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The treatment effects and safety of ear acupressure EAP for patients with allergic rhinitis AR have yet to be clarified. Systematic review of published studies. We performed literature inclusion, data extraction, and trial quality evaluations. Methodological quality was assessed according to the Cochrane Handbook. A total of trials were identified and eleven studies involved participants aged 3—70 years. EAP was better than control group interventions in terms of effectiveness risk ratio RR : 0.

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• The Repression of Atoh1 by Neurogenin1 during Inner Ear Development
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Both genes are induced early in development, but the expression of Atoh1 is counteracted by Neurog1. As a result, HC development is prevented during neurogenesis. This work aimed at understanding the molecular basis of this interaction. Reporter assays on chick embryos and P19 cells show that Neurog1 hampers the autoactivation of Atoh1, the effect being cell autonomous and independent on Notch activity. Neurog1 requires the regions flanking the class A E-box to show its repressor effect, however, it does not require binding to DNA for Atoh1 repression.

This depends on the dimerization domains Helix-1 and Helix-2 and the reduction of Atoh1 protein levels. The results point towards the acceleration of Atoh1 mRNA degradation as the potential mechanism for the reduction of Atoh1 levels.

Such a mechanism dissociates the prevention of Atoh1 expression in neurosensory progenitors from the unfolding of the neurogenic program. Hair cells HCs of the inner ear are sensory mechanoreceptors that transduce hearing and balance stimuli into electrical signals. They are part of the functional unit of the inner ear, which is also composed of supporting cells SCs and neurons. In amniotes, multipotent neurosensory progenitors generate the three cell types with a tight time sequence.

Neurons are specified first and delaminate from the otic epithelium and only later on in development, sensory precursors differentiate into HCs and SCs Raft et al. Interestingly, the regulatory networks operating during development reactivate during HC regeneration. Birds are able to regenerate auditory HCs after damage and this ability relies on the competence of SCs to reactivate the expression of Atoh1 Cafaro et al.

In mammals, Atoh1 is also able to drive HC regeneration, but this ability is lost after early post-natal life White et al. The expression of Atoh1 in HCs depends on several factors but it is ultimately established by an autoregulatory loop by which Atoh1 sustains its own expression Helms et al. Both Atoh1 and Neurog1 are induced very early in development, but Atoh1 is repressed during neurogenesis and during the expansion of the prospective sensory organs Puligilla et al.

This, results in the delay of HC development with respect to neuronal production. The mutual exclusion between neurogenesis and sensorigenesis is paralleled by the antagonism between Neurog1 and Atoh1 Matei et al.

Yet, the molecular mechanisms underlying this interaction are largely unknown. Atoh1 expression in the inner ear is accounted for by a 1. The goal of this work was to understand how Neurog1 counteracts the function of Atoh1. Instead, the repressor function of Neurog1 depends on the H1-helix heterodimerization domain and results in the reduction of Atoh1 protein levels.

Protein extract from electroporated HH chicken otic vesicles was prepared using Reporter Lysis buffer EA, Promega 24 h after electroporation Petrovic et al. Detailed point mutations are shown in Figure 1C. Figure 1. The forward oligonucleotide contains a NheI site, while the reverse oligonucleotide contains a BglII site.

P19 cells embryonic carcinoma cells derived from teratocarcinoma mice; Castro et al. Ninety-six well dishes were seeded with 10 4 cells and transfected at 24 h with Fugene HD E, Promega , 75 pg of each expression plasmids, 75 pg luciferase reporter plasmid, and 30 pg pRenilla-TK vector Promega as internal control.

The resulting library was sequenced in Illumina Hi-seq pair-end lane. Reads were aligned with Bowtie2 Software Langmead and Salzberg, , using mouse July mm9 as reference genome. Duplicated pairs or those ones separated by more than 2 Kb were removed. Starting material for immunoprecipitation was 5—10 mg. Dynabeads protG beads previously blocked 0.

Secondary antibodies were Alexa Fluor , , , and conjugated anti-mouse, anti-goat and anti-rabbit Molecular Probes Invitrogen, Western blot was performed as in Neves et al. In vitro cultures of otic vesicles were performed as described in Neves et al. However, given the small size of the samples, and following Halsey et al.

The expression of Atoh1 during inner ear development relies on an enhancer located 3. Reporter activity of this enhancer is detected within the inner ear neurosensory domain Neves et al. However, Atoh1 transcription is silent during neurogenesis and it is not expressed until later stages Lumpkin et al. As shown by Helms et al. The region containing these three E-box binding sites is referred hereafter as the CAN region.

In otic vesicles, the activity of the enhancer was restricted to the neurosensory domain Figure 2Ab ; Neves et al. Cotransfection of P19 cells with Atoh1 together with decreasing amounts of Neurog1 showed that the latter was able to prevent Atoh1 autoactivation even at a concentration ratio of Figure 2D. Figure 2.

D Neurog1 is able to repress Atoh1 autoactivation at low concentrations in P19 cells. Mouse otocysts enriched in neurosensory tissue were analyzed at two different stages of development: E A set of E Figure 3. Middle and lower lanes are from samples corresponding to E In all conditions readings are mainly present at the position of EnhB, EnhA showing very little accessibility. To further analyze the contribution of each enhancer to Atoh1 regulation, separate multimer constructs of either Enhancer A or B 4xEnhA or 4xEnhB were electroporated and their activity measured in otic vesicles.

The spatial activity of 4xEnh A and B was strikingly different in chick otic vesicle. Quantitation of reporter activity showed undetectable endogenous activity of 4xEnhA, and no activation by Atoh1 or Sox2 data not shown. This contrasted with the intense activity of 4xEnhB Figure 4B.

Next, we studied whether Enhancer B was also repressed by Neurog1. This indicates that Enhancer B accounts for the repression by Neurog1. Figure 4. EnhB contains the essential elements for the repression by Neurog1. A EnhA shows no activity but regulates that of EnhB. Luciferase activity corresponding to EnhB in the three conditions indicated in abscissa.

D Atoh1 and Neurog1 activated the isolated E-box A. In agreement, they activated the 4xEboxA multimer Figure 4D , the mixture of both being additive. From the above results, there may be three major and not mutually exclusive mechanisms for the repression of Atoh1 by Neurog1. First, the direct interaction of Neurog1 with the CAN region, secondly, the interaction Neurog1 with Atoh1protein or with essential cofactors for Atoh1 autoactivation and, finally, the post-transcriptional modification of Atoh1 at mRNA or protein levels.

This suggests that Neurog1 does not interfere with Atoh1 autoactivation by competing with Atoh1 for DNA binding or by the transcriptional activation of a repressor factor. Figure 5. Neurog1 does not require DNA-binding to repress Atoh1. Neurog1 upper row or Neurog1-AQ lower row were electroporated in ovo E3. Cells electroporated with Neurog1 adopted neuronal fate a—c , cvg: cochleo-vestibular ganglion , while those with Neurog1-AQ d—h turned into supporting cells SCs; arrows in f,g.

Bars represent the number of cells counted in two consecutive frames of electroporated macula sacularis, from three independent embryos. Cell types were identified with the markers described above. Otic vesicles were electroporated at the prosensory stage E3. Electroporation of Neurog1 resulted in a massive neuronal commitment Figure 5Fa electroprated cells in non-neural domains were also forced to become neurons Figure 5Fb.

No electroporated cells were observed in the sensory epithelium after 3-days and HC patterning was not substantially affected Figure 5Fc. Contrarily, electroporation of Neurog1-AQ caused a strong blockade of neuronal formation Figure 5Fd , suggesting that it acts as a dominant-negative for Neurog1.

After 6 h otic vesicles were dissected, and incubated with or without the Notch inhibitor LY for another 16 h. As shown, Neurog1-AQ repression was similar in both cases Figure 6A , suggesting Notch signaling is not necessary for the repressor effect of Neurog1. Figure 6. Neurog1 Helix-1 dimerization domain is essential for Atoh1 repression.

A Neurog1 does not require Notch signaling for Atoh1 repression. Left: diagram of the different constructs tested. Right: reporter activity in P19 cells shown in the conditions indicated in abscissa. To gain insight into the mechanism of action of Neurog1, we analyzed the functionality of different modified Neurog1 constructs carrying selective deletions of the Helix-1, Helix-2 or the C-terminal domains.

Deletion of Helix-1 restored almost completely Atoh1 autoactivation, and Helix-2 only partially Figure 6B. The deletion of the C-terminal domain, which contains phosphorylation sites required for their activity and stability Cundiff et al. Therefore, Helix-1 and Helix-2, which are dimerization domains, are crucial for the repressor function of Neurog1. We tested the ability of these E-proteins to rescue Atoh1 repression by Neurog1, and the results showed that none of them was able to revert the effect of Neurog1 Figure 6C.

Therefore, Neurog1 does not seem to act by sequestering necessary transcriptional co-factors. We next questioned whether Neurog1 binds directly to Atoh1 forming a non-functional heterodimer. This procedure provides also information on other possible proteins that interact with Atoh1. Atoh1 was immunoprecipitated with an anti-FLAG antibody and the bound proteins identified by mass spectrometry. Neurog1 targeted several types of genes including genes that control regulation of transcription, signal transduction and cytoskeleton rearrangement, but with relative paucity of transcription factors Supplementary Figure S3, see also Seo et al.

TCF4 E2. The profile of the molecular function of both interactomes was very similar as well Supplementary Figure S3. Figure 7. Neurog1 reduces Atoh1 protein levels. Diagrams illustrate the number of identified proteins pulled down in the conditions indicated above.

The Repression of Atoh1 by Neurogenin1 during Inner Ear Development

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Granzyme B inhibition reduces disease severity in autoimmune blistering diseases

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Gli EAR come il CD e il nuovo sono costruiti da me personalmente mentre i trasformatori sono fatti dai miei collaboratori sotto le mie precise ed accurate istruzioni. La costruzione di un EAR necessita approssimativamente di un tempo 5 volte superiore a quello necessario per la costruzione di un EAR Mi auguro quindi che i clienti capiscano che valga la pena aspettare per poi poter usufruire di vera musica" Grazie e buon ascolto Tim De Paravicini. E' in occasione dell'incontro con la Luxman Corporation che, nel , viene invitato ad Osaka, in Giappone, dove gli fu offerto di lavorare come designer audio.

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Building on the success of the EAR with increase power output and better control of operating conditions irrespective of valve parameters and age. When it was launched in the early s, originally as a kit offered through Hi-Fi News magazine and subsequently as a regular EAR product, the EAR integrated amplifier caused quite a stir. Because it was designed by Tim de Paravicini, the man who almost single-handedly started the so-called valve renaissance in England. Normal triode-connected pentodes have the screen grid connected to the anode, but Tim turned things upside down and connected the control grid to the cathode, using the screen grid as the input. This turned out to give better linearity, higher power rating and much better reliability than alternatives, and the went on to become a classic amplifier, winning plaudits throughout the world. Hence the the basic output topology of the with a slightly revised output transformer, plus a modified input stage with one extra small-signal valve. This has allowed a small but significant increase in output power to 15W per channel, and even better control of operating conditions irrespective of valve parameters meaning better consistency as valves age or are replaced.

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