.
Various pre- and postnatal risk factors, which act additively or synergistically induce an injurious inflammatory response in the airways and the pulmonary interstitium of preterm infants with bronchopulmonary dysplasia. This inflammatory response is characterized by an accumulation of neutrophils and macrophages as well as an arsenal of proinflammatory mediators that affect the endothelium and alveolar-capillary integrity. Besides proinflammatory cytokines and toxic oxygen radicals, lipid mediators as well as potent proteases may be responsible for acute lung injury. There is increasing evidence that an imbalance between pro- and anti-inflammatory factors, which should protect the alveoli and lung tissue, are key features in the pathogenesis of bronchopulmonary dysplasia. In addition, a subnormal generation of growth factors may affect alveolarization and vascular development in preterm infants with bronchopulmonary dysplasia. In this condensed review article, the current concepts on the possible role of inflammation in the evolution of bronchopulmonary dysplasia will be summarized.
Blood-Air Barrier↗
[Congenital skin lesions in occult spinal dysraphism--what is typical?].
Occult spinal dysraphism (OSD) includes a group of spinal malformations covered by intact skin. Neurological sequelae include paresis and sensory deficits in the lower limbs, neurogenic bladder and bowel disturbances, pain and neuro-orthopaedic syndrome as well as a high risk for secondary neurological deterioration. In up to 80 % of the cases, OSD is accompanied by lumbosacral skin anomalies. In this article, an overview on the main forms of OSD and characteristic skin lesions is given, which can guide the clinician to early diagnosis and appropriate diagnostic work-up and, if necessary, therapeutic intervention.
Humans↗
Factor VIII is a positive regulator of platelet function.
FVIII is an important cofactor in the tenase coagulation factor complex, lack of FVIII causes severe bleeding, whereas high FVIII levels seem to be associated with venous and arterial thromboembolism. Resting platelets do not bind FVIII, but activated platelets bind unactivated FVIII if vWF is not present. We investigated a possible influence of platelet bound FVIII on platelet function itself as it is unclear if there is a direct effect of FVIII on platelet function. The influence of FVIII on platelet function was investigated by flow cytometric analysis of P-selectin expression (CD62P) and PAC-1 binding before and after submaximal stimulation with TRAP-6 (5 microM final concentration), by confocal microscopy and by platelet aggregometry. For flow cytometry and confocal microscopy, washed platelets were incubated with human recombinant FVIII for 5 min at 37 degrees C. Analysis of platelet surface area was measured by computerized image analysis. Treatment with FVIII only caused no changes in P-selectin expression or PAC-1 binding, respectively. Stimulation of platelets with TRAP-6 increased the expression of P-selectin (445%) and PAC-1 binding (934%) as expected. These effects were further increased when platelets were stimulated with TRAP-6 and FVIII (P-selectin 499%, difference not significant; PAC-1 1626%, P < 0.05. Values were expressed in%, related to unstimulated, buffer treated platelets). Platelet spreading on fibrinogen was significantly increased when platelets were treated with FVIII and TRAP-6 compared to TRAP-6 alone (368 vs. 307 average pixel/platelet, P<0.05). In addition platelet aggregation was enhanced when platelets were stimulated with FVIII and TRAP-6 compared to TRAP-6 alone. FVIII can act as a positive regulator of platelet function in TRAP-co-stimulated platelets. We hypothesize that FVIII induced increase in platelet activation might contribute to venous and even arterial thrombus formation in patients with high FVIII levels.
Dual Specificity Phosphatase 2↗
Cerebral mass in a 13-year-old girl following long-term sojourn in the Tropics.
Cysticercosis of the central nervous system is the main cause of late-onset epilepsy in tropical countries. The case of a 13-year-old German girl with a generalized seizure following long-term sojourns in the Tropics is reported. Cranial imaging showed two cerebral lesions with central calcifications. Serological, molecular and cultural examination of cerebrospinal fluid and blood was negative for various parasites, fungi and bacteria including mycobacteria. Histopathological examination after neurosurgical resection revealed calcareous bodies pathognomonic for platyhelminths, in particular tapeworms. Taken together, the radiological and histopathological findings indicate infection with cysticerci, the larvae of Taenia solium.
Adolescent↗
Freeze-thawing of breast milk does not prevent cytomegalovirus transmission to a preterm infant.
Freezing human milk is recommended to inactivate cytomegalovirus (CMV). A case of a preterm infant exclusively receiving frozen breast milk from his CMV seropositive mother showed that storage of breast milk for two months at -20 degrees C did not prevent symptomatic postnatal CMV infection.
Cryopreservation↗
[Pharmacological prophylaxis and treatment of bronchopulmonary dysplasia].
Treatment with prenatal steroids, prophylactic or early therapeutic surfactant substitution, application of early nasal CPAP, minimizing of mechanical ventilation, early treatment of PDA and avoiding nosocomial infections are the main measures to prevent the development of bronchopulmonary dysplasia (BPD) in high-risk pre-term neonates. Beside these strategies, several pharmacologic interventions to prevent or to treat BPD have been investigated. So far, clear evidence for effective prevention has only been demonstrated for the administration of vitamin A and vaccinations. The administration of oxygen is the only effective treatment modality. Unfortunately, the upper and lower limits for the dosage of oxygen are still not clear. In patients with established BPD, a transient therapeutic effect is observed following treatment with systemic diuretics, inhaled steroids, and inhaled bronchodilators. However, treatment with these drugs has no documented long-term effect on the course of the disease. Systemic steroids only play a role as rescue treatment in life-threatening situations. Treatment with inhaled or systemic pulmonary vasodilatative may have a place in the treatment of pulmonary hypertension in severely affected infants. However, long-term experience in this treatment modality is still lacking.
Adrenal Cortex Hormones↗
[Aseptic meningitis after intrathecal infusion of a parenteral nutrition solution: examples of rare malpositions of central venous catheters in preterm neonates].
BACKGROUND: Central venous catheters are an indispensable part of intensive care. In the management of preterm neonates, these are introduced after puncture of a peripheral subcutaneous vein. The catheters are supposed to be pushed forward with the venous flow. A chest X-ray is usually performed for verification of the position of the catheter. Localization of the tip of the catheter is often very difficult because of its extremely small diameter. METHODS: A malposition of a central venous catheter resulting in intrathecal infusion of parenteral nutrition and subsequent aseptic meningitis in a preterm neonate is presented. Further cases of catheter malpositions leading to arthrography, arteriography and incorrect position in various parts of the venous system are discussed. DISCUSSION AND CONCLUSION: The case reports demonstrate that wire-guided central venous catheters are not only advanced by the forward blood flow but can also inadvertently end up in undesired sites and may thus induce serious side effects.
Catheterization, Peripheral↗
[Inhaled nitric oxide in neonatology: state of the art].
In the late 1970 s it was demonstrated that nitric oxide (NO) was involved in the regulation of vasomotor tone. In Europe inhaled NO (iNO) was approved as a therapy option for the treatment of pulmonary hypertension in term and slightly preterm (> 34 weeks of gestation) neonates. Therapy by iNO mainly reduces the necessity for treatment by extracorporeal membrane oxygenation. However, the mortality of the underlying disease is not affected. According to our current knowledge iNO therapy for term and slightly preterm (> 34 weeks of gestation) neonates does not represent an additional risk factor for the neurological development. Today, iNO therapy constitutes the gold standard for pulmonary hypertension in new-born babies. However, the 30 % non-responders warrant a continued search for alternative treatment concepts. Prophylactic therapy according to a risk profile has not yet proved to be meaningful. An indication for the treatment of preterm neonates of less than 34 weeks of gestation has not yet been confirmed.
Administration, Inhalation↗
[Breast feeding of very preterm infants of HCMV-seropositive mothers].
Preterm infants can be infected with human cytomegalovirus (HCMV) transmitted via breast milk of their HCMV-seropositive mothers, 96 % of whom reactivate the virus during lactation. 38 % of exposed VLBW infants become infected, with 48 % of these developing at least one symptom. Whether priority should be given to the multiple advantages of breast milk feeding or to the avoidance of a possible HCMV infection by exclusive formula feeding still cannot be decided due to insufficient data on the long-term outcome of infected infants. Inactivation of HCMV in breast milk can be achieved safely only via heat treatment, but the clinical consequences resulting from the use of pasteurized breast milk are unknown. Given the above situation, the authors decided to continue breast-feeding of VLBW and ELBW infants in their units after obtaining informed parenteral consent, until data for an evidence-based decision become available.
Breast Feeding↗
[Differential diagnosis of bullous skin lesions in neonates: pemphigoid gestationis].
The clinical relevance of bullous skin diseases in newborns varies widely. We present the case of a preterm, 35 weeks of gestation, infant who was admitted to our hospital with skin lesions on face, thorax and plantae. There were no other pathological findings on clinical and neurological examinations. During another pregnancy the mother of the child had already suffered from pemphigoid gestationis. In the blood of the newborn complement-fixing auto-antibodies against BP180, the common antigen of pemphigoid gestationis and bullous pemphigoid, were detected. The skin lesions disappeared after a few days of local antiseptic therapy. Pemphigoid gestations is a rare autoimmune dermatosis in pregnancy. The frequency of skin lesions in newborns of mothers with pemphigoid gestationis is estimated to about 5 -- 10 %.
Diagnosis, Differential↗
Apoptosis and proliferation in lungs of human fetuses exposed to chorioamnionitis.
AIMS: To determine whether chorioamnionitis has an impact on the extent of apoptosis and proliferation in fetal lungs. Fetuses exposed to chorioamnionitis have an increased risk of aquiring lung tissue damage in utero. METHODS AND RESULTS: Lung tissue sections from 35 stillborn fetuses were used in this study. Chorioamnionitis-exposed fetuses were subdivided depending on whether pneumonia was diagnosed (n = 13) or not (n = 10); 12 unaffected fetuses served as controls. Apoptotic and proliferating cells were determined by in-situ terminal deoxytransferase-mediated dUTP nick end labelling (TUNEL) assay and by anti-Ki67 immunohistochemistry, and quantified. The median apoptotic index in lungs of chorioamnionitis-exposed fetuses increased 2.4-fold compared with chorioamnionitis-negative stillborn controls (P = 0.043) and rose 21.6-fold when chorioamnionitis-exposed fetuses additionally developed pneumonia (P < 0.001). Compared with the proliferation index of the control group (PI = 2.3), the median percentage of proliferating cells in the lungs of chorioamnionitis-exposed fetuses decreased (PI = 1.4) (P = 0.036), but increased 1.8-fold (P = 0.036) in fetal lungs of the chorioamnionitis/pneumonia group. By double labellings combining the TUNEL assay or the Ki67 antigen with cell marker proteins, we identified distal airway epithelial cells as the cell type undergoing apoptosis in chorioamnionitis-exposed fetal lungs, while epithelial, endothelial and smooth muscle cells proliferated. Immunolabellings of cleaved caspases -8 and -9 revealed that apoptosis is mediated via initiator caspase-8. CONCLUSION: Chorioamnionitis induces apoptosis of distal airway epithelial cells via the caspase-8 pathway and interferes with the normal proliferative activity of epithelial, endothelial, and smooth muscle cells in fetal lungs. Thus, apoptosis and proliferation are an important feature of chorioamnionitis-associated lung injury in utero.
Antigens, CD34↗
Apoptosis and proliferation in lungs of ventilated and oxygen-treated preterm infants.
Apoptosis and proliferation and the effect of exogenous surfactant on these processes were investigated in the lungs of mechanically ventilated/oxygen-treated preterm infants with respiratory distress syndrome and stillborn foetuses. Apoptotic and proliferation indices were determined in lung tissue sections from 27 ventilated/oxygen-treated preterm infants and 29 stillborn foetuses. The effect of exogenous surfactant on apoptosis and proliferation was studied in 16 ventilated preterm infants; 11 untreated infants served as control. Apoptotic and proliferating cells were identified by double labelling combining terminal deoxynucleotidyltransferase-mediated deoxyuridine triphosphate nick end-labelling or Ki-67 with cell marker proteins. Pathways to cell death were explored by immunolabelling of cleaved caspases-3, -8 and -9. In the lungs of ventilated/oxygen-treated preterm infants, the numbers of apoptotic and proliferating cells increased significantly compared to the respective numbers in the lungs of stillborn foetuses. Apoptosis was detected in alveolar epithelial cells, whereas epithelial, endothelial and smooth muscle cells proliferated. Surfactant treatment reduced apoptosis induced by ventilation/oxygen-treatment; however, the decrease was not significant. Caspases-8 and -9 do not contribute to ventilation-induced apoptosis, whereas caspase-3 is involved. In conclusion, ventilation/oxygen-treatment induces epithelial cell apoptosis and proliferation of epithelial, endothelial and smooth muscle cells in the lungs of preterm infants.
Apoptosis↗
Association of histologic chorioamnionitis, increased levels of cord blood cytokines, and intracerebral hemorrhage in preterm neonates.
The objective of this study was to investigate in a prospective study whether histological chorioamnionitis (ChA) is a risk factor predisposing for intracerebral hemorrhage (ICH), and whether ICH is associated with a systemic fetal inflammation in preterm neonates with a gestational age <32 weeks. 106 neonates were studied; 20 (18.9%) suffered from ICH. ChA occurred significantly more often in neonates with ICH compared to neonates without ICH (70.0 vs. 36.0%, p = 0.006). Neonates with ICH had significantly higher median levels of proinflammatory cytokines (IL-1beta, IL-6 and IL-8) compared to neonates without ICH (p < 0.001 for all comparisons). We conclude that the development of ICH in preterm infants is associated with both ChA and high levels of proinflammatory cytokines at birth.
Cerebral Hemorrhage↗
The current role of colony-stimulating factors in prevention and treatment of neonatal sepsis.
OBJECTIVES: To review the role of colony-stimulating factors as adjuncts in the therapy of neonatal sepsis. DATA SUMMARY: Data provided by animal experiments and in vitro experiments in human neonates demonstrate the inability of newborn infants to significantly upregulate colony-stimulating factor expression during infectious challenge. In a few clinical trials, exogenous administration of colony-stimulating factors has been associated with reduced neonatal morbidity and mortality. However, reviewing the existing data on colony-stimulating factor administration in neonates, evidence for efficacy and benefit of these adjuncts in treating neonatal sepsis still appears to be poor. CONCLUSION: Further randomized, placebo-controlled clinical trials, particularly for the subgroups of premature infants or infants with neutropenia, are urgently warranted before routine application of these cytokines can be recommended.
Animals↗
Cytomegalovirus infection of extremely low-birth weight infants via breast milk.
In addition to seroprevalence and transmission rate, the clinical symptoms of postnatal cytomegalovirus (CMV) infection in infants with a very low birth weight (VLBW; <1500 g; <32 weeks gestational age at birth) were assessed in a 3-year prospective study. CMV monitoring included serologic testing (of the mother and child) and virus culture and PCR (of samples of both breast milk and the infant's urine). Within 3 weeks of the initial virus detection in the infant, clinical and laboratory parameters were evaluated. Of 170 infants, no CMV transmission was found in the 80 infants of seronegative mothers and in the 3 infants of seropositive mothers who did not shed CMV DNA into breast milk. Transmission occurred in 33 of the 87 CMV-exposed infants, 16 of whom presented with such symptoms as hepatopathy, neutropenia, thrombocytopenia, and sepsis-like deterioration. Low birth weight and early postnatal virus transmission were risk factors for symptomatic infection. VLBW infants of CMV-seropositive mothers are at high risk of acquiring a symptomatic CMV infection postnatally via breast milk.
Cytomegalovirus Infections↗
Double-outlet right ventricle and overriding tricuspid valve reflect disturbances of looping, myocardialization, endocardial cushion differentiation, and apoptosis in TGF-beta(2)-knockout mice.
BACKGROUND: Transforming growth factor-beta(2) (TGF-beta(2)) is a member of a family of growth factors with the potential to modify multiple processes. Mice deficient in the TGF-beta(2) gene die around birth and show a variety of defects of different organs, including the heart. METHODS AND RESULTS: We studied the hearts of TGF-beta(2)-null mouse embryos from 11.5 to 18.5 days of gestation to analyze the types of defects and determine which processes of cardiac morphogenesis are affected by the absence of TGF-beta(2). Analysis of serial sections revealed malformations of the outflow tract (typically a double-outlet right ventricle) in 87.5%. There was 1 case of common arterial trunk. Abnormal thickening of the semilunar valves was seen in 4.2%. Associated malformations of the atrioventricular (AV) canal were found in 62.5% and were composed of perimembranous inlet ventricular septal defects (37.5%), AV valve thickening (33.3%), overriding tricuspid valve (25.0%), and complete AV septal defects (4.2%). Anomalies of the aorta and its branches were seen in 33.3%. Immunohistochemical staining showed failure of myocardialization of the mesenchyme of the atrial septum and the ventricular outflow tract as well as deficient valve differentiation. Morphometry documented this to be associated with absence of the normal decrease of total endocardial cushion volume in the older stages. Apoptosis in TGF-beta(2)-knockout mice was increased, although regional distribution was normal. CONCLUSIONS: TGF-beta(2)-knockout mice exhibited characteristic cardiovascular anomalies comparable to malformations seen in the human population.
Animals↗
Epidemiology of transmission of cytomegalovirus from mother to preterm infant by breastfeeding.
BACKGROUND: Breastfeeding practices strongly influence the epidemiology of human cytomegalovirus infection. By contrast with term neonates, few data are available on transmission of infection from mothers to preterm infants during breastfeeding. METHODS: 151 mothers and their 176 preterm infants (gestational age at birth <32 weeks or birthweight <1500 g) were prospectively screened for cytomegalovirus infection by serology, virus culture, and PCR. The roles of cell-free and cell-associated cytomegalovirus excretion during lactation were analysed longitudinally in relation to transmission, by maximum-likelihood estimates. FINDINGS: Of the 69 seronegative breastfeeding control mothers, none had detectable cytomegalovirus DNA in breastmilk and none of their 80 infants shed the virus in urine. The proportion of cytomegalovirus reactivation in seropositive breastfeeding mothers was 96% (73 of 76). The early appearance of viral DNA in milk whey (median 3.5 days post partum in transmitters; 8 days in non-transmitters; p=0.025) and infectious virus in milk whey (10 days and 16 days, respectively; p=0.005) were risk factors for transmission. The cumulative rate of transmission was 37% (27 of 73 mothers; 33 infants). The infection of the neonates had a mean incubation time of 42 days (95% CI 28-69). About 50% of the infected infants had no symptoms, but four had sepsis-like symptoms. INTERPRETATION: The proportion of cytomegalovirus reactivation during lactation almost equals maternal seroprevalence. Breastfeeding as a source of postnatal cytomegalovirus infection in preterm infants has been underestimated and may be associated with a symptomatic infection.
Breast Feeding↗