one shot six centres a new strategy in ultrasound guided paravertebralblock

The paravertebral block (PVB) is the technique of injecting local anaesthetic alongside the vertebral body close to where the spinal nerves emerge from the intervertebral foramen. This produces unilateral, segmental, somatic, and sympathetic nerve blockade in multiple contiguous thoracic dermatomes which is effective for managing acute and chronic pain. Recently PVB has also been used for surgical anaesthesia in patients undergoing several surgical procedures with improved postoperative outcomes. Unfortunately the spread of local anaesthetic and the anaesthetic effect is sometime unpredictable, even with a standardized ultrasound-guided technique. The aim of this study is to show a new approach for the Paravertebral block ultrasound-guided and confirmed by ENS using a single injection. This new approach allows an easy visualization and accurate puncture of the paravertebral space, ensuring good anaesthesia of reproducibility, productivity and effectiveness. In this study we obtained six dermatomes anaesthesia, with a single shot injection in all patients

Holographic Renormalization and Ward Identities with the Hamilton-Jacobi Method

A systematic procedure for performing holographic renormalization, which makes use of the Hamilton-Jacobi method, is proposed and applied to a bulk theory of gravity interacting with a scalar field and a U(1) gauge field in the Stueckelberg formalism. We describe how the power divergences are obtained as solutions of a set of "descent equations" stemming from the radial Hamiltonian constraint of the theory. In addition, we isolate the logarithmic divergences, which are closely related to anomalies. The method allows to determine also the exact one-point functions of the dual field theory. Using the other Hamiltonian constraints of the bulk theory, we derive the Ward identities for diffeomorphisms and gauge invariance. In particular, we demonstrate the breaking of U(1)_R current conservation, recovering the holographic chiral anomaly recently discussed in hep-th/0112119 and hep-th/0202056.Comment: 31 pages; v2: references added. Version published in Nuclear Physics

Molecular mechanisms and physiological changes behind benign tracheal and subglottic stenosis in adults.

Laryngotracheal stenosis (LTS) is a complex and heterogeneous disease whose pathogenesis remains unclear. LTS is considered to be the result of aberrant wound-healing process that leads to fibrotic scarring, originating from different etiology. Although iatrogenic etiology is the main cause of subglottic or tracheal stenosis, also autoimmune and infectious diseases may be involved in causing LTS. Furthermore, fibrotic obstruction in the anatomic region under the glottis can also be diagnosed without apparent etiology after a comprehensive workup; in this case, the pathological process is called idiopathic subglottic stenosis (iSGS). So far, the laryngotracheal scar resulting from airway injury due to different diseases was considered as inert tissue requiring surgical removal to restore airway patency. However, this assumption has recently been revised by regarding the tracheal scarring process as a fibroinflammatory event due to immunological alteration, similar to other fibrotic diseases. Recent acquisitions suggest that different factors, such as growth factors, cytokines, altered fibroblast function and genetic susceptibility, can all interact in a complex way leading to aberrant and fibrotic wound healing after an insult that acts as a trigger. However, also physiological derangement due to LTS could play a role in promoting dysregulated response to laryngo-tracheal mucosal injury, through biomechanical stress and mechanotransduction activation. The aim of this narrative review is to present the state-of-the-art knowledge regarding molecular mechanisms, as well as mechanical and physio-pathological features behind LTS

Hypoalbuminemia as a predictor of acute kidney injury during colistin treatment

This study aimed to assess the predictors of acute kidney injury (AKI) during colistin therapy in a cohort of patients with bloodstream infections (BSI) due to colistin-susceptible Gram-negative bacteria, focusing on the role of serum albumin levels. The study consisted of two parts: (1) a multicentre retrospective clinical study to assess the predictors of AKI during colistin therapy, defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria; and (2) bioinformatic and biochemical characterization of the possible interaction between human serum albumin and colistin. Among the 170 patients included in the study, 71 (42%), 35 (21%), and 11 (6%) developed KDIGO stage 1 (K1-AKI), KDIGO stage 2 (K2-AKI), and KDIGO stage 3 (K3-AKI), respectively. In multivariable analyses, serum albumin <2.5 g/dL was independently associated with K1-AKI (subdistribution hazard ratio [sHR] 1.85, 95% confidence interval [CI] 1.17\u20132.93, p = 0.009) and K2-AKI (sHR 2.37, 95% CI 1.15\u20134.87, p = 0.019). Bioinformatic and biochemical analyses provided additional information nurturing the discussion on how hypoalbuminemia favors development of AKI during colistin therapy. In conclusion, severe hypoalbuminemia independently predicted AKI during colistin therapy in a large cohort of patients with BSI due to colistin-susceptible Gram-negative bacteria. Further study is needed to clarify the underlying causal pathways