Impressive Nasal Septum Regeneration after Cord Blood Platelet Gel (CBPG) in Extreme Premature Neonate with Non-Invasive Ventilation: A Case Report.

BACKGROUND: We evaluated the efficacy of Cord Blood Platelet Gel (CBPG) in the regenerative reconstruction of the nasal septal tissue of a preterm infant undergoing non-invasive ventilation. METHODS: A CBPC treatment was used to enhance the regeneration of the nasal septum of a premature patient in an experimental way, evaluating the efficacy described in the literature (selective bibliographic search in PubMed) of the use of blood products for non-transfusion purposes. RESULTS: A partial but satisfactory regeneration of the patient's nasal septum was observed. Using the free NIH Image J online software, we were able to calculate the regenerated surface (about 83% of the destroyed cartilage). CONCLUSIONS: The use of platelet gel has been a promising alternative to surgical treatment in patients with severe damage to the nasal septum.

Prolotherapy: Regenerative Medicine for Lateral Epicondylitis.

Lateral epicondylitis (LE) is a degenerative disease of the tendons, spurred by repetitive microtrauma leading to an attempt by the body to heal by upregulating local angiogenesis and fibroblast proliferation. Prolotherapy (PT) is the injection of dextrose around the injured tissues to stimulate their spontaneous regeneration. Herein, we have described a case of lateral epicondylitis, diagnosed with clinical and ultrasound (US) examination, where local steroid injections provided relief only for a limited time. We treated the patient with US-guided PT, following which the pain disappeared and the tendon was restored.

Ultrasound-guided erector spinae block for post-thoracotomy pain syndrome in video-assisted thoracic surgery.

This article describes our experience with 5 patients with post-thoracotomy pain syndrome after video-assisted thoracoscopic lobectomies, treated with weekly erector spinae plane block. We injected corticosteroid and local anesthetic. At the end of the treatment period, pain scores decreased significantly. Our experience suggests that erector spinae plane block may have a role in the treatment of post-thoracoscopy pain syndrome.

Can diaphragmatic ultrasonography performed during the T-tube trial predict weaning failure? The role of diaphragmatic rapid shallow breathing index.

BACKGROUND: The rapid shallow breathing index (RSBI), which is the ratio between respiratory rate (RR) and tidal volume (VT), is one of the most widely used indices to predict weaning outcome. Whereas the diaphragm plays a fundamental role in generating VT, in the case of diaphragmatic dysfunction the inspiratory accessory muscles may contribute. If this occurs during a weaning trial, delayed weaning failure is likely since the accessory muscles are more fatigable than the diaphragm. Hence, we hypothesised that the traditional RSBI could be implemented by substituting VT with the ultrasonographic evaluation of diaphragmatic displacement (DD). We named the new index the diaphragmatic-RSBI (D-RSBI). The aim of this study was to compare the ability of the traditional RSBI and D-RSBI to predict weaning failure in ready-to-wean patients. METHODS: We performed a prospective observational study. During a T-tube spontaneous breathing trial (SBT) we simultaneously evaluated right hemidiaphragm displacement (i.e., DD) by using M-mode ultrasonography as well as the RSBI. Outcome of the weaning attempt, length of mechanical ventilation, length of intensive care unit and hospital stay, and hospital mortality were recorded. Receiver operator characteristic (ROC) curves were used to evaluate the diagnostic accuracy of D-RSBI and RSBI. RESULTS: We enrolled 51 patients requiring mechanical ventilation for more than 48 h who were ready to perform a SBT. Most of the patients, 34 (66 %), were successfully weaned from mechanical ventilation. When considering the 17 patients that failed the weaning attempt, 11 (64 %) had to be reconnected to the ventilator during the SBT, three (18 %) had to be re-intubated within 48 h of extubation, and three (18 %) required non-invasive ventilation support within 48 h of extubation. The areas under the ROC curves for D-RSBI and RSBI were 0.89 and 0.72, respectively (P = 0.006). CONCLUSIONS: D-RSBI (RR/DD) was more accurate than traditional RSBI (RR/VT) in predicting the weaning outcome. TRIAL REGISTRATION: Our clinical trial was retrospectively registered with ClinicalTrials.gov (identifier: NCT02696018 ). ClinicalTrials.gov processed our record on 25 February 2016.

Activation of phospholipase A(2) and MAP kinases by oxidized low-density lipoproteins in immortalized GP8.39 endothelial cells.

In immortalized rat brain endothelial cells (GP8.39), we have previously shown that oxidized LDL (oxLDL), after 24-h treatment, stimulates arachidonic acid release and phosphatidylcholine hydrolysis by activation of cytosolic phospholipase A(2) (cPLA(2)). A putative role for MAPKs in this process has emerged. Here, we studied the contribution of Ca(2+)-independent phospholipase A(2) (iPLA(2)), and the role of the MAP kinase family as well as both cPLA(2) and iPLA(2) mRNA expression by RT-PCR in oxLDL toxicity to GP8.39 cells in vitro. The activation of extracellular signal-regulated kinases ERK1/2, p38 and c-Jun NH(2)-terminal kinase (JNK) was assessed with Western blotting and kinase activity assays. iPLA(2) activity, which was found as a membrane-associated enzyme, was more stimulated by oxLDL compared with native LDL. The phosphorylation of ERK1/2, p38 and JNKs was also significantly enhanced in a dose-dependent manner. PD98059, an ERK inhibitor, SB203580, a p38 inhibitor, and SP600125, an JNK inhibitor, abolished the stimulation of all three members of the MAPK family by oxLDL. Confocal microscopy analysis and subcellular fractionation confirmed either an increase in phosphorylated form of ERKs, p38 and JNKs, or their nuclear translocation upon activation. A strong inhibition of MAPK activation was also observed when endothelial cells were treated with GF109203X, a PKC inhibitor, indicating the important role of both PKC and all three MAPKs in mediating the maximal oxLDL response. Finally, compared with samples untreated or treated with native LDL, treatment with oxLDL (100 muM hydroperoxides) for 24 h significantly increased the levels of constitutively expressed iPLA(2) protein (by 5.1-fold) and mRNA (by 3.1-fold), as well as cPLA(2) protein (by 4.4-fold) and mRNA (by 1.5-fold). Together, these data link the stimulation of PKC-ERK-p38-JNK pathways and PLA(2) activity by oxLDL to the prooxidant mechanism of the lipoprotein complex, which may initially stimulate the endothelial cell reaction against noxious stimuli as well as metabolic repair, such as during inflammation and atherosclerosis.