Cross-reactivity to olive tree pollen and orchard grass pollen in patients with pollinosis

We studied 92 patients with allergic rhinitis in Syodoshima, Japan, during the pollen season between April and June to evaluate the cross-reactivity to different antigens, including pollen from the olive tree (Olea europaea) and orchard grass (Dactylis glomerata). Olive tree pollen was present in the atmosphere for 23 days, from May 19 to June 12, 1994. Specific IgE antibodies for olive tree pollen antigen were present in 21 (26.9%) of the 78 patients with allergic rhinitis. Nine (24.3%) of the 37 patients with allergic rhinitis exhibited positive skin reactivity to an extract of olive tree pollen. Fifteen (88.2 %) of the 17 patients who had IgE reactivity in their sera to olive tree pollen antigen demonstrated allergic reactions to an extract of olive tree pollen. Specific IgE antibodies for orchard grass pollen antigen were present in 43 (48.3%) of the 89 patients with allergic rhinitis and 20 (95.2%) of the 21 patients who had IgE reactivity in their sera to olive tree pollen antigen. The inhibition test using the CAP System revealed that the reactivity of the IgE antibody specific for olive tree pollen antigen was inhibited dose-dependently by an extract of orchard grass pollen. These findings show that there is a reaction in some patients with grass (Gramineae) pollinosis that might be induced by olive tree pollen.</p

IP3R-driven increases in mitochondrial Ca2+ promote neuronal death in NPC disease

Ca2+ is the most ubiquitous second messenger in neurons whose spatial and temporal elevations are tightly controlled to initiate and orchestrate diverse intracellular signaling cascades. Numerous neuropathologies result from mutations or alterations in Ca2+ handling proteins; thus, elucidating molecular pathways that shape Ca2+ signaling is imperative. Here, we report that loss-of-function, knockout, or neurodegenerative disease-causing mutations in the lysosomal cholesterol transporter, Niemann-Pick Type C1 (NPC1), initiate a damaging signaling cascade that alters the expression and nanoscale distribution of IP3R type 1 (IP3R1) in endoplasmic reticulum membranes. These alterations detrimentally increase Gq-protein coupled receptor-stimulated Ca2+ release and spontaneous IP3R1 Ca2+ activity, leading to mitochondrial Ca2+ cytotoxicity. Mechanistically, we find that SREBP-dependent increases in Presenilin 1 (PS1) underlie functional and expressional changes in IP3R1. Accordingly, expression of PS1 mutants recapitulate, while PS1 knockout abrogates Ca2+ phenotypes. These data present a signaling axis that links the NPC1 lysosomal cholesterol transporter to the damaging redistribution and activity of IP3R1 that precipitates cell death in NPC1 disease and suggests that NPC1 is a nanostructural disease

A New Dissolution Effect of DMO on Human Pancreatic Stone : In vitro Study

In this study, we examined the dissolution effect of dimethadione (DMO) on pancreatic stones, when kept at 37°C in a DMO 0.05 M NaHC03 saline solution which was replaced once a week, were partially dissolved during a 12-week period. The decreasing stone weight ratios were 38% (1.0 g/1 DMO), 41% (0.5 g/1), 7% (0.1 g/1), and 2% (control). The DMO solution induced a concentration-dependent increase in the solubility of the pancreatic stones associated with a concentration-dependent fall in the solution pH. The eluted calcium concentration in the solution was measured after one week\u27s incubation, and then the decrease in stone weight in theory was calculated. The decrease in stone weight in practice, however, was more than the calculated weight in theory. To determine the reason for this discrepancy, we examined the solution microscopically for sediment and found amorphous substances indicating a concentration-dependent increase in the amount of sediment. These substances resembled artificially broken pancreatic stones and they were dissolved by bubbles following the addition of acetic acid. This phenomenon suggests that these substances and pancreatic stones consist of CaC03. Therefore, it appears DMO has the potency not only to dissolve CaCO3, but also to break pancreatic stones into small pieces

Regulation of young-adult neurogenesis and neuronal differentiation by neural cell adhesion molecule 2 (NCAM2)

Adult neurogenesis persists in mammals in the neurogenic zones, where newborn neurons are incorporated into preexisting circuits to preserve and improve learning and memory tasks. Relevant structural elements of the neurogenic niches include the family of cell adhesion molecules (CAMs), which participate in signal transduction and regulate the survival, division, and differentiation of radial glial progenitors (RGPs). Here we analyzed the functions of neural cell adhesion molecule 2 (NCAM2) in the regulation of RGPs in adult neurogenesis and during corticogenesis. We characterized the presence of NCAM2 across the main cell types of the neurogenic process in the dentate gyrus, revealing different levels of NCAM2 amid the progression of RGPs and the formation of neurons. We showed that Ncam2 overexpression in adult mice arrested progenitors in an RGP-like state, affecting the normal course of young-adult neurogenesis. Furthermore, changes in Ncam2 levels during corticogenesis led to transient migratory deficits but did not affect the survival and proliferation of RGPs, suggesting a differential role of NCAM2 in adult and embryonic stages. Our data reinforce the relevance of CAMs in the neurogenic process by revealing a significant role of Ncam2 levels in the regulation of RGPs during young-adult neurogenesis in the hippocampus

DU-PAN 2 Antigen in Sera of Patients with Liver Diseases

To evaluate the usefulness of serum DU-PAN 2 (an antigen defined by a monoclonal antibody raised against human pancreatic carcinoma cells), serum specimens from 370 cases of hepatobiliary and pancreatic diseases along with 31 normal controls were studied using an enzyme immunoassay. Elevated levels of serum DU-PAN 2 were detected in the serum of 28.3% of the cases with chronic hepatitis (15/53), 36.5% of those with liver cirrhosis (27/74), 48.4% of the hepatocellular carcinoma cases (61/126) and 50% of primary biliary cirrhosis (4/8). Significant differences were noted between patients with chronic inactive hepatitis (17 cases mean 201.4 U/ml) and chronic active hepatitis (36 cases; mean 394.5 U/ml) and, more distinctly, between patients with compensated liver cirrhosis (41 cases; mean 225.1 U/ml) and, those with decompensated liver cirrhosis (33 cases; mean 564.7 U/ml). The highest median levels were seen in patients with primary biliary cirrhosis (922.7 U/ml), and then in those with hepatocellular carcinoma (551.4 U/ml). Using an immunoperoxidase technique on formalin-fixed, deparaffinized liver sections, we showed that DU-PAN 2 reacted with bile-duct epithelium but never stained hepatoma cells. These results suggest that the determination of serum DU-PAN 2 can be useful in evaluating chronic liver diseases