No abstract available.
Ear, Middle* ; Eustachian Tube*

No abstract available.

No abstract available.

No abstract available.

No abstract available.
Ear, Middle*

No abstract available.

Adult-onset egg allergy is rare compared to child-onset egg allergy, and the component-resolved diagnosis test is effective in evaluating food allergy. We herein report a 24-year-old woman with late-onset egg-yolk allergy diagnosed as bird-egg syndrome. The prolonged exposure to pet parrots' dander or dropping through the respiratory system caused sensitization to the Gal d 5 component and resulted in a cross-reaction to egg yolk. Since the patient was suspected of the syndrome by her history, the skin prick test, ISAC ImmunoCAP, and serum ImmunoCAP test were performed. By confirming Gal d 5 component by ISAC ImmunoCAP, the patient was diagnosed with the syndrome. In patients with newly adult-onset food allergy, the clinician must identify the environmental conditions which can cause cross-sensitization and perform the causative component test.

To evaluate the efficacy of oplyhexamethylene biguanide(PHMB) in Staphylococcus aureus (S. aureus) keratitis model, 10microliter of S. sureus bacterial suspension(1x10(5) colony-forming unit(cfu)/ml) were infected intrastromally into rabbit corneas. 18 rabbits were divided into three treatment groups : balanced salt solution (BSS) group(n=18 eyes), PHMB(0.02%, 200microgram/ml) group(n=9), cefazolin(40 microgram/ml) group(n=9). Topical antibiotic drops were given hourly starting at 24 hours after inoculation. A subconjunctival injection was given every 24 hours for the study duration(96 hours). The severity of keratitis was scored in masked fashion every 12 hours. Corneal buttons were excised and homogenized at the end of the study to determine viable bacterial counts. In the S. aureus keratitis model, there was no difference of clinical scores between BSS, cefazolin, PHMB group at 72 hours, and the number of viable bacteria recovered from the corneal button in log(10) cfu was 2.65+/-1.85, 3.30+/-0.85, 2.86+/-1.36, in BSS, cefazolin, PHMB group respectively. No differences in either clinical scores or bacterial counts were found between the PHMB and BSS groups. PHMB appears to be ineffective against S. aureus in this model of experimental keratitis.
Bacteria ; Bacterial Load ; Cefazolin ; Cornea ; Keratitis* ; Masks ; Rabbits ; Staphylococcus aureus* ; Staphylococcus*

PURPOSE: The objective of this study was to observe the neurodevelopmental outcomes of the surviving very low birth weight infants (VLBWIs) and to identify the perinatal risk factors having influences on to poor neurodevelopmental outcomes . METHODS: The VLBWIs weighing 500 to 1,499 g at birth who had survived to discharge from one NICU during about a 2 year period were followed-up and assessed with using the Baley Scales of Infant Development-Second Edition (BSID-II) test and neurologic examinations when the infants corrected age was between 12 and 24 months. Developmental delay was defined as a MDI less than 70 or a PDI less than 70. The birthweight specific rates of developmental delay and cerebral palsy were examined. The perinatal data were retrospectively collected from the medical records to identify peinatal risk factors that had an influence on poor neurologic outcomes. RESULTS: Thirty three (42.9%) of the 77 VLBWIs were assessed with the BSID-II and neurologic examination, when their corrected age was between 12 and 24 months. The rate of developmental delay and cerebral palsy in the assessed infants was 15.2% and 21.2%, respectively. Extremely low birth weight infants (ELBWIs) had high rates of developmental delay (30.8%) and cerebral palsys (30.8%). Maternal old age (>35 years, odds ratio=18.0, 95% CI, 1.2-262.7, P=0.035) and periventricular leukomalacia (PVL, odds ratio=12.6, 95% CI, 1.1-148.1, P=0.044) were independently associated with developmental delay and cerebral palsy, respectively. CONCLUSION: Significant poor neurodevelopmental outcome for the VLBW infants needs a more extended follow-up study for development, and especially for the ELBWIs.
Cerebral Palsy ; Follow-Up Studies ; Humans ; Infant* ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Very Low Birth Weight* ; Leukomalacia, Periventricular ; Medical Records ; Neurologic Examination ; Parturition ; Retrospective Studies ; Risk Factors ; Weights and Measures

During angiogenesis, binding of urokinase plasminogen activator(uPA) and its receptor(uPAR) has been implicated as an important component of the angiogenesis pathway. We have produced a high-affinity competitive antagonist for the uPA receptor consisting of a fusion protein linking the endothelial growth factor(EGF)-like domain of uPA(residues 1-48) to the Fc domain of IgG. To determine whether this recombinant murine uPA1-48-IgG fusion protein could interfere with angiogenesis, we studied the effect of this compound on rat corneal angiogenesisinduced by basic fibroblast growth factor(bFGF). A hydrogel disk containing 250ng of bFGF and 4.2ug of uPA1-48-IgG fusiong protein in seven eyes, 250ug of bFGF and 4.2ug of phosphate-buffered saline(PBS) in another sseven eyes were implanted intrastromally 1.5mm from the superior limbus. At five days post-implantation of bFGF disk, the eyes treated with uPA1-48IgG fusion protein had reduced angiogenesis (mean score=3.1) compared with the PBS-treated controls(mean score=6.1)(P<0.05, Wilcoxon rank sum test). In a rat corneal pocket assay, murine uPA1-48-IgG fusion protein appears to inhibit bFGF-induced angiogenesis. Compounds that block uPAR binding of uPA may have therapeutic potential as anti-angiogenic agents.
Animals ; Corneal Neovascularization* ; Fibroblast Growth Factor 2* ; Fibroblasts ; Hydrogel ; Immunoglobulin G ; Plasminogen Activators* ; Plasminogen* ; Rats* ; Urokinase-Type Plasminogen Activator*