The subependymal zone (SEZ) of the lateral ventricles is one of the areas of the adult brain where new neurons are continuously generated from neural stem cells (NSCs), via rapidly dividing precursors. This neurogenic niche is a complex cellular and extracellular microenvironment, highly vascularized compared to non-neurogenic periventricular areas, within which NSCs and precursors exhibit distinct behavior. Here, we investigate the possible mechanisms by which extracellular matrix molecules and their receptors might regulate this differential behavior. We show that NSCs and precursors proceed through mitosis in the same domains within the SEZ of adult male mice-albeit with NSCs nearer ependymal cells-and that distance from the ventricle is a stronger limiting factor for neurogenic activity than distance from blood vessels. Furthermore, we show that NSCs and precursors are embedded in a laminin-rich extracellular matrix, to which they can both contribute. Importantly, they express differential levels of extracellular matrix receptors, with NSCs expressing low levels of ␣61 integrin, syndecan-1, and lutheran, and in vivo blocking of 1 integrin selectively induced the proliferation and ectopic migration of precursors. Finally, when NSCs are activated to reconstitute the niche after depletion of precursors, expression of laminin receptors is upregulated. These results indicate that the distinct behavior of adult NSCs and precursors is not necessarily regulated via exposure to differential extracellular signals, but rather via intrinsic regulation of their interaction with their microenvironment.
Although a ‘vascular stem cell’ population has not been identified or generated, vascular endothelial and mural cells (smooth muscle cells and pericytes) can be derived from currently known pluripotent stem cell sources including human embryonic stem cells and induced pluripotent stem cells. We review the vascular potential of these human pluripotent stem cells, the mechanisms by which they are induced to differentiate toward a vascular endothelial cell fate, and their applications in regenerative medicine.
INTRODUCTION: Dunbar Syndrome, also known as median arcuate ligament syndrome (MALS), is a rare condition with a reported incidence of 2 per 100,000. It is characterized by an extrinsic compression of the celiac trunk, and should be considered when evaluating patients with abdominal pain of unknown etiology. CASE DESCRIPTION/METHODS: A 78 year old female presented with a complaint of epigastric discomfort that was post-prandial in nature, with associated weakness and early satiety. Her symptoms had been persistent for one year. Workup prior to her presentation included a normal nuclear medicine (NM) gastric emptying scan and normal NM hepatobiliary scan with CCK. A detailed history revealed that her pain was particularly worse after eating and was associated with early satiety. Laboratory results on admission were unremarkable. Contrast-enhanced CT scan of the abdomen and pelvis showed external compression and indentation of the superior aspect of the proximal celiac axis with post-stenotic dilation. Further diagnostic evaluation utilized end-inspiratory phase CT angiography of the abdomen, which showed an approximately 1 cm length segment of proximal celiac arterial narrowing, measuring 70% maximally at its origin. She was diagnosed with MALS after review of the CTA reconstructive images which showed moderate external compression of the celiac artery. DISCUSSION: MALS predominantly affects women between the ages of 30 and 50 and is marked by the hallmark feature of postprandial abdominal pain. Other signs and symptoms may include nausea, vomiting, and consequent weight loss from an inability to tolerate oral intake. Symptoms are thought to have both a vascular (mesenteric ischemia) as well as neurogenic component (somatic pain thought to originate from the splanchnic plexus). CT angiography and conventional angiography are considered to be gold standard imaging modalities for Dunbar syndrome. They demonstrate focal stenosis that has a characteristic hooked appearance due to the indentation of the celiac trunk on its superior surface. Imaging for an accurate diagnosis should ideally be performed during the end-inspiratory phase, as indentation of the celiac trunk may be seen normally during expiration. Additional imaging features may include post-stenotic dilation, prominent collateral vessels, and thickening of the median arcuate ligament. Treatment includes endovascular transluminal angioplasty and stent placement, as well as laparoscopic division of the arcuate ligament and resection of the celiac plexus.
INTRODUCTION: Colchicine, a commonly prescribed medication for numerous medical conditions, is notorious for causing harm in the stomach and small intestine. Less commonly, damage can occur in other organs, such as the esophagus. CASE DESCRIPTION/METHODS: A 72-year-old male with a history of gout presented to the gastroenterology clinic with a several month progression of pyrosis and dysphagia. Upper endoscopy was performed which revealed erosive esophagitis. Biopsies were obtained which revealed mitotic arrest of the cells in metaphase. On review of his medications, he had been on long-term colchicine therapy for management of his gout. DISCUSSION: Colchicine, an anti-inflammatory medication, acts at the cellular level by interrupting mitosis. This is achieved through disrupting neutrophil microtubules and ultimately preventing neutrophil migration and adhesion, thus, decreasing the inflammation associated with diseases, such as gout. Microscopically, mitotic arrest is commonly seen in metaphase with evidence of ringed mitoses, glandular cell apoptosis, and epithelial pseudostratification. Within the gastrointestinal tract, colchicine is most notable for causing side effects such as diarrhea and nausea. However, due to its prevention of cellular division, it can cause injury to rapidly proliferating cells within the gastrointestinal tract. Most commonly, this occurs in the small bowel and gastric antrum. We present a rare case in which evidence of colchicine toxicity is identified within the esophagus. In our patient, colchicine was discontinued and he was treated with proton pump inhibitor therapy with improvement of his symptoms.
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