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Background: Abdominal aortic aneurysms and atheromatous plaques are well-established potential culprits in the development of cholesterol embolization. This embolic phenomenon can result in the occlusion of peripheral arteries in the forefoot or toes, commonly referred to as "trash foot". Case: A 61-year old patient exhibited severe symptoms and signs of lower limb and mesenteric ischemia, represented clinically by abdominal pain, hematochezia, and bilateral plantar necrotic lesions, attributed to embolization from a previously unknown large infrarenal abdominal aortic aneurysm. Diagnosis was confirmed by performing angio-CT of the abdomen, an angiologic examination, as well as colonoscopy. The patient underwent open surgical repair of the aortic aneurysm and received intravenous prostanoids, resulting in a successful outcome with resolution of bowel ischemia and complete recovery of bilateral foot lesions with no tissue loss. Conclusion: Cholesterol embolization syndrome seldom manifests with its complete clinical spectrum. Identifying and addressing the underlying cause is crucial, with a focus on potential abdominal aortic aneurysms. A combined approach involving surgical repair and prostanoid therapy may offer a viable option for patients experiencing severe manifestations. [ABSTRACT FROM AUTHOR]

Introduction: Critically ill patients suffer from a wide variety of clinical events, most of them leading to pro-inflammatory states such as sepsis or simply as consequence of major surgery. Many of these patients develop forms of acute kidney injury, heart or acute liver failure during intensive care. Lipid signaling is critically involved in triggering systemic inflammation processes, pain and vascular tone. We therefore hypothesized that fatty-acid-derived lipid mediators might be regulated during inflammatory stages and other clinical events in critically ill patients and might serve as potential biomarker candidates. Methods and study design: Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), we determined the levels of 53 lipid mediators in plasma from nine patients. These patients were hospitalized at Frankfurt University Hospital's intensive care unit (ICU) after cardiac surgery. Inflammatory stages were illustrated over time using clinically established biomarkers such as interleukin-6 (IL-6) and leukocyte count. Normal range values of the lipids were obtained from healthy volunteers. Results: Plasma levels clearly outside the normal range were observed for 22 of 53 lipid mediators, of which 13 were increased (including ceramides Cer (d18:0/18:0), Cer (d18:1/16:0), Cer (d18:1/18:1), glucosyl-ceramide GluCer (d18:1/24:1), lactosylceramide LacCer (d18:1/18:0), and LacCer (d18:1/24:1), 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), 11,12- and 14,15-DHET and 1- and 2-arachidonoyl glycerol (1-AG and 2-AG), Sphingosine SPH (d18:1) and 20-HETE. Furthermore, nine lipids were decreased (Cer (d18:1/24:0), LacCer (d18:1/16:0), LacCer (d18:1/24:0), sphingosine-1-phosphate S1P (d18:1), S1P (d18:0), the lysophosphatidic acids LPA (16:0), LPA (18:0), LPA (18:1) and 9-HODE. Among increased lipids, the remarkable changes in 1-AG, 2-AG, and to a lower extent of 6-keto-PGF1-alpha plasma levels showed a certain agreement with inflammatory phases. Furthermore, 6-keto-PGF1alpha had its peak shortly before initiation of continuous veno-venous hemodialysis (at least in 5 of the observed patients), 2-AG was elevated in all our nine patients during (right) heart failure in the context of either re-opening patient's chest, implementation of veno-arterial ECMO or at least while significantly increasing the amount of catecholamines. Discussion: In this pilot trial we identified several evaluated lipids in critically ill patients representing either potentially (patho-) physiologically relevant mediators of the pro-inflammatory processes and during heart failure or possible markers preceding veno-venous hemodialysis. [ABSTRACT FROM AUTHOR]

The skin is a barrier that protects the human body against environmental factors (physical, including solar radiation, chemicals, and pathogens). The integrity and, consequently, the effective metabolic activity of skin cells is ensured by the cell membrane, the important structural and metabolic elements of which are phospholipids. Phospholipids are subject to continuous transformation, including enzymatic hydrolysis (with the participation of phospholipases A, C, and D) to free polyunsaturated fatty acids (PUFAs), which under the influence of cyclooxygenases (COX1/2), lipoxygenases (LOXs), and cytochrome P450 (CYPs P450) are metabolized to various classes of oxylipins, depending on the type of PUFA being metabolized and the enzyme acting. The most frequently analyzed oxylipins, especially in skin cells, are eicosanoids, which are derivatives of arachidonic acid (AA). Their level depends on both environmental factors and endogenous metabolic disorders. However, they play an important role in homeostasis mechanisms related to the structural and functional integrity of the skin, including maintaining redox balance, as well as regulating inflammatory processes arising in response to endogenous and exogenous factors reaching skin cells. Therefore, it is believed that dysregulation of eicosanoid levels may contribute to the development of skin diseases, such as psoriasis or atopic dermatitis, which in turn suggests that targeted control of the generation of specific eicosanoids may have diagnostic significance and beneficial therapeutic effects. This review is the first systemic and very detailed approach presenting both the causes and consequences of changes in phospholipid metabolism leading to the generation of eicosanoids, changes in the level of which result in specific metabolic disorders in skin cells leading to the development of various diseases. At the same time, existing literature data indicate that further detailed research is necessary to understand a clear relationship between changes in the level of specific eicosanoids and the pathomechanisms of specific skin diseases, as well as to develop an effective diagnostic and therapeutic approach. [ABSTRACT FROM AUTHOR]

The urothelium and lamina propria (LP) contribute to sensations of bladder fullness by releasing multiple mediators, including prostaglandins (PGs) and adenosine 5′-triphosphate (ATP), that activate or modulate functions of cells throughout the bladder wall. Mediators that are simultaneously released in response to bladder distention likely influence each other's mechanisms of release and action. This study investigated whether PGs could alter the extracellular hydrolysis of ATP by soluble nucleotidases (s-NTDs) released in the LP of nondistended or distended bladders. Using an ex vivo murine detrusor-free bladder model to access the LP during bladder filling and a sensitive HPLC-FLD detection methodology, we evaluated the decrease in ATP and the increase in adenosine 5′-diphosphate (ADP), adenosine 5′-monophosphate (AMP), and adenosine by s-NTDs released in the LP. Endogenous PGE2 increased the spontaneous but not the distention-induced release of s-NTD via EP2 and EP3 prostanoid receptors, whereas exogenous PGE2 increased the spontaneous s-NTD release via EP3, EP4, and FP receptors and the distention-induced s-NTD release via EP1-4 and FP receptors. Endogenous PGF2α, PGD2, and PGI2 did not change the s-NTD release. Exogenous PGD2 increased the spontaneous s-NTD release via DP2 receptors and the distention-induced s-NTD release via DP1 and DP2 receptors. Exogenous PGF2α increased the spontaneous but not the distention-induced release of s-NTD via FP receptors. It is possible that higher concentrations of PGE2, PGF2α, and PGD2 (as expected in inflammation, bladder pain syndrome, or overactive bladder) potentiate the release of s-NTDs and the consecutive degradation of ATP as a safeguard mechanism to prevent the development of excessive bladder excitability and overactivity by high amounts of extracellular ATP. [ABSTRACT FROM AUTHOR]

Objective Prostaglandins (PGs) play a major role in maintaining patency of the ductal arteriosus (DA). Pulmonary 15-hydroxyprostaglandin dehydrogenase (PGDH), which is ecoded by the hydroxyprostaglandin dehydrogenase (HPGD) gene, is the primary enzyme responsible for PG breakdown. Animal studies have shown HPGD -knockout mice have significantly higher prostaglandin E2 levels and no ductal remodeling. Functional variants of the HPGD gene that alter PG breakdown have not been studied in preterm infants with patent ductus arteriosus (PDA). Study Design This was an observational cohort study including extreme low birth weight (ELBW) infants classified as having spontaneous, medical, or procedural (transcatheter or surgical ligation) closure of their DA. Urine prostaglandin E metabolite (PGEM) levels were measured in ELBW infants following ibuprofen treatment using competitive ELISA. HPGD genetic variants rs8752, rs2612656, and rs9312555 were analyzed. Kruskal–Wallis, Fisher's exact, chi square, logistic regression, and Wilcoxon signed-rank tests were used; p < 0.05 was considered significant. Results Infants in the procedural closure group had a younger gestational age (GA). The incidence of spontaneous closure or medical closure was higher compared to procedural closure in the presence of any minor allele of rs8752 (67 and 27%, respectively; p = 0.01), when adjusted for GA and gender. Haplotype analysis of three variants of HPGD revealed differences when comparing the spontaneous and medical closure group to the procedural group (p < 0.05). Urinary PGEM levels dropped significantly in those ELBW infants who responded to ibuprofen (p = 0.003) in contrast to those who did not respond (p = 0.5). Conclusion There was a different genotype distribution for the rs8752 genetic variant of the HPGD gene—as it relates to the mode of treatment for ELBW infants with PDA. We speculate that medical management in the presence of this variant facilitated additional PG breakdown, significantly abrogating the need for procedural closure. Additionally, differences in genotype and haplotype distributions implicate a specific HPGD genetic foundation for DA closure in ELBW infants. Key Points PGs and their metabolism play a major role in PDA patency or closure. Genetic variants of the HPGD gene influence mode of treatment of PDA in ELBW infants. ELBW infants with PDA that responded to medical closure had significantly decreased urine PGEM levels. [ABSTRACT FROM AUTHOR]

Purpose: Nonsteroidal anti-inflammatory drugs (NSAID) are associated with increased stress fracture risk, potentially due to inhibiting the adaptive bone formation responses to exercise. This study investigated if a single, maximal dose of three different NSAID alters bone formation biomarker response to strenuous exercise. Methods: In a randomized, counterbalanced order, 12 participants (10 male, 2 female), performed four bouts of plyometric jumps, each separated by at least 1 wk. Two hours before exercise, participants consumed either placebo or NSAID: ibuprofen (800 mg), celecoxib (200 mg), flurbiprofen (100 mg). Blood was collected before (PRE), and at 0, 15, 60, 120, and 240 min postexercise. Parathyroid hormone, ionized calcium, procollagen type 1 N-terminal propeptide, bone alkaline phosphatase, osteocalcin, C-terminal telopeptide of type 1 collagen, tartrate-resistant acid phosphatase, and sclerostin were measured. Prostaglandin E2 metabolite and creatinine were measured in urine. Data were analyzed using repeated-measures ANOVA and area under the curve analysis. Data are mean ± SD. Results: There was an exercise effect for procollagen type 1 N-terminal propeptide, bone alkaline phosphatase, osteocalcin, C-terminal telopeptide of type 1 collagen, tartrate-resistant acid phosphatase, sclerostin, osteoprotegerin, parathyroid hormone, and ionized calcium (all P < 0.05), but no NSAID treatment effect for any biomarker (all P > 0.05). Area under the curve analyses were not different for any biomarker (P > 0.05). Prostaglandin E2 metabolite was higher during the placebo trial (322 ± 153 pg·mg−1 creatinine, P < 0.05) compared with ibuprofen (135 ± 83 pg·mg−1), celecoxib (202 ± 107 pg·mg−1), and flurbiprofen (159 ± 74 pg·mg−1). Conclusions: Plyometric exercise induced changes in bone metabolism, but the responses were unaltered by consuming NSAID 2 h before exercise. [ABSTRACT FROM AUTHOR]

One of the signs of puberty experienced by young women is menstruation, some young women experience pain known as dysmenorrhea during menstruation. Iron is one of the essential nutrients for adolescent reproduction, and its deficiency can increase the risk of dysmenorrhea. Stress can also affect Dysmenorrhea, as stress can lead to hormonal imbalances and the secretion of prostaglandin hormones produced by stress. The purpose of this study was to analyze the relationship between iron intake and stress levels with the incidence of primary dysmenorrhea in adolescent girls at PB Soedirman Islamic High School Bekasi. This study uses an observational analytic method with a cross-sectional design, and data collection using consecutive sampling techniques with 100 respondents. Data were collected through semi-quantitative food frequency questionnaires (SQ-FFQ) and Perceived Stress Scale (PSS) and determining the incidence of dysmenorrhea using dysmenorrhea questionnaires. The results measured by Chi-square test, showed p-values for iron intake (0.010) and stress levels (0.002). This study found a significant correlation between stress levels and iron intake in adolescent girls in PB Soedirman Islamic High School Bekasi. [ABSTRACT FROM AUTHOR]

The prevalence of dysmenorrhea in the world is still quite high. Primary dysmenorrhea occurs due to an increase in prostaglandin F2α (PGF2α). Cyclooxigenase-2 (COX-2) is a crucial component that controls the synthesis of prostaglandins. A key target for reducing menstrual pain is COX-2. This study aimed to investigate the effect of curcumin on COX-2 expression and PGF2α expression in uterine tissue in mice model primary dysmenorrhea. The study involved a randomized post-test control group design using non-pregnant female Balb/c mice as a model of primary dysmenorrhea induced by estradiol benzoate and oxytocin. Five groups of mice (n = 7 each group) were randomly assigned: Sham group (SG), which received placebo; Ibuprofen group (IG), which received ibuprofen 100 mg/kg; C100, which received 100 mg/kg of curcumin; C200, which received 200 mg/kg of curcumin; and C400, which received 400 mg/kg of curcumin. The intervention was administered orally twice a day for 7 days. For ten days, estradiol benzoate was injected subcutaneously, and on day 11, oxytocin was injected intraperitoneally. COX-2 expression was examined by Western blot and prostaglandin expression by immunohistochemistry. The data was analysed using a One-way analysis of variance (ANOVA) and Tukey's test. Curcumin significantly decreased COX-2 and PGF2α expression in uterine tissues of primary dysmenorrhea models compared with the SG (p<0.05). There is no significant difference in COX-2 and PGF2α expression between IG and C400 (p>0.05). Curcumin effectively reduces COX-2 and PGF2α expression in uterine tissues in mice models of primary dysmenorrhea. [ABSTRACT FROM AUTHOR]

IntroductionCritically ill patients suffer from a wide variety of clinical events, most of them leading to pro-inflammatory states such as sepsis or simply as consequence of major surgery. Many of these patients develop forms of acute kidney injury, heart or acute liver failure during intensive care. Lipid signaling is critically involved in triggering systemic inflammation processes, pain and vascular tone. We therefore hypothesized that fatty-acid-derived lipid mediators might be regulated during inflammatory stages and other clinical events in critically ill patients and might serve as potential biomarker candidates.Methods and study designUsing liquid chromatography-tandem mass spectrometry (LC-MS/MS), we determined the levels of 53 lipid mediators in plasma from nine patients. These patients were hospitalized at Frankfurt University Hospital’s intensive care unit (ICU) after cardiac surgery. Inflammatory stages were illustrated over time using clinically established biomarkers such as interleukin-6 (IL-6) and leukocyte count. Normal range values of the lipids were obtained from healthy volunteers.ResultsPlasma levels clearly outside the normal range were observed for 22 of 53 lipid mediators, of which 13 were increased (including ceramides Cer (d18:0/18:0), Cer (d18:1/16:0), Cer (d18:1/18:1), glucosyl-ceramide GluCer (d18:1/24:1), lactosylceramide LacCer (d18:1/18:0), and LacCer (d18:1/24:1), 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), 11,12- and 14,15-DHET and 1- and 2-arachidonoyl glycerol (1-AG and 2-AG), Sphingosine SPH (d18:1) and 20-HETE. Furthermore, nine lipids were decreased (Cer (d18:1/24:0), LacCer (d18:1/16:0), LacCer (d18:1/24:0), sphingosine-1-phosphate S1P (d18:1), S1P (d18:0), the lysophosphatidic acids LPA (16:0), LPA (18:0), LPA (18:1) and 9-HODE. Among increased lipids, the remarkable changes in 1-AG, 2-AG, and to a lower extent of 6-keto-PGF1-alpha plasma levels showed a certain agreement with inflammatory phases. Furthermore, 6-keto-PGF1alpha had its peak shortly before initiation of continuous veno-venous hemodialysis (at least in 5 of the observed patients), 2-AG was elevated in all our nine patients during (right) heart failure in the context of either re-opening patient’s chest, implementation of veno-arterial ECMO or at least while significantly increasing the amount of catecholamines.DiscussionIn this pilot trial we identified several evaluated lipids in critically ill patients representing either potentially (patho-) physiologically relevant mediators of the pro-inflammatory processes and during heart failure or possible markers preceding veno-venous hemodialysis.

Inflammation is a biological process in response to injury, resulting in altered blood flow, increased vascular permeability, tissue destruction, and the production of reactive oxygen species (ROS) and inflammatory mediators. Zygophyllum simplex L., a medicinal plant traditionally used in the Arabian Peninsula for inflammatory disorders, has demonstrated promising in vitro anti-inflammatory activity due to its phenolic content. Additionally, the ethyl acetate fraction has exhibited notable in vivo anti-inflammatory effects. This research aimed to evaluate the in vivo anti-inflammatory effects of a Z. simplex plant extract and its principal ethyl acetate isolate, isorhamnetin-3- O -β-D-glucoside (Isor-3-Glu). The study seeks to develop a straightforward and robust HPLC method for quantifying Isor-3-Glu within the total methanolic extract of Z. simplex. The total methanol extract of Z. simplex was successively partitioned with a variety of organic solvents and the ethyl acetate fraction was used to isolate Isor-3-Glu on a Sephadex LH-20 column. The in vivo anti-inflammatory activity was investigated using carrageenan-triggered inflammation in rats. Histological features and immunohistochemical expression of cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-α) were analyzed, and the levels of interleukins (IL-1β and IL-6) as well as prostaglandin E2 (PGE2) of the paw tissues were examined by qRT-PCR and ELISA, respectively. Quantification of Isor-3-Glu was achieved using an HPLC-PDA method. Isor-3-Glu considerably (p < 0.05) lowered the weight of the paw edema. The histological abnormalities were improved, and the percentage of the COX-2 and TNF-α immunoreactive cells substantially decreased in the Isor-3-Glu-treated group in comparison with the positive control and Z. simplex extract group. Isor-3-Glu significantly ameliorated PGE2, IL-1β, and IL-6 levels. A straightforward and dependable HPLC technique was established for quantifying Isor-3-Glu in the total extract. The proposed methodology effectively determined Isor-3-Glu in less than 5 min. The calibration curve exhibited a linear relationship over the concentration range of 1.0–40.0 μg/mL, with a correlation coefficient (r) ≥ 0.9995. The developed method demonstrated a high level of sensitivity, with a detection limit as low as 0.139 μg/mL. The concentration of Isor-3-Glu in the total extract of Z. simplex was determined to be 0.05% w/w of dry extract. Isor-3-Glu could be considered a promising anti-inflammatory compound that necessitates future clinical research. Isor-3-Glu was accurately quantified using a meticulously developed and optimized HPLC-PDA technique. [Display omitted] • Zygophyllum simplex is used as an anti-inflammatory plant in the Arabian Peninsula. • Isorhamnetin-3-glucoside is a main component of this plant. • Isorhamnetin-3-glucoside considerably lowered the weight of the paw edema in rats. • It ameliorated PGE2, IL-1 β and IL-6 level and decreased COX-2 and TNF- α expression. • Its analysis was successfully conducted using a developed simple HPLC-PDA method. [ABSTRACT FROM AUTHOR]

The corpus luteum is a temporary endocrine gland that is crucial for pregnancy, as it produces the progesterone needed to maintain optimal uterine conditions for implantation. In the absence of a conceptus, the corpus luteum becomes non-functional and undergoes rapid tissue remodeling to regress into a fibrotic corpus albicans. Early luteal regression is characterized by increased cytokine release. Because the role of fibroblasts in the bovine corpus luteum remains to be elucidated, the aim of this study was to elucidate the response of bovine luteal fibroblasts to inflammatory cytokines, tumor necrosis factor α (TNFα), and interleukin 1β (IL1β). Both cytokines induced canonical mitogen activated protein kinase (MAPK) signaling in luteal fibroblasts by phosphorylation of ERK1/2, p38 MAPK, and JNK. IL1β elevated expression and phosphorylation of cytosolic phospholipase A2 (cPLA 2), an enzyme that mobilizes arachidonic acid for prostanoid synthesis. IL1β also elevated expression of prostaglandin-endoperoxide synthase 2 (PTGS2), another enzyme needed to synthesize prostanoids. IL1β increased PGF2α and PGE 2 levels in the culture medium over 20-fold. Inhibition of MAPKs with small-molecule inhibitors abrogated the stimulatory effects of IL1β. IL1β also induced prostaglandin production in steroidogenic cells; however, there was no elevation in cPLA 2. Therefore, actions of IL1β differ based on ovarian cell type. All together, we have identified luteal fibroblasts as potential inflammatory mediators during luteal regression. [Display omitted] • Bovine luteal fibroblasts are responsive to the inflammatory cytokines IL1β and TNFα. • IL1β, but not TNFα, increases luteal fibroblast production of PGF2α and PGE 2. • IL1β elevates cPLA 2 in luteal fibroblasts but not in steroidogenic cells. • Bovine luteal fibroblasts contribute lipid mediators to the microenvironment during luteal regression. [ABSTRACT FROM AUTHOR]

Background: Sustained-release prostaglandin intracameral implants are new targeted treatment options for open-angle glaucoma or ocular hypertension that lower intraocular pressure (IOP) and reduce or eliminate the need for topical eye drops. Objective: To summarize evidence supporting prostaglandin intracameral implants for treatment of ocular hypertension or open angle glaucoma and identify patient populations most likely to benefit from these treatments. Data sources: A PubMed search (1/1/2016 to 10/1/2024) was conducted to identify randomized, controlled clinical trials for bimatoprost 10-μg and travoprost 75-μg intracameral implants. Manufacturer prescribing information, formulary dossiers, Food and Drug Administration (FDA) clinical reviews and glaucoma clinical treatment guidelines were also reviewed. Study selection and data extraction: English-language randomized controlled trials involving bimatoprost 10-μg or travoprost 75-μg intracameral implants were included. Data synthesis: Bimatoprost and travoprost intracameral implants demonstrated noninferior IOP reduction compared to timolol eye drops in phase 3 trials, with sustained effects up to 12 and 36 months, respectively. The FDA-approved implants are limited to a single administration to the affected eye to minimize corneal risks. The travoprost implant contains a titanium reservoir and requires surgical placement, while the bimatoprost implant is biodegradable and can be placed in a clinic setting. There are no studies directly comparing the safety and efficacy of the two intracameral implants. Conclusions: Prostaglandin intracameral implants are a novel approach to reducing medication burden while delivering sustained IOP reducing effects. Pharmacists should be aware of efficacy and safety considerations of these implants relative to available topical treatments for ocular hypertension or open angle glaucoma., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2025.)

The analysis of prostaglandin urinary metabolites is valuable for assessing physiological processes and identifying disease biomarkers. These metabolites, derived from the breakdown of prostaglandins, offer a noninvasive means to gauge prostaglandin production and its potential impact on various biological functions. We report an efficient LC-MS method of four commonly analyzed prostaglandin urinary metabolites including tetranor-PGEM (derived from PGE 2 ), tetranor-PGDM, 11β-PGF 2α , and 2,3-dinor-11β-PGF 2α (derived from PGD 2 ). Each metabolite possesses distinct characteristics and clinical applications, collectively contributing to our understanding of prostaglandin-mediated pathways., (© 2025. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)