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Pain and spasms of urinary and biliary tracts are conditions causing poor quality of life. Treatment with analgesic drugs such as non-steroidal anti-inflammatory drugs and modulators of the parasympathetic system are not always tolerated, and often additional therapeutic options are necessary. The present analysis aimed to evaluate the pharmacokinetics and effectiveness of oral and parenteral preparations based on phloroglucinol in reducing pain and spasms associated with renal or biliary colic in phase 3, multicentre, open-label, randomized, comparative studies on clinical effectiveness and safety.

We aimed to examine the risk of cardiovascular adverse events by tricyclic antidepressant (TCA) dosage among patients with chronic pain.

In humans, persistent pain often leads to decreased appetite. However, the neural circuits underlying this behaviour remain unclear. Here, we show that a circuit arising from glutamatergic neurons in the anterior cingulate cortex (Glu) projects to glutamatergic neurons in the lateral hypothalamic area (Glu) to blunt food intake in a mouse model of persistent pain. In turn, these Glu neurons project to pro-opiomelanocortin neurons in the hypothalamic arcuate nucleus (POMC), a well-known neuronal population involved in decreasing food intake. In vivo calcium imaging and multi-tetrode electrophysiological recordings reveal that the Glu → Glu → Arc circuit is activated in mouse models of persistent pain and is accompanied by decreased feeding behaviour in both males and females. Inhibition of this circuit using chemogenetics can alleviate the feeding suppression symptoms. Our study indicates that the Glu → Glu → Arc circuit is involved in driving the suppression of feeding under persistent pain through POMC neuronal activity. This previously unrecognized pathway could be explored as a potential target for pain-associated diseases.

Advances have been made in the search for new multi-target modulators to control pain and inflammation. Therefore, compound 3,5-di-tert-butyl-4-hydroxyphenyl)(4-methylpiperazin-1-yl)methanone (LQFM202) was synthesised and evaluated. First, in vitro assays were performed for COX-1, COX-2, and 5-LOX enzymes. Subsequently, adult female Swiss albino mice treated orally with LQFM202 at doses of 25-200 mg/kg were subjected to acetic acid-induced writhing, formalin-induced pain, carrageenan-induced hyperalgesia, carrageenan- or zymosan-induced paw oedema, or pleurisy. LQFM202 inhibited COX-1, COX-2, and LOX-5 (IC = 3499 µM, 1565 µM, and 1343 µM, respectively). In acute animal models, LQFM202 (50, 100, or 200 mg/kg) decreased the amount of abdominal writhing (29%, 52% and 48%, respectively). Pain in the second phase of the formalin test was reduced by 46% with intermediate dose. LQFM202 (100 mg/kg) reduced the difference in nociceptive threshold in all 4 h evaluated (46%, 37%, 30%, and 26%, respectively). LQFM202 (50 mg/kg) decreased the carrageenan-oedema from the second hour (27%, 31% and 25%, respectively); however, LQFM202 (100 mg/kg) decreased the carrageenan-oedema in all hours evaluated (35%, 42%, 48% and 50%, respectively). When using zymosan, LQFM202 (50 mg/kg) decreased the oedema in all hours evaluated (33%, 32%, 31% and 20%, respectively). In the carrageenan-pleurisy test, LQFM202 (50 mg/kg) reduced significantly the number of polymorphonuclear cells (34%), the myeloperoxidase activity (53%), TNF-α levels (47%), and IL-1β levels (58.8%). When using zymosan, LQFM202 (50 mg/kg) reduced the number of polymorphonuclear and mononuclear cells (54% and 79%, respectively); and the myeloperoxidase activity (46%). These results suggest antinociceptive and anti-inflammatory effects of LQFM202.

Tietze syndrome is a rare form of chest wall costochondritis with joint swelling which can cause significant chest pain and decline in ability of daily activities. There is no standardized treatment protocol. The aim of this study was to assess the efficacy of adding oral steroids in addition to other non- steroidal treatment in improvement of pain and quality of life (QOL) in patients with Tietze syndrome.

The outcomes and morbidity following treatment for persistent or varicocele recurrence remain controversial.

The prevalence and harm associated with inadvertent neuraxial cardiovascular (CV) medication administration errors are unknown. This review aims to analyze neuraxial CV drug administration errors and associated clinical consequences. The secondary objective is to identify the causes and contributory factors in order to prevent future incidents. The author reviewed reports of accidental administration of CV medications via neuraxial routes during spinal or epidural anesthesia or analgesia published in the last 5 decades (1972-2022). Twenty-seven publications reported neuraxial administration of 10 different CV drugs among patients aged 1 to 81. Seventeen of the 33 errors occurred via the epidural route. Digoxin (9 patients), ephedrine (6), metaraminol (4), labetalol (4), and dopamine (3) were frequently involved in the incidents. Intrathecal digoxin (8 patients) was associated with paraplegia and encephalopathy, of whom 4 pregnant women scheduled for elective cesarean delivery sustained permanent lower limb neurologic deficits. Reversible systemic hemodynamic changes were predominant following the administration of epidural inotropes (dobutamine, dopamine, and epinephrine) and vasopressors (ephedrine and metaraminol). Most administrations (30 out of 32) were only bolus injections. All were preventable skill-based errors. The human factor analysis classification system (HFACS) identified poor organizational climate, inadequate supervision of junior doctors, deficiencies in neuraxial task processes, and incorrect visual perception of objects. The HFACS suggests CV medication safety strategies should include better education and training of junior doctors, modifications in neuraxial anesthesia practices, and careful handling of the CV drug ampoules and syringes.

Plantar fasciitis is one of the most common pathologies addressed by foot and ankle surgeons. Despite advances and overall success rates for conservative therapy, many of the recalcitrant cases proceed to require surgical correction. Partial to complete release of the fascia is often performed altering foot biomechanics and severing the windlass mechanism. Endoscopic debridement of the plantar fascia allows for direct visualization and removal of the inflammatory tissue while leaving the fascia and its function intact. A total of 125 feet were evaluated with a minimum follow-up time of 5 years. Gender, body mass index, and duration of symptoms were all evaluated and documented. Visual analog scale scores (VAS), American Orthopedic Foot and Ankle Score (AOFAS), and Foot Function Index (FFI) were collected both pre- and postoperatively. AOFAS, FFI, and VAS scores improved from a pre-operative mean of 57.6, 89.4%, and 8.6-89.1, 13.4%, and 0.7 respectively (p < .05) at final follow-up. Of the 125 patients, 98% stated they were satisfied with the operative outcome and would undergo the procedure again. At final follow-up, no patient suffered rupture of the fascia or recurrence. Patients were able to bear weight immediately following the surgery in a walking boot and on average patients were able to return to work at 3.4 days following surgery. This is a novel technique that does not compromise the plantar fascia or alter foot biomechanics with promising 5-year outcomes.

To improve patient safety and pain management, the Centers for Disease Control and Prevention (CDC) released the Guideline for Prescribing Opioids for Chronic Pain (CDC Guideline). Recognizing that issuing a guideline alone is insufficient for transforming practice, CDC supported an Opioid Quality Improvement (QI) Collaborative, consisting of 10 health care systems that represented more than 120 practices across the United States. The research team identified factors related to implementation success using domains described by the integrated Promoting Action on Research Implementation in Health Services (iPARIHS) implementation science framework.

The morbidity rate of ulcerative colitis (UC) in the world is increasing year by year, recurrent episodes of diarrhea, mucopurulent and bloody stools, and abdominal pain are the main symptoms, reducing the quality of life of the patient and affecting the productivity of the society. In this study, we sought to develop robust diagnostic biomarkers for UC, to uncover potential targets for anti-TNF-ɑ drugs, and to investigate their associated pathway mechanisms. We collected single-cell expression profile data from 9 UC or healthy samples and performed cell annotation and cell communication analysis. Revealing the possible pathogenesis of ulcerative colitis by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) analysis. Based on the disease-related modules obtained from weighted correlation network analysis (WGCNA) analysis, we used Lasso regression analysis and random forest algorithm to identify the genes with the greatest impact on disease (EPB41L3, HSD17B3, NDRG1, PDIA5, TRPV3) and further validated the diagnostic value of the model genes by various means. To further explore the relationship and mechanism between model genes and drug sensitivity, we collected gene expression profiles of 185 UC patients before receiving anti-tumor necrosis factor drugs, and we performed functional analysis based on the results of differential analysis between NR tissues and R tissues, and used single-sample GSEA (ssGSEA) and CIBERSORT algorithms to explore the important role of immune microenvironment on drug sensitivity. The results suggest that our model is not only helpful in aiding diagnosis, but also has implications for predicting drug efficacy; in addition, model genes may influence drug sensitivity by affecting immune cells. We suggest that this study has developed a diagnostic model with higher specificity and sensitivity, and also provides suggestions for clinical administration and drug efficacy prediction.