Business Recovery Status Report #13: Presidential Disaster #1763, October 3, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #14: Presidential Disaster #1763, October 10, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #15: Presidential Disaster #1763, October 17, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #16: Presidential Disaster #1763, October 24, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #17: Presidential Disaster #1763, October 31, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #18: Presidential Disaster #1763, November 7, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #19: Presidential Disaster #1763, November 14, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

Business Recovery Status Report #20: Presidential Disaster #1763, November 21, 2008

Safeguard Iowa Partnership launched a survey to the business community to capture the impact from the 2008 disasters. Five hundred eighty surveys were completed and compiled for the report submitted to the Rebuild Iowa Office Economic and Workforce Development Task Force on August 20, 2008.

CD47 knockout mice exhibit improved recovery from spinal cord injury.

Recent data have implicated thrombospondin-1 (TSP-1) signaling in the acute neuropathological events that occur in microvascular endothelial cells (ECs) following spinal cord injury (SCI) (Benton et al., 2008b). We hypothesized that deletion of TSP-1 or its receptor CD47 would reduce these pathological events following SCI. CD47 is expressed in a variety of tissues, including vascular ECs and neutrophils. CD47 binds to TSP-1 and inhibits angiogenesis. CD47 also binds to the signal regulatory protein (SIRP)α and facilitates neutrophil diapedesis across ECs to sites of injury. After contusive SCI, TSP-1(-/-) mice did not show functional improvement compared to wildtype (WT) mice. CD47(-/-) mice, however, exhibited functional locomotor improvements and greater white matter sparing. Whereas targeted deletion of either CD47 or TSP-1 improved acute epicenter vascularity in contused mice, only CD47 deletion reduced neutrophil diapedesis and increased microvascular perfusion. An ex vivo model of the CNS microvasculature revealed that CD47(-/-)-derived microvessels (MVs) prominently exhibit adherent WT or CD47(-/-) neutrophils on the endothelial lumen, whereas WT-derived MVs do not. This implicates a defect in diapedesis mediated by the loss of CD47 expression on ECs. In vitro transmigration assays confirmed the role of SIRPα in neutrophil diapedesis through EC monolayers. We conclude that CD47 deletion modestly, but significantly, improves functional recovery from SCI via an increase in vascular patency and a reduction of SIRPα-mediated neutrophil diapedesis, rather than the abrogation of TSP-1-mediated anti-angiogenic signaling.

Psychophysiological activation during preparation, performance, and recovery in high- and low-anxious music students

The present study provides a comprehensive view of (a) the time dynamics of the psychophysiological responding in performing music students (n = 66) before, during, and after a private and a public performance and (b) the moderating effect of music performance anxiety (MPA). Heart rate (HR), minute ventilation (VE), and all affective and somatic self-report variables increased in the public session compared to the private session. Furthermore, the activation of all variables was stronger during the performances than before or after. Differences between phases were larger in the public than in the private session for HR, VE, total breath duration, anxiety, and trembling. Furthermore, while higher MPA scores were associated with higher scores and with larger changes between sessions and phases for self-reports, this association was less coherent for physiological variables. Finally, self-reported intra-individual performance improvements or deteriorations were not associated with MPA. This study makes a novel contribution by showing how the presence of an audience influences low- and high-anxious musicians' psychophysiological responding before, during and after performing. Overall, the findings are more consistent with models of anxiety that emphasize the importance of cognitive rather than physiological factors in MPA.

Visual activity predicts auditory recovery from deafness after adult cochlear implantation.

Modern cochlear implantation technologies allow deaf patients to understand auditory speech; however, the implants deliver only a coarse auditory input and patients must use long-term adaptive processes to achieve coherent percepts. In adults with post-lingual deafness, the high progress of speech recovery is observed during the first year after cochlear implantation, but there is a large range of variability in the level of cochlear implant outcomes and the temporal evolution of recovery. It has been proposed that when profoundly deaf subjects receive a cochlear implant, the visual cross-modal reorganization of the brain is deleterious for auditory speech recovery. We tested this hypothesis in post-lingually deaf adults by analysing whether brain activity shortly after implantation correlated with the level of auditory recovery 6 months later. Based on brain activity induced by a speech-processing task, we found strong positive correlations in areas outside the auditory cortex. The highest positive correlations were found in the occipital cortex involved in visual processing, as well as in the posterior-temporal cortex known for audio-visual integration. The other area, which positively correlated with auditory speech recovery, was localized in the left inferior frontal area known for speech processing. Our results demonstrate that the visual modality's functional level is related to the proficiency level of auditory recovery. Based on the positive correlation of visual activity with auditory speech recovery, we suggest that visual modality may facilitate the perception of the word's auditory counterpart in communicative situations. The link demonstrated between visual activity and auditory speech perception indicates that visuoauditory synergy is crucial for cross-modal plasticity and fostering speech-comprehension recovery in adult cochlear-implanted deaf patients.

Ectopic pacing at physiological rate improves postanoxic recovery of the developing heart.

Recently, rapid and transient cardiac pacing was shown to induce preconditioning in animal models. Whether the electrical stimulation per se or the concomitant myocardial ischemia affords such a protection remains unknown. We tested the hypothesis that chronic pacing of a cardiac preparation maintained in a normoxic condition can induce protection. Hearts of 4-day-old chick embryos were electrically paced in ovo over a 12-h period using asynchronous and intermittent ventricular stimulation (5 min on-10 min off) at 110% of the intrinsic rate. Sham (n = 6) and paced hearts (n = 6) were then excised, mounted in vitro, and subjected successively to 30 min of normoxia (20% O(2)), 30 min of anoxia (0% O(2)), and 60 min of reoxygenation (20% O(2)). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout the experiment. Reoxygenation-induced chrono-, dromo-, and inotropic disturbances, incidence of arrhythmias, and changes in electromechanical delay (EMD) in atria and ventricle were systematically investigated in sham and paced hearts. Under normoxia, the isolated heart beat spontaneously and regularly, and all baseline functional parameters were similar in sham and paced groups (means +/- SD): heart rate (190 +/- 36 beats/min), P-R interval (104 +/- 25 ms), mechanical atrioventricular propagation (20 +/- 4 mm/s), ventricular shortening velocity (1.7 +/- 1 mm/s), atrial EMD (17 +/- 4 ms), and ventricular EMD (16 +/- 2 ms). Under anoxia, cardiac function progressively collapsed, and sinoatrial activity finally stopped after approximately 9 min in both groups. During reoxygenation, paced hearts showed 1) a lower incidence of arrhythmias than sham hearts, 2) an increased rate of recovery of ventricular contractility compared with sham hearts, and 3) a faster return of ventricular EMD to basal value than sham hearts. However, recovery of heart rate, atrioventricular conduction, and atrial EMD was not improved by pacing. Activity of all hearts was fully restored at the end of reoxygenation. These findings suggest that chronic electrical stimulation of the ventricle at a near-physiological rate selectively alters some cellular functions within the heart and constitutes a nonischemic means to increase myocardial tolerance to a subsequent hypoxia-reoxygenation.

Examining chemical compound biodegradation at low concentrations through bacterial cell proliferation.

We show proof of principle for assessing compound biodegradation at 1-2 mg C per L by measuring microbial community growth over time with direct cell counting by flow cytometry. The concept is based on the assumption that the microbial community will increase in cell number through incorporation of carbon from the added test compound into new cells in the absence of (as much as possible) other assimilable carbon. We show on pure cultures of the bacterium Pseudomonas azelaica that specific population growth can be measured with as low as 0.1 mg 2-hydroxybiphenyl per L, whereas in mixed community 1 mg 2-hydroxybiphenyl per L still supported growth. Growth was also detected with a set of fragrance compounds dosed at 1-2 mg C per L into diluted activated sludge and freshwater lake communities at starting densities of 10(4) cells per ml. Yield approximations from the observed community growth was to some extent in agreement with standard OECD biodegradation test results for all, except one of the examined compounds.

Potential use of a chemical leaching reject from a kaolin industry as agricultural fertilizer

The industrial refining of kaolin involves the removal of iron oxides and hydroxides along with other impurities that cause discoloration of the final product and depreciate its commercial value, particularly undesirable if destined to the paper industry. The chemical leaching in the industrial processing requires treatments with sodium hyposulfite, metallic zinc, or sulfuric and phosphoric acids, in order to reduce, dissolve and remove ferruginous compounds. To mitigate the environmental impact, the acidic effluent from the leaching process must be neutralized, usually with calcium oxide. The resulting solid residue contains phosphorous, zinc, and calcium, among other essential nutrients for plant growth, suggesting its use as a macro and micronutrient source. Samples of such a solid industrial residue were used here to evaluate their potential as soil fertilizer in an incubation greenhouse experiment with two soil samples (clayey and medium-textured). The small pH shift generated by applying the residue to the soil was not a limiting factor for its use in agriculture. The evolution of the concentrations of exchangeable calcium, and phosphorous and zinc extractability by Mehlich-1 extractant during the incubation period confirms the potential use of this industrial residue as agricultural fertilizer.

Botulinum neurotoxin type A blocks the morphological changes induced by chemical stimulation on the presynaptic membrane of Torpedo synaptosomes.

The action of botulinum neurotoxin on acetylcholine release, and on the structural changes at the presynaptic membrane associated with the transmitter release,was studied by using a subcellular fraction of cholinergic nerve terminals (synaptosomes) isolated from the Torpedo electric organ. Acetylcholine and ATP release were continuously monitored by chemiluminescent methods.To catch the membrane morphological changes, the quick-freezing method was applied. Our results show that botulinum neurotoxin inhibits the release of acetylcholine from these isolated nerve terminals in a dose-dependent manner, whereas ATP release is not affected. The maximal inhibition (70%) is achieved at neurotoxin concentrations as low as 125 pM with an incubation time of 6 min. This effect is not linked to an alteration of the integrity of the synaptosomes since, after poisoning by botulinum neurotoxin type A, they show a nonmodified occluded lactate dehydrogenase activity. Moreover, membrane potential is not altered by the toxin with respect to the control, either in resting condition or after potassium depolarization. In addition to acetylcholine release inhibition, botulinum neurotoxin blocks the rearrangement of the presynaptic intramembrane particles induced by potassium stimulation. The action of botulinum neurotoxin suggests that the intramembrane particle rearrangement is related to the acetylcholine secretion induced by potassium stimulation in synaptosomes isolated from the electric organ of Torpedo marmorata.