Rejected

Lumbar radiofrequency ablation is indicated for the treatment of chronic axial low back pain that is mediated by facet arthropathy which has failed more conservative treatment options. This article details proper equipment and medications, patient positioning and setup, step-by-step instructions for multiplanar fluoroscopic visualization, cannula placement, and postoperative management. Pearls and pitfalls are also discussed. In addition, an instructional procedure video (Supplemental Digital Content 1, http://links.lww.com/CLINSPINE/A90) accompanies this paper.

Crohn's disease (CD) and ulcerative colitis (UC) are chronic, inflammatory bowel diseases (IBD). Each class and type of medication available for the treatment of IBD has distinct characteristics and long-term effects that a patient may consider. We present the results of qualitative research that aimed to develop a descriptive framework that outlines the most relevant disease and/or treatment attributes for IBD treatment decisions and focuses on the patient perspective.

Contemporary interventional treatment of primary chronic venous disease (CVD) is mainly focused on the treatment of venous reflux. The long-term results of endovenous ablation (EVA) and high ligation and stripping are not different with respect to varicose vein recurrence, and this recurrence appears to be a manifestation of disease progression. Since inflammation is one of the key mechanisms of CVD development and progression, efforts to minimize inflammation and angiogenic potential in endovenous and surgical procedures are worthwhile. As techniques continue to be refined, surgery remains a valid option; in particular, the techniques that minimize trauma can be beneficial regarding recurrence. Medical treatment with venoactive drug therapy such as micronized purified flavonoid fraction (MPFF; Daflon), which has proven clinical benefits in patients with CVD, can be used before and after EVA or surgery to minimize inflammation, pain, hemorrhage, and reduce CVD symptoms.

Effective analgesia after joint replacement allows for earlier mobilization, decreased length of stay, and reduced opioid use. The injection of the surgical area with ketorolac (Toradol) prior to closure has changed pain management in joint replacement surgery.

P53 mutations are responsible for drug-resistance of tumour cells which impacts on the efficacy of treatment. Alternative tumour suppressor pathways need to be explored to treat p53- deficient tumours. The E3 ubiquitin ligase, ITCH, negatively regulates the tumour suppressor protein TP73, providing a therapeutic target to enhance the sensitivity of the tumour cells to the treatment. In the present study, two p53-mutant neuroblastoma cell lines were used as in vitro models. Using immunostaining, western blot and qPCR methods, we firstly identified that ITCH was expressed on p53-mutant neuroblastoma cell lines. Transfection of these cell lines with ITCH siRNA could effectively silence the ITCH expression, and result in the stabilization of TP73 protein, which mediated the apoptosis of the neuroblastoma cells upon irradiation treatment. Finally, in vivo delivery of the ITCH siRNA using nanoparticles to the neuroblastoma xenograft mouse model showed around 15-20% ITCH silencing 48 hours after transfection. Our data suggest that ITCH could be silenced both in vitro and in vivo using nanoparticles, and silencing of ITCH sensitizes the tumour cells to irradiation treatment. This strategy could be further explored to combine the chemotherapy/radiotherapy treatment to enhance the therapeutic effects on p53-deficient neuroblastoma.

The objective of the study was to analyse patient-reported outcome measures (PROMs), seroma formation, long-term recurrence and chronic pain after closure of the fascial defect in patients undergoing laparoscopic umbilical hernia mesh repair.

Pectoral block (PECS)-based anesthesia without opioids decreases analgesic requirement, pain scores and post-operative nausea vomiting (PONV) compared to conventional opioid-based general anesthesia in patients undergoing modified radical mastectomy and axillary dissection (MRM-AD). We compared PECS versus Paravertebral Block (PVB) in providing an opioid free, nerve block-based regimen. Outcomes of interest were post-operative analgesic requirement, duration of analgesia, PONV and patient and surgeon satisfaction.

Emerging studies indicate that the immune system can regulate systemic metabolism. Here, we show that thymic stromal lymphopoietin (TSLP) stimulates T cells to induce selective white adipose loss, which protects against obesity, improves glucose metabolism, and mitigates nonalcoholic steatohepatitis. Unexpectedly, adipose loss was not caused by alterations in food intake, absorption, or energy expenditure. Rather, it was induced by the excessive loss of lipids through the skin as sebum. TSLP and T cells regulated sebum release and sebum-associated antimicrobial peptide expression in the steady state. In human skin, expression correlated directly with sebum-associated gene expression. Thus, we establish a paradigm in which adipose loss can be achieved by means of sebum hypersecretion and uncover a role for adaptive immunity in skin barrier function through sebum secretion.

To evaluate whether a simple health and wellness coaching (HWC) program embedded within routine clinical practice resulted in improved opioid weaning and discontinuation.

Pancreatic cancer (PC) is a fatal malignancy in the human abdominal cavity that prefers to invade the surrounding nerve/nerve plexus and even the spine, causing devastating and unbearable pain. The limitation of available in vitro models restricts revealing the molecular mechanism of pain and screening pain-relieving strategies to improve the quality of life of end-stage PC patients. Here, we report a PC nerve invasion model that merged human brain organoids (hBrO) with mouse PC organoids (mPCO). After merging hBrOs with mPCOs, we monitored the structural crosstalk, growth patterns, and mutual interaction dynamics of hBrO with mPCOs for 7 days. After 7 days, we also analyzed the pathophysiological statuses, including proliferation, apoptosis and inflammation. The results showed that mPCOs tend to approximate and intrude into the hBrOs, merge entirely into the hBrOs, and induce the retraction/shrinking of neuronal projections that protrude from the margin of the hBrOs. The approximating of mPCOs to hBrOs accelerated the proliferation of neuronal progenitor cells, intensified the apoptosis of neurons in the hBrOs, and increased the expression of inflammatory molecules in hBrOs, including NLRP3, IL-8, and IL-1β. Our system pathophysiologically replicated the nerve invasions in mouse GEMM (genetically engineered mouse model) primary and human PCs and might have the potential to be applied to reveal the molecular mechanism of nerve invasion and screen therapeutic strategies in PCs.