Histidine decarboxylase (HDC) synthesizes histamine from histidine in mammals. To evaluate the role of histamine, we generated HDC-deficient mice using a gene targeting method. The mice showed a histamine deficiency and lacked histaminesynthesizing activity from histidine. These HDC-deficient mice are viable and fertile but exhibit a decrease in the numbers of mast cells while the remaining mast cells show an altered morphology and reduced granular content. The amounts of mast cell granular proteases were tremendously reduced. The HDCdeficient mice provide a unique and promising model for studying the role of histamine in a broad range of normal and disease processes. ß

The Mini-International Neuropsychiatric Interview (MINI) is a short, structured diagnostic interview used as a tool to diagnose 16 axis I (Diagnostic and Statistical Manual) DSM-IV disorders and one personality disorder. Its original version was developed by Sheehan and Lecrubier. We translated the MINI into Japanese, and investigated the reliability and validity of the Japanese version of MINI. Eighty-two subjects participated in the validation of the MINI versus the Structured Clinical Interview for DSM-III-R (SCID-P). One hundred and sixty-nine subjects participated in the validation of the MINI versus an expert's professional opinion. Seventy-seven subjects were interviewed by two investigators and subsequently readministered by a third interviewer blind to the results of initial evaluation 1-2 days later. In general, kappa values indicated good or excellent agreement between MINI and SCID-P diagnoses. Kappa values indicated poor agreement between MINI and expert's diagnoses for most diagnoses. Interrater and test-retest reliabilities were good or excellent. The mean durations of the interview were 18.8 min for MINI and 45.4 min for corresponding sections of SCID-P. Overall, the results suggest that the MINI Japanese version succeeds in reliably and validly eliciting symptom criteria used in making DSM-III-R diagnoses, and can be performed in less than half the time required for the SCID-P.

Microenvironment-based alterations in phenotypes of mast cells influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast-cell maturation via PGD2 receptor DP1. Mice lacking PLA2G3, L-PGDS or DP1, mast cell–deficient mice reconstituted with PLA2G3-null or DP1-null mast cells, or mast cells cultured with L-PGDS–ablated fibroblasts exhibited impaired maturation and anaphylaxis of mast cells. Thus, we describe a lipid-driven PLA2G3–L-PGDS–DP1 loop that drives mast cell maturation.

Complementary DNA (cDNA) clones specific for phospholamban of sarcoplasmic reticulum membranes have been isolated from a canine cardiac cDNA library. The amino acid sequence deduced from the cDNA sequence indicates that phospholamban consists of 52 amino acid residues ,and lacks an amino-terminal signal sequence. The protein has an. inferred mol wt 6,080 that is in agreement with its apparent monomeric mol wt 6,000, estimated previously by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Phospholamban contains two distinct domains, a hydrophilic region at the amino terminus (domain I) and a hydrophobic region at the carboxy terminus (domain II). We propose that domain I is localized at the cytoplasmic surface and offers phosphorylatable sites whereas domain II is anchored into the sarcoplasmic reticulum membrane.

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