scholarly journals Modern Myoma Treatment in the Last 20 Years: A Review of the Literature

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Ahmed El-Balat ◽  
Rudy Leon DeWilde ◽  
Iryna Schmeil ◽  
Morva Tahmasbi-Rad ◽  
Sandra Bogdanyova ◽  
...  

Myomas, also known as fibroids, are a specific characteristic of the human species. No other primates develop fibroids. At a cellular level, myomas are benign hyperplastic lesions of uterine smooth muscle cells. There are interesting theoretical concepts that link the development of myomas in humans with the highly specific process of childbirth from an upright position and the resulting need for greatly increased “expulsive” forces during labor. Myomas might be the price our species pays for our bipedal and highly intelligent existence. Myomas affect, with some variability, all ethnic groups and approximately 50% of all women during their lifetime. While some remain asymptomatic, myomas can cause significant and sometimes life-threatening uterine bleeding, pain, infertility, and, in extreme cases, ureteral obstruction and death. Traditionally, over 50% of all hysterectomies were performed for fibroids, leading to a significant healthcare burden. In this article, we review the developments of the past 20 years with regard to multiple new treatment strategies that have evolved during this time.

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5227
Author(s):  
Annarita Del Gatto ◽  
Michele Saviano ◽  
Laura Zaccaro

Multiple sclerosis (MS) belongs to demyelinating diseases, which are progressive and highly debilitating pathologies that imply a high burden both on individual patients and on society. Currently, several treatment strategies differ in the route of administration, adverse events, and possible risks. Side effects associated with multiple sclerosis medications range from mild symptoms, such as flu-like or irritation at the injection site, to serious ones, such as progressive multifocal leukoencephalopathy and other life-threatening events. Moreover, the agents so far available have proved incapable of fully preventing disease progression, mostly during the phases that consist of continuous, accumulating disability. Thus, new treatment strategies, able to halt or even reverse disease progression and specific for targeting solely the pathways that contribute to the disease pathogenesis, are highly desirable. Here, we provide an overview of the recent literature about peptide-based systems tested on experimental autoimmune encephalitis (EAE) models. Since peptides are considered a unique therapeutic niche and important elements in the pharmaceutical landscape, they could open up new therapeutic opportunities for the treatment of MS.


2019 ◽  
Vol 14 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Yingjuan Li ◽  
Guangchun Dai ◽  
Liu Shi ◽  
Yucheng Lin ◽  
Minhao Chen ◽  
...  

Aging is a key dangerous factor for the occurrence and severity of tendon injury, but the exact cognition of the relationship is elusive at present. More previous studies suggest age-related changes occur at tendon mechanical properties, structure and composition, but the pathological alternations may be overlooked, which might be a cause for the structure and function variations, and even speed up the progress of age-related disorders. Recently, the presence of tendon stem/progenitor cells (TSPCs) would provide new insights for the pathogenesis of tendon aging. In this review, the tendon mechanical properties, structure and composition are presented in brief, then, the pathological changes of the aging tendon are described firstly, and the latest researches on alterations of TSPCs in the pathogenesis of tendon aging have also been analyzed. At a cellular level, the hypothetical model of altered TSPCs fate for tendon aging is also proposed. Moreover, the regulation of TSPCs as a potential way of the therapies for age-related tendon diseases is discussed. Therefore, reversing the impaired function of TSPCs and promoting the tenogenic differentiation of TSPCs could become hot spots for further study and give the opportunity to establish new treatment strategies for age-related tendon injuries.


Author(s):  
Thomas Gasser

Over the past few years, genetic findings have changed our views on the molecular pathogenesis of Parkinson disease (PD), as mutations in a growing number of genes have been found to cause monogenic forms of the disorder. These mutations cause neuronal dysfunction and neurodegeneration either by a toxic gain of function, as in the case of the dominant forms of monogenic PD caused by mutations in the genes for α-synuclein or LRRK2, or by a loss of an intrinsic protective function, as is likely for the recessive PD genes parkin (PRKN), PINK1 and DJ-1. Evidence is emerging that at least some of the pathways uncovered in the rare monogenic forms of PD may play a direct role in the aetiology of the common sporadic disorder and that variants of the respective genes contribute to the risk of developing the disease. These findings will allow the search for new treatment strategies that focus on the underlying molecular pathophysiology, rather than simply on ameliorating symptoms.


Blood ◽  
2008 ◽  
Vol 111 (5) ◽  
pp. 2503-2503
Author(s):  
Irene M. Ghobrial ◽  
Kenneth C. Anderson

For the past several decades, multiple myeloma (MM), the second most common hematologic malignancy, has been considered a fatal disease with a median survival of 5 years. However, recent advances in the understanding of the molecular pathogenesis of MM have led to new treatment strategies.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 240 ◽  
Author(s):  
Luis Sifuentes-Dominguez ◽  
Ashish S. Patel

Ulcerative colitis (UC) is a relapsing and remitting disease with significant phenotypic and genotypic variability. Though more common in adults, UC is being increasingly diagnosed in childhood. The subsequent lifelong course of disease results in challenges for the patient and physician. Currently, there is no medical cure for UC. Even though surgical removal of the colon can be curative, complications including infertility in females make colectomy an option often considered only when the disease presents with life-threatening complications or when medical management fails. One of the greatest challenges the clinician faces in the care of patients with UC is the inability to predict at diagnosis which patient is going to respond to a specific therapy or will eventually require surgery. This therapeutic conundrum frames the discussion to follow, specifically the concept of individualized or personalized treatment strategies based on genetic risk factors. As we move to therapeutics, we will elucidate traditional approaches and discuss known and novel agents. As we look to the future, we can expect increasing integrated approaches using several scientific disciplines to inform how genetic interactions shape and mold the pathogenesis and therapeutics of UC.


Pathogens ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 52 ◽  
Author(s):  
Patricia Otieno-Odhiambo ◽  
Sean Wasserman ◽  
J. Claire Hoving

Pneumocystis is a ubiquitous atypical fungus that is distributed globally. The genus comprises morphologically similar but genetically heterogeneous species that have co-evolved with specific mammalian hosts as obligate intra-pulmonary pathogens. In humans, Pneumocystis jirovecii is the causative organism of Pneumocystis pneumonia (PCP) in immunocompromised individuals, a serious illness frequently leading to life-threatening respiratory failure. Initially observed in acquired immunodeficiency syndrome (AIDS) patients, PCP is increasingly observed in immunocompromised non-AIDS patients. The evolving epidemiology and persistently poor outcomes of this common infection will require new strategies for diagnosis and treatment. A deeper understanding of host immune responses and of the cells that mediate them will improve the chance of developing new treatment strategies. This brief review provides an update on recent studies on the role of host immunity against Pneumocystis.


2006 ◽  
Vol 20 (11) ◽  
pp. 735-739 ◽  
Author(s):  
Marc Bilodeau ◽  
Daniel Lamarre

Treatment of hepatitis C virus infection is currently based on a combination of pegylated interferon and ribavirin. Because efficacy of this therapy remains suboptimal and side effects sometimes problematic, major efforts have been put forward by scientists and the pharmaceutical industry to develop alternative treatments for this chronic infection. Over the past few years, clinical studies performed with some of these new agents have been presented at major international meetings. The present paper aims to review the rationale underlying the development of these new forms of treatment as well as the current available data concerning their clinical efficacy.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 72 ◽  
Author(s):  
Michael S. Kapiloff ◽  
Craig A. Emter

The prevalence of heart failure is expected to increase almost 50% in the next 15 years because of aging of the general population, an increased frequency of comorbidities, and an improved survival following cardiac events. Conventional treatments for heart failure have remained largely static over the past 20 years, illustrating the pressing need for the discovery of novel therapeutic agents for this patient population. Given the heterogeneous nature of heart failure, it is important to specifically define the cellular mechanisms in the heart that drive the patient’s symptoms, particularly when considering new treatment strategies. This report highlights the latest research efforts, as well as the possible pitfalls, in cardiac disease translational research and discusses future questions and considerations needed to advance the development of new heart failure therapies. In particular, we discuss cardiac remodeling and the translation of animal work to humans and how advancements in our understanding of these concepts relative to disease are central to new discoveries that can improve cardiovascular health.


2020 ◽  
Author(s):  
T. Prescott Atkinson ◽  
William M. Geisler ◽  
Ken B. Waites

The class Mollicutes includes organisms in the genera Mycoplasma and Ureaplasma. They are prokaryotes that lack a cell wall, and are among the smallest known living organisms in both cellular dimensions and genome sizes. At least 17 different species inhabit the mucosae of the respiratory and urogenital tracts of humans, several of which are pathogenic in a variety of clinical illnesses. Their fastidious nature and often slow growth in vitro have hampered understanding of their roles as agents of human disease. Mycoplasma pneumoniae is an important cause of community acquired respiratory infections that occur endemically and epidemically worldwide in persons of all ages and ranges in severity from mild to life-threatening. Molecular-based laboratory techniques have resulted in increased understanding of the pathogenesis and epidemiology M. pneumoniae infections as well as improved means for laboratory detection. Resistance of M. pneumoniae to macrolide antimicrobials has emerged worldwide over the past several years, complicating treatment strategies. This review contains 2 figures, 1 table and 58 references Key Words: Antimicrobial Resistance, Ciliated respiratory epithelium, Community Acquired Pneumonia, Cytadherence, Mycoplasma pneumoniae, Reinfections


2020 ◽  
Vol 40 (02) ◽  
pp. 192-200
Author(s):  
J. Nicholas Brenton ◽  
Ryan Kammeyer ◽  
Lauren Gluck ◽  
Teri Schreiner ◽  
Naila Makhani

AbstractMultiple sclerosis is being increasingly recognized and diagnosed in children. In the past several years, advances have been made in diagnosing multiple sclerosis in children, identifying new genetic and environmental risk factors, delineating underlying immunobiology, characterizing imaging findings, and implementing new treatment strategies. In this review, we discuss these advances. Future research into the determinants of multiple sclerosis in children and into new treatment options will be aided by continued international collaboration.


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