Ocular infarction following ethanol sclerotherapy of an arteriovenous malformation.

PURPOSE: To illustrate a case of ocular infarction following percutaneous ethanol sclerotherapy of an orbital arteriovenous malformation. OBSERVATIONS: The patient is a 31-year-old female who developed ocular infarction of the left eye with light perception vision, proptosis, ophthalmoplegia, and a cherry red spot following sclerotherapy of an orbital arteriovenous malformation. Fluorescein angiography demonstrated decreased arteriolar filling with vascular leakage, indocyanine green angiography showed decreased choroidal perfusion, and optical coherence tomography revealed full thickness retinal edema. Magnetic resonance angiography and venography were negative for venous sinus thrombosis or intracranial vascular compromise. CONCLUSIONS AND IMPORTANCE: Ocular infarction is a rare and devastating disorder that may result in permanent vision loss. Ethanol sclerotherapy has been reported to be effective in treating arteriovenous malformations. To the best of our knowledge, this is the first report in the literature of ocular infarction following percutaneous ethanol sclerotherapy to highlight this disease with multimodal imaging.

MTBP inhibits the Erk1/2-Elk-1 signaling in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and the prognosis of HCC patients, especially those with metastasis, remains extremely poor. This is partly due to unclear molecular mechanisms underlying HCC metastasis. Our previous study indicates that MDM2 Binding Protein (MTBP) suppresses migration and metastasis of HCC cells. However, signaling pathways regulated by MTBP remain unknown. To identify metastasis-associated signaling pathways governed by MTBP, we have performed unbiased luciferase reporter-based signal array analyses and found that MTBP suppresses the activity of the ETS-domain transcription factor Elk-1, a downstream target of Erk1/2 MAP kinases. MTBP also inhibits phosphorylation of Elk-1 and decreases mRNA expression of Elk-1 target genes. Reduced Elk-1 activity is caused by inhibited nuclear translocation of phosphorylated Erk1/2 (p-Erk) by MTBP and subsequent inhibition of Elk-1 phosphorylation. We also reveal that MTBP inhibits the interaction of p-Erk with importin-7/RanBP7 (IPO7), an importin family member which shuttles p-Erk into the nucleus, by binding to IPO7. Moreover, high levels of MTBP in human HCC tissues are correlated with cytoplasmic localization of p-Erk1/2. Our study suggests that MTBP suppresses metastasis, at least partially, by down-modulating the Erk1/2-Elk-1 signaling pathway, thus identifying a novel regulatory mechanism of HCC metastasis by regulating the subcellular localization of p-Erk.

Roles of p53 in extrinsic factor-induced liver carcinogenesis.

Liver cancer remains one of the most common human cancers with a high mortality rate. Therapies for hepatocellular carcinoma (HCC) remain ineffective, due to the heterogeneity of HCC with regard to both the etiology and mutation spectrum, as well as its chemotherapy resistant nature; thus surgical resection and liver transplantation remain the gold standard of patient care. The most common etiologies of HCC are extrinsic factors. Humans have multiple defense mechanisms against extrinsic factor-induced carcinogenesis, of which tumor suppressors play crucial roles in preventing normal cells from becoming cancerous. The tumor suppressor p53 is one of the most frequently mutated genes in liver cancer. p53 regulates expression of genes involved in cell cycle progression, cell death, and cellular metabolism to avert tumor development due to carcinogens. This review article mainly summarizes extrinsic factors that induce liver cancer and potentially have etiological association with p53, including aflatoxin B1, vinyl chloride, non-alcoholic fatty liver disease, iron overload, and infection of hepatitis viruses.

Cold air drainage and modeled nocturnal leaf water potential in complex forested terrain.

Spatial variation in microclimate caused by air temperature inversions plays an important role in determining the timing and rate of many physical and biophysical processes. Such phenomena are of particular interest in mountainous regions where complex physiographic terrain can greatly complicate these processes. Recent work has demonstrated that, in some plants, stomata do not close completely at night, resulting in nocturnal transpiration. The following work was undertaken to develop a better understanding of nocturnal cold air drainage and its subsequent impact on the reliability of predawn leaf water potential (Psi(pd)) as a surrogate for soil water potential (Psi(s)). Eight temperature data loggers were installed on a transect spanning a vertical distance of 155 m along a north facing slope in the Mica Creek Experimental Watershed (MCEW) in northern Idaho during July and August 2004. Results indicated strong nocturnal temperature inversions occurring from the low- to upper-mid-slope, typically spanning the lower 88 m of the vertical distance. Based on mean temperatures for both months, inversions resulted in lapse rates of 29.0, 27.0 and 25.0 degrees C km(-1) at 0000, 0400 and 2000 h, respectively. At this scale (i.e., < 1 km), the observed lapse rates resulted in highly variable nighttime vapor pressure deficits (D) over the length of the slope, with variable impacts on modeled disequilibrium between soil and leaf water potential. As a result of cold air drainage, modeled Psi(pd) became consistently more negative (up to -0.3 MPa) at higher elevations during the night based on mean temperatures. Nocturnal inversions on the lower- and mid-slopes resulted in leaf water potentials that were at least 30 and 50% more negative over the lower 88 m of the inversion layer, based on mean and maximum temperatures, respectively. However, on a cloudy night, with low D, the maximum decrease in Psi(pd) was -0.04 MPa. Our results indicate that, given persistent cold air drainage and nighttime stomatal opening, serious errors will result if Psi(s) is estimated from Psi(pd).