A case of milk allergy that presented anaphylaxis after cutaneous contact with allergen

ABSTRACTMilk allergy in a 1-year and 8-month-old boy is reported. At 1 year and 1 month of age, the patient presented with anaphylaxis, including erythema, which was initially localized to the contact site of the anterior chest, and wheezing accompanied by dyspnea, 5 min after contact with milk allergen through his atopic skin. These symptoms continued for 50 min. Seventy minutes after the disappearance of the initial erythema, the patient developed subsequent erythematous lesions distributed throughout the neck and head area that persisted for as long as 24 h. On another occasion, he also exhibited a pale face and generalized erythema immediately after an accidental oral ingestion of milk at the age of 1 year and 8 months. He had been unsettled for several hours when an intravenous steroid was administered. His serum IgE was 590 IU/mL and the radioallergosorbent test (RAST) scores against milk, α-lactoalbumin, β-lactoglobulin, casein and cheese were 5, 2, 3, 5 and 5, respectively. This is a rare case of a patient with milk allergy who fell into anaphylaxis following both cutaneous contact with and oral ingestion of the offending milk protein. Care should be taken with patients with food allergies because cutaneous contact with the offending food may cause adverse reactions, including anaphylaxis

Evx2-Hoxd13 Intergenic Region Restricts Enhancer Association to Hoxd13 Promoter

Expression of Hox genes is tightly regulated in spatial and temporal domains. Evx2 is located next to Hoxd13 within 8 kb on the opposite DNA strand. Early in development, the pattern of Hoxd13 expression resembles that of Evx2 in limb and genital buds. After 10 dpc, however, Evx2 begins to be expressed in CNS as well. We analyzed the region responsible for these differences using ES cell techniques, and found that the intergenic region between Evx2 and Hoxd13 behaves as a boundary element that functions differentially in space and time, specifically in the development of limbs, genital bud, and brain. This boundary element comprises a large sequence spanning several kilobases that can be divided into at least two units: a constitutive boundary element, which blocks transcription regulatory influences from the chromosomal environment, and a regulatory element, which controls the function of the constitutive boundary element in time and space

Structure-activity relationship study of the neuritogenic potential of the glycan of starfish ganglioside LLG-3

LLG-3 is a ganglioside isolated from the starfish Linchia laevigata. To clarify the structure-activity relationship of the glycan of LLG-3 toward rat pheochromocytoma PC12 cells in the presence of nerve growth factor, a series of mono- to tetrasaccharide glycan derivatives were chemically synthesized and evaluated in vitro. The methyl group at C8 of the terminal sialic acid residue was crucial for neuritogenic activity, and the terminal trisaccharide moiety was the minimum active motif. Furthermore, the trisaccharide also stimulated neuritogenesis in human neuroblastoma SH-SY5Y cells via mitogen-activated protein kinase (MAPK) signaling. Phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was rapidly induced by adding 1 or 10 nM of the trisaccharide. The ratio of phosphorylated ERK to ERK reached a maximum 5 min after stimulation, and then decreased gradually. However, the trisaccharide did not induce significant Akt phosphorylation. These effects were abolished by pretreatment with the MAPK inhibitor U0126, which inhibits enzymes MEK1 and MEK2. In addition, U0126 inhibited the phosphorylation of ERK 1/2 in response to the trisaccharide dose-dependently. Therefore, we concluded that the trisaccharide promotes neurite extension in SH-SY5Y cells via MAPK/ERK signaling, not Akt signaling

Figure 6

<p>Position-effect blocker activity of the XB fragment. (A) Constructs introduced into the NIH3T3 cell line. Construct I (top) contains a CAGGS promoter-driven fluorescent protein (Venus) and a neomycin-resistance gene, enabling G418 selection of stable transformant colonies of transfected NIH3T3 cells. Construct II (bottom) is organized similarly, except it contains XB blocker fragments bordering both sides of the Venus expression marker gene. (B) Experimental scheme illustrating the transfection scenario. Stable transformants of both constructs were selected using G418. Colonies were maintained in culture for one year. We selected samples from each colony after 1, 6, and 12 months for FACS analyses. (C) Fluorescence assessment of 12 colonies harboring either Construct I or Construct II. Fewer fluorescent cells were observed in colonies lacking the XB fragment, while numerous fluorescent cells were observed in colonies harboring the XB fragment, indicating that the XB construct (Construct II) maintained Venus expression.</p

Figure 4

<p>Methylation profile of insulator fragment. (A) Hindbrain and forelimbs were dissected from 11 dpc embryos to obtain the DNA used for the methylation assays. (B) Map of the tested fragment. Red line represents the insulator (XB fragment) and blue line represents the regulator (BB fragment). Bisulfite-treated genomic DNA was subjected to PCR using three sets of primers (indicated by arrows; see Experimental Procedures). Primer pairs for one PCR reaction have matching arrow color. (C) Ten clones from each PCR product were sequenced. Their methylation status is shown here. White circles represent methylated cytosine residues, while black circles represent non-methylated cytosine residues.</p

Figure 3

<p>Insulation activity is spatially dependent. (A) Design of two targeted transgenic mice. XNs and XB as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000175#pone-0000175-g002" target="_blank">Figure 2A</a>. (B) Expression pattern of XNs- and XB-transgenic mouse embryos. XNs 11 dpc embryos expressed lacZ in the limbs and genital bud, whereas XB embryos did not. Limbs are shown in the boxed areas and genital buds are shown in the middle panels. (C) Scheme illustrating the regulation underlying enhancer-promoter interaction. Within the CNS, the XB fragment prevents interaction between the enhancer and <i>Hoxd13</i> promoter, while the BB fragment blocks the insulator activity of the XB fragment within the limbs and genital bud.</p

Figure 5

<p>Premature expression of <i>Hoxd13</i> observed in XB-targeted transgenic mice. (A) <i>Hoxd13</i> expression in 7 dpc embryos was specifically upregulated. Sample RNA levels were normalized according to β-actin mRNA levels. W1–W3, samples from three litters arising from wild-type mice; B1–B6, samples from six litters arising from internally bred BB-transgenic mice; X1–X8, samples from eight litters arising from internally bred XB-transgenic mice. (B) Hypothetical scheme for premature expression of these genes in XB-transgenic mice. The region downstream of <i>Evx2</i> recruits repression over the <i>Hox</i> complex before the 7-dpc embryonic stage in preparation for <i>Hox</i> expression in wild-type and BB-targeted transgenic mice. The XB fragment disrupts repression, preventing the repressor region downstream of <i>Evx2</i> from recruiting repression into the <i>HoxD</i> complex.</p