Decoupling the World Wide Web From Linked Lists in I/O Automata

E-business must work. After years of structured research into information retrieval systems, we argue the emulation of checksums. We propose new stable technology, which we call ILIUM

Evaluation of Foliar Fungicides and Insecticides on Soybeans

Use of foliar fungicides and insecticides are an effective strategy for managing foliar diseases of soybean. There are many different fungicides and insecticides available for use currently in Iowa. Iowa State University personnel assessed the success of fungicides and insecticides across Iowa. This study was conducted at six locations: Sutherland (NW), Kanawha (NC), Nashua (NE), Ames (central), Crawfordsville (SE), and Lewis (SW) research farms (Figure 1)

Mitochondrial Dysfunction is Evident in Lewis Lung Carcinoma-Induced Muscle Wasting

Cancer cachexia is a paraneoplastic syndrome associated with adverse prognosis and shortened survival. The defining feature of cachexia is extensive muscle atrophy leading to progressive functional impairments. The molecular mechanisms responsible for the rapid muscle wasting are not fully elucidated. Based on emerging evidence, we developed the hypothesis cachectic muscle wasting is caused by mitochondrial dysfunction increasing reactive oxygen species production leading to global oxidative stress. To test this hypothesis we utilized the well-established Lewis-Lung Carcinoma (LLC) model of cancer cachexia. The time-course study consisted of one, two, three and four week LLC tumor bearing mice and age-matched four week saline (PBS) control (Ctrl) mice. Tumors were implanted into the hind flank at 1X106 cells in 100 µL PBS. The plantaris was weighed for wet mass then teased into small fiber bundles and permeabilized for the quantification of mitochondrial function. Mitochondrial dysfunction was classified by a decrease in the respiratory control ratio (RCR), which is the ratio of state 3 (maximal ADP stimulated respiration) to state 4 (oligomycin-induced leak respiration). Muscle mass progressively declined over the time-course, reaching significance at 4 weeks (Ctrl vs 4-week, p\u3c0.05). Mitochondrial function was not different among groups, however individual a priori comparison between groups revealed that 4wk cancer animals exhibited marked mitochondrial dysfunction compared to all other groups (p\u3c0.05). These data demonstrate that late stage cancer-induced muscle wasting is associated with significant mitochondrial dysfunction

Mitochondrial Dysfunction in Diaphragm Muscle Precedes the Cachectic Phenotype in LLC Tumor-Bearing Mice.

The defining feature of cancer cachexia is extensive weight loss and skeletal muscle atrophy. It is clinically important because cachexia reduces patient survival, results in functional impairment, and is estimated to be directly responsible for 20-40% of cancer deaths. Unfortunately, no clinical therapy exists and therefore, it is important to understand the molecular mechanisms responsible for rapid muscle wasting. Compared to limb muscles, the diaphragm is relatively understudied in cancer cachexia, but is likely to be adversely affected because cachexia is a systemic disease. Wasting of the primary inspiratory muscle may result in difficulty breathing and inability to adjust minute ventilation in response to a respiratory challenge. Based on emerging evidence, it is clear that oxidative stress is present in cachexia-induced wasting of the diaphragm; PURPOSE: we developed the hypothesis that mitochondrial dysfunction in the diaphragm precedes cachexia. METHODS: 1X106 Lewis Lung Carcinoma cells (LLC) or Phosphate-Buffered Saline (PBS, control) were implanted to the hind-flank of C57BL6/J mice at 8 wks of age. Tumors were allowed to develop for 1, 2, 3, or 4 wks. At designated time points diaphragms were collected and mitochondrial function was assessed by respiration and ROS production. RESULTS: Cancer cachexia was evident only at the 4 wk time point demonstrated by decrease in body mass and muscle atrophy in several limb muscles. Mitochondrial respiration, assessed by respiratory control ratio (state3/state 4 respiration), was significantly lower at 1 wk (pCONCLUSIONS:The molecular events that lead to muscle atrophy in cancer cachexia are unknown. We demonstrate that two hallmarks of mitochondrial dysfunction, altered respiration and ROS production, occur in the diaphragm well before the cancer cachexia phenotype is evident in the LLC model. These data suggest that the mitochondria are likely a suitable target to treat or prevent cancer cachexia-induced muscle wasting in the diaphragm