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Objective To investigate the efficacy of medical glue in halting fluid extravasation at needle insertion sites in patients with severe edema. Methods Sixty patients with severe edema were recruited between June 2022 and June 2023 and randomly allocated into either the control group or the experimental group, with 30 cases in each. In the experimental group, after intramuscular injection, medical glue was administered at the needle insertion site, and covered with gauze dressing upon curing, and subsequently subjected to pressure bandaging. Patients were instructed to limit their activity. Meanwhile, the control group received conventional nursing procedures involving pressure bandaging and activity restriction. The effectiveness of nursing interventions in halting exudation, duration of hospitalization, duration of exudation, nursing expenses, skin complications (infection, rash, abrasion, abnormal sensation, etc.), and patient satisfaction with nursing care were monitored. Results Comparison between the two groups revealed statistically significant differences in several aspects: the success rate of halting exudation, duration of exudation, total skin complication rate, and overall satisfaction [83.3% vs. 20.0%, (2.20 ± 2.76) days vs. (7.33 ± 3.28) days, 6.67% vs. 33.33%, 80.00% vs. 36.67%, P  < 0.05]. However, there were no statistically significant differences in hospitalization time and nursing expenses [(14.50 ± 5.17) days vs. (14.00 ± 3.95) days, (537.53 ± 264.19) yuan vs. (661.97 ± 305.55) yuan, P  > 0.05]. Conclusion Medical glue demonstrates effectiveness in halting fluid extravasation at needle insertion sites among patients experiencing severe edema. Additionally, it reduces the duration of exudation, diminishes skin complications resulting from exudation, and significantly enhances patient satisfaction with nursing care. Given these benefits, its clinical adoption and application are highly recommended.

Purpose This study aims to evaluate the role of intraoperative control of the watertightness of vesicourethral anastomosis extravasation control (VUAEC) in predicting vesicourethral anastomosis (VUA) healing and early postoperative outcomes in patients undergoing robot-assisted radical prostatectomy (RARP). Methods 100 patients who underwent RARP between October 2020 and May 2023 were consecutively included in the study. Preoperatively, the patients were randomized to undergo VUAEC ( Group-A ) or not ( Group-B ). Patients in Group-A were evaluated in 2 subgroups: those with no extravasation observed during VUAEC ( Group-A1 ; n  = 31 (62%)) and those with extravasation ( Group-A2 ; n  = 19 (38%)). On the 8th post-operative day, a gravity cystogram (GC) was performed on all patients to assess VUA healing. Results There was no statistically significant difference between the groups in terms of clinical features, drain removal time, length of hospital stay, extravasation on GC, catheter removal time and postoperative complications ( p  > 0.05, for each). There was also no statistically significant difference between the subgroups in terms of drain removal time, length of hospital stays, catheter removal time ( p  > 0.05, for each). In Group-A2 , urinary extravasation on GC was found in a greater percentage, but the difference remained statistically insignificant ( p  = 0.082). Conclusions Performing intraoperative VUAEC did not have a significant role in the prediction of VUA healing and early postoperative outcomes in patients undergoing RARP. The current study did not identify a substantial clinical benefit of routine intraoperative VUAEC.

Need for a review Guidelines for management and prevention of contrast media extravasation have not been updated recently. In view of emerging research and changing working practices, this review aims to inform update on the current guidelines. Areas covered In this paper, we review the literature pertaining to the pathophysiology, diagnosis, risk factors and treatments of contrast media extravasation. A suggested protocol and guidelines are recommended based upon the available literature. Key Points • Risk of extravasation is dependent on scanning technique and patient risk factors. • Diagnosis is mostly clinical, and outcomes are mostly favourable. • Referral to surgery should be based on clinical severity rather than extravasated volume.

While most cancer nanomedicine is designed to eliminate cancer, the nanomaterial per se can lead to the formation of micrometre-sized gaps in the blood vessel endothelial walls. Nanomaterials-induced endothelial leakiness (NanoEL) might favour intravasation of surviving cancer cells into the surrounding vasculature and subsequently extravasation, accelerating metastasis. Here, we show that nanoparticles induce endothelial leakiness through disruption of the VE-cadherin–VE-cadherin homophilic interactions at the adherens junction. We show that intravenously injected titanium dioxide, silica and gold nanoparticles significantly accelerate both intravasation and extravasation of breast cancer cells in animal models, increasing the extent of existing metastasis and promoting the appearance of new metastatic sites. Our results add to the understanding of the behaviour of nanoparticles in complex biological systems. The potential for NanoEL needs to be taken into consideration when designing future nanomedicines, especially nanomedicine to treat cancer.Nanoparticles used in nanomedicine can induce increased vascular leakiness and therefore accelerate intravasation and extravasation of cancer cells, exacerbating existing metastasis and promoting the appearance of new metastatic sites.

The ketogenic diet is a high-fat, low-carbohydrate regimen that forces ketone-based rather than glucose-based cellular metabolism. Clinically, maintenance on a ketogenic diet has been proven effective in treating pediatric epilepsy and type II diabetes, and recent basic research provides evidence that ketogenic strategies offer promise in reducing brain injury. Cellular mechanisms hypothesized to be mobilized by ketone metabolism and underlying the success of ketogenic diet therapy, such as reduced reactive oxygen species and increased central adenosine, suggest that the ketolytic metabolism induced by the diet could reduce pain and inflammation. To test the effects of a ketone-based metabolism on pain and inflammation directly, we fed juvenile and adult rats a control diet (standard rodent chow) or ketogenic diet (79% fat) ad libitum for 3-4 weeks. We then quantified hindpaw thermal nociception as a pain measure and complete Freund's adjuvant-induced local hindpaw swelling and plasma extravasation (fluid movement from the vasculature) as inflammation measures. Independent of age, maintenance on a ketogenic diet reduced the peripheral inflammatory response significantly as measured by paw swelling and plasma extravasation. The ketogenic diet also induced significant thermal hypoalgesia independent of age, shown by increased hindpaw withdrawal latency in the hotplate nociception test. Anti-inflammatory and hypoalgesic diet effects were generally more robust in juveniles. The ketogenic diet elevated plasma ketones similarly in both age groups, but caused slowed body growth only in juveniles. These data suggest that applying a ketogenic diet or exploiting cellular mechanisms associated with ketone-based metabolism offers new therapeutic opportunities for controlling pain and peripheral inflammation, and that such a metabolic strategy may offer significant benefits for children and adults.

Significance The cancer biology seed-and-soil paradigm recognizes the existence of organ-specific patterns of metastasization that drive the spread of selected primary tumors toward specific secondary loci. However, despite efforts to model the organotypic microenvironment, the organ specificity of cancer metastases needs to be elucidated. The relevance of this study lies in the generation of a human vascularized organ-specific microenvironment, which can be used to investigate and tune the extravasation process of metastatic tumor cells. Furthermore, beyond mimicking the pro- or antimetastatic signatures of different microenvironments, our microfluidic model provides insights into different properties of organ-specific endothelia. This study paves the way toward advanced in vitro models to screen for highly tailored organ-specific therapeutics and investigate key molecular pathways involved in organ-specific metastases. A key aspect of cancer metastases is the tendency for specific cancer cells to home to defined subsets of secondary organs. Despite these known tendencies, the underlying mechanisms remain poorly understood. Here we develop a microfluidic 3D in vitro model to analyze organ-specific human breast cancer cell extravasation into bone- and muscle-mimicking microenvironments through a microvascular network concentrically wrapped with mural cells. Extravasation rates and microvasculature permeabilities were significantly different in the bone-mimicking microenvironment compared with unconditioned or myoblast containing matrices. Blocking breast cancer cell A ₃ adenosine receptors resulted in higher extravasation rates of cancer cells into the myoblast-containing matrices compared with untreated cells, suggesting a role for adenosine in reducing extravasation. These results demonstrate the efficacy of our model as a drug screening platform and a promising tool to investigate specific molecular pathways involved in cancer biology, with potential applications to personalized medicine.

Solitary chemosensory cells (SCCs) of the nasal cavity are specialized epithelial chemosensors that respond to irritants through the canonical taste transduction cascade involving Gα-gustducin and transient receptor potential melastatin 5. When stimulated, SCCs trigger peptidergic nociceptive (or pain) nerve fibers, causing an alteration of the respiratory rate indicative of trigeminal activation. Direct chemical excitation of trigeminal pain fibers by capsaicin evokes neurogenic inflammation in the surrounding epithelium. In the current study, we test whether activation of nasal SCCs can trigger similar local inflammatory responses, specifically mast cell degranulation and plasma leakage. The prototypical bitter compound, denatonium, a well-established activator of SCCs, caused significant inflammatory responses in WT mice but not mice with a genetic deletion of elements of the canonical taste transduction cascade, showing that activation of taste signaling components is sufficient to trigger local inflammation. Chemical ablation of peptidergic trigeminal fibers prevented the SCC-induced nasal inflammation, indicating that SCCs evoke inflammation only by neural activity and not by release of local inflammatory mediators. Additionally, blocking nicotinic, but not muscarinic, acetylcholine receptors prevents SCC-mediated neurogenic inflammation for both denatonium and the bacterial signaling molecule 3-oxo-C12-homoserine lactone, showing the necessity for cholinergic transmission. Finally, we show that the neurokinin 1 receptor for substance P is required for SCC-mediated inflammation, suggesting that release of substance P from nerve fibers triggers the inflammatory events. Taken together, these results show that SCCs use cholinergic neurotransmission to trigger peptidergic trigeminal nociceptors, which link SCCs to the neurogenic inflammatory pathway.

Background To evaluate the clinical significance of contrast extravasation observed on post-ablation computed tomography (CT) performed immediately following thermal ablation of hepatic tumors. Methods Between October 2014 and December 2023, 1,274 patients with 1,745 primary or metastatic hepatic tumors underwent ablation, including radiofrequency ablation, microwave ablation, and cryoablation. Among them, 30 patients (median age: 66 years) with contrast extravasation observed on post-ablation CT scans were retrospectively analyzed. The pre- and post-ablation hemoglobin and hematocrit levels were measured. Local tumor progression-free survival (LTPFS) and overall survival (OS) rates were evaluated. Results Among the 30 patients, angiography was performed in 6 patients. Contrast extravasation was observed on angiography in only two patients; contrast extravasation from the right inferior phrenic artery and intercostal artery was noted, and successful transarterial embolization was achieved. Conservative management was considered adequate without additional treatment in 28 of 30 patients. No significant differences were observed between the 1 day before and after ablation hemoglobin (12.9 g/dL; 12.0–13.8 g/dL vs. 12.5 g/dL; 11.5–13.8 g/dL, P  = 0.102) and hematocrit (38.3%; 36.0–40.1% vs. 37.0%; 34.8–39.2%, P  = 0.100) levels. During a mean follow up period of 23.3 ± 17.8 months, the LTPFS rates were 96.4% and 84.3% at 1 and 2 years, respectively. The OS rate after the procedure was 96.7%. Conclusion The presence of contrast extravasation on post-ablation CT was not clinically significant, when extravasation confined to intrahepatic or venous origins. However, transarterial embolization is required if contrast extravasation is detected in the extrahepatic arteries.

The etiology of migraine pain involves sensitized meningeal afferents that densely innervate the dural vasculature. These afferents, with their cell bodies located in the trigeminal ganglion, project to the nucleus caudalis, which in turn transmits signals to higher brain centers. Factors such as chronic stress, diet, hormonal fluctuations, or events like cortical spreading depression can generate a state of “sterile inflammation” in the intracranial meninges resulting in the sensitization and activation of trigeminal meningeal nociceptors. This sterile inflammatory phenotype also referred to as neurogenic inflammation is characterized by the release of neuropeptides (such as substance P, calcitonin gene related peptide) from the trigeminal innervation. This release leads to vasodilation, plasma extravasation secondary to capillary leakage, edema, and mast cell degranulation. Although neurogenic inflammation has been observed and extensively studied in peripheral tissues, its role has been primarily investigated in the genesis and maintenance of migraine pain. While some aspects of neurogenic inflammation has been disregarded in the occurrence of migraine pain, targeted analysis of factors have opened up the possibilities of a dialogue between the neurons and immune cells in driving such a sterile neuroinflammatory state in migraine pathophysiology.