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T Juven

Publications and source records attributed to T Juven.

6 recordsLinked to original sources
PubMed2005

Radiographic follow-up of pneumonia in children.

This study assessed the clinical value of routine follow-up chest radiographs in hospitalized children with community-acquired pneumonia. The study population consisted of 196 children hospitalized for community-acquired pneumonia diagnosed between 1993-1995. Seventeen infective agents (10 viruses and 7 bacteria) were sought. Chest radiographs were taken on admission and 3-7 weeks later. All children were treated with antibiotics. Data on the course of illness over the following 8-10 years were obtained from patient files and questionnaires sent to parents. A potential causative agent was found in 165 (84%) of 196 cases. On follow-up chest radiographs, residual or new changes were seen in 30% of cases. The residual changes tended to be more common after mixed viral-bacterial infection (43%) than after sole viral (25%) or sole bacterial (20%) infection. Interstitial infiltrates (66%), atelectasis (46%), and enlarged lymph nodes were the most common sequelae seen on follow-up. Residual findings on follow-up radiographs did not affect the treatment of the children. No further chest radiographs were taken. During the 8-10-year follow-up of 194 children, no illnesses appeared that were associated with previous pneumonia. Twenty-six children had a new episode of pneumonia, 7 of them had asthma, and 6 had different underlying illnesses. In conclusion, routine follow-up chest radiographs are not needed in childhood community-acquired pneumonia if the child has a clinically uneventful recovery.

Adolescent↗
PubMed2002

Differentiation of bacterial and viral pneumonia in children.

BACKGROUND: A study was undertaken to investigate the differential diagnostic role of chest radiographic findings, total white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and serum C reactive protein (CRP) in children with community acquired pneumonia of varying aetiology. METHODS: The study population consisted of 254 consecutive children admitted to hospital with community acquired pneumonia diagnosed between 1993 and 1995. WBC, ESR, and CRP levels were determined on admission. Seventeen infective agents (10 viruses and seven bacteria) were searched for. Chest radiographs were retrospectively and separately reviewed by three paediatric radiologists. RESULTS: A potential causative agent was found in 215 (85%) of the 254 cases. Bacterial infection was found in 71% of 137 children with alveolar infiltrates on the chest radiograph, while 72% of the 134 cases with a bacterial pneumonia had alveolar infiltrates. Half of the 77 children with solely interstitial infiltrates on the chest radiograph had evidence of bacterial infection. The proportion of patients with increased WBC or ESR did not differ between bacterial and viral pneumonias, but differences in the CRP levels of >40 mg/l, >80 mg/l, and >120 mg/l were significant although the sensitivity for detecting bacterial pneumonia was too low for use in clinical practice. CONCLUSIONS: Most children with alveolar pneumonia, especially those with lobar infiltrates, have laboratory evidence of a bacterial infection. Interstitial infiltrates are seen in both viral and bacterial pneumonias.

Blood Sedimentation↗
PubMed1993

mdm2 expression is induced by wild type p53 activity.

We have recently characterized a 95 kDa protein, p95, which exhibits enhanced binding to temperature-sensitive p53 (ts-p53) when cells are shifted down to 32.5 degrees C, a temperature at which ts-p53 possesses wild-type (wt)-like activities. In the present study we show that p95 is a product of the mdm2 putative proto-oncogene. The enhanced complex formation of mdm2 with ts-p53 in cells maintained at 32.5 degrees C is due to an elevation in total mdm2 protein levels following the temperature shift. We further demonstrate that the induction of mdm2 expression by t p53 activity is at the mRNA level. The induction occurs with very rapid kinetics and does not require de novo protein synthesis, suggesting a direct involvement of p53 in the process. Based on these data and on recent findings implicating p53 as a transcription factor, we suggest that the mdm2 gene is a target for activation by wt p53. In view of the ability of mdm2 to act as a specific antagonist of p53 activity, this induction process may serve to tightly autoregulate p53 activity in living cells.

Animals↗
PubMed1993

Wild type p53 can mediate sequence-specific transactivation of an internal promoter within the mdm2 gene.

The p53 tumor suppressor gene product can complex with polypeptides encoded by the mdm2 putative protoncogene. In addition, mdm2 mRNA levels have been shown to increase following the activation of wild type (wt) p53. To determine the basis for the effect of wt p53 on mdm2 mRNA, we studied the interaction of the mdm2 gene with p53. We report that wt p53 can bind sequence-specifically to a DNA region residing downstream to exon 1 of the mdm2 gene. This is correlated with a pronounced p53-dependent transcriptional activation. Efficient p53-dependent transactivation can be obtained with an mdm2 genomic DNA fragment lacking the putative mdm2 promoter. These findings suggest that p53 can induce transcription from an internal promoter located within the mdm2 gene. These findings raise the possibility that, in addition to increasing the overall levels of mdm2 mRNA, wt p53 may also modulate the repertoire of mdm2 transcripts present within the cell.

Animals↗