Prolonging the Shelf Life of Homemade Gelatin Ultrasound Phantoms.

A significant limitation of homemade phantoms is shelf life. Our goal was to compare the impact on shelf life of easily obtained additives. Fifteen additives were mixed into a gelatin-psyllium hydrophilic mucilloid fiber phantom; three of these additives were used as a layer on top of the phantom. The mixtures were stored in the refrigerator and at room temperature. The samples were evaluated daily for microbial growth and phantom degradation. A 4% of chlorhexidine gluconate layer on top of the phantom quickly made the phantom unusable. The addition of benzoic acid and bleach to the mixture negatively affected phantom appearance with ultrasound imaging. The addition of household bleach or 4% chlorhexidine gluconate to the mixture or a 10% povidone-iodine layer on top of the phantom was the best way to preserve samples stored at room temperature. The refrigerated sample outlasted the paired room temperature sample in every case, with most room temperature samples becoming unusable by day 10 and most refrigerated samples lasting past 50 days.

Po2 cycling protects diaphragm function during reoxygenation via ROS, Akt, ERK, and mitochondrial channels.

Po2 cycling, often referred to as intermittent hypoxia, involves exposing tissues to brief cycles of low oxygen environments immediately followed by hyperoxic conditions. After experiencing long-term hypoxia, muscle can be damaged during the subsequent reintroduction of oxygen, which leads to muscle dysfunction via reperfusion injury. The protective effect and mechanism behind Po2 cycling in skeletal muscle during reoxygenation have yet to be fully elucidated. We hypothesize that Po2 cycling effectively increases muscle fatigue resistance through reactive oxygen species (ROS), protein kinase B (Akt), extracellular signal-regulated kinase (ERK), and certain mitochondrial channels during reoxygenation. Using a dihydrofluorescein fluorescent probe, we detected the production of ROS in mouse diaphragmatic skeletal muscle in real time under confocal microscopy. Muscles treated with Po2 cycling displayed significantly attenuated ROS levels (n = 5; P < 0.001) as well as enhanced force generation compared with controls during reperfusion (n = 7; P < 0.05). We also used inhibitors for signaling molecules or membrane channels such as ROS, Akt, ERK, as well as chemical stimulators to close mitochondrial ATP-sensitive potassium channel (KATP) or open mitochondrial permeability transition pore (mPTP). All these blockers or stimulators abolished improved muscle function with Po2 cycling treatment. This current investigation has discovered a correlation between KATP and mPTP and the Po2 cycling pathway in diaphragmatic skeletal muscle. Thus we have identified a unique signaling pathway that may involve ROS, Akt, ERK, and mitochondrial channels responsible for Po2 cycling protection during reoxygenation conditions in the diaphragm.

Nitric oxide in cancer metastasis.

Cancer metastasis is the spread and growth of tumor cells from the original neoplasm to further organs. This review analyzes the role of nitric oxide (NO), a signaling molecule, in the regulation of cancer formation, progression, and metastasis. The action of NO on cancer relies on multiple factors including cell type, metastasis stage, and organs involved. Various chemotherapy drugs cause cells to release NO, which in turn induces cytotoxic death of breast, liver, and skin tumors. However, NO has also been clinically connected to a poor cancer prognosis because of its role in angiogenesis and intravasation. This supports the claim that NO can be characterized as both pro-metastatic and anti-metastatic, depending on specific factors. The inhibition of cell proliferation and anti-apoptosis pathways by NO donors has been proposed as a novel therapy to various cancers. Studies suggest that NO-releasing non-steroidal anti-inflammatory drugs act on cancer cells in several ways that may make them ideal for cancer therapy. This review summarizes the biological significance of NO in each step of cancer metastasis, its controversial effects for cancer progression, and its therapeutic potential.