[Diagnosis and treatment of pneumatosis cystoides intestinalis].

Pneumatosis cystoides intestinalis (PCI) is a rare disease, which is characterized by the accumulation of gas cysts located in the submucosa or subserosa of the gastrointestinal tract. It can occur in the whole or part of the gastrointestinal tract from the esophagus to the rectum, but clinically the main involved sites are the colon and small intestine. PCI can also appear in other sites such as mesentery, the greater omentum and the hepatogastric ligament. In recent years, with the renewal of imaging method, the detection rate of PCI has been on the rise. Most patients with PCI have no obvious symptoms or only non-specific symptoms of the digestive tract like abdominal distension, abdominal pain, diarrhea, hematochezia, etc. The atypical clinical symptoms of PCI can easily lead to missed diagnosis or misdiagnosis. A small amount of patients would have complications like peritonitis and even perforation of the digestive tract. The therapeutic principle for these patients is different from that for patients with acute abdomen. The prognosis of PCI depends on its severity and comorbidities. In this article, a literature review would be conducted on the epidemiological characteristics, etiology and pathogenesis, clinical manifestations, diagnosis and treatment of PCI, which might help clinical doctors with diagnosis and treatment of the disease.

Testis-specific expression of an intronless gene encoding a human poly(A) polymerase.

A mouse intronless gene, encoding a testis-specific poly(A) polymerase (mPAPT), was previously identified. mPAPT may play a role as a putative enzyme that is responsible for polyadenylation regulation during mouse spermatogenesis. In order to understand how PAPT genes are conserved in mammals, we isolated a human cDNA homolog encoding a human PAPT (hPAPT), which was specifically expressed in the testis. The structure of hPAPT was very similar to that of mPAPT. The about 100 residues at the C-terminal region of a nuclear poly(A) polymerase, PAP II, were missing in both PAPT proteins. An analysis of the genomic DNA showed that the hPAPT gene is an intronless gene that is similar to the mPAPT gene. Interestingly, the sequence homology between hPAPT and mPAPT was much lower than the homology between hPAP II and mPAP II. The phylogenetic analysis suggests that PAPTs arose through retrotransposition after the amphibian-amniote split during evolution.

Hypoxia-induced bFGF gene expression is mediated through the JNK signal transduction pathway.

Although the synthesis of angiogenic factors in hypoxic regions of solid tumors is recognized as one of the critical steps in tumor growth and metastasis, the signal transduction pathway involved in hypoxic induction of basic fibroblast growth factor (bFGF) gene expression is still obscure. In the study described here, we investigated the intracellular responses to hypoxia and the mechanisms triggering the initiation of angiogenic activity in drug-resistant human breast carcinoma MCF-7/ADR cells. Northern blots showed an increase in the level of c-jun, c-fos, and bFGF mRNA during hypoxia. Gel mobility-shift analysis of nuclear extracts from hypoxia-exposed cells showed an increase in AP-1 binding activity. In addition, hypoxic treatment strongly activated c-Jun N-terminal kinase 1 (JNK1), leading to phosphorylation and activation of c-Jun. Expression of a dominant negative mutant of JNK1 suppressed hypoxia-induced JNK1 activation as well as bFGF gene expression. Taken together, hypoxia-induced bFGF gene expression is mediated through the stress-activated protein kinase (SAPK) signal transduction pathway.