Detection of air trapping in chronic obstructive pulmonary disease by low frequency ultrasound

<p>Abstract</p> <p>Background</p> <p>Spirometry is regarded as the gold standard for the diagnosis of COPD, yet the condition is widely underdiagnosed. Therefore, additional screening methods that are easy to perform and to interpret are needed. Recently, we demonstrated that low frequency ultrasound (LFU) may be helpful for monitoring lung diseases. The objective of this study was to evaluate whether LFU can be used to detect air trapping in COPD. In addition, we evaluated the ability of LFU to detect the effects of short-acting bronchodilator medication.</p> <p>Methods</p> <p>Seventeen patients with COPD and 9 healthy subjects were examined by body plethysmography and LFU. Ultrasound frequencies ranging from 1 to 40 kHz were transmitted to the sternum and received at the back during inspiration and expiration. The high pass frequency was determined from the inspiratory and the expiratory signals and their difference termed ΔF. Measurements were repeated after inhalation of salbutamol.</p> <p>Results</p> <p>We found significant differences in ΔF between COPD subjects and healthy subjects. These differences were already significant at GOLD stage 1 and increased with the severity of COPD. Sensitivity for detection of GOLD stage 1 was 83% and for GOLD stages worse than 1 it was 91%. Bronchodilator effects could not be detected reliably.</p> <p>Conclusions</p> <p>We conclude that low frequency ultrasound is cost-effective, easy to perform and suitable for detecting air trapping. It might be useful in screening for COPD.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT01080924">NCT01080924</a></p

PifC and Osa, Plasmid Weapons against Rival Conjugative Coupling Proteins

Bacteria display a variety of mechanisms to control plasmid conjugation. Among them, fertility inhibition (FI) systems prevent conjugation of co-resident plasmids within donor cells. Analysis of the mechanisms of inhibition between conjugative plasmids could provide new alternatives to fight antibiotic resistance dissemination. In this work, inhibition of conjugation of broad host range IncW plasmids was analyzed in the presence of a set of co-resident plasmids. Strong FI systems against plasmid R388 conjugation were found in IncF/MOBF12 as well as in IncI/MOBP12 plasmids, represented by plasmids F and R64, respectively. In both cases, the responsible gene was pifC, known also to be involved in FI of IncP plasmids and Agrobacterium T-DNA transfer to plant cells. It was also discovered that the R388 gene osa, which affects T-DNA transfer, also prevented conjugation of IncP-1/MOBP11 plasmids represented by plasmids RP4 and R751. Conjugation experiments of different mobilizable plasmids, helped by either FI-susceptible or FI-resistant transfer systems, demonstrated that the conjugative component affected by both PifC and Osa was the type IV conjugative coupling protein. In addition, in silico analysis of FI proteins suggests that they represent recent acquisitions of conjugative plasmids, i.e., are not shared by members of the same plasmid species. This implies that FI are rapidly-moving accessory genes, possibly acting on evolutionary fights between plasmids for the colonization of specific hosts

Antisense reduction of tau in adult mice protects against seizures

Tau, a microtubule-associated protein, is implicated in the pathogenesis of Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hyperexcitability. The genetic ablation of tau substantially reduces hyperexcitability in AD mouse lines, induced seizure models, and genetic in vivo models of epilepsy. These data demonstrate that tau is an important regulator of network excitability. However, developmental compensation in the genetic tau knock-out line may account for the protective effect against seizures. To test the efficacy of a tau reducing therapy for disorders with a detrimental hyperexcitability profile in adult animals, we identified antisense oligonucleotides that selectively decrease endogenous tau expression throughout the entire mouse CNS—brain and spinal cord tissue, interstitial fluid, and CSF—while having no effect on baseline motor or cognitive behavior. In two chemically induced seizure models, mice with reduced tau protein had less severe seizures than control mice. Total tau protein levels and seizure severity were highly correlated, such that those mice with the most severe seizures also had the highest levels of tau. Our results demonstrate that endogenous tau is integral for regulating neuronal hyperexcitability in adult animals and suggest that an antisense oligonucleotide reduction of tau could benefit those with epilepsy and perhaps other disorders associated with tau-mediated neuronal hyperexcitability

Implicating Calpain in Tau-Mediated Toxicity In Vivo

Alzheimer's disease and other related neurodegenerative disorders known as tauopathies are characterized by the accumulation of abnormally phosphorylated and aggregated forms of the microtubule-associated protein tau. Several laboratories have identified a 17 kD proteolytic fragment of tau in degenerating neurons and in numerous cell culture models that is generated by calpain cleavage and speculated to contribute to tau toxicity. In the current study, we employed a Drosophila tauopathy model to investigate the importance of calpain-mediated tau proteolysis in contributing to tau neurotoxicity in an animal model of human neurodegenerative disease. We found that mutations that disrupted endogenous calpainA or calpainB activity in transgenic flies suppressed tau toxicity. Expression of a calpain-resistant form of tau in Drosophila revealed that mutating the putative calpain cleavage sites that produce the 17 kD fragment was sufficient to abrogate tau toxicity in vivo. Furthermore, we found significant toxicity in the fly retina associated with expression of only the 17 kD tau fragment. Collectively, our data implicate calpain-mediated proteolysis of tau as an important pathway mediating tau neurotoxicity in vivo

THE EVOLUTIONARY ANALYSIS AND TRANSCRIPTIONAL CHARACTERIZATION OF PABB.

THE EVOLUTIONARY ANALYSIS AND TRANSCRIPTIONAL CHARACTERIZATION OF PABB

Nicholas Goncharoff letter to Thomas Bernard (January 3, 1985)

This is a letter from Nicholas T. Goncharoff, Director of Special Programs at the YMCA of the USA, to Thomas L. Bernard, the Executive Director of YMCA Studies and a professor of education at Springfield College. It is dated January 3, 1985. The letter thanks Mr. Bernard, on behalf of the YMCA of the USA, for the "brilliant" idea of creating a YMCA Hall of Fame at Springfield College. He also talks about the possibility of working with the statesmanship program and a scholar-in-residence program at Springfield College.Thomas L. Bernard held many roles at Springfield college between when he first arrived in 1974 till he retired in 1999. He was a professor of education and psychology at Springfield College, the head of the Division of Community Education for eight years, Executive Director of the YMCA Studies during which he created the YMCA Hall of Fame, and the Director of the Graduate Education Programs for 22 years.The original letter is not within the collection. The letter was scanned and a facsimile was placed in the collection. The original letter was returned to Thomas L. Bernard

Process of interplay with loose material in the feeding unit of a gravitation-rotary type

Виконано теоретичний аналіз взаємодії ротора з сипким матеріалом, що надходить у нього з матеріалопроводу постачального пристрою. Отримано залежності для визначення вихідних параметрів потоку матеріалу після взаємодії з ротором: швидкості і напряму рухуAs a result of the analysis of movement of a flow of a free-flowing material in a rotor of the having device are received of analytical dependences for definition of target parameters of a flow of a material after interaction with a rotor: speed and direction of movemen