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The Journal of Sexual Medicine Apr 2021Female genital mutilation (FGM) can leave a lasting mark on the lives and minds of those affected. (Meta-Analysis)
Meta-Analysis
BACKGROUND
Female genital mutilation (FGM) can leave a lasting mark on the lives and minds of those affected.
AIM
To assess the consequences of FGM on women's sexual function in women who have undergone FGM compared to women who have not undergone FGM.
METHODS
A systematic review and meta-analysis were conducted from 3 databases; inclusion and exclusion criterions were determined. Studies included adult women having undergone FGM and presenting sexual disorders assessed by the Female Sexual Function Index (FSFI).
RESULTS
Of 129 studies, 5 that met the criteria were selected. The sexual function of mutilated women, based on the FSFI total score and its different domains, was compared to the sexual function of non-mutilated women. There was a significant decrease in the total FSFI scores of mutilated women compared to non-mutilated women. However, the results obtained for the different domains were not the same for all authors. The meta-analysis highlighted a high heterogeneity with inconsistency and true variance in effect size between-studies.
CONCLUSION
Analysis of studies showed that there is a significant decrease in the total FSFI score, indicating that FGM of any type may cause impaired sexual functioning. But a firm conclusion on this topic is not yet achievable because the results of this analysis do not allow to conclude a cause and effect relationship of FGM on sexual function. Nzinga A-M, De Andrade Castanheira S, Herklmann J, et al. Consequences of Female Genital Mutilation on Women's Sexual Health - Systematic Review and Meta-Analysis. J Sex Med 2021;18:750-760.
Topics: Adult; Circumcision, Female; Female; Humans; Sexual Behavior; Sexual Dysfunction, Physiological; Sexual Health; Women's Health
PubMed: 33618990
DOI: 10.1016/j.jsxm.2021.01.173 -
Neuroscience and Biobehavioral Reviews Jun 2021Olfactory impairment is a common clinical motif across neurodevelopmental disorders, suggesting olfactory circuits are particularly vulnerable to disease processes and... (Review)
Review
Olfactory impairment is a common clinical motif across neurodevelopmental disorders, suggesting olfactory circuits are particularly vulnerable to disease processes and can provide insight into underlying disease mechanisms. The mouse olfactory bulb is an ideal model system to study mechanisms of neurodevelopmental disease due to its anatomical accessibility, behavioral relevance, ease of measuring circuit input and output, and the feature of adult neurogenesis. Despite the clinical relevance and experimental benefits, olfactory testing across animal models of neurodevelopmental disease has been inconsistent and non-standardized. Here we performed a systematic literature review of olfactory function testing in mouse models of neurodevelopmental disorders, and identified intriguing inconsistencies that include evidence for both increased and decreased acuity in odor detection in various mouse models of Autism Spectrum Disorder (ASD). Based on our identified gaps in the literature, we recommend direct comparison of different mouse models of ASD using standardized tests for odor detection and discrimination. This review provides a framework to guide future olfactory function testing in mouse models of neurodevelopmental diseases.
Topics: Adult; Animals; Autism Spectrum Disorder; Humans; Mice; Neurogenesis; Olfaction Disorders; Olfactory Bulb; Smell
PubMed: 33610612
DOI: 10.1016/j.neubiorev.2021.02.024 -
Frontiers in Immunology 2020The Long Pentraxin 3 (PTX3) is a multifunctional glycoprotein released by peripheral blood leukocytes and myeloid dendritic cells in response to primary pro-inflammatory...
The Long Pentraxin 3 (PTX3) is a multifunctional glycoprotein released by peripheral blood leukocytes and myeloid dendritic cells in response to primary pro-inflammatory stimuli, that acts as a non-redundant component of the humoral arm of innate immunity. In addition to the primary role in the acute inflammatory response, PTX3 seems to be involved in other physiological and pathological processes. Indeed, PTX3 seems to play a pivotal role in the deposition and remodeling of bone matrix during the mineralization process, promoting osteoblasts differentiation and activity. Recently, PTX3 was seen to be involved in the ectopic calcifications' formation in breast cancer disease. In this regard, it has been observed that breast cancer tumors characterized by high expression of PTX3 and high amount of Breast Osteoblast Like Cells (BOLCs) showed several Hydroxyapatite (HA) microcalcifications, suggesting a likely role for PTX3 in differentiation and osteoblastic activity in both bone and extra-bone sites. Furthermore, given its involvement in bone metabolism, several studies agree with the definition of PTX3 as a molecule significantly involved in the pathogenesis of age-related bone diseases, such as osteoporosis, both in mice and humans. Recent results suggest that genetic and epigenetic mechanisms acting on gene are also involved in the progression of these diseases. Based on these evidences, the aim of our systemic review was to offer an overview of the variety of biological processes in which PTX3 is involved, focusing on bone mineralization, both in a physiological and pathological context.
Topics: Aging; Animals; C-Reactive Protein; Calcification, Physiologic; Humans; Mice; Nerve Tissue Proteins; Osteoporosis; Serum Amyloid P-Component
PubMed: 33584725
DOI: 10.3389/fimmu.2020.622772 -
Stem Cell Research & Therapy Feb 2021To repair bone defects, a variety of bone substitution materials have been used, such as ceramics, metals, natural and synthetic polymers, and combinations thereof. In... (Review)
Review
INTRODUCTION
To repair bone defects, a variety of bone substitution materials have been used, such as ceramics, metals, natural and synthetic polymers, and combinations thereof. In recent decades, a wide range of synthetic polymers have been used for bone regeneration. These polymers have the advantages of biocompatibility, biodegradability, good mechanical properties, low toxicity, and ease of processing. However, when used alone, they are unable to achieve ideal bone formation. Incorporating zinc (Zn) into synthetic polymers has been considered, as previous studies have shown that Zn promotes stem cell osteogenesis and mineral deposition. The purpose of this systematic review was to provide an overview of the application and effectiveness of Zn in synthetic polymers for bone regeneration, whether used alone or in combination with other biomaterials. This study was performed according to the PRISMA guidelines.
MATERIALS AND METHODS
A search of the PubMed, Embase, and the Cochrane Library databases for articles published up to June 2020 revealed 153 relevant studies. After screening the titles, abstracts, and full texts, 13 articles were included in the review; 9 of these were in vitro, 3 were in vivo, and 1 included both in vitro and in vivo experiments.
RESULTS
At low concentrations, Zn promoted cell proliferation and osteogenic differentiation, while high-dose Zn resulted in cytotoxicity and inhibition of osteogenic differentiation. Additionally, one study showed that Zn reduced apatite formation in simulated body fluid. In all of the in vivo experiments, Zn-containing materials enhanced bone formation.
CONCLUSIONS
At appropriate concentrations, Zn-doped synthetic polymer materials are better able to promote bone regeneration than materials without Zn.
Topics: Biocompatible Materials; Bone Regeneration; Osteogenesis; Polymers; Zinc
PubMed: 33579372
DOI: 10.1186/s13287-021-02195-y -
Fitoterapia Apr 2021Members of the botanical families Apiaceae/Umbelliferae, Asteraceae, Fabaceae/Leguminosae, and Thymelaeaceae are rich in coumarins and have traditionally been used as...
BACKGROUND
Members of the botanical families Apiaceae/Umbelliferae, Asteraceae, Fabaceae/Leguminosae, and Thymelaeaceae are rich in coumarins and have traditionally been used as ethnomedicines in many regions including Europe, Asia, and South America. Coumarins are a class of secondary metabolites that are widely present in plants, fungi, and bacteria and exhibit several pharmacological, biochemical, and therapeutic effects. Recently, many plants rich in coumarins and their derivatives were found to affect bone metabolism.
OBJECTIVE
To review scientific literature describing the mechanisms of action of coumarins in osteoclastogenesis and bone resorption.
MATERIALS AND METHODS
For this systematic review, the PubMed, Scopus, and Periodical Capes databases and portals were searched. We included in vitro research articles published between 2010 and 2020 that evaluated coumarins using osteoclastogenic markers.
RESULTS
Coumarins have been reported to downregulate RANKL-RANK signaling and various downstream signaling pathways required for osteoclast development, such as NF-κB, MAPK, Akt, and Ca signaling, as well as pathways downstream of the nuclear factor of activated T-cells (NFATc1), including tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), and matrix metalloproteinase 9 (MMP-9).
CONCLUSIONS
Coumarins primarily inhibit osteoclast differentiation and activation by modulating different intracellular signaling pathways; therefore, they could serve as potential candidates for controlled randomized clinical trials aimed at improving human bone health.
Topics: Animals; Bone Resorption; Cells, Cultured; Coumarins; Humans; Osteogenesis; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Signal Transduction
PubMed: 33556550
DOI: 10.1016/j.fitote.2021.104842 -
Drug Design, Development and Therapy 2021Caffeic acid is a metabolite of hydroxycinnamate and phenylpropanoid, which are commonly synthesized by all plant species. It is present in various food sources that are...
PURPOSE
Caffeic acid is a metabolite of hydroxycinnamate and phenylpropanoid, which are commonly synthesized by all plant species. It is present in various food sources that are known for their antioxidant properties. As an antioxidant, caffeic acid ameliorates reactive oxygen species, which have been reported to cause bone loss. Some studies have highlighted the effects of caffeic acid against bone resorption.
METHODS
A systematic review of the literature was conducted to identify relevant studies on the effects of caffeic acid on bone. A comprehensive search was conducted from July to November 2020 using PubMed, Scopus, Cochrane Library and Web of Science databases. Cellular, animal and human studies reporting the effects of caffeic acid, as a single compound, on bone cells or bone were considered.
RESULTS
The literature search found 226 articles on this topic, but only 24 articles met the inclusion criteria and were included in this review. The results showed that caffeic acid supplementation reduced osteoclastogenesis and bone resorption, possibly through its antioxidant potential and increased expression of osteoblast markers. However, some studies showed that caffeic acid did not affect bone resorption in ovariectomized rats and might impair bone mechanical properties in normal rats.
CONCLUSION
Caffeic acid potentially regulates the bone remodelling process by inhibiting osteoclastogenesis and bone resorption, as well as osteoblast apoptosis. Thus, it has medicinal values against bone diseases.
Topics: Animals; Bone Resorption; Bone and Bones; Caffeic Acids; Humans; Osteogenesis
PubMed: 33519191
DOI: 10.2147/DDDT.S287280 -
Medicine and Science in Sports and... Jun 2021This study aimed to analyze the effect of resistance training (RT) performed until volitional failure with low, moderate, and high loads on muscle hypertrophy and muscle... (Meta-Analysis)
Meta-Analysis
PURPOSE
This study aimed to analyze the effect of resistance training (RT) performed until volitional failure with low, moderate, and high loads on muscle hypertrophy and muscle strength in healthy adults and to assess the possible participant-, design-, and training-related covariates that may affect the adaptations.
METHODS
Using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, MEDLINE, CINAHL, EMBASE, SPORTDiscus, and Web of Science databases were searched. Including only studies that performed sets to volitional failure, the effects of low- (>15 repetitions maximum (RM)), moderate- (9-15 RM), and high-load (≤8 RM) RTs were examined in healthy adults. Network meta-analysis was undertaken to calculate the standardized mean difference (SMD) between RT loads in overall and subgroup analyses involving studies deemed of high quality. Associations between participant-, design-, and training-related covariates with SMD were assessed by univariate and multivariate network meta-regression analyses.
RESULTS
Twenty-eight studies involving 747 healthy adults were included. Although no differences in muscle hypertrophy between RT loads were found in overall (P = 0.113-0.469) or subgroup analysis (P = 0.871-0.995), greater effects were observed in untrained participants (P = 0.033) and participants with some training background who undertook more RT sessions (P = 0.031-0.045). Muscle strength improvement was superior for both high-load and moderate-load compared with low-load RT in overall and subgroup analysis (SMD, 0.60-0.63 and 0.34-0.35, respectively; P < 0.001-0.003), with a nonsignificant but superior effect for high compared with moderate load (SMD, 0.26-0.28, P = 0.068).
CONCLUSIONS
Although muscle hypertrophy improvements seem to be load independent, increases in muscle strength are superior in high-load RT programs. Untrained participants exhibit greater muscle hypertrophy, whereas undertaking more RT sessions provides superior gains in those with previous training experience.
Topics: Adult; Female; Humans; Male; Muscle Strength; Network Meta-Analysis; Resistance Training; Skeletal Muscle Enlargement
PubMed: 33433148
DOI: 10.1249/MSS.0000000000002585 -
Head and Neck Pathology Sep 2021Odontomas and ameloblastic fibro-odontomas (AFOs) are the result of a developmental anomaly of odontogenic tissues. A literature review of proteins immunoexpressed in...
Odontomas and ameloblastic fibro-odontomas (AFOs) are the result of a developmental anomaly of odontogenic tissues. A literature review of proteins immunoexpressed in odontomas and AFOs was conducted in order to determine which proteins are involved in the pathogenesis of these lesions. AFO was changed to early odontoma in the 2017 WHO classification and will also be discussed in this article. A literature search was performed in the following electronic databases: PubMed/MEDLINE, Web of Science, Scopus, EMBASE, Lilacs, Cochrane Collaboration Library, and Science Direct. The research question was developed according to the population, intervention, comparison, and outcome (PICO) framework: Which proteins are related to the differentiation of odontomas and what is their interrelationship with AFOs? Thirty articles met all inclusion criteria and were selected for this systematic review, totaling 355 cases of odontomas and 43 cases of AFO. Similar immunoexpression was observed in odontomas and AFOs. Immunoexpression of proteins involved in cell differentiation was higher in compound odontomas than in complex odontomas. Proteins involved in histodifferentiation and enamel formation were more frequent in odontomas. The immunoexpression of enamel matrix proteins differs between odontomas and tooth germs, with their persistence being related to the development of odontomas. Compound odontomas exhibit the highest immunoexpression of proteins involved in cellular histodifferentiation and the Wnt/beta-catenin pathway is involved in tumor formation.
Topics: Animals; Humans; Odontogenesis; Odontoma; Proteomics
PubMed: 33394370
DOI: 10.1007/s12105-020-01260-x -
Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth.The Cochrane Database of Systematic... Dec 2020Respiratory morbidity including respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Respiratory morbidity including respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and disability. Despite early evidence indicating a beneficial effect of antenatal corticosteroids on fetal lung maturation and widespread recommendations to use this treatment in women at risk of preterm delivery, some uncertainty remains about their effectiveness particularly with regard to their use in lower-resource settings, different gestational ages and high-risk obstetric groups such as women with hypertension or multiple pregnancies. This updated review (which supersedes an earlier review Crowley 1996) was first published in 2006 and subsequently updated in 2017.
OBJECTIVES
To assess the effects of administering a course of corticosteroids to women prior to anticipated preterm birth (before 37 weeks of pregnancy) on fetal and neonatal morbidity and mortality, maternal mortality and morbidity, and on the child in later life.
SEARCH METHODS
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (3 September 2020), ClinicalTrials.gov, the databases that contribute to the WHO International Clinical Trials Registry Platform (ICTRP) (3 September 2020), and reference lists of the retrieved studies.
SELECTION CRITERIA
We considered all randomised controlled comparisons of antenatal corticosteroid administration with placebo, or with no treatment, given to women with a singleton or multiple pregnancy, prior to anticipated preterm delivery (elective, or following rupture of membranes or spontaneous labour), regardless of other co-morbidity, for inclusion in this review.
DATA COLLECTION AND ANALYSIS
We used standard Cochrane Pregnancy and Childbirth methods for data collection and analysis. Two review authors independently assessed trials for inclusion, assessed risk of bias, evaluated trustworthiness based on predefined criteria developed by Cochrane Pregnancy and Childbirth, extracted data and checked them for accuracy, and assessed the certainty of the evidence using the GRADE approach. Primary outcomes included perinatal death, neonatal death, RDS, intraventricular haemorrhage (IVH), birthweight, developmental delay in childhood and maternal death.
MAIN RESULTS
We included 27 studies (11,272 randomised women and 11,925 neonates) from 20 countries. Ten trials (4422 randomised women) took place in lower- or middle-resource settings. We removed six trials from the analysis that were included in the previous version of the review; this review only includes trials that meet our pre-defined trustworthiness criteria. In 19 trials the women received a single course of steroids. In the remaining eight trials repeated courses may have been prescribed. Fifteen trials were judged to be at low risk of bias, two had a high risk of bias in two or more domains and we ten trials had a high risk of bias due to lack of blinding (placebo was not used in the control arm. Overall, the certainty of evidence was moderate to high, but it was downgraded for IVH due to indirectness; for developmental delay due to risk of bias and for maternal adverse outcomes (death, chorioamnionitis and endometritis) due to imprecision. Neonatal/child outcomes Antenatal corticosteroids reduce the risk of: - perinatal death (risk ratio (RR) 0.85, 95% confidence interval (CI) 0.77 to 0.93; 9833 infants; 14 studies; high-certainty evidence; 2.3% fewer, 95% CI 1.1% to 3.6% fewer), - neonatal death (RR 0.78, 95% CI 0.70 to 0.87; 10,609 infants; 22 studies; high-certainty evidence; 2.6% fewer, 95% CI 1.5% to 3.6% fewer), - respiratory distress syndrome (RR 0.71, 95% CI 0.65 to 0.78; 11,183 infants; studies = 26; high-certainty evidence; 4.3% fewer, 95% CI 3.2% to 5.2% fewer). Antenatal corticosteroids probably reduce the risk of IVH (RR 0.58, 95% CI 0.45 to 0.75; 8475 infants; 12 studies; moderate-certainty evidence; 1.4% fewer, 95% CI 0.8% to1.8% fewer), and probably have little to no effect on birthweight (mean difference (MD) -14.02 g, 95% CI -33.79 to 5.76; 9551 infants; 19 studies; high-certainty evidence). Antenatal corticosteroids probably lead to a reduction in developmental delay in childhood (RR 0.51, 95% CI 0.27 to 0.97; 600 children; 3 studies; moderate-certainty evidence; 3.8% fewer, 95% CI 0.2% to 5.7% fewer). Maternal outcomes Antenatal corticosteroids probably result in little to no difference in maternal death (RR 1.19, 95% CI 0.36 to 3.89; 6244 women; 6 studies; moderate-certainty evidence; 0.0% fewer, 95% CI 0.1% fewer to 0.5% more), chorioamnionitis (RR 0.86, 95% CI 0.69 to 1.08; 8374 women; 15 studies; moderate-certainty evidence; 0.5% fewer, 95% CI 1.1% fewer to 0.3% more), and endometritis (RR 1.14, 95% CI 0.82 to 1.58; 6764 women; 10 studies; moderate-certainty; 0.3% more, 95% CI 0.3% fewer to 1.1% more) The wide 95% CIs in all of these outcomes include possible benefit and possible harm.
AUTHORS' CONCLUSIONS
Evidence from this updated review supports the continued use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk of preterm birth. Treatment with antenatal corticosteroids reduces the risk of perinatal death, neonatal death and RDS and probably reduces the risk of IVH. This evidence is robust, regardless of resource setting (high, middle or low). Further research should focus on variations in the treatment regimen, effectiveness of the intervention in specific understudied subgroups such as multiple pregnancies and other high-risk obstetric groups, and the risks and benefits in the very early or very late preterm periods. Additionally, outcomes from existing trials with follow-up into childhood and adulthood are needed in order to investigate any longer-term effects of antenatal corticosteroids. We encourage authors of previous studies to provide further information which may answer any remaining questions about the use of antenatal corticosteroids without the need for further randomised controlled trials. Individual patient data meta-analyses from published trials are likely to provide answers for most of the remaining clinical uncertainties.
Topics: Adrenal Cortex Hormones; Betamethasone; Bias; Cerebral Intraventricular Hemorrhage; Developmental Disabilities; Dexamethasone; Female; Fetal Organ Maturity; Humans; Hydrocortisone; Infant, Newborn; Lung; Maternal Death; Perinatal Death; Pregnancy; Premature Birth; Prenatal Care; Randomized Controlled Trials as Topic; Respiratory Distress Syndrome, Newborn
PubMed: 33368142
DOI: 10.1002/14651858.CD004454.pub4 -
Cells Nov 2020Cardiovascular calcification is highly prevalent and associated with increased morbidity in chronic kidney disease (CKD). This review examines the impact of uremic...
Cardiovascular calcification is highly prevalent and associated with increased morbidity in chronic kidney disease (CKD). This review examines the impact of uremic toxins, which accumulate in CKD due to a failing kidney function, on cardiovascular calcification. A systematic literature search identified 41 uremic toxins that have been studied in relation to cardiovascular calcification. For 29 substances, a potentially causal role in cardiovascular calcification was addressed in in vitro or animal studies. A calcification-inducing effect was revealed for 16 substances, whereas for three uremic toxins, namely the guanidino compounds asymmetric and symmetric dimethylarginine, as well as guanidinosuccinic acid, a calcification inhibitory effect was identified in vitro. At a mechanistic level, effects of uremic toxins on calcification could be linked to the induction of inflammation or oxidative stress, smooth muscle cell osteogenic transdifferentiation and/or apoptosis, or alkaline phosphatase activity. For all middle molecular weight and protein-bound uremic toxins that were found to affect cardiovascular calcification, an increasing effect on calcification was revealed, supporting the need to focus on an increased removal efficiency of these uremic toxin classes in dialysis. In conclusion, of all uremic toxins studied with respect to calcification regulatory effects to date, more uremic toxins promote rather than reduce cardiovascular calcification processes. Additionally, it highlights that only a relatively small part of uremic toxins has been screened for effects on calcification, supporting further investigation of uremic toxins, as well as of associated post-translational modifications, on cardiovascular calcification processes.
Topics: Alkaline Phosphatase; Animals; Apoptosis; Calcinosis; Cardiomyopathies; Humans; Inflammation; Molecular Weight; Osteogenesis; Oxidative Stress; Renal Insufficiency, Chronic; Signal Transduction; Toxins, Biological; Uremia
PubMed: 33172085
DOI: 10.3390/cells9112428