Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021843 (bowel obstruction)
 9,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and histopathologic features in seven patients with intestinal lymphoma are reported. Three of these presented with ulcerative jejunitis and four with overt lymphomas. A short history of abdominal pain with weight loss followed by intestinal obstruction, hemorrhage, or perforation characterized all the patients except one in whom a nine year history of malabsorption preceded the acute phase of the disease. Malabsorption was demonstrated in four of the patients, and all showed villous atrophy with crypt hyperplasia of the jejunum remote from areas of ulceration or frank lymphoma. The malignant lymphoma cells showed varying degrees of pleomorphism and exhibited phagocytosis of platelets, red cells, and cell debris. The accompanying infiltrate of inflammatory cells often overshadowed the neoplastic histiocytes, and in those cases showing little pleomorphism these cells could be easily overlooked. In the intestine the tumor cells were usually present as a diffuse infiltrate in the lamina propria or within the bases of ulcers and in five of seven cases did not give rise to macroscopic tumor masses. In all patients dissemination of tumor cells to the lymph nodes, liver, spleen, and bone marrow was evident, the infiltrate in all these organs resembling that seen in malignant histiocytosis. The morphology of the tumor cells, their phagocytic nature, the diffuse character of the tumor infiltrate, and the pattern of dissemination suggest that this lesion should be designated malignant histiocytosis of the intestine rather than histiocytic lymphoma (reticulum cell sarcoma). It is suggested that the tumor may arise from cells of monocyte-histiocyte lineage normally present in the lamina propria of the gut and that a prolonged cryptic phase accompanied, and often overshadowed, by an inflammatory reaction may give rise to malabsorption and ulcerative jejunitis before overt lymphoma is manifest.
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PMID:Malignant histiocytosis of the intestine. Its relationship to malabsorption and ulcerative jejunitis. 73 Jan 48

Computed tomography was performed on a patient presenting with cryptic small bowel obstruction. A correct preoperative diagnosis of obturator foramen hernia was arrived at based on the recognition of a loop of ileum protruding between the pectineus and external obturator muscles.
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PMID:Computed tomographic diagnosis of obturator foramen hernia. 664 57

Recently we have created a mouse model of cystic fibrosis (CF) by insertional gene targeting to exon 10. In common with CF subjects, this model displays a low incidence of meconium ileus. This contrasts strikingly with the very high level of fatal intestinal obstruction in the three other CF mouse models so far described. We investigate here the molecular basis of this difference in phenotype. We show that the partial duplication consequent upon insertional gene targeting allows exon skipping and aberrant splicing to produce normal Cftr mRNA, but at levels greatly reduced compared with wild-type mice. Furthermore, instead of the predicted mutant Cftr transcript, a novel mRNA is produced that utilizes cryptic splice sites in the disrupting plasmid sequence. However, we have previously shown that these mice display the ion transport defect characteristic of CF, and mutant animals can be distinguished from their normal littermates on this basis. Consistent with this, residual CFTR function has recently been observed for several "mild" mutations in CF individuals who display pancreatic sufficiency but still develop lung disease. We conclude that (i) residual wild-type mRNA in the exon 10 insertional mutant mouse ameliorates the severity of the intestinal phenotype observed in the absolute "null" CF mice, (ii) the presence of low-level residual wild-type Cftr mRNA does not correct the CF ion transport defect, and (iii) the long-term survival of this insertional mutant mouse provides the opportunity to address the factors important in development of lung disease.
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PMID:Long-term survival of the exon 10 insertional cystic fibrosis mutant mouse is a consequence of low level residual wild-type Cftr gene expression. 794 29