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Biomedical subjects

M J Lentze

Publications and source records attributed to M J Lentze.

At least 19 recordsLinked to original sources
PubMed2006

[Human Metapneumovirus in hospitalized children - a review].

The human Metapneumovirus (HMPV) has been discovered by von den Hoogen et al. in 2001 and seems to play an important role as etiologic agent in childhood respiratory tract infections in particular involving infants after the 6th month of life and toddlers. Duly considering the hitherto published studies and retrospective analysis of two HMPV seasons (2002-2004) at our institution this review focuses on children, who had to be hospitalized due to HMPV infection. The analysis confirmed, that among those patients there is a high proportion of children with pre-existing risk factors for a complicated clinical course, a high proportion of children with bronchiolitis or pneumonia and a relevant proportion of children with HMPV related apnoeas, most prevalent in the prematurely born. Although the first HMPV infection takes place somewhat later in infancy, the data do not show that HMPV infection is in general milder than RSV infection in hospitalized children. Clinical symptoms and radiological signs do not permit tentative conclusions on the causative agent. This underlines the necessity of specific diagnostic efforts (in case of HMPV with PCR). HMPV may cause lobar or segmental pneumonias difficult to distinguish from bacterial lower respiratory tract infection. Children admitted to the hospital with an acute exacerbation of asthma bronchiale or cystic fibrosis should not only be tested for RSV but also for HMPV. Prospective studies investigating specific therapeutic interventions or describing the impact and prevention of nosocomial HMPV in fection are awaited for. There has been one report of a meningoencephalitis possibly related to HMPV. Thus, liquor samples in such cases should be tested for HMPV too.

Child, Preschool↗
PubMed2004

[Nutrition of children and adolescents. Results of the DONALD Study].

In this paper, the actual diet of children and adolescents is characterized by food group intake. Age-dependent dietary patterns and long-term dietary trends are described and commented on against the background of the optimized mixed diet, a preventive total diet concept for German children and adolescents. Dietary intake data come from 3-day dietary records obtained in the DONALD Study (Dortmund Nutritional and Anthropometrical Longitudinally Designed Study), an ongoing mixed longitudinal cohort study conducted at the Research Institute of Child Nutrition since 1985. The actual diet of the observed children and adolescents differed to some extent from the optimized mixed diet. For example, the intake of vegetables was lower and the intake of meat/sausage and confectionary was higher than recommended. The three rules for food selection of the optimized mixed diet (consume plant foods and beverages liberally, animal foods moderately, and high-fat, high-sugar foods occasionally) show a practical way to improve unfavorable dietary habits of children and adolescents without fundamental changes of food intake patterns and taste properties of the actual diet. The partly favorable and partly unfavorable dietary trends observed in the DONALD Study should continue to be critically considered.

Adolescent↗
PubMed2004

Induction of T lymphocyte apoptosis by sulphasalazine in patients with Crohn's disease.

BACKGROUND: Lamina propria T lymphocytes (LPL) of the intestinal mucosa are chronically activated in Crohn's disease (CD). Defective apoptosis of activated LPL was proposed as a key pathogenic mechanism. In fact, increased expression of antiapoptotic molecules was observed in CD LPL. In the present work, we aimed to analyse the effects and underlying molecular mechanisms of 5-amino salicylic acid (5-ASA) and derivatives on apoptosis of LPL and peripheral blood lymphocytes (PBL) in patients with CD compared with ulcerative colitis (UC) and in non-inflammatory controls. METHODS: PBL and LPL were isolated by Ficoll-Hypopaque gradient centrifugation and the EGTA-collagenase method, respectively. PBL/LPL were stimulated with FasL, 5-ASA, sulphapyridine, and sulphasalazine for 24/48 hours and apoptosis was quantified by flow cytometry (annexin V- propidium iodide method) and immunofluorescence. The molecular mechanisms of drug induced apoptosis were analysed in wild-type and FADD-/- Jurkat T cells using western blots and caspase assays. RESULTS: While PBL displayed a normal apoptosis pattern after Fas stimulation in patients with active CD, LPL from inflammatory areas were highly resistant. Comparable resistance to apoptosis was observed in LPL of UC patients. In contrast with 5-ASA, which did not induce apoptosis in lymphocytes, sulphasalazine proved to be a potent proapoptotic agent. Sulphasalazine induced T lymphocyte apoptosis was independent of the Fas pathway but associated with marked downregulation of antiapoptotic bcl-xl and bcl2, activation of the mitochondrial apoptosis signalling pathway, and subsequent activation of caspase-9 and caspase-3. CONCLUSION: The beneficial effect of sulphasalazine in treating inflammatory bowel disease is at least in part attributable to its proapoptotic effects on LPL which allows potent downregulation of lymphocyte activation.

Adolescent↗
PubMed2003

Antibiotic-associated diarrhea: therapeutic aspects and practical guidelines--an interdisciplinary approach to a common problem.

Antibiotic-associated diarrhea (AAD) is a common complication of antibiotic treatment, most often seen in non-hospitalised patients. In principle, such diarrhea can be triggered by any antibiotic. An interdisciplinary working group discussed the different aspects of AAD in view of its gastroenterological, microbiological, paediatric, general medical and pharmaceutical implications, also in consideration of the position of patients and health insurance funds. This paper implies therapeutic aspects and practical guidelines to raise awareness of these problems also in routine situations and to enable the persons and institutions involved on the various levels of the health-care system (patients, pharmacists, family doctors, specialists and hospitals) to handle the problem of AAD more easily in a standardised way as far as diagnostics, therapy and prevention are concerned.

Adult↗
PubMed2003

Antibiotic-associated diarrhea: incidence, risk factors of antibiotics and patients, pathophysiology and differential diagnosis--an interdisciplinary approach to a common problem.

Antibiotic-associated diarrhea (AAD) is a common complication of antibiotic treatment, most often seen in non-hospitalised patients. In principle, such diarrhea can be triggered by any antibiotic. An interdisciplinary working group discussed the different aspects of AAD in view of its gastroenterological, microbiological, paediatric, general medical and pharmaceutical implications, also in consideration of the position of patients and health insurance funds. The incidence, risk factors of antibiotics and patients, the pathophysiology of the various types of AAD and the differential diagnosis are reviewed.

Adolescent↗
PubMed2003

Butyrate induced Caco-2 cell apoptosis is mediated via the mitochondrial pathway.

BACKGROUND: During the process of tumorigenesis most colon cancer cells acquire resistance to apoptosis. The short chain fatty acid butyrate is well established as an antitumour agent which selectively induces apoptosis in colon cancer cells but not in normal intestinal epithelial cells. AIMS: To analyse the signalling pathway of butyrate induced apoptosis. METHODS: Using Caco-2 cells we focused on the bcl family of proteins, mitochondrial pathway, and caspase signalling cascade involved in butyrate induced apoptosis. Techniques employed included western blots, immunofluorescence, as well as experiments with peptide inhibitors of specific caspases. RESULTS: Butyrate induced a clear shift of the mitochondrial bcl rheostat towards a proapoptotic constellation, as demonstrated by upregulation of proapoptotic bak accompanied by reduced antiapoptotic bcl-x(L) levels. This was associated with translocation of cytochrome-c from the mitochondria to the cytosol, resulting in activation of the caspase cascade via caspase-9. Key executioner enzymes were caspases-3 and -1. No effect of butyrate on regulatory proteins of the inhibitor of apoptosis family was observed. CONCLUSIONS: Butyrate induced Caco-2 cell apoptosis via the mitochondrial pathway. Upregulation of bak and translocation of cytochrome-c were upstream of the caspase cascade. Subsequently, this cascade was activated via the formation of an apoptosome.

Apoptosis↗
PubMed2002

The susceptibility to Fas-induced apoptosis in normal enterocytes is regulated on the level of cIAP1 and 2.

Various members of the tumor necrosis factor receptor superfamily are implicated in the regulation of enterocyte apoptosis. Previously, we observed that human intestinal epithelial cells are rather unsusceptible to Fas-induced apoptosis. In the present study we analyzed these protective mechanisms in the human intestinal epithelial cell line HIEC, focusing on antiapoptotic molecules of the IAP family which block apoptosis at the level of the caspase cascade. HIEC expressed all key molecules required to trigger Fas-induced apoptosis. However, no apoptosis occurred after activation of Fas, whereas an upregulation of antiapoptotic cIAP1 and 2 was observed. Suppression of this upregulation with the proteasome inhibitor MG132 or the protein synthesis inhibitor cycloheximide highly sensitized HIEC toward Fas-induced apoptosis. Western blot analyses revealed that both inhibitors potently suppressed endogenously produced cIAP1 and 2. No effect was observed on XIAP expression. These data indicate that enterocytes are particularly protected against Fas-induced apoptosis on the level of executionary caspases.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Lipopolysaccharide modulation of normal enterocyte turnover by toll-like receptors is mediated by endogenously produced tumour necrosis factor alpha.

BACKGROUND: Circulating levels of endotoxin (or lipopolysaccharide (LPS)) and anti-endotoxin antibodies are increased in patients with inflammatory bowel disease, supporting the hypothesis of a role for endogenous bacterial products in the pathogenesis of these disorders. AIM: The aim of this study was to analyse the direct effects of LPS on intestinal epithelial cell turnover. METHODS AND RESULTS: LPS significantly inhibited growth of the human non-transformed immature crypt cell line (HIEC), whereas IEC-6 cell proliferation was stimulated by LPS. As LPS is a physiological inducer of tumour necrosis factor alpha (TNFalpha) in various cell systems and this cytokine exerted similar anti-proliferative (HIEC) or growth stimulatory (IEC-6 cells) effects, the study thus tested the hypothesis that endogenously produced TNFalpha in response to LPS mediates this growth modulatory effect in an autoparacrine/paracrine way. Therefore, during LPS stimulation, the biological activity of TNFalpha was blocked using neutralising anti-TNFalpha antibodies, as well as inhibitory, antagonistic antibodies directed against the p55 TNF receptor, signalling the antimitotic TNFalpha effect in HIEC. Both experimental approaches completely abolished the growth modulatory effects of LPS in HIEC/IEC-6 cells. Production and secretion of TNFalpha by HIEC/IEC-6 cells in response to LPS was confirmed on mRNA and protein level by reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay. LPS signalling was independent of CD14 in HIEC, as these cells lack this receptor. However, HIEC expressed TLR4 and MD2 resulting in a fully functional signalling complex as demonstrated by RT-PCR, western blot, and immunofluorescence analyses. CONCLUSION: These results support the hypothesis that LPS induced changes of intestinal epithelial cell turnover may directly contribute to the pathogenesis of inflammatory epithelial cell lesions by endogenous TNFalpha production by enterocytes.

Antibodies, Monoclonal↗
PubMed2002

The beta2-microglobulin/cystatin C ratio--a potential marker of post-transplant lymphoproliferative disease.

BACKGROUND: As a consequence of more intensified immunosuppression, post-transplant lymphoproliferative disease (PTLD) is increasingly observed in patients after solid-organ transplantation. Beta2-microglobulin, a low-molecular weight protein (MW 11.8 kDa), is produced by all nucleated cells as part of the HLA complex. Its serum concentration is directly correlated with prognosis in patients with lymphatic neoplasms. Like other low-molecular weight proteins, beta2-microglobulin is eliminated by glomerular filtration. This complicates its use as a tumor marker in renal insufficiency. Cystatin C, a low-molecular weight protein of 13.3 kDa, is a new marker of kidney function largely unaffected by extrarenal disease. We, therefore, sought to assess the potential of the beta2-microglobulin/cystatin C ratio (beta2M/Cys) as a marker of lymphoproliferation. PATIENTS AND METHODS: Beta2M/Cys was determined by particle-enhanced immunonephelometry in sera from 132 children with different degrees of renal insufficiency, 5 of whom had lymphoproliferative disease. Renal function was assessed using the Schwartz formula. RESULTS: Beta2M/Cys was constant between 1.2 and 2.4 mg/mg for Schwartz GFR > or = 40 ml/min x 1.73 m2. With lower GFR, beta2M/Cys rose progressively, maximum values being found in the hemodialysis patients (4.85-11.73). Healthy renal transplant recipients had beta2M/Cys comparable to controls. With acute lymphoproliferative disease, all but one patient had significantly elevated beta2M/Cys between 2.68 and 3.68 mg/mg, which returned to normal in remission (1.67-2.35 mg/mg). The sensitivity of a beta2M/Cys ratio > 2.4 mg/mg for the detection of PTLD was 80%, the specificity 100%, positive predictive value 100%, negative predictive value 90%. CONCLUSION: The beta2-microglobulin/cystatin C ratio is a promising parameter of lymphoproliferation in patients with normal or mildly impaired renal function.

Biomarkers↗
PubMed2001

Prolonged awakening and pulmonary edema after general anesthesia and naphazoline application in an infant.

IMPLICATIONS: Naphazoline intoxication by intrabronchial overdose caused prolonged unconsciousness of an 18-mo-old child after general anesthesia for tracheal rigid bronchoscopy. The leading symptoms were side effects involving the cardiovascular, pulmonary, and central nervous systems. Intensive care unit admission with the need for mechanical ventilation was necessary. Recovery was uneventful.

Adrenergic alpha-Agonists↗
PubMed2000

Mutation screening of the chromosome 8q24.3-human activity-regulated cytoskeleton-associated gene (ARC) in idiopathic generalized epilepsy.

Idiopathic generalized epilepsy (IGE) comprises a heterogeneous group of disorders, in which a high genetic predisposition and a complex mode of inheritance have been suggested. However, genes, which confer liability to common IGE subtypes including juvenile myoclonic epilepsy (JME) and childhood absence epilepsy (CAE) have not been identified so far. Here, we tested the hypothesis that genetic variation in the human homolog of the <<< >>> (ARC) contributes to the etiology of common IGE disorders. The gene has recently been mapped to chromosome 8q24.3, a region which spans previously identified major IGE susceptibility loci. A systematic search for mutations was performed in 143 patients with a known family history of IGE. However, no evidence for functional variants was found in the ARC coding sequence. Nevertheless, we detected a novel common C489T single nucleotide polymorphism, which provides a useful marker in genetic linkage and association studies. By performing a population- and family-based study we however failed to show significant association between this novel single nucleotide polymorphism and IGE, a finding, which most likely rules out that genetic variation in or close to the ARC gene confers liability to common IGE subtypes.

Adult↗
PubMed2000

Transient abnormal neurologic signs (TANS) in a longitudinal study of very low birth weight preterm infants.

OBJECTIVE AND METHODS: In the Bonn Longitudinal Study (BLS), the course of neurologic development was analysed with regard to transient abnormal neurologic signs (TANS). Abnormal neurologic signs (ANS) are defined when present in at least one developmental area at one examination. From birth to adulthood (mean 23 years) 108 preterm infants, 81% of very low birth weight (VLBW) were examined with regard to their psychological, neurologic and physical development: 62 appropriate for gestational age (AGA), 46 small for gestational age (SGA), 27 with postnatal catch-up growth of head circumference (group A) and 19 without catch-up (group B); 73 full terms served as controls. The dropout rate was 7.6%. RESULTS: ANS showed a great inter- and intraindividual variability. Episodes of neurologic abnormalities changed with those of normality. ANS reappeared when new abilities developed. ANS were observed mainly during the first year. The incidence was higher in preterms (AGA 49%, SGA A 63%, SGA B 61%) than in full terms (15%). Transient ANS (TANS) were diagnosed in 42% of AGA, 63% of SGA A, 33% of SGA B preterms and 12% of full terms. The recovery rate, i.e., the TANS to ANS percentage, was higher in AGA (86%), SGA A (100%) and full terms (82%) than in SGA B (55%) preterms. CONCLUSION: It is impossible to predict early on whether ANS will be transient, i.e. TANS. Longitudinal analyses are needed. The outcome depends on recovery from or persistence in ANS.

Blindness↗