The presence of pharmaceuticals in aquatic ecosystems implies the need for efficient and sustainable treatment processes for their removal. This paper reports an innovative adsorption-regeneration process of a heat-resistant montmorillonite/sand composite (Mnt/sand) used to remove phenazopyridine (PHY) from aqueous media. Unlike other adsorption-thermolysis processes, which mostly use fine clay particles, this composite entraps the adsorptive Mnt phase within a fine sand matrix to improve the performance of the adsorbent. A maximum adsorption of 8.98 mg g[-1] was achieved using the total weight of the Mnt/sand composite, whereas 44.90 mg g[-1] was calculated on the basis of the weight of the active Mnt phase only. Kinetic studies revealed that the adsorption process occurs via pseudo-second-order kinetics (R [2] = 0.997), suggesting that the rate-limiting step in the process is due to surface interactions. The equilibrium data followed the Langmuir isotherm model, indicating that monolayer adsorption occurred on homogeneous sites, whereas thermodynamic calculations revealed that the process was spontaneous and endothermic (ΔG° < 0, ΔH° > 0). Furthermore, the Mnt/sand composite was tested under continuous flow conditions using a fixed-bed column. In the case of the breakthrough run with a nominal C 0 = 20 mg L[-1], Q = 2 mL min[-1] and m = 3.0 g, breakthrough was observed at 33.75 min, with a breakthrough capacity of 0.439 mg g[-1]. The kinetic parameters obtained from the Thomas model are k Th = 5.14 × 10[-3] L mg[-1] min[-1], q Th = 0.758 mg g[-1], and R [2] = 0.963, representing an efficiency of the bed usage of 57.9% compared with the theoretical saturation capacity. The experiments on thermal regeneration revealed highly efficient restoration of the adsorption capacity of the material at approximately 550 °C, with stable performance throughout multiple cycles (87-90%). From the point of view of computational research, the adsorption of PHY molecules on Mnt is energetically favorable (E ads = -0.1273 hartree = -334.25 kJ mol[-1] = -3.46 eV), accompanied by structural modification of PHY, which could be helpful for the thermal degradation of PHY.

Pharmaceutical salts are commonly used to enhance the bioavailability of poorly water-soluble drugs. The maximum solubility in water and the physical stability of a salt are closely linked to its pHmax, the pH at which both the free form (acid or base) and the salt can coexist. However, several aspects related to pHmax are only partially addressed or unexplored: (1) before salt screening, which usually consumes significant materials and efforts, whether pHmax can be predicted based on molecular properties; (2) whether salt disproportionation proceeds via a solid-state or water-mediated mechanism; and (3) whether disproportionation risk can be graded systematically and predicted. In this work, the relationship between pHmax and the physical properties of the basic compounds was examined, and a regression model was constructed based on their correlations. The pHmax values of 106 monosalts for 35 basic drugs were compiled from the literature. In the data set examined, the pHmax is strongly correlated with the pKa of the drug (2-10), but not significantly with the pKa of the counter-acid (-8 to 5), and is slightly influenced by the molecular weights of the drug and counter-acid. Accordingly, before salt screening, pHmax of a monosalt can be predicted as a function of the drug pKa and the relevant molecular weights. Across a pH range of 1-11, for the 106 monosalts studied, 74% of the predicted pHmax values were found to be within experimental errors. To determine whether disproportionation between pharmaceutical salts of basic drugs and basic excipients is a solid-state reaction or not, differential scanning calorimetry (DSC) is performed. The results showed that a solid-state reaction did not occur even at high temperatures where the excipient either melted or was liquefied above its glass transition temperature. Disproportionation risk levels were systematically defined based on development requirements and were exemplified using model HCl salts (sertraline, prazosin, phenazopyridine, and pioglitazone) across a wide pHmax range. The risk level shows a strong correlation with the pH difference between the equilibrium pH of the excipient (pHee) and the pHmax of the salt. Notably, the risk level increases more sharply with the pH difference (pHee - pHmax) for highly hygroscopic excipients. A prediction workflow for disproportionation risk level is proposed based on the above correlation and the self-disproportionation type of pharmaceutical salts.

Finding effective materials for the removal of pollutants from wastewater has become an essential requirement in environmental protection and the development of advanced water-treatment technologies. In this study, Ti3C2T x -MXene was synthesized using two methods (i.e., sol-gel and hydrothermal). The influence of synthesis parameters, including etching agent (i.e., LiF and NaF), temperature (i.e. 38, 80 and 90 °C), and reaction time (i.e., 3 and 7 days), on the structural characteristics and pollutant-removal performance of MXene was systematically investigated. The synthesized samples were evaluated for the removal of dye and pharmaceutical contaminants, including methylene blue (MB), tetracycline (TC), carbamazepine (CBZ), and phenazopyridine (PhP). The results revealed that the sample synthesized using LiF (i.e., LTi2) as an etchant at 90 °C possessed the highest specific surface area and exhibited higher adsorption efficiency compared to other samples. At an initial concentration of 10 ppm, LTi2 removed more than 93% of MB and 88% of PhP within 60 min through adsorption. At a concentration of 40 ppm, adsorption efficiencies of approximately 48%, 29%, and 18% were obtained for MB, TC, and CBZ, respectively. Under subsequent visible-light irradiation, further pollutant removal was observed, resulting in total removal efficiencies exceeding 98% for MB and 93% for PhP at 10 ppm, while overall removal efficiencies of 59%, 64%, and 37% were achieved for MB, TC, and CBZ, respectively, at 40 ppm. These findings demonstrated that careful control of the synthesis conditions was an effective strategy for tailoring the MXene structure and improving its adsorption-dominated and visible light assisted pollutant removal performance.

Phenazopyridine is a urinary analgesic widely available as both a prescription and over-the-counter medication, yet its appropriate clinical use, safety profile, and limitations remain poorly understood among patients and clinicians alike. This activity examines the pharmacology, approved indications, pharmacokinetics, dosing recommendations, adverse effects, and monitoring considerations associated with phenazopyridine. Particular attention is given to the drug's role as an adjuvant therapy in uncomplicated urinary tract infections, its contraindications in renal and hepatic impairment, and the risks associated with prolonged or inappropriate use. The activity also addresses the importance of patient education regarding the drug's symptomatic, not anti-infective, properties. By completing this activity, clinicians will be better equipped to counsel patients appropriately, recognize serious adverse effects, such as methemoglobinemia and hemolytic anemia, and apply evidence-based guidelines to optimize the safe and effective use of phenazopyridine in clinical practice.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic X-linked recessive disorder that results from mutations in the G6PD gene, which provides instructions for manufacturing the G6PD enzyme. G6PD deficiency primarily impacts red blood cells. This deficiency can result in hemolytic anemia (HA), in which rapid destruction of red blood cells occurs due to the vulnerability of erythrocytes to reactive oxygen species. It is most commonly found in males and affects 1 in 10 Black males in the United States. Persons with G6PD deficiency may exhibit symptoms such as pallor, jaundice, dark urine, fatigue, tachycardia, shortness of breath, and splenomegaly. Exposure to certain medications such as rasburicase, sulfonamides, nitrofurantoin, antimalarials, dapsone, chloramphenicol, high-dose aspirin, methylene blue, and phenazopyridine may trigger a hemolytic crisis in those with G6PD deficiency. Tests used in the diagnosis of HA include the Coombs test, haptoglobin, complete blood count, urinalysis, lactate dehydrogenase, bone marrow tests, and a peripheral blood smear. This article summarizes the case of a patient who developed HA after an infusion of rasburicase and offers management strategies.

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme found in the cytoplasm of all cells in the body. It is a housekeeping enzyme that plays a vital role in the prevention of cellular damage from reactive oxygen species (ROS). It does this by providing substrates to prevent oxidative damage. Erythrocytes are particularly vulnerable to ROS due to their role in oxygen transport and inability to replace cellular proteins as mature cells. Inherited deficiencies of G6PD can result in acute hemolytic anemia during times of increased ROS production. This may be caused by stress or exposure to certain foods that contain high amounts of oxidative substances, for example, fava beans, or certain medications.  In particular, anti-malarial agents have a strong association with inducing hemolytic anemia in patients with G6PD deficiency. Below are medications more commonly used in the United States that have been shown to trigger a hemolytic crisis in those with G6PD deficiency; however, a more comprehensive list of medications to be avoided has been published by the Italian G6PD Deficiency Association and can be found at www.g6pd.org.[1][2][3][4] Common medications to be avoided or used with caution in G6PD-deficient patients include: Acetaminophen. Acetylsalicylic acid. Chloramphenicol. Chloroquine. Colchicine. Diaminodiphenyl sulfone. Diphenhydramine. Glyburide. Isoniazid. L-Dopa. Methylene blue. Nitrofurantoin. Phenazopyridine. Primaquine. Rasburicase. Streptomycin. Sulfacetamide. Sulfanilamide. Sulfapyridine. Sulfacytine. Sulfadiazine. Sulfaguanidine. Sulfamethoxazole. Sulfisoxazole. Trimethoprim. Tripelennamine. Vitamin K.

Methemoglobinemia is a rare but serious condition affecting the blood's ability to carry oxygen. Symptoms at presentation are often nonspecific. We describe the case of a 58-year-old female presenting with unexplained central cyanosis and severe hypoxia despite preserved respiratory effort and seemingly reassuring lab values. Further questioning revealed recent ingestion of a large quantity of phenazopyridine, an over-the-counter urinary analgesic known to cause oxidative stress. Co-oximetry confirmed significant elevation of methemoglobin levels. Methylene blue is well-regarded as the gold standard, and its use in treatment of this patient led to favorable clinical and laboratory improvement. Clinicians must maintain a high index of suspicion for dyshemoglobinemias in patients with unexplained cyanosis refractory to oxygen therapy, particularly when conventional metrics of oxygenation are inconsistent with the overall clinical picture.

Liquid-liquid phase separation (LLPS) has been linked to the initiation and progression of cancers. This study aimed to investigate the LLPS-related molecular features and develop a prognostic signature for hepatocellular carcinoma (HCC). Single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data were obtained from open-source repositories. The Seurat package was used for processing and analyzing scRNA-seq data. LLPS-related genes (LLPSRGs) were identified by integrating scRNA-seq and bulk RNA-seq data. Univariate Cox and LASSO regression analyses were employed to construct an LLPS-related prognostic risk model. A predictive nomogram was also developed based on the risk score and clinicopathologic features. Additionally, correlations between clinicopathological features, biological functions, and tumor mutations with prognostic risk were explored. Experimental validation included cell transfection, wound healing, and transwell assays. Fourteen distinct cell clusters were identified, with malignant hepatocytes exhibiting the highest LLPS score. High-LLPS hepatocytes strongly interacted with other cells, showing elevated expression of EGFR-ERGF, EGFR-AREG, MIF-CD44, and MIF-CXCR4 interactions. The LLPS score was associated with malignant differentiation of hepatocytes. Ten LLPSRGs were identified as part of the LLPS-related risk signature, and potential agents were predicted: Olitigaltin and Lactose for LGALS3, and Sitamaquine, Phenazopyridine, Sulfanilamide, Pamaquine, Sodium ascorbate, and Co-trimoxazole for G6PD. Knockdown of LGALS3 inhibited HCC cell migration and invasion. LLPS-related molecular characteristics were identified, and an LLPS-related prognostic model was developed, offering novel insights into HCC research and providing potential therapeutic targets.

Phenazopyridine is an azo dye analgesic routinely used in the management of urinary tract infections. An overdose of this pharmaceutical agent causes methemoglobinemia and renal failure across all age groups. There is limited knowledge regarding the implications of early phenazopyridine exposure, whether via medicinal use or inadvertent contact, or its toxicity in specific organs in living organisms. Moreover, 40-50 % of this drug gets eliminated in its native form and hence it contributes to the pharmaceutical burden in the environment. In this study, we used zebrafish, a versatile model system for assessing drug-induced toxicity, to investigate the effects of phenazopyridine exposure on embryonic development and hematopoiesis. Zebrafish embryos exposed to sublethal doses showed distinct toxicological manifestations including cardiotoxicity, delayed hatching, and absence of swim bladder, which are indicative of developmental anomalies associated with the phenazopyridine exposure. Phenazopyridine-exposed embryos also had a significant reduction in blood cell population and defective vascularization, indicating an effect on hematopoiesis. Investigation of molecular mechanisms in the treated embryos revealed elevated ROS signals and downregulation of key genes involved in host's antioxidant response, suggesting the induction of oxidative stress upon phenazopyridine exposure. While the results of this study clearly demonstrate the developmental toxicity associated with phenazopyridine exposure in living systems, the use of zebrafish, which is an aquatic organism, also highlights the long-term implications of this pharmaceutical contaminant on the life forms in the aquatic environment, given that this medication is a frequently used over-the-counter analgesic.

Key aspects of pain syndrome in urology, including its classification, pathogenesis, and current treatment approaches, are discussed in the article. Special attention is given to the phenomenon of chronic pelvic pain, defined as persistent pain lasting at least three months, accompanied by dysfunction of the genitourinary system and emotional disorders. The main pathogenetic mechanisms underlying pain syndrome determine its complex multisystem nature, which requires a comprehensive approach to both diagnosis and treatment. Various etiologies of urologic chronic pain syndrome are described. Particular emphasis is given on urological causes such as bacterial cystitis and interstitial cystitis/bladder pain syndrome (IC/BPS). Clinical phenotypes of IC/BPS are discussed, along with individualized treatment approaches for each phenotype. The impact of pain syndrome in bacterial cystitis on quality of life and the role of phenazopyridine in pain relief are also highlighted. The importance of an interdisciplinary approach and the combination of different therapeutic methods to achieve good outcomes in the management of pain syndrome is emphasized.

This work introduces a sustainable and innovative water purification technique that uses thermally stable natural clay to remove hazardous organic contaminants and nitrate ions from water. The method integrates adsorption and thermal regeneration to ensure both high removal efficiency and reusability. The contaminants investigated include pharmaceutical compounds (phenazopyridine and tetracycline), industrial dyes (methyl orange and methylene blue), and nitrate ions, which are selected on the basis of their persistence, toxicity, and resistance to conventional treatment methods. Batch adsorption experiments conducted under optimized conditions (pH ≈ 4, 25 °C, and pollutant concentrations ranging from 10 to 40 mg/L) revealed high removal efficiencies, ranging between 84% and 93% for organic pollutants and 89% for nitrate. To assess practical applicability, a continuous-flow column system was employed, confirming the robust performance of the clay under dynamic conditions. A thermal decomposition step at 600 °C effectively regenerated the spent clay by completely mineralizing the adsorbed pollutants into harmless byproducts such as carbon dioxide and water vapor, with no observable secondary waste. The regenerated clay maintained adsorption efficiencies above 85% through five successive reuse cycles, and the reuse experiments were conducted in triplicate to ensure the repeatability and reliability of the application. Comprehensive characterization via X-ray diffraction, scanning electron microscopy, thermogravimetric analysis, and elemental analysis confirmed the high crystallinity, porous structure, and thermal robustness of the clay-properties essential for its dual adsorption-thermolysis functionality. The novelty of this work lies in combining low-cost, thermally stable natural clay with complete thermal decomposition of adsorbed contaminants, achieving both high reusability and pollutant mineralization without secondary waste. This dual-action purification method offers a cost-effective, reusable, and environmentally friendly alternative to conventional water treatment technologies. The results position thermally regenerated natural clay as a promising candidate for large-scale applications in water purification, particularly in resource-limited settings.

INTRODUCTION: Significant cases of methemoglobinemia will cause a signal interference in traditional dual-wavelength pulse oximetry leading to the classic finding of “refractory hypoxemia”. As smartwatches begin to incorporate pulse oximetry capabilities, it is unclear whether these devices will demonstrate the same type of interference in the presence of methemoglobinemia. This article reports a case where a patient’s Apple Watch© reported a hypoxemia alert in the setting of phenazopyridine induce methemoglobinemia. CASE REPORT: This is a case report of a 71-year-old female whose Apple Watch© reported a hypoxemia alarm in the setting of methemoglobinemia caused by phenazopyridine use. The patient’s smartwatch began signaling hypoxemia alerts the day before she noticed clinical cyanosis. 24 hours after the hypoxemia alerts began, she presented to the Emergency Department (ED) with shortness of breath and blue discoloration of skin. The Apple Watch© recorded oxygen saturation readings between 73% and 86%. Upon arrival to the ED, the patient’s SpO2 was 84% on traditional hospital-grade dual-wavelength pulse oximetry and her methemoglobin level was 19.8%. Her symptoms and methemoglobinemia resolved after administration of 1 mg/kg of IV methylene blue. CONCLUSION: Pulse oximetry used in smartwatch technology can trigger a hypoxemia alarm in the presence of drug-induced methemoglobinemia. If demonstrated to be a reproducible finding, smartwatch technology has the potential to be used as part of an early detection system for clinically significant methemoglobinemia.