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The main objective was to analyse the use of rigid laryngotracheoscopy under general anaesthesia (GA) and endoscopic surgery in the management of inspiratory stridor in patients referred to a paediatric ENT outpatient clinic. The secondary objective was to analyse the aetiological diagnoses made and their therapeutic management. This is a prospective study including all newborns and infants, corresponding to 190 patients, presenting for the first time in consultation for inspiratory stridor from January 2015 to December 2017. A consultation form was filled out after each consultation and added to a database; a management algorithm was used to determine which patients required a rigid laryngotracheoscopy. A 17.9% (n = 34) of the patients required rigid laryngotracheoscopy, of whom 12.6% (n = 24) underwent concomitant endoscopic surgery. A 65.8% (n = 125) of the patients were diagnosed with laryngomalacia, 21.1% (n = 40) with isolated posterior excess of mucosa, 9.5% (n = 18) with another diagnosis and 3.7% (n = 7) with a normal examination. The presence of comorbidity was associated (p less then 0.001) with the use of rigid laryngotracheoscopy and endoscopic surgery.Conclusion Rigid laryngotracheoscopy under GA was required in one in five to six patients. Conservative management with strict follow-up may be appropriate in a large number of patients, especially those with laryngomalacia. What is Known • Previous research has established that laryngomalacia is the main aetiology of stridor. Selleckchem TP-1454 • Comorbidities are linked with a poor tolerance of stridor. What is new • About one in five to six patients seen in consultation for stridor will require a trip to the operative room (and one in eight will require endoscopic surgery). • Laryngomalacia and isolated posterior excess of mucosa account for 85-90% of the patients seen in consultation for stridor.To boost the healing process in a full-thickness wound, a simple and efficient strategy based on adipose-derived mesenchymal stem cells (ADSCs) transplantation is described in this work. To increase the chance of ADSCs immobilization in the wound bed and prevent its migration, these cells are fully grown on the surface of a thermoresponsive dressing membrane under in vitro condition. Then, the cells sheet with their secreted extracellular matrix (ECM) is transferred to the damaged skin with the help of this dressing membrane. This membrane remains on wound bed and acts both as a cell sheet transfer vehicle, after external reduction of temperature, and protect wound during the healing process like a common wound dressing. The visual inspection of wounded skin (rat animal model) at selected time intervals shows a higher wound closure rate for ADSCs treated group. For this group of rats, the better quality of reconstructed tissue is approved by results of histological and immunohistochemical analysis since the higher length of the new epidermis, the higher thickness of re-epithelialization layer, a higher level of neovascularization and capillary density, and the least collagen deposition are detected in the healed tissue.The bed nucleus of the stria terminalis (BNST) is a forebrain structure, involved in the modulation of neuroendocrine, cardiovascular and autonomic responses. One of the responses is baroreflex activity, which consists in a neural mechanism responsible for keeping the blood pressure within a narrow range of variation. It has been reported that blockade of BNST α1-adrenoceptors increased the bradycardic component of baroreflex. In addition, such receptors are able to modulate glutamate release in this structure. Interestingly, BNST NMDA receptor antagonism and neuronal nitric oxide synthase (nNOS) inhibition led to the same effect of the α1-adrenoceptors blockade on baroreflex bradycardic response. Therefore, the hypothesis of the present study is that BNST noradrenergic transmission interacts with NMDA/NO pathway through α1 adrenoceptors to modulate the baroreflex activity. Male Wistar rats had stainless steel guide cannulas bilaterally implanted in the BNST. Subsequently, a catheter was inserted into the femoral artery for cardiovascular recordings, and into the femoral vein for assessing baroreflex activation. Injection of the noradrenaline reuptake inhibitor reboxetine in the BNST did not modify the tachycardic, but significantly decreased the bradycardic component of baroreflex. Administration of an α1, but not an α2 antagonist into the BNST prior to reboxetine prevented this effect. Likewise, previous injection of NMDA/NO pathway blockers inhibited the effect of reboxetine on bradycardic response. In conclusion, it was demonstrated for the first time the existence of an interaction between BNST noradrenergic, glutamatergic and nitrergic neurotransmissions in the modulation of bradycardic baroreflex response.
Adrenomedullin (AM) is a bioactive peptide having many pleiotropic effects, including mucosal healing and immunomodulation. AM has shown beneficial effects in rodent models and in preliminary study for patients with ulcerative colitis (UC). We performed a clinical trial to investigate the efficacy and safety of AM in patients with UC.
This was a multi-center, double-blind, placebo-controlled phase-2a trial evaluating 28 patients in Japan with steroid-resistant UC. Patients were randomly assigned to four groups and given an infusion of 5, 10, 15ng/kg/min of AM or placebo for 8h per day for 14days. The primary endpoint was the change in Mayo scores at 2weeks. Main secondary endpoints included the change in Mayo scores and the rate of clinical remission at 8weeks, defined as a Mayo score 0.
No differences in the primary or secondary endpoints were observed among the four groups at 2weeks. Despite the insufficient tracking rate, the Mayo score at 8 weeks was only significantly decreased in the high-dose AM group (15ng/kg/min) compared with the placebo group (-9.3 ± 1.2 vs. -3.0 ± 2.8, P = 0.035), with its rate of clinical remission at 8 weeks being significantly higher (3/3, 100% vs. 0/2, 0%, P = 0.025). We noted mild but no serious adverse events caused by the vasodilatory effect of AM.
In this double-blind randomized trial, we observed the complete remission at 8 weeks in patients with steroid-resistant UC receiving a high dose of AM.
JAPIC clinical trials information; Japic CTI-205255 (200410115290). https//www.clinicaltrials.jp/cti-user/trial/Search.jsp .
JAPIC clinical trials information; Japic CTI-205255 (200410115290). https//www.clinicaltrials.jp/cti-user/trial/Search.jsp .
Homepage: https://www.selleckchem.com/products/tp-1454.html
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