Maximal sterile barrier precautions independently contribute to decreased central line-associated bloodstream infection in very low birth weight infants: A prospective multicenter observational study.

BACKGROUND: The use of peripherally inserted central catheters (PICCs) in neonates differs among various institutions and countries because there are no random controlled trials or large observational studies regarding maximal sterile barrier (MSB) precautions in neonatal intensive care units. Our objective was to investigate the association of MSB implementation with central line-associated bloodstream infection (CLABSI) in very low birth weight infants. METHODS: This was a prospective multicenter observational study in Japan of infants with birth weight less than 1501 grams and in whom a PICC was placed for the first time between October 2014 and March 2017. Risk factors for CLABSI, both related and unrelated to MSB, were assessed by the mixed-effects Cox proportional hazards model, with the neonatal center variable as the random effect. RESULTS: In total, 33,713 catheter-days among 2383 infants were included. We observed 70 cases of CLABSI. MSB precautions were implemented in 13.9% of insertions and were associated with a lower CLABSI risk (adjusted hazard ratio, 0.20; 95% confidence interval, 0.05-0.84). CONCLUSIONS: We found that MSB implementation during PICC insertion in infants with birth weight less than 1501 grams independently contributed to a decrease in CLABSI risk.

A novel PAX3 rearrangement in embryonal rhabdomyosarcoma.

Rhabdomyosarcoma is the most common soft tissue tumor seen in children and young adults, and it can be classified into 2 major histological subtypes, alveolar and embryonal. In the alveolar subtype, 2 recurrent chromosomal translocations, t(2;13)(q35;q14) and its variant t(1;13)(p36;q14), have been identified as the specific cytogenetic abnormalities. These translocations produce the PAX3-FOXO1 and PAX7-FOXO1 fusion genes, respectively. In the embryonal subtype, however, no recurrent chromosomal abnormalities have been identified. In this study, we analyzed the complex chromosomal translocation in one case with embryonal rhabdomyosarcoma by means of spectral karyotyping (SKY) and identified a novel translocation involving chromosome band 2q35, which is the locus of PAX3 gene. Furthermore, we identified the novel PAX3 rearrangement using fluorescence in situ hybridization (FISH) analysis. Additional identification of the partner gene may help disclose the molecular mechanism of the development of this embryonal subtype.

Nutrient-enriched Diet in the Early Neonatal Period Influences the 3†year-old Height in Very Low Birth Weight Infants.

Nutrient-enriched milk has been advocated to enhance premature infants'growth and early nutritional intervention is effective for growth failure in very low birth weight infants (VLBWI). We studied the 3-yr-old physical growth of VLBWI who received nutrient enriched diets in the early neonatal period. VLBWI, who were born in 1996, received nutrient enriched milk around 1 mo of age. By contrast, in VLBWI born in 1998, nutrient enriched milk was started at 1-2 wk after birth. The daily calorie intake of VLBWI in 1998 had a tendency to be high compared to that of VLBWI in 1996. Height and body weight SD of 3-yr-old children who were born in 1998 tended to be greater than those of children who were born in 1996 (mean ± SD, -0.27 ± 0.54 vs. -1.01 ± 0.67; p=0.043, -0.47 ± 0.61 vs. -0.97 ± 1.10; p=0.31). Our study suggests that early feeding of nutrient-enriched milk for VLBWI in the neonatal period may affect their growth.

A new chromosome banding technique, spectral color banding (SCAN), for full characterization of chromosomal abnormalities.

We have developed spectral color banding (SCAN) as a new chromosome banding technique based on spectral analysis of differentially labeled chromosome band-specific painting probes. In this study, we succeeded in displaying a multicolor banding pattern for chromosome 3, which was almost identical to the pattern obtained with the corresponding G-banding. We applied this method to metaphase cells from different normal male donors with various levels of G-banding resolution, ranging from 250 to 850 bands per haploid set. The same multicolor banding pattern was observed in all samples regardless of the length of the chromosomes or the quality of the G-banding. We then used SCAN in a diffuse large B-cell lymphoma case for a complete analysis of the intrachromosomal change for chromosome 3, which could not be fully characterized by G-banding or even by spectral karyotyping (SKY). SCAN could detect the duplicated segment and identify the origin of the chromosome band on the basis of the specific spectral color of each band. This study demonstrates that SCAN is a useful tool for full characterization of chromosomal abnormalities not identified by SKY.

Rearrangement of the MOZ gene in pediatric therapy-related myelodysplastic syndrome with a novel chromosomal translocation t(2;8)(p23;p11).

In this study, we examined a pediatric case of therapy-related myelodysplastic syndrome (tMDS). The symptoms developed 17 months after treatment for acute myeloblastic leukemia (AML, M2 subtype according to the French-American-British [FAB] classification) involving a chromosome abnormality at t(8;21)(q22;q22). Upon diagnosis of tMDS, spectral karyotyping analysis detected a new chromosomal translocation at t(2;8)(p23;p11.2). In addition, fluorescence in situ hybridization analysis suggested a rearrangement in the monocytic leukemia zinc finger (MOZ) gene, located in the 8p11 region of chromosome 8. However, no partner gene on 2p23 could be identified. To our knowledge, this is the first report of tMDS associated with a rearrangement of the MOZ gene. MOZ-linked fusion proteins such as MOZ-CBP (CREB binding protein), MOZ-TIF2 (transcriptional intermediary factor 2), and MOZ-p300 (adenoviral E1A-associated protein) are associated with AML chromosomal abnormalities at t(8;16)(p11;p13), inv(8)(p11q13), and t(8;22)(p11;q13), respectively, and are thought to account for leukemogenesis occurring through the aberrant regulation of histone acetylation. Through a similar mechanism, we believe that MOZ, fused to an unidentified partner gene at 2p23, may have caused an alteration in histone acetylation, resulting in the development of tMDS in this patient.