Alkali-related ocular burns: a case series and review.

Alkali burns are known to possess high pathological potential because of their inherent ability to lyse cell membranes and penetrate intraocular structures with devastating results. The authors aimed to evaluate the most common cause of this presentation, the current treatment approaches to injury, and eventual outcome as related to severity. The authors performed a retrospective review of all patients who sustained chemical-related ocular injuries seen at the Concord Hospital Burns Unit, Australia between January 2005 and March 2012.

Loss of p21Waf1/Cip1/Sdi1 enhances intestinal stem cell survival following radiation injury.

The microcolony assay following gamma irradiation (IR) is a functional assay of intestinal stem cell fate. The cyclin-dependent kinase (CDK) inhibitor p21(Waf1/Cip1/Sdi1) (p21) regulates cell cycle arrest following DNA damage. To explore the role of p21 on stem cell fate, we examined the effects of p21 deletion on intestinal crypt survival following IR and expression of the stem/progenitor cell marker Musashi-1 (Msi-1) and the antiapoptotic gene survivin.

Knockdown of RNA binding protein musashi-1 leads to tumor regression in vivo.

Background & Aims: In the gut, tumorigenesis is thought to arise from the stem cell population located near the base of intestinal and colonic crypts. The RNA binding protein musashi-1 (Msi-1) is a putative intestinal and progenitor/stem cell marker. Msi-1 expression is increased during rat brain development and in APC(min/+) mice tumors.

EP4 mediates PGE2 dependent cell survival through the PI3 kinase/AKT pathway.

The anti-apoptotic effect of PGE(2) was examined in Jurkat cells (human T-cell leukemia) by incubation with PGE(2) (5 nM) prior to treatment with the cancer chemotherapeutic agent camptothecin. Apoptosis was evaluated by caspase-3 activity in cell extracts and flow cytometry of propidium iodide-labeled cells. Pre-incubation with PGE(2) reduced camptothecin-induced caspase activity by 30% and apoptosis by 35%, respectively.

Azoxymethane protects intestinal stem cells and reduces crypt epithelial mitosis through a COX-1-dependent mechanism.

Azoxymethane (AOM) is a potent DNA-damaging agent and carcinogen that induces intestinal and colonic tumors in rodents. Evaluation of the stem cell population by colony formation assay reveals that, within 8 h after treatment, AOM (10 mg/kg) elicited a prosurvival response. In wild-type (WT) mice, AOM treatment induced a 2.