In this narrative review article, the authors discuss the anatomy, nomenclature, history, approaches (posterior vs. lateral vs. subcostal), techniques, pharmacology, indications, and complications of transversus abdominis plane blocks, as well as possible alternative truncal blocks.Despite the scarcity of evidence and contradictory findings, certain clinical suggestions can nonetheless be made. Overall transversus abdominis plane blocks appear most beneficial in the setting of open appendectomy (posterior or lateral approach). Lateral transversus abdominis plane blocks are not suggested for laparoscopic hysterectomy, laparoscopic appendectomy, or open prostatectomy. However, transversus abdominis plane blocks could serve as an analgesic option for Cesarean delivery (posterior or lateral approach) and open colorectal section (subcostal or lateral approach) if there exist contraindications to intrathecal morphine and thoracic epidural analgesia, respectively.Future investigation is required to compare posterior and subcostal transversus abdominis plane blocks in clinical settings. Furthermore, posterior transversus abdominis plane blocks should be investigated for surgical interventions in which their lateral counterparts have proven not to be beneficial (e.g., laparoscopic hysterectomy/appendectomy, open prostatectomy). More importantly, because posterior transversus abdominis plane blocks can purportedly provide sympathetic blockade and visceral analgesia, they should be compared with thoracic epidural analgesia for open colorectal surgery. Finally, transversus abdominis plane blocks should be compared with newer truncal blocks (e.g., erector spinae plane and quadratus lumborum blocks) with well-designed and adequately powered trials.

/pdf/transversus-abdominis-plane-block-a-narrative-review-5fme75ckj4.pdf

Transversus Abdominis Plane Block: A Narrative Review

Cancer is a leading cause of death worldwide. In many cases, the treatment of the disease is limited due to the metastasis of cells to distant locations of the body through the blood and lymphatic drainage. Most of the anticancer therapeutic options focus mainly on the inhibition of tumor cell growth or the induction of cell death, and do not consider the molecular basis of metastasis. The aim of this work is to provide a comprehensive review focusing on cancer metastasis and the mitogen-activated protein kinase (MAPK) pathway (ERK/JNK/P38 signaling) as a crucial modulator of this process.

https://www.mdpi.com/1422-0067/23/7/3847/pdf?version=1648707778

Metastasis and MAPK Pathways

Cleft lip and palate.

Understanding and targeting anoikis in metastasis for cancer therapies

Abstract Breast cancer exhibits the highest global incidence among all tumor types. Regardless of the type of breast cancer, metastasis is a crucial cause of poor prognosis. Anoikis, a form of apoptosis initiated by cell detachment from the native environment, is an outside-in process commencing with the disruption of cytosolic connectors such as integrin-ECM and cadherin-cell. This disruption subsequently leads to intracellular cytoskeletal and signaling pathway alterations, ultimately activating caspases and initiating programmed cell death. Development of an anoikis-resistant phenotype is a critical initial step in tumor metastasis. Breast cancer employs a series of stromal alterations to suppress anoikis in cancer cells. Comprehensive investigation of anoikis resistance mechanisms can inform strategies for preventing and regressing metastatic breast cancer. The present review first outlines the physiological mechanisms of anoikis, elucidating the alterations in signaling pathways, cytoskeleton, and protein targets that transpire from the outside in upon adhesion loss in normal breast cells. The specific anoikis resistance mechanisms induced by pathological changes in various spatial structures during breast cancer development are also discussed. Additionally, the genetic loci of targets altered in the development of anoikis resistance in breast cancer, are summarized. Finally, the micro-RNAs and targeted drugs reported in the literature concerning anoikis are compiled, with keratocin being the most functionally comprehensive. 

Anoikis resistance––protagonists of breast cancer cells survive and metastasize after ECM detachment

Purpose of Review. Transversus abdominis plane (TAP) block is a regional technique for analgesia of the anterolateral abdominal wall. This review highlights the nomenclature system and recent advances in TAP block techniques and proposes directions for future research. Recent Findings. Ultrasound guidance is now considered the gold standard in TAP blocks. It is easy to acquire ultrasound images; it can be used in many surgeries involving the anterolateral abdominal wall. However, the efficacy of ultrasound-guided TAP blocks is not consistent, which might be due to the use of different approaches. The choice of technique influences the involved area and block duration. To investigate the actual analgesic effects of TAP blocks, we unified the nomenclature system and clarified the definition of each technique. Although a single-shot TAP block is limited in duration, it is still the candidate of the analgesic standard for abdominal wall surgery because the use of the catheter technique and liposomal bupivacaine may overcome this limitation. Summary. Ultrasound-guided TAP blocks are commonly used. With the unified nomenclature and the development of catheter technique and/or liposomal local anesthetics, TAP blocks can be applied more appropriately to achieve better pain control.

/pdf/transversus-abdominis-plane-block-an-updated-review-of-53xppwaa30.pdf

Transversus Abdominis Plane Block: An Updated Review of Anatomy and Techniques.

Anoikis resistance has been observed in various types of cancers in which anchorage-independent growth is a crucial step for cancer metastasis. Therefore, agents interfering with this specific cancer cell behavior may be integrated into novel antimetastatic strategies. Monascin (MS), a secondary metabolite found in Monascus species, is a known potent chemopreventive compound used for treating metabolic complications; however, the effect of MS on anoikis resistance has not been investigated. In this study, 4T1 breast cells were treated with MS under either suspension or adhesion conditions. The higher cytotoxicity of MS was more potent against suspended cells than against adherent cells. This selective cytotoxicity was due to the induction of anoikis, which was evidenced by changes in cell aggregation, caspase activity, and Annexin V/propidium iodide binding as well as the results of systemic metastasis in an animal model. Furthermore, MS inhibited E-cadherin and β-catenin expression in the cells; the treated cells formed spherical aggregates, which suggested that anchorage-independent growth was prevented by MS. These results provide new insights into the mechanisms underlying the growth-preventing effect of MS on cancer cells and indicate the potential ability of MS to suppress metastasis.

/pdf/monascin-accelerates-anoikis-in-circulating-tumor-cells-and-4it69st0oo.pdf

Monascin accelerates anoikis in circulating tumor cells and prevents breast cancer metastasis.

Background: This study aimed to explore the effects of netrin-1 on hypobaric hypoxia-induced lung injury in mice. Methods: We exposed 6–8-week-old C57BL/6 mice to hypobaric stress at 340 m...

Netrin-1 Dampens Hypobaric Hypoxia-Induced Lung Injury in Mice.

Posterior reversible encephalopathy syndrome as a rare cause of reversible postoperative Quadriplegia

The effects of clinically relevant concentrations of lidocaine on epithelial-mesenchymal transition (EMT) and associated lung cancer behaviors have rarely been investigated. The aim of the present study was to assess the impact of lidocaine on EMT and its related phenomena, including chemoresistance. Lung cancer cell lines (A549 and LLC.LG) were incubated with various concentrations of lidocaine, 5-fluorouracil (5-FU) or both to test their effects on cell viability. Subsequently, the effects of lidocaine on various cell behaviors were assessed in vitro and in vivo using Transwell migration, colony-formation and anoikis-resistant cell aggregation assays, and human tumor cell metastasis in a chorioallantoic membrane (CAM) model quantitated by PCR analysis. Prototypical EMT markers and their molecular switch were analyzed using western blotting. In addition, a conditioned metastasis pathway was generated through Ingenuity Pathway Analysis. Based on these measured proteins (slug, vimentin and E-cadherin), the molecules involved and the alteration of genes associated with metastasis were predicted. Of note, clinically relevant concentrations of lidocaine did not affect lung cancer cell viability or alter the effects of 5-FU on cell survival; however, at this dose range, lidocaine attenuated the 5-FU-induced inhibitory effect on cell migration and promoted EMT. The expression levels of vimentin and Slug were upregulated, whereas the expression of E-cadherin was downregulated. EMT-associated anoikis resistance was also induced by lidocaine administration. In addition, portions of the lower CAM with a dense distribution of blood vessels exhibited markedly increased Alu expression 24 h following the inoculation of lidocaine-treated A549 cells on the upper CAM. Thus, at clinically relevant concentrations, lidocaine has the potential to aggravate cancer behaviors in non-small cell lung cancer cells. The phenomena accompanying lidocaine-aggravated migration and metastasis included altered prototypical EMT markers, anoikis-resistant cell aggregation and attenuation of the 5-FU-induced inhibitory effect on cell migration.

Lidocaine induces epithelial‑mesenchymal transition and aggravates cancer behaviors in non‑small cell lung cancer A549 cells

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