Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma levels of atrial natriuretic peptide (ANP) were determined with radioimmunoassay in 23 cases of advanced schistosomiasis, 16 cases of chronic schistosomiasis and 16 normal subjects. The results were: the plasma ANP level in advanced schistosomiasis (286.6 +/- 13.0 ng/L) was significantly higher than that in of chronic schistosomiasis (196.7 +/- 17.3 ng/L) and normal controls (157.2 +/- 16.0 ng/L) (P < 0.01 respectively). Among advanced schistosomiasis, the plasma ANP level in 12 cases with ascites (256.5 +/- 16.8 ng/L) was significantly lower than that in 11 cases with splenomegaly but without ascites (320.5 +/- 20.0 ng/L) (P < 0.05). There was no significant difference between the levels in chronic schistosomiasis and normal control (P > 0.05), the results suggested that ANP played a role in maintaining homeostasis of sodium and fluid in advanced schistosomiasis.
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PMID:[The detection and significance of plasma atrial natriuretic peptide in advanced schistosomiasis patients]. 811 47

Mast cells participate in pathophysiological processes that range from antimicrobial defense to anaphylaxis and inflammatory arthritis. Much of the groundwork for the understanding of mast cells was established in mice that lacked mast cells through defects in either stem cell factor or its receptor, Kit. Among available strains, C57BL/6-Kit(W-sh) (W(sh)) mice are experimentally advantageous because of their background strain and fertility. However, the genetic inversion responsible for the W(sh) phenotype remains poorly defined, and its effects beyond the mast cell have been incompletely characterized. We report that W(sh) animals exhibit splenomegaly with expanded myeloid and megakaryocyte populations. Hematopoietic abnormalities extend to the bone marrow and are reflected by neutrophilia and thrombocytosis. In contrast, mast cell-deficient WBB6F1-Kit(W)/Kit(W-v) (W/W(v)) mice display mild neutropenia, but no changes in circulating platelet numbers. To help define the basis for the W(sh) phenotype, a "DNA walking" strategy was used to identify the precise location of the 3' breakpoint, which was found to reside 67.5 kb upstream of Kit. The 5' breakpoint disrupts corin, a cardiac protease responsible for the activation of atrial natriuretic peptide. Consistent with this result, transcription of full-length corin is ablated and W(sh) mice develop symptoms of cardiomegaly. Studies performed using mast cell-deficient strains must consider the capacity of associated abnormalities to either expose or compensate for the missing mast cell lineage.
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PMID:Genetic inversion in mast cell-deficient (Wsh) mice interrupts corin and manifests as hematopoietic and cardiac aberrancy. 1898 2