Action Of Prostaglandins Research Articles

Prostaglandins in the Inflamed Central Nervous System: Potential Therapeutic Targets.

The global burden of neurological disorders is evident, yet there remains limited efficacious therapeutics for their treatment. There is a growing recognition of the role of inflammation in diseases of the central nervous system (CNS); among the numerous inflammatory mediators involved, prostaglandins play a crucial role. Prostaglandins are small lipid mediators derived from arachidonic acid via multi-enzymatic pathways. The actions of prostaglandins are varied, with each prostaglandin having a specific role in maintaining homeostasis. In the CNS, prostaglandins can have neuroprotective or neurotoxic properties depending on their specific G-protein receptor. These G-protein receptors have varying subfamilies, tissue distribution, and signal transduction cascades. Further studies into the impact of prostaglandins in CNS-based diseases may contribute to the clarification of their actions, hopefully leading to the development of efficacious therapeutic strategies. This review focuses on the roles played by prostaglandins in neural degeneration, with a focus on Alzheimer's Disease, Multiple Sclerosis, and Amyotrophic Lateral Sclerosis in both preclinical and clinical settings. We further discuss current prostaglandin-related agonists and antagonists concerning suggestions for their use as future therapeutics.

Nanoemulsion of Ethanolic Extract of Centella asiatica (NanoSECA)Ameliorates Learning and Memory Performance by EnhancingCholinergic Activities, Increasing Antioxidative Levels, and AttenuatingOxidative Stress Markers in Adult Rats.

Centella asiatica (C. asiatica) has long been traditionally used as a memory enhancer. Nanoemulsion of ethanolic extract C. asiatica (NanoSECA) has been developed to improve brain functions. However, the effect of NanoSECA on enhancing memory and cognitive functions remains unexplored. This research aimed to investigate the potential of NanoSECA on cognitive tasks and memory enhancement pathways in a normal adult rat model. Thirty male Sprague Dawley rats (7-8 weeks old) were randomly subjected to five groups (n=six per group). Treatment groups were supplemented with NanoSECA and ethanolic extract of C. asiatica (SECA) for 28 days by oral gavages. Different brain sections were isolated, homogenized, and tested for acetylcholinesterase, antioxidants (glutathione and malondialdehyde), and anti-inflammatory agents (nitric oxide, tumour necrosis factor-α, and prostaglandin E2). NanoSECA supplementation markedly enhanced the acetylcholine, glutathione levels and reduced a distinct diminution in plasma activities of acetylcholinesterase, malondialdehyde, nitric oxide, prostaglandin E, and tumor necrosis factor-α levels. NanoSECA can be used as a memory enhancer through enhanced cholinergic activity, increased antioxidant level, and reduced oxidative stress.

Retraction: Interleukin-6 Synthesis in Human Chondrocytes Is Regulated via the Antagonistic Actions of Prostaglandin (PG)E2 and 15-deoxy-Δ12,14-PGJ2.

Retraction: Interleukin-6 Synthesis in Human Chondrocytes Is Regulated via the Antagonistic Actions of Prostaglandin (PG)E2 and 15-deoxy-Δ12,14-PGJ2.

PPARG is dispensable for bovine embryo development up to tubular stages†.

Following blastocyst hatching, ungulate embryos undergo a prolonged preimplantation period termed conceptus elongation. Conceptus elongation constitutes a highly susceptible period for embryonic loss, and the embryonic requirements during this process are largely unknown, but multiple lipid compounds have been identified in the fluid nourishing the elongating conceptuses. Peroxisome proliferator-activated receptors mediate the signaling actions of prostaglandins and other lipids, and, between them, PPARG has been pointed out to play a relevant role in conceptus elongation by a functional study that depleted PPARG in both uterus and conceptus. The objective of this study has been to determine if embryonic PPARG is required for bovine embryo development. To that aim, we have generated bovine PPARG knock-out embryos in vitro using two independent gene ablation strategies and assessed their developmental ability. In vitro development to Day 8 blastocyst was unaffected by PPARG ablation, as total, inner cell mass, and trophectoderm cell numbers were similar between wild-type and knock-out D8 embryos. In vitro post-hatching development to D12 was also comparable between different genotypes, as embryo diameter, epiblast cell number, embryonic disk formation, and hypoblast migration rates were unaffected by the ablation. The development of tubular stages equivalent to E14 was assessed in vivo, following a heterologous embryo transfer experiment, observing that the development of extra-embryonic membranes and of the embryonic disk was not altered by PPARG ablation. In conclusion, PPARG ablation did not impaired bovine embryo development up to tubular stages.

Cellular mechanism underlying leptin-induced anion secretion of rat epididymal epithelial cells.

A large number of studies have shown that leptin plays an important role in the regulation of fertility via the hypothalamus-pituitary-gonad axis. However, its peripheral function in epididymis was still elusive. The purpose of this study was to determine the pro-secretion effect of leptin on the rat epididymal epithelium. In the present study, real-time quantitative polymerase chain reaction, western blot, and immunohistochemical analysis were employed to detect the expression pattern of leptin receptors in rat epididymis. The pro-secretion effect of leptin on epididymal epithelial cells was measured by short-circuit current, and the prostaglandin E2 and cyclic adenosine monophosphate level was evaluated by enzyme-linked immunosorbent assay. We verified that the leptin receptor was located on the epididymal epithelium, with a relatively high expression level in corpus and cauda epididymis. Ussing chamber experiments showed that leptin stimulated a significant rise of the short-circuit current in rat epididymal epithelial cells, which could be abolished by the specific leptin receptor antagonist peptide Allo-aca, or by removing the ambient Cl- and HCO3 -. Furthermore, the leptin-stimulated short-circuit current response could be abrogated by blocking the apical cystic fibrosis transmembrane regulator or the basolateral Na+-K+-2Cl- cotransporter. Our pharmacological experiments manifested that interfering with the prostaglandin H synthase-2-prostaglandin E2-EP2/EP4-adenylate cyclase pathways could significantly blunt the cystic fibrosis transmembrane regulator-mediated anion secretion induced by leptin. The enzyme-linked immunosorbent assay demonstrated that leptin could induce a substantial increase in prostaglandin E2 release and cyclic adenosine monophosphate synthesis of primary cultured rat cauda epididymal epithelial cells. Our data also suggested that JAK2, ERK, and PI3K-dependent phosphorylation may be involved in the activation of prostaglandin H synthase-2 and the subsequent prostaglandin E2 production. The present study demonstrated the pro-secretion function of leptin in rat epididymal epithelium via the activation of cystic fibrosis transmembrane regulator and Na+-K+-2Cl- cotransporter, which was dependent on the paracrine/autocrine prostaglandin E2 stimulated EP2/EP4-adenylate cyclase pathways, and thus contributed to the formation of an appropriate microenvironment essential for sperm maturation.

Leptin signalling regulates transcriptional differences in granulosa cells from genetically obese mice but not the activation of NLRP3 inflammasome

Obesity is associated with increased ovarian inflammation and the establishment of leptin resistance. We presently investigated the role of impaired leptin signalling on transcriptional regulation in granulosa cells (GCs) collected from genetically obese mice. Furthermore, we characterised the association between ovarian leptin signalling, the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome and macrophage infiltration in obese mice. After phenotype characterisation, ovaries were collected from distinct group of animals for protein and mRNA expression analysis: (i) mice subjected to a diet-induced obesity (DIO) protocol, where one group was fed a high-fat diet (HFD) and another a standard chow diet (CD) for durations of 4 or 16 weeks; (ii) mice genetically deficient in the long isoform of the leptin receptor (ObRb; db/db); (iii) mice genetically deficient in leptin (ob/ob); and (iv) mice rendered pharmacologically hyperleptinemic (LEPT). Next, GCs from antral follicles isolated from db/db and ob/ob mice were subjected to transcriptome analysis. Transcriptional analysis revealed opposing profiles in genes associated with steroidogenesis and prostaglandin action between the genetic models, despite the similarities in body weight. Furthermore, we observed no changes in the mRNA and protein levels of NLRP3 inflammasome components in the ovaries of db/db mice or in markers of M1 and M2 macrophage infiltration. This contrasted with the downregulation of NLRP3 inflammasome components and M1 markers in ob/ob and 16-wk HFD-fed mice. We concluded that leptin signalling regulates NLRP3 inflammasome activation and the expression of M1 markers in the ovaries of obese mice in an ObRb-dependent and ObRb-independent manner. Furthermore, we found no changes in the expression of leptin signalling and NLRP3 inflammasome genes in GCs from db/db and ob/ob mice, which was associated with no effects on macrophage infiltration genes, despite the dysregulation of genes associated with steroidogenesis in homozygous obese db/db. Our results suggest that: (i) the crosstalk between leptin signalling, NLRP3 inflammasome and macrophage infiltration takes place in ovarian components other than the GC compartment; and (ii) transcriptional changes in GCs from homozygous obese ob/ob mice suggest structural rearrangement and organisation, whereas in db/db mice the impairment in steroidogenesis and secretory activity.

Elucidating miR-146a-3p as a key player in autophagy and lipid metabolism in Leishmania major infection

Autophagy is a key step involved in many unicellular eukaryotic diseases, including leishmaniasis, for cellular remodelling and differentiation during parasite's lifecycle. Lipids play a significant role in the infection process that begins with Leishmania major invading host cells. MicroRNAs (miRNAs), a family of small, 22–24 nucleotide noncoding regulatory RNAs, target mRNAs to modify gene expression and, subsequently, proteome output may have a regulatory role in altering the host cell processes. We observed miR-146a-3p expression increases in a time-dependent manner post Leishmania major infection. Transfecting miR-146a-3p mimic increases the expression of ATG7, an autophagy gene that encodes an E1-like enzyme in two ubiquitin-like conjugation systems required for autophagosome progression. HPGD (15-hydroxyprostaglandin dehydrogenase) operates as an enzyme, converting prostaglandin to its non-active form. Microarray data and western studies reveal that miR-146a-3p targets and inhibits HPGD, thereby increasing prostaglandin activity in lipid droplets. Herein, our research focuses on miR-146a-3p, which boosts ATG7 expression while reducing HPGD post Leishmania major infections helping us comprehend the intricate network of microRNA, autophagy, and lipid metabolism in leishmaniasis.

The influence of physical activity, body mass index and urinary levels of prostaglandin (PGF2α) with the incidence of primary dysmenorrhea in adolescents.

This study aims to investigate the effect of physical activity, body mass index (BMI), and levels of prostaglandins (PGF2α) urine on the occurrence of dysmenorrhea in adolescents. A total of 128 female students included in the study. The study was conducted from January to March 2023 using a cross-sectional design. This study utilized the Menstrual Symptom Questionnaire (MSQ) and gynecological examination with ultrasonography. The urinary prostaglandin (PGF2α) was measured using the enzyme linked immuno sorbent assay (ELISA). Data were analyzed using the chi-square test and logistic regression test. The age range of the participants included in the study was 14-17, with a mean age of 15.85 ± 0.65. There was an correlation between physical activity, BMI, and urinary prostaglandin (PGF2α) levels with the incidence of dysmenorrhea in adolescents (p < 0.001). In multivariate analysis, it revealed that underweight, and had a high urinary prostaglandin significant correlated to primary dysmenorrhea with odds ratio 4.78 (95% confidence interval [CI] 1.98-11.54) and 4.88 (95% CI 1.98-12.08), respectively. High physical activity and overweight was not associated with incidence of dysmenorrhea in adolescents. This study provides valuable insights into the correlation between physical activity, BMI, and levels of prostaglandins (PGF2α) in urine. A high level of urinary prostaglandin was found to be the most influential factor in the incidence of primary dysmenorrhea in adolescents. By addressing factors associated with dysmenorrhea in adolescents, healthcare professionals can potentially enhance well-being by reducing menstrual pain and encouraging a healthy lifestyle to prevent dysmenorrhea.

Abstract 12249: Activation of Prostaglandin E Receptor 4 Ameliorates Perivascular Inflammation and Pulmonary Hypertension in Rats

Introduction: Perivascular inflammation is involved in the progression of vascular remodeling and pulmonary arterial hypertension (PAH). Activation of prostaglandin E receptor 4 (EP 4 ) has recently been reported to reduce inflammation in ulcerative colitis and osteoarthritis, but there are no reports on perivascular inflammation in PAH. Hypothesis: EP 4 agonist ameliorate perivascular inflammation, vascular remodeling and pulmonary hypertension (PH). Methods and Results: We investigated the effects of EP 4 agonist (KAG-308) on hemodynamics and pulmonary artery remodeling in a monocrotaline (MCT)-exposed rat model of PH. Immunohistochemistry detected predominant expression of EP4 proteins in the macrophages and endothelial layer of pulmonary arteries in the lungs of normal and MCT-exposed rats. Compared to normal rats, MCT-exposed rats had increased nuclear factor kappa B (NFκB) activation and significantly higher interleukin 6 ( IL -6) mRNA levels (1.0±0.4 vs 62.3±39.7, p &lt; 0.05) in the lungs, and showed elevated right ventricular systolic pressure (RVSP; 29.7±1.8 vs 81.0±18.5 mmHg, p &lt; 0.0001), total pulmonary vascular resistance index (TPRI; 91.0±12.1 vs 161.4 ± 37.0 mmHg/mL/min/g, p &lt; 0.001) and RV hypertrophy (0.32±0.02 vs 0.57±0.10, p &lt; 0.0001), together with medial wall thickening and perivascular macrophage accumulation on day 21 after MCT injection. Oral administration of EP 4 agonist KAG-308 (1 mg/kg, twice daily, by gavage, day 0 to 21) significantly reduced NFκB activation and interleukin-6 mRNA levels (6.8 ± 2.5, p &lt; 0.05) in the lungs. Furthermore, KAG-308 prevented the elevated RVSP (53.1 ± 9.3 mmHg, p &lt; 0.01), TPRI (112.0 ± 16.6 mmHg/mL/min/g, p &lt; 0.05) and RV hypertrophy (0.47 ± 0.04, p &lt; 0.05) by inhibiting medical wall thickening and macrophage accumulation. Conclusion: EP 4 agonist ameliorated inflammation, vascular remodeling and PH in MCT-exposed rat. The EP 4 agonist KAG-308 is a potential therapeutic agent for the treatment of PAH.

Regulations of Tumor Microenvironment by Prostaglandins.

Prostaglandins, the bioactive lipids generated from the metabolism of arachidonic acid through cyclooxygenases, have potent effects on many constituents of tumor microenvironments. In this review, we will describe the formation and activities of prostaglandins in the context of the tumor microenvironment. We will discuss the regulation of cancer-associated fibroblasts and immune constituents by prostaglandins and their roles in immune escapes during tumor progression. The review concludes with future perspectives on improving the efficacy of immunotherapy through repurposing non-steroid anti-inflammatory drugs and other prostaglandin modulators.

AROMATERAPI BITTER ORANGE

Labor is a series of physiological and psychological processes that can cause labor pain, anxiety and fatigue. One of the non-pharmacological therapies to reduce labor pain is aromatherapy. Aromatherapy is a non-pharmacological therapy that uses pure essential oils. Aromatherapy Bitter Orange is a non-pharmacological therapy to reduce or relieve pain in mothers who give birth during the first period.Citrus Aurantium or better known as Bitter Orange (bitter orange) contains limonene, linalool, linalyl acetate, geranyl acetate, geraniol, nerol, and neryl acetate. This oil has a reactive, anti-septic, anti-spasmodic and mild sedative effect. Limonele found in bitter orange (Citrus Aurantium) oil controls cyclooxygenase I and II, prevents prostaglandin activity and reduces pain. Based on several studies, it can be concluded that bitter orange (Citrus Aurantium) aromatherapy can reduce labor pain during the 1st stage of the active phase.

Abstract 6333: Repurposing NSAIDs for chemo-immunotherapy: mechanisms beyond COX inhibition

Abstract It has been well-established that some nonsteroidal anti-inflammatory drugs (NSAIDs) have antitumor activities. The beneficial effects of these NSAIDs are mainly attributed to their ability to inhibit the production and activity of cyclooxygenases (COX1 and COX2) and prostaglandin (PGE2), which are known to promote tumor progression, angiogenesis, metastasis and immunosuppression. We recently reported that administration of indomethacin, a prototypical NSAID, can enhance the antitumor efficacy of adoptive T cell therapy in animal models. However, currently adoptive T cell therapy as a treatment option is only suitable for selected patients with certain types of cancer. Here, we set out to explore the utility of indomethacin in a chemo-immunotherapy setting that is readily applicable to a wide range of cancers. Cyclophosphamide (CTX) is a widely used antineoplastic chemotherapeutic agent with immunostimulatory activities when used at low-medium doses. We show that indomethacin had no impact on tumor growth but can significantly enhance the antitumor effect of CTX in multiple mouse tumor models. The beneficial effect of indomethacin was diminished in immunodeficient mice or CD8 T cell-depleted wild-type mice, indicating the requirement for the host immunity. Furthermore, the CTX and indomethacin regimen can sensitize tumors to anti-PD1 immunotherapy. scRNAseq analysis of tumor samples revealed the impact of indomethacin on the tumor microenvironment. Our data also indicate that the immunopotentiating effect of indomethacin can be independent of PGE2 inhibition, and involves the TRAIL-DR5 axis in promoting tumor regression. Other potential mechanisms, including modulation of chronic interferon signaling in tumor cells, have also been investigated. Altogether, our study sheds light on the multiple mechanisms underlying indomethacin’s beneficial effects, and highlights the potential of NSAID administration as a readily applicable and cost-effective approach to augment the efficacy of chemo-immunotherapy. Citation Format: Ogacheko D. Okoko, Md Y. Gazi, Xin Wang, Caitlin Brandle, Mercy Kehinde-Ige, Gary A. Piazza, Huidong Shi, Gang Zhou. Repurposing NSAIDs for chemo-immunotherapy: mechanisms beyond COX inhibition [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6333.

A pilot study to compare propranolol and misoprostol versus misoprostol and placebo for induction of labor in primigravidae; a randomized, single-blinded, placebo-controlled trial

BackgroundThe Induction of labor is the most common obstetric procedure in daily practice. Introducing propranolol as a new drug to augment the action of prostaglandins will help in the induction process and decrease CS rates. Several researchers have used propranolol in the augmentation of labor.AimThis pilot study compares propranolol and misoprostol versus misoprostol alone for labor induction in primigravids.MethodsThis is a Randomized clinical trial, single-blinded, placebo-controlled trial at Ain Shams University Maternity hospital. This study included 128 pregnant full-term primigravid women candidates for labor induction, randomized into two groups. All candidates underwent labor induction with 25 µg of vaginal misoprostol. Group I received 20 mg of oral propranolol tablets, while group II received sugary pills as a placebo. Candidates who responded successfully to induction were assessed for possible augmentation of labor by amniotomy or oxytocin infusion. The Primary outcome was induction to delivery interval, while the secondary outcomes were the duration of the latent phase, mode of delivery, and APGAR score of the neonate.ResultsThe induction-delivery time was (11.8 ± 8.1 h. vs. 12.6 ± 8.9 h., P value = 0.027) and the duration of the latent phase of labor (7.9 ± 5.6 h. vs. 9.2 ± 6.03 h., P value = 0.017) were significantly shorter in the group of misoprostol and propranolol compared to the group of misoprostol and placebo. There was no statistically significant difference between both groups’ mode of delivery, indications for cesarean section, misoprostol, and oxytocin doses, or neonatal outcome. (P value > 0.05).ConclusionPropranolol, when used with misoprostol for induction of labor, results in augmentation of action of misoprostol and a significantly shorter induction-delivery interval.Trial registrationWe retrospectively registered this trial in clinicaltrial.gov on 01/09/2020 (NCT04533841). https://clinicaltrials.gov/ct2/show/NCT04533841

Sex-differences in prostaglandin signaling: a semi-systematic review and characterization of PTGDS expression in human sensory neurons

There is increasing evidence of sex differences in underlying mechanisms causing pain in preclinical models, and in clinical populations. There are also important disconnects between clinical pain populations and the way preclinical pain studies are conducted. For instance, osteoarthritis pain more frequently affects women, but most preclinical studies have been conducted using males in animal models. The most widely used painkillers, nonsteroidal anti-inflammatory drugs (NSAIDs), act on the prostaglandin pathway by inhibiting cyclooxygenase (COX) enzymes. The purpose of this study was to analyze the preclinical and clinical literature on the role of prostaglandins and COX in inflammation and pain. We aimed to specifically identify studies that used both sexes and investigate whether any sex-differences in the action of prostaglandins and COX inhibition had been reported, either in clinical or preclinical studies. We conducted a PubMed search and identified 369 preclinical studies and 100 clinical studies that matched our inclusion/exclusion criteria. Our analysis shows that only 17% of preclinical studies on prostaglandins used both sexes and, out of those, only 19% analyzed or reported data separated by sex. In contrast, 79% of the clinical studies analyzed used both sexes. However, only 6% of those reported data separated by sex. Interestingly, 14 out of 15 preclinical studies and 5 out of 6 clinical studies that analyzed data separated by sex have identified sex-differences. This builds on the increasing evidence of sex-differences in prostaglandin signaling and the importance of sex as a biological variable in data analysis. The preclinical literature identifies a sex difference in prostaglandin D2 synthase (PTGDS) expression where it is higher in female than in male rodents in the nervous system. We experimentally validated that PTGDS expression is higher in female human dorsal root ganglia (DRG) neurons recovered from organ donors. Our semi-systematic literature review reveals a need for continued inclusivity of both male and female animals in prostaglandins studies and data analysis separated by sex in preclinical and clinical studies. Our finding of sex-differences in neuronal PTGDS expression in humans exemplifies the need for a more comprehensive understanding of how the prostaglandin system functions in the DRG in rodents and humans.

Expression and regulation of visfatin/NAMPT in the porcine corpus luteum during the estrous cycle and early pregnancy

Visfatin/NAMPT creates a hormonal link between energy metabolism and female reproduction. A recent study documented visfatin expression in the ovary and its action on follicular cells; however, the expression of visfatin in luteal cells is still unknown. The aim of this study, therefore, was to investigate the transcript and protein expression of visfatin as well as its immunolocalization in the corpus luteum (CL) and to examine the involvement of extracellular signal-regulated kinases (ERK1/2) in the regulation of visfatin level in response to LH, insulin, progesterone (P4), prostaglandin E2 (PGE2) and F2α (PGF2α). Corpora lutea were harvested from gilts on days 2–3, 10–12 and 14–16 of the estrous cycle and on days 10–11, 12–13, 15–16 and 27–28 of pregnancy. The current study demonstrated that visfatin expression depends on hormonal status related to the phase of the estrous cycle or early pregnancy. Visfatin was immunolocalized to the cytoplasm of small and large luteal cells. Moreover, visfatin protein abundance was increased by P4, and decreased by both prostaglandins, while LH and insulin have modulatory effects, depending on the phase of the cycle. Interestingly, LH, P4 and PGE2 effects were abolished in response to the inhibition of ERK1/2 kinase. Thus, this study demonstrated that expression of visfatin in the porcine CL is determined by the endocrine status related to the estrous cycle and early pregnancy and by the action of LH, insulin, P4 and prostaglandins via activation of the ERK1/2 pathway.

Prostaglandins limit nuclear actin to control nucleolar function during oogenesis.

Prostaglandins (PGs), locally acting lipid signals, regulate female reproduction, including oocyte development. However, the cellular mechanisms of PG action remain largely unknown. One cellular target of PG signaling is the nucleolus. Indeed, across organisms, loss of PGs results in misshapen nucleoli, and changes in nucleolar morphology are indicative of altered nucleolar function. A key role of the nucleolus is to transcribe ribosomal RNA (rRNA) to drive ribosomal biogenesis. Here we take advantage of the robust, in vivo system of Drosophila oogenesis to define the roles and downstream mechanisms whereby PGs regulate the nucleolus. We find that the altered nucleolar morphology due to PG loss is not due to reduced rRNA transcription. Instead, loss of PGs results in increased rRNA transcription and overall protein translation. PGs modulate these nucleolar functions by tightly regulating nuclear actin, which is enriched in the nucleolus. Specifically, we find that loss of PGs results in both increased nucleolar actin and changes in its form. Increasing nuclear actin, by either genetic loss of PG signaling or overexpression of nuclear targeted actin (NLS-actin), results in a round nucleolar morphology. Further, loss of PGs, overexpression of NLS-actin or loss of Exportin 6, all manipulations that increase nuclear actin levels, results in increased RNAPI-dependent transcription. Together these data reveal PGs carefully balance the level and forms of nuclear actin to control the level of nucleolar activity required for producing fertilization competent oocytes.

Role of the Midwife in Hemorrhage Management

Severe hemorrhage occurs in less than 1% of all pregnancies; however, it remains one of the important causes of maternal morbidity and mortality. Although the importance of hemorrhage has been recognized in obstetric circles for years, in the last decade or so, research has been conducted that has disproven long-held beliefs. Nurse-midwives must be knowledgeable about the etiology, management, and treatment of postpartum hemorrhage. This article presents an overview of postpartum hemorrhage and its pharmacologic and nurse-midwifery management. The overview includes definitions of postpartum hemorrhage, identifies risk factors for hemorrhage, and addresses problems associated with estimation of blood loss. The mechanisms of action of ergots, oxytocin, and prostaglandins are described, and criteria for selecting a medication are presented. Herbal remedies for hemorrhage are discussed briefly. Also discussed are the optimal time for drawing the hematocrit and what this laboratory value can tell the nurse-midwife.

Giving Warm Compresses with Progressive Muscle Relaxation Techniques Can Reduce Pain Intensity in Dysmenorrhea

Background: Dysmenorrhea is a menstrual disorder in the form of severe pain or tenderness in the lower abdomen caused by the activity of prostaglandins, during menstruation the damaged uterine lining is expelled by new compounds called prostaglandins. Intervention in adolescent girls who experience dysmenorrhea can be done by non-pharmacological techniques, namely by warm compresses and progressive muscle relaxation. Objectives: To determine the effectiveness of giving compressed warm with progressive muscle relaxation techniques to intense pain in dysmenorrhea. Methods: This study used a quasi-experimental with a pre-posttest approach, and a non-equivalent control group design. The research instrument used on the compress variable warm with progressive muscle relaxation techniques, namely SOP (Standard Operational Procedure) and pain intensity variable, namely using the NRS (Numeric Rating Scale). The population in this study found 95 female students, the samples were taken using purposive sampling, and samples in research this group collects 54 female students who are calculated using the formula slovin and drop out a formula. Results: Based on the results of statistical tests, namely the Mann Withney. Test obtained p-value 0.187&gt;0.05. Conclusion: In this study, there were no significant differences between the warm compress intervention and the technique of progressive muscle relaxation or both have an effect on a decrease in pain intensity in the incidences of dysmenorrhea.

Endometrial and luteal gene expression of putative gene regulators of the equine maternal recognition of pregnancy

Our understanding of the temporal changes in endometrial and luteal gene transcripts related to the actions of oxytocin and prostaglandin during early equine pregnancy is incomplete. Additionally, the role of oxytocinase, also known as Leucyl-cystinyl aminopeptidase (LNPEP), during early pregnancy in mares has not been previously investigated. Luteal and endometrial biopsies were obtained on Day (D)8, D10, D12 and D15 post-ovulation in pregnant (PREG) and diestrus (DIEST) mares for real-time qPCR. Differences in endometrial gene expression occurred over time in: SLC2A4, SLC2A1, PTGES, OXTR and LNPEP. PTGFR and PLA2G2C had lower relative abundance in PREG D15 endometrium compared to D10. OXT and OXTR were increased on D10 and 15 PREG, respectively. Regarding luteal mRNA relative abundance, ESR1, PTGS2, PTGFR, and PTGES had higher relative abundance in D12 of DIEST and PREG. Luteal expression of OXTR and OXT had higher relative abundance in D15 compared to D8, and LNPEP had higher relative abundance in D10 and 12. Endometrial and luteal PTGES had an increased mRNA abundance in both D12 DIEST and PREG mares, which may lead to additional luteoprotective prostaglandin E2 (PGE2) secretion. Furthermore, luteal SLC2A1 had higher relative abundance in pregnancy, and likely supports the high metabolic activity of luteal tissue by increasing glucose uptake. Oxytocinase is present in endometrial and luteal tissue and its role in oxytocin induced prostaglandin secretion is uncertain.

On the prospects for the use of undenatured type II collagen in the treatment of osteoarthritis and other joint diseases

Standardized extracts of undenatured type II collagen (UC-II) are used as alternative approaches to the treatment of osteoarthritis (OA). The effect of UC-II extracts is associated with the modulation of the mechanisms of innate and acquired immunity, a decrease in the activity of proinflammatory cytokines and prostaglandins. Epitopes of native collagen in the structure of UC-II contribute to a decrease in the activity of autoimmune reactions that stimulate cartilage degradation. Interacting with discoidin receptors, UC-II accelerates the reconstruction of cartilage connective tissue and inhibits the pro-inflammatory effects of endogenous collagens. Experimental and clinical studies confirm the effectiveness of the use of standardized substances UC-II for acceleration of cartilage regeneration and reduce pain in OA and subclinical joint dysfunction.