KTP laser: An important tool in refractory recurrent tracheo-esophageal fistula in children

Secondary tracheo-oesophageal fistula in delayed primary repair of oesophageal atresia is rare. This paper reports the successful use of the KTP laser in the treatment of this condition in a refractory case. It also recommends the use of direct laryngotracheobronchoscopy (DLTB) in the diagnosis. We recommend the use of this laser in cases of recurrent tracheo-esophageal fistula especially when other means have failed.     

Neurological examination of the infant

Clinicians are required to perform neurological examinations on infants to ensure they meet developmental milestones. A full neurological examination includes evaluating motor and sensory function, assessing the status of the cranial nerves, testing primitive reflexes, and atypical responses to further evaluate any developmental pathologies. The difficulty in maintaining infants' cooperation requires resourcefulness on the clinician's part to understand what is being tested and in what way to complete the examination. This literature will provide clinicians with guidance on the way to conduct a thorough neurological examination of infants. Clin. Anat. 32:770–777, 2019. © 2019 Wiley Periodicals, Inc.     

Psychological Distress among Syrian Refugee Women and a Control Group in an Urban Settlement in Beirut- a Pilot Study

Psychiatric Quarterly - The Syrian conflict has created approximately five million refugees. Of these, more than one million have settled in Lebanon. This project aimed to determine the prevalence...     

De novo methicillin-resistant Staphylococcus aureus vs. methicillin-sensitive Staphylococcus aureus infections of the spine,similar clinical outcome,despite more severe presentation in surgical patients

Neurosurgical Review - Vertebral osteomyelitis (VO) is a severe infection of the vertebral body and the adjacent disc space, where Staphylococcus aureus is most commonly isolated. The objective of...     

Patients with high bone mass phenotype exhibit enhanced osteoblast differentiation and inhibition of adipogenesis of human mesenchymal stem cells.

Genetic mutations in the LRP5 gene affect Wnt signaling and lead to changes in bone mass in humans. Our in vivo and in vitro results show that activated mutation T253I of LRP5 enhances osteogenesis and inhibits adipogenesis. Inactivating mutation T244M of LRP5 exerts opposite effects. INTRODUCTION: Mutations in the Wnt co-receptor, LRP5, leading to decreased or increased canonical Wnt signaling, result in osteoporosis or a high bone mass (HBM) phenotype, respectively. However, the mechanisms whereby mutated LRP5 causes changes in bone mass are not known. MATERIALS AND METHODS: We studied bone marrow composition in iliac crest bone biopsies from patients with the HBM phenotype and controls. We also used retrovirus-mediated gene transduction to establish three different human mesenchymal stem cell (hMSC) strains stably expressing wildtype LRP5 (hMSC-LRP5(WT)), LRP5(T244) (hMSC-LRP5(T244), inactivation mutation leading to osteoporosis), or LRP5(T253) (hMSC-LRP5(T253), activation mutation leading to high bone mass). We characterized Wnt signaling activation using a dual luciferase assay, cell proliferation, lineage biomarkers using real-time PCR, and in vivo bone formation. RESULTS: In bone biopsies, we found increased trabecular bone volume and decreased bone marrow fat volume in patients with the HBM phenotype (n = 9) compared with controls (n = 5). The hMSC-LRP5(WT) and hMSC-LRP5(T253) but not hMSC-LRP5(T244) transduced high level of Wnt signaling. Wnt3a inhibited cell proliferation in hMSC-LRP5(WT) and hMSC-LRP5(T253), and this effect was associated with downregulation of DKK1. Both hMSC-LRP5(WT) and hMSC-LRP5(T253) showed enhanced osteoblast differentiation and inhibited adipogenesis in vitro, and the opposite effect was observed in hMSC-LRP5(T244). Similarly, hMSC-LRP5(WT) and hMSC-LRP5(T253) but not hMSC-LRP5(T244) formed ectopic mineralized bone when implanted subcutaneously with hydroxyapatite/tricalcium phosphate in SCID/NOD mice. CONCLUSIONS: LRP5 mutations and the level of Wnt signaling determine differentiation fate of hMSCs into osteoblasts or adipocytes. Activation of Wnt signaling can thus provide a novel approach to increase bone mass by preventing the age-related reciprocal decrease in osteogenesis and increase in adipogenesis.     

Isolation and Differentiation of Chondrocytic Cells Derived from Human Embryonic Stem Cells Using dlk1/FA1 as a Novel Surface Marker

Few surface markers are available to monitor lineage differentiation during chondrogenesis. Recently, delta-like1/fetal antigen1 (dlk1/FA1), a transmembrane protein of the Notch/Delta/Serrata family, was shown to be essential for inducing early chondrogenesis. Thus, we investigated the possible use of dlk1/FA1 as a novel surface marker for chondroprogenitor cells during hESC differentiation. We found that, Dlk1/FA1 is expressed specifically in cells undergoing transition from proliferating to prehypertrophic chondrocytes during endochondral ossification of the mouse limb. In hESC cells, dlk1/FA1 was not expressed by undifferentiated hESC, but expressed during in vitro embryoid bodies (hEBs) formation upon down-regulation of undifferentiated markers e.g. Oct 3/4. Similarly, dlk1/FA1 was expressed in chondrocytic cells during in vivo teratoma formation. Interestingly, treatment of hEBs with Activin B, a member of TGF-ß family, markedly increased Dlk1 expression in association with up-regulation of the mesoderm-specific markers (e.g. FOXF1, KDR and VE-cadherin) and SOX9. dlk1/FA1⁺ cells isolated by fluorescence activated cell sorting (FACS) were capable of differentiating into chondrocytic cells when cultured as micromass pellets in a xeno-free system containing TGFβ1. In conclusion, we identified dlk1/FA1 as a novel marker of chondroprogenitor cells that undergo embryonic lineage progression from proliferation to the prehypertrophic stage. Tracking dlk1/FA1 expression as a mesoderm/chondroprogenitor surface marker provides a novel strategy for designing clinically relevant protocols to direct the differentiation of hESC into chondrocytes.