Journal articles on the topic 'ASM dysfunction'
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1
Khan, Shah Dupesh, and N. Pandiyan. "Ejaculatory Dysfunction—A Mini Review." Advances in Sexual Medicine 05, no. 02 (2015): 39–42. http://dx.doi.org/10.4236/asm.2015.52005.
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El-Tahlawi, Samar, Noha Ezzat Mohammad, Asmaa Younes Elsary, Noha Mohamed Yousef, and Talal Abdelreheem. "Female Sexual Dysfunction in Elfayoum Governorate." Advances in Sexual Medicine 08, no. 01 (2018): 1–13. http://dx.doi.org/10.4236/asm.2018.81001.
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Jesudason, E. C., N. P. Smith, M. G. Connell, D. G. Spiller, M. R. H. White, D. G. Fernig, and P. D. Losty. "Peristalsis of airway smooth muscle is developmentally regulated and uncoupled from hypoplastic lung growth." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L559—L565. http://dx.doi.org/10.1152/ajplung.00498.2005.
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Prenatal airway smooth muscle (ASM) peristalsis appears coupled to lung growth. Moreover, ASM progenitors produce fibroblast growth factor-10 (FGF-10) for lung morphogenesis. Congenital diaphragmatic hernia (CDH) is associated with lung hypoplasia, FGF-10 deficiency, and postnatal ASM dysfunction. We hypothesized ASM dysfunction emerges in tandem with, and may contribute toward, the primordial lung hypoplasia that precedes experimental CDH. Spatial origin and frequency of ASM peristaltic waves were measured in normal and hypoplastic rat lungs cultured from day 13.5 of gestation (lung hypoplasia was generated by nitrofen dosing of pregnant dams). Longitudinal lung growth was assayed by bud counts and tracing photomicrographs of cultures. Coupling of lung growth and peristalsis was tested by stimulation studies using serum, FGF-10, or nicotine and inhibition studies with nifedipine or U0126 (MEK1/2 inhibitor). In normal lung, ASM peristalsis is developmentally regulated: proximal ASM becomes quiescent (while retaining capacity for cholinergic-stimulated peristalsis). However, in hypoplastic lung, spontaneous proximal ASM activity persists. FGF-10 corrects this aberrant ASM activity in tandem with improved growth. Stimulation and inhibition studies showed that, unlike normal lung, changes in growth or peristalsis are not consistently accompanied by parallel modulation of the other. ASM peristalsis undergoes FGF-10-regulated spatiotemporal development coupled to lung growth: this process is disrupted early in lung hypoplasia. ASM dysfunction emerges in tandem with and may therefore contribute toward lung hypoplasia in CDH.
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Alidu, Huseini, W. K. B. A. Owiredu, Nafiu Amidu, Peter Paul Mwinsanga Dapare, Ahmed Tijani Bawah, Christian Kofi Gyasi-Sarpong, and Christian Obirikorang. "The Metabolic Syndrome and Sexual Dysfunction in a State of Inflammation." Advances in Sexual Medicine 07, no. 02 (2017): 82–96. http://dx.doi.org/10.4236/asm.2017.72006.
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Dumbraveanu, Ion, Iurie Arian, Andrei Munteanu, Daniela Catereniuc, and Adrian Tanase. "Erectile Dysfunction in Male with Glans Penis Apocrine Hydrocystoma: Organic or Psychogenic?" Advances in Sexual Medicine 07, no. 03 (2017): 131–38. http://dx.doi.org/10.4236/asm.2017.73010.
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Eyada, Moustafa M. K., Alaa-Aldin S. Abd-Elhamid, Riham A. F. Elboghdady, Ahmed M. Gadallah, and Mohamed Azab. "Assessment of Female Sexual Dysfunction in Patients with Premenopausal Female Pattern Hair Loss." Advances in Sexual Medicine 10, no. 03 (2020): 86–103. http://dx.doi.org/10.4236/asm.2020.103006.
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Keeler, Allison M., Donghai Liu, Marina Zieger, Lang Xiong, Jeffrey Salemi, Karl Bellvé, Barry J. Byrne, David D. Fuller, Ronghua ZhuGe, and Mai K. ElMallah. "Airway smooth muscle dysfunction in Pompe (Gaa−/−) mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 6 (June 1, 2017): L873—L881. http://dx.doi.org/10.1152/ajplung.00568.2016.
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Pompe disease is an autosomal recessive disorder caused by a deficiency of acid α-glucosidase (GAA), an enzyme responsible for hydrolyzing lysosomal glycogen. Deficiency of GAA leads to systemic glycogen accumulation in the lysosomes of skeletal muscle, motor neurons, and smooth muscle. Skeletal muscle and motor neuron pathology are known to contribute to respiratory insufficiency in Pompe disease, but the role of airway pathology has not been evaluated. Here we propose that GAA enzyme deficiency disrupts the function of the trachea and bronchi and this lower airway pathology contributes to respiratory insufficiency in Pompe disease. Using an established mouse model of Pompe disease, the Gaa−/− mouse, we compared histology, pulmonary mechanics, airway smooth muscle (ASM) function, and calcium signaling between Gaa−/− and age-matched wild-type (WT) mice. Lysosomal glycogen accumulation was observed in the smooth muscle of both the bronchi and the trachea in Gaa−/− but not WT mice. Furthermore, Gaa−/− mice had hyporesponsive airway resistance and bronchial ring contraction to the bronchoconstrictive agents methacholine (MCh) and potassium chloride (KCl) and to a bronchodilator (albuterol). Finally, calcium signaling during bronchiolar smooth muscle contraction was impaired in Gaa−/− mice indicating impaired extracellular calcium influx. We conclude that GAA enzyme deficiency leads to glycogen accumulation in the trachea and bronchi and impairs the ability of lower ASM to regulate calcium and respond appropriately to bronchodilator or constrictors. Accordingly, ASM dysfunction may contribute to respiratory impairments in Pompe disease.
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Rodríguez-Sureda, Víctor, Francesca Crovetto, Stefania Triunfo, Olga Sánchez, Fátima Crispi, Elisa Llurba, Eduard Gratacós, Francesc Figueras, and Carmen Domínguez. "Increased secretory sphingomyelinase activity in the first trimester of pregnancy in women later developing preeclampsia: a nested case-control study." Biological Chemistry 397, no. 3 (March 1, 2016): 269–79. http://dx.doi.org/10.1515/hsz-2015-0266.
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Abstract The pathogenic basis of abnormal placentation and dysfunction in preeclampsia (PE) is highly complex and incompletely understood. Secretory sphyngomyelinase activity (S-ASM) was analyzed in plasma samples from 158 pregnant women developing PE and 112 healthy pregnant controls. Serum PlGF, sFlt-1, s-Endoglin and sVCAM were measured. Results showed S-ASM activity to be higher in women who later developed PE than in those with uncomplicated pregnancies (40.6% and 28.8% higher in the late- and early-onset groups, respectively). Plasma S-ASM activity correlated significantly with circulating markers of endothelial damage in the late-PE group (endoglin and sVCAM-1), with plasma cholesterol and total lipid levels. However, these significant associations were not observed in the early-PE or control groups. This work provides the first evidence of significantly elevated circulating S-ASM activity in the first trimester of pregnancy in women who go on to develop PE; thus, it may be deduced that the circulating form of ASM is biologically active in PE and could contribute to promoting endothelial dysfunction and cardiovascular programming. Plasma S-ASM measurement may have clinical relevance as a further potential biomarker contributing to the earliest identification of women at risk of developing preeclampsia.
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Nkumu, Matthieu Marc Loposso, Christian Kane Kapinga, Mafuta Tsita Alpha, Dieu Donné Moningo Molamba, Nkodila Aliosha, Augustin Punga Maole Monga-Lembe, Jean Paul Esika Mokumo, Diangienda Nkutima Pablo, Mujinga Lukusa Elisabeth, and Dirk De Ridder. "A Cross-Sectional Study According to Risk Factors Associated with Erectile Dysfunction in Men." Advances in Sexual Medicine 10, no. 03 (2020): 104–18. http://dx.doi.org/10.4236/asm.2020.103007.
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Bao, Jun-Xiang, Min Xia, Justin L. Poklis, Wei-Qing Han, Christopher Brimson, and Pin-Lan Li. "Triggering role of acid sphingomyelinase in endothelial lysosome-membrane fusion and dysfunction in coronary arteries." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 3 (March 2010): H992—H1002. http://dx.doi.org/10.1152/ajpheart.00958.2009.
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The present study determined whether activation of acid sphingomyelinase (ASM) drives membrane proximal lysosomes to fuse to the cell surface, facilitating membrane lipid rafts (LRs) clustering in coronary arterial endothelial cells (CAECs) and leading to endothelial dysfunction. By confocal microscopy, the activators of ASM, phosphatidylinositol (PI), and bis (monoacylglyceryl) phosphate (Bis), and an inducer of ASM, butyrate, were found to increase LRs clustering in bovine CAECs, which was blocked by lysosome fusion inhibitor vacuolin-1. However, arsenic trioxide (Ars), an inducer of de novo synthesis of ceramide, had no such effect. Similarly, vacuolin-1-blockable effects were observed using fluorescence resonance energy transfer detection. Liquid chromatography-electrospray ionization-tandem mass spectrometry analysis demonstrated that all of these treatments, even Ars, increased ceramide production in CAECs. When ASM gene was silenced, all treatments except Ars no longer increased ceramide levels. Furthermore, dynamic fluorescence monitoring in live cells showed that PI and Bis stimulated lysosome-membrane fusion in CAECs. Functionally, PI and Bis impaired endothelium-dependent vasodilation in perfused coronary arteries, which was blocked by vacuolin-1 and a lysosome function inhibitor, bafilomycine. FasL (Fas ligand), a previously confirmed lysosome fusion stimulator as a comparison, also produced a similar effect. It is concluded that ASM activation serves as a triggering mechanism and driving force, leading to fusion of membrane proximal lysosomes into LR clusters on the cell membrane of CAECs, which represents a novel mechanism mediating endothelial dysfunction during death receptor activation or other pathological situation.
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Kambou, Timothée, Cyprien Zaré, Abdoul Karim Paré, Adama Ouattara, Youombèviel Ludovic Somé, and Bakary Gustave Sanon. "Erectile Dysfunction among Diabetic Men in Two Medical Centers in Burkina Faso: Epidemiological, Diagnosis and Therapeutic Aspects." Advances in Sexual Medicine 04, no. 01 (2014): 1–5. http://dx.doi.org/10.4236/asm.2014.41001.
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Lee, Jong Kil, Hee Kyung Jin, Min Hee Park, Bo-ra Kim, Phil Hyu Lee, Hiromitsu Nakauchi, Janet E. Carter, Xingxuan He, Edward H. Schuchman, and Jae-sung Bae. "Acid sphingomyelinase modulates the autophagic process by controlling lysosomal biogenesis in Alzheimer’s disease." Journal of Experimental Medicine 211, no. 8 (July 21, 2014): 1551–70. http://dx.doi.org/10.1084/jem.20132451.
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In Alzheimer’s disease (AD), abnormal sphingolipid metabolism has been reported, although the pathogenic consequences of these changes have not been fully characterized. We show that acid sphingomyelinase (ASM) is increased in fibroblasts, brain, and/or plasma from patients with AD and in AD mice, leading to defective autophagic degradation due to lysosomal depletion. Partial genetic inhibition of ASM (ASM+/−) in a mouse model of familial AD (FAD; amyloid precursor protein [APP]/presenilin 1 [PS1]) ameliorated the autophagocytic defect by restoring lysosomal biogenesis, resulting in improved AD clinical and pathological findings, including reduction of amyloid-β (Aβ) deposition and improvement of memory impairment. Similar effects were noted after pharmacologic restoration of ASM to the normal range in APP/PS1 mice. Autophagic dysfunction in neurons derived from FAD patient induced pluripotent stem cells (iPSCs) was restored by partial ASM inhibition. Overall, these results reveal a novel mechanism of ASM pathogenesis in AD that leads to defective autophagy due to impaired lysosomal biogenesis and suggests that partial ASM inhibition is a potential new therapeutic intervention for the disease.
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Jurado, Ana Rosa, Mirian Jouda-Benazouz, Loreto Mendoza-Huertas, and Nicolás Mendoza. "The Use of Natural Products for the Treatment of Female Sexual Dysfunction: A Systematic Review of Randomized Clinical Trials." Advances in Sexual Medicine 10, no. 02 (2020): 56–69. http://dx.doi.org/10.4236/asm.2020.102004.
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Jang, Joyce Hojin, Alice Panariti, Michael J. O’Sullivan, Melissa Pyrch, Chris Wong, Anne-Marie Lauzon, and James G. Martin. "Characterization of cystic fibrosis airway smooth muscle cell proliferative and contractile activities." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 5 (November 1, 2019): L690—L701. http://dx.doi.org/10.1152/ajplung.00090.2019.
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Cystic fibrosis (CF) is a genetic disease that causes multiple airway abnormalities. Two major respiratory consequences of CF are airway hyperresponsiveness (AHR) and airway remodeling. Airway smooth muscle (ASM) is hypothesized to be responsible for the airway dysfunction, since their thickening is involved in remodeling, and excessive contraction by the ASM may cause AHR. It is unclear whether the ASM is intrinsically altered to favor increased contractility or proliferation or if microenvironmental influences induce pathological behavior in vivo. In this study, we examined the contractile and proliferative properties of ASM cells isolated from healthy donor and CF transplant lungs. Assays of proliferation showed that CF ASM proliferates at a higher rate than healthy cells. Through calcium analysis, no differences in contractile activation in response to histamine were found. However, CF ASM cells lagged in their reuptake of calcium in the sarcoplasmic reticulum. The combination CFTR corrector and potentiator, VX-809/770, used to restore CFTR function in CF ASM, resulted in a reduction in proliferation and in a normalization of calcium reuptake kinetics. These results show that impaired CFTR function in ASM cells causes intrinsic changes in their proliferative and contractile properties.
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Ikegami, Machiko, Rajwinder Dhami, and Edward H. Schuchman. "Alveolar lipoproteinosis in an acid sphingomyelinase-deficient mouse model of Niemann-Pick disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 3 (March 1, 2003): L518—L525. http://dx.doi.org/10.1152/ajplung.00258.2002.
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Types A and B Niemann-Pick disease (NPD) are lipid storage disorders caused by the deficient activity of acid sphingomyelinase (ASM). In humans, NPD is associated with the dysfunction of numerous organs including the lung. Gene targeting of the ASM gene in transgenic mice produced an animal model with features typical of NPD, including pulmonary inflammation. To assess mechanisms by which ASM perturbed lung function, we studied lung morphology, surfactant content, and metabolism in ASM-deficient mice in vivo. Pulmonary inflammation, with increased cellular infiltrates and the accumulation of alveolar material, was associated with alterations in surfactant content. Saturated phosphatidylcholine (SatPC) content was increased twofold, and sphingomyelin content was increased 5.5-fold in lungs of the ASM knockout (ASMKO) mice. Additional sphingomyelin enhanced the sensitivity of surfactant inhibition by plasma proteins. Clearance of SatPC from the lungs of ASMKO mice was decreased. Catabolism of SatPC by alveolar macrophages from the ASMKO mouse was significantly decreased, likely accounting for decreased pulmonary SatPC in vivo. In summary, ASM is required for normal surfactant catabolism by alveolar macrophages in vivo. Alterations in surfactant composition, including increased sphingomyelin content, contributed to the abnormal surfactant function observed in the ASM-deficient mouse.
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Novikova, Elena, Vera Selyatitskaya, Igor Mitrofanov, Boris Pinkhasov, and Ani Karapetyan. "Association of Erectile Dysfunction and Hypogonadism with Metabolic Syndrome in Men with Lower Urinary Tract Symptoms of Younger and Older Age Groups." Advances in Sexual Medicine 04, no. 04 (2014): 55–64. http://dx.doi.org/10.4236/asm.2014.44009.
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Janssen, Luke J. "Membrane Currents in Airway Smooth Muscle: Mechanisms and Therapeutic Implications." Canadian Respiratory Journal 4, no. 1 (1997): 13–20. http://dx.doi.org/10.1155/1997/253424.
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Electrophysiological and pharmacological techniques were used to characterize the membrane conductance changes underlying spasmogen-evoked depolarization in airway smooth muscle (ASM). Changes included a transient activation of chloride ion channels and prolonged suppression of potassium ion channels; both changes are triggered by release of internally sequestered calcium ion and in turn cause opening of voltage-dependent calcium channels. The resultant influx of calcium ions contributes to contraction as well as to refilling of the internal calcium ion pool. Bronchodilators, on the other hand, act in part through activation of potassium channels, with consequent closure of calcium channels. The tools used to study ion channels in ASM are described, and the investigations of the roles of ion channels in ASM physiology (autacoid-evoked depolarization and hyperpolarization) and pathophysiology (airway hyperresponsiveness) are summarized. Finally, how the relationship between ion channels and ASM function/dysfunction may relate to the treatment of asthma and related breathing disorders is discussed.
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West, Adrian R., Nishat Zaman, Darren J. Cole, Matthew J. Walker, Wesley R. Legant, Thomas Boudou, Christopher S. Chen, et al. "Development and characterization of a 3D multicell microtissue culture model of airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 1 (January 1, 2013): L4—L16. http://dx.doi.org/10.1152/ajplung.00168.2012.
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Airway smooth muscle (ASM) cellular and molecular biology is typically studied with single-cell cultures grown on flat 2D substrates. However, cells in vivo exist as part of complex 3D structures, and it is well established in other cell types that altering substrate geometry exerts potent effects on phenotype and function. These factors may be especially relevant to asthma, a disease characterized by structural remodeling of the airway wall, and highlights a need for more physiologically relevant models of ASM function. We utilized a tissue engineering platform known as microfabricated tissue gauges to develop a 3D culture model of ASM featuring arrays of ∼0.4 mm long, ∼350 cell “microtissues” capable of simultaneous contractile force measurement and cell-level microscopy. ASM-only microtissues generated baseline tension, exhibited strong cellular organization, and developed actin stress fibers, but lost structural integrity and dissociated from the cantilevers within 3 days. Addition of 3T3-fibroblasts dramatically improved survival times without affecting tension development or morphology. ASM-3T3 microtissues contracted similarly to ex vivo ASM, exhibiting reproducible responses to a range of contractile and relaxant agents. Compared with 2D cultures, microtissues demonstrated identical responses to acetylcholine and KCl, but not histamine, forskolin, or cytochalasin D, suggesting that contractility is regulated by substrate geometry. Microtissues represent a novel model for studying ASM, incorporating a physiological 3D structure, realistic mechanical environment, coculture of multiple cells types, and comparable contractile properties to existing models. This new model allows for rapid screening of biochemical and mechanical factors to provide insight into ASM dysfunction in asthma.
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Aravamudan, Bharathi, Alexander Kiel, Michelle Freeman, Philippe Delmotte, Michael Thompson, Robert Vassallo, Gary C. Sieck, Christina M. Pabelick, and Y. S. Prakash. "Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 9 (May 1, 2014): L840—L854. http://dx.doi.org/10.1152/ajplung.00155.2013.
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The balance between mitochondrial fission and fusion is crucial for mitochondria to perform its normal cellular functions. We hypothesized that cigarette smoke (CS) disrupts this balance and enhances mitochondrial dysfunction in the airway. In nonasthmatic human airway smooth muscle (ASM) cells, CS extract (CSE) induced mitochondrial fragmentation and damages their networked morphology in a concentration-dependent fashion, via increased expression of mitochondrial fission protein dynamin-related protein 1 (Drp1) and decreased fusion protein mitofusin (Mfn) 2. CSE effects on Drp1 vs. Mfn2 and mitochondrial network morphology involved reactive oxygen species (ROS), activation of extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), protein kinase C (PKC) and proteasome pathways, as well as transcriptional regulation via factors such as NF-κB and nuclear erythroid 2-related factor 2. Inhibiting Drp1 prevented CSE effects on mitochondrial networks and ROS generation, whereas blocking Mfn2 had the opposite, detrimental effect. In ASM from asmatic patients, mitochondria exhibited substantial morphological defects at baseline and showed increased Drp1 but decreased Mfn2 expression, with exacerbating effects of CSE. Overall, these results highlight the importance of mitochondrial networks and their regulation in the context of cellular changes induced by insults such as inflammation (as in asthma) or CS. Altered mitochondrial fission/fusion proteins have a further potential to influence parameters such as ROS and cell proliferation and apoptosis relevant to airway diseases.
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Kramer, Elizabeth L., Rhonda Szczesniak, Weiji Su, Satish Madala, Kristin Hudock, Cynthia Davidson, Alicia Ostmann, Lauren Strecker, and John P. Clancy. "3123 TGFbeta, Early Cytokine Dysregulation, and Airway Smooth Muscle Dysfunction in Cystic Fibrosis." Journal of Clinical and Translational Science 3, s1 (March 2019): 22–23. http://dx.doi.org/10.1017/cts.2019.55.
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OBJECTIVES/SPECIFIC AIMS: This study aims to first describe the unique cytokine profile and TGFbeta levels of young children with CF, then understand the pathologic effects of TGFbeta on lung function in a CF animal model. These powerful translational studies linking observations in clinical disease with a transgenic mouse model allow us a unique opportunity to investigate the role of TGFbeta in early CF lung disease. METHODS/STUDY POPULATION: Cytokine levels (TGFbeta, TNFalpha, IL-8, IL-6, HNE, and IL-1beta) in bronchoalveolar lavage fluid (BALF) from CF patients (n = 15) and non-CF control patients (n = 21) under 6 years old were determined by ELISA and Luminex assay. Tracheotomized patients without significant underlying lung disease were chosen as non-CF inflamed control patients, as they had similar levels of neutrophilic inflammation and infection as CF patients. The percentage of BAL neutrophils (% PMNs) in each sample was assessed. The relationships between cytokines were analyzed using linear regression and principal components analysis. In animal studies, CF and non-CF mice (n = 4-5 per group) were treated with intratracheal adenoviral TGFbeta1 vector, an empty vector control, or PBS. After one week, animals were collected; lung function, response to the bronchoconstrictor methacholine, and rescue with albuterol were measured utilizing a FlexiVent machine. Lungs were collected for histology. Immunohistochemistry for alpha-SMA was performed and pictures of all cross-sectional airways were obtained. Burden of ASM was assessed by dividing the square root of alpha-SMA stained airway smooth muscle by the basement membrane perimeter length of each airway. RESULTS/ANTICIPATED RESULTS: Patient characteristics of CF and non-CF inflamed control patients were similar in terms of age (3.6 yrs vs 3.3 yrs respectively, p = 0.49), positive BAL culture (13% vs 14%, p = 0.94), and % PMNs (65% vs 56%, p = 0.64). Despite these similarities, TGFbeta levels were 2-fold higher in CF versus non-CF BAL (p = 0.034). Analysis of BAL cytokines from both patient groups showed that three principal components describe 86% of total variance across the cytokine variables. These components represent different contributions from the cytokines, with TGFbeta, IL6, and % PMNs comprising one component of similarly regulated inflammatory markers. These components can distinguish CF versus non-CF patients with 77% accuracy (area under the curve: 0.77). TGFbeta concentrations were uniquely associated with increased IL-6 in CF samples (r = 0.74; p = 0.0015) but did not demonstrate association with other cytokines. After TGFbeta exposure, CF mice demonstrated greater abnormalities in airway resistance than non-CF mice, with heightened response to methacholine. Importantly, this increase in airway obstruction in CF mice was reversible with albuterol treatment, indicating airway smooth muscle dysfunction as a principal driver of lung function abnormalities. Furthermore, TGFbeta induced an increased ASM burden on lung histology in both CF and non-CF mice (p<0.05). IL-6 levels in the BAL of CF mice showed greater increases after TGFbeta treatment compared to non-CF mice (p<0.05). Empty vector control treatment did not cause lung pathology. DISCUSSION/SIGNIFICANCE OF IMPACT: Young children with CF have a unique pattern of pulmonary inflammation compared to inflamed non-CF control patients. In CF, TGFbeta pulmonary levels are uniquely associated with IL-6, a driver of ASM dysfunction in other pulmonary diseases. We followed up this clinical observation study by investigating the effect of TGFbeta on pulmonary disease in a mouse model. CF mice demonstrate increased pulmonary IL-6, airway obstruction, and ASM dysfunction after TGFbeta exposure. This study provides evidence that TGFbeta is associated with a distinct cytokine pattern that may promote ASM dysfunction in early CF lung disease. Understanding the mechanism of early CF pathophysiology will be critical in developing targeted therapeutics that can prevent early lung damage.
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Ghanem, Sassine, Gwenalyn Garcia, Liu Ying, Matthew Hurford, and Marcel Odaimi. "Systemic Mastocytosis with Smoldering Multiple Myeloma: Report of a Case." Case Reports in Oncological Medicine 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/3161768.
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Systemic mastocytosis (SM) is a disease characterized by a clonal infiltration of mast cells affecting various tissues of the body. It is grouped into six different subtypes according to the World Health Organization classification. It is called indolent systemic mastocytosis (ISM) when there is no evidence of end organ dysfunction, while the presence of end organ dysfunction defines aggressive systemic mastocytosis (ASM). When SM coexists with a clonal hematological disorder, it is classified as systemic mastocytosis with associated clonal hematological nonmast cell lineage disease (SM-AHNMD). Over 80% of SM-AHNMD cases involve disorders of the myeloid cell lines. To our knowledge, there are only 8 reported cases to date of SM associated with a plasma cell disorder. We report a patient with ISM who was found to have concomitant smoldering multiple myeloma. His disease later progressed to ASM. We discuss this rare association between SM and a plasma cell disorder, and potential common pathophysiologic mechanisms linking the two disorders will be reviewed. We also discuss prognostic factors in SM as well as the management options considered during the evolution of the patient’s disease.
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Avraham, Tomer, Alan Yan, Jamie C. Zampell, Sanjay V. Daluvoy, Adriana Haimovitz-Friedman, Andrew P. Cordeiro, and Babak J. Mehrara. "Radiation therapy causes loss of dermal lymphatic vessels and interferes with lymphatic function by TGF-β1-mediated tissue fibrosis." American Journal of Physiology-Cell Physiology 299, no. 3 (September 2010): C589—C605. http://dx.doi.org/10.1152/ajpcell.00535.2009.
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Although radiation therapy is a major risk factor for the development of lymphedema following lymphadenectomy, the mechanisms responsible for this effect remain unknown. The purpose of this study was therefore to determine the effects of radiation on lymphatic endothelial cells (LECs) and lymphatic function. The tails of wild-type or acid sphingomyelinase (ASM)-deficient mice were treated with 0, 15, or 30 Gy of radiation and then analyzed for LEC apoptosis and lymphatic function at various time points. To analyze the effects of radiation fibrosis on lymphatic function, we determined the effects of transforming growth factor (TGF)-β1 blockade after radiation in vivo. Finally, we determined the effects of radiation and exogenous TGF-β1 on LECs in vitro. Radiation caused mild edema that resolved after 12–24 wk. Interestingly, despite resolution of tail edema, irradiated animals displayed persistent lymphatic dysfunction. Radiation caused loss of capillary lymphatics and was associated with a dose-dependent increase in LEC apoptosis. ASM−/− mice had significantly less LEC apoptosis; however, this finding did not translate to improved lymphatic function at later time points. Short-term blockade of TGF-β1 function after radiation markedly decreased tissue fibrosis and significantly improved lymphatic function but did not alter LEC apoptosis. Radiation therapy decreases lymphatic reserve by causing depletion of lymphatic vessels and LECs as well as promoting soft tissue fibrosis. Short-term inhibition of TGF-β1 activity following radiation improves lymphatic function and is associated with decreased soft tissue fibrosis. ASM deficiency confers LEC protection from radiation-induced apoptosis but does not prevent lymphatic dysfunction.
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O'Reilly, Megan, Stuart B. Hooper, Beth J. Allison, Sharon J. Flecknoe, Ken Snibson, Richard Harding, and Foula Sozo. "Persistent bronchiolar remodeling following brief ventilation of the very immature ovine lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 5 (November 2009): L992—L1001. http://dx.doi.org/10.1152/ajplung.00099.2009.
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Children and adults who were mechanically ventilated following preterm birth are at increased risk of reduced lung function, suggesting small airway dysfunction. We hypothesized that short periods of mechanical ventilation of very immature lungs can induce persistent bronchiolar remodeling that may adversely affect later lung function. Our objectives were to characterize the effects of brief, positive-pressure ventilation per se on the small airways in very immature, surfactant-deficient lungs and to determine whether the effects persist after the cessation of ventilation. Fetal sheep (0.75 of term) were mechanically ventilated in utero with room air (peak inspiratory pressure 40 cmH2O, positive end-expiratory pressure 4 cmH2O, 65 breaths/min) for 6 or 12 h, after which tissues were collected; another group was studied 7 days after 12-h ventilation. Age-matched unventilated fetuses were controls. The mean basement membrane perimeter of airways analyzed was 548.6 ± 8.5 μm and was not different between groups. Immediately after ventilation, 21% of airways had epithelial injury; in airways with intact epithelium, there was more airway smooth muscle (ASM) and less collagen, and the epithelium contained more mucin-containing and apoptotic cells and fewer proliferating cells. Seven days after ventilation, epithelial injury was absent but the epithelium was thicker, with greater cell turnover; there were increased amounts of bronchiolar collagen and ASM and fewer alveolar attachments. The increase in ASM was likely due to cellular hypertrophy rather than hyperplasia. We conclude that brief mechanical ventilation of the very immature lung induces remodeling of the bronchiolar epithelium and walls that lasts for at least 7 days; such changes could contribute to later airway dysfunction.
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Motil, Igor, Ivan Kubis, and Tatana Sramkova. "Treatment of Vasculogenic Erectile Dysfunction with Piezowave2 Device. Application of Low Intensity Shockwaves Using Novel Linear Shockwave Tissue Coverage (LSTC-ED<sup>®</sup>) Technique. A Prospective, Multicentric, Placebo-Controlled Study." Advances in Sexual Medicine 06, no. 02 (2016): 15–18. http://dx.doi.org/10.4236/asm.2016.62002.
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Britt, Rodney D., Michael A. Thompson, Ine Kuipers, Alecia Stewart, Elizabeth R. Vogel, James Thu, Richard J. Martin, Christina M. Pabelick, and Y. S. Prakash. "Soluble guanylate cyclase modulators blunt hyperoxia effects on calcium responses of developing human airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 6 (September 15, 2015): L537—L542. http://dx.doi.org/10.1152/ajplung.00232.2015.
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Exposure to moderate hyperoxia in prematurity contributes to subsequent airway dysfunction and increases the risk of developing recurrent wheeze and asthma. The nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic GMP (cGMP) axis modulates airway tone by regulating airway smooth muscle (ASM) intracellular Ca2+ ([Ca2+]i) and contractility. However, the effects of hyperoxia on this axis in the context of Ca2+/contractility are not known. In developing human ASM, we explored the effects of novel drugs that activate sGC independent of NO on alleviating hyperoxia (50% oxygen)-induced enhancement of Ca2+ responses to bronchoconstrictor agonists. Treatment with BAY 41–2272 (sGC stimulator) and BAY 60-2770 (sGC activator) increased cGMP levels during exposure to 50% O2. Although 50% O2 did not alter sGCα1 or sGCβ1 expression, BAY 60-2770 did increase sGCβ1 expression. BAY 41-2272 and BAY 60-2770 blunted Ca2+ responses to histamine in cells exposed to 50% O2. The effects of BAY 41-2272 and BAY 60-2770 were reversed by protein kinase G inhibition. These novel data demonstrate that BAY 41-2272 and BAY 60-2770 stimulate production of cGMP and blunt hyperoxia-induced increases in Ca2+ responses in developing ASM. Accordingly, sGC stimulators/activators may be a useful therapeutic strategy in improving bronchodilation in preterm infants.
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Oudaert, Inge, Sylvia Faict, Ludovic D'Auria, Jonas Dehairs, Ken Maes, Philip Vlummens, Lotte Jacobs, et al. "The Exosomal Transfer of Acid Sphingomyelinase Contributes to Drug Resistance in Multiple Myeloma." Blood 134, Supplement_1 (November 13, 2019): 3058. http://dx.doi.org/10.1182/blood-2019-122857.
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Introduction Multiple myeloma (MM) is well-known for the development of drug resistance, leading to the need for multiple treatment lines at times of relapse or progression. Even then, most patients ultimately will succumb to this cancer. Therefore, there is a need for new therapeutic strategies to conquer this drug resistance. Lipidomics has recently gained more attention in the search for new cancer therapies. Lipids are mainly found in biological membranes and function as building blocks, but are also important metabolites that can influence energy, structure and signaling cascades. Lipid dysfunction has been correlated to other cancers, like prostate and breast cancer. In this study, we identified changes in lipid content in MM patients and further investigated this altered metabolism in vitro. Methods We performed a lipidomics assay to compare plasma from healthy volunteers to MM patients. For all in vitro experiments, we used four human MM cell lines (JJN3, OPM2, LP1, U266) and primary CD138+ patient samples, isolated by MACS. Differential mRNA expression (SMPD1 = acid sphingomyelinase, ASM) was measured by qRT-PCR and ASM protein levels by western blot. Exosomes were isolated by exoquick, while changes in secretion were measured by nanoparticle tracking analysis. Viability was measured by CellTiter Glo and apoptosis rates for melphalan, bortezomib and ASM inhibitor (amitriptyline) were measured by flow cytometry (annexinV-FITC/7-AAD staining). Drug efficacy of amitriptyline was also confirmed on primary CD138+ samples by CellTiter Glo. Results Lipidomics analysis revealed an increase in ceramides and a decrease in sphingomyelin. Therefore, we believe that the enzyme sphingomyelinase, which converts sphingomyelin into ceramide, is upregulated in MM, which we confirmed on primary CD138+ MM cells for ASM. We also observed an increase in SMPD1 expression by qRT-PCR and ASM levels by western blot after melphalan and bortezomib treatment. Furthermore, we also investigated effects of these drugs on exosome secretion, where we found an increase in the number of exosomes secreted, as well as higher ASM levels in these exosomes. U266-derived exosomes, containing high amounts of ASM, were able to transfer their resistance to ASM-low JJN3 cells as an increase in viability was measured. Inhibition of ASM by amitriptyline, combined with melphalan and bortezomib, increased apoptotic cell death by upregulating cleaved PARP and caspase 3 levels. Combination therapy of amitriptyline with melphalan and bortezomib was also successfully tested on primary CD138+ MM cells. Conclusion This study is the first to identify changes in sphingolipids in plasma of MM patients, where we matched the observed difference to an upregulation of ASM in MM cells. Standard-of-care drugs stimulated ASM expression and production, and cells were able to transfer their resistance to other cells by ASM-rich exosomes. Enzyme inhibition by amitriptyline, a cheap tricyclic antidepressant drug frequently used to combat neuropathic pain in MM, increased drug efficacy of standard-of-care drugs. This study therefore provides a rationale to add ASM-targeting drugs to current combination therapies in MM patients. Disclosures No relevant conflicts of interest to declare. OffLabel Disclosure: Amitriptyline is a tricyclic antidepressant, which is also often used to treat neuropathic pain in Multiple Myeloma patients. Here we describe additive effects of amitriptyline on bortezomib and melphalan treatment in MM.
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Sathish, Venkatachalem, Michelle R. Freeman, Emma Long, Michael A. Thompson, Christina M. Pabelick, and Y. S. Prakash. "Cigarette Smoke and Estrogen Signaling in Human Airway Smooth Muscle." Cellular Physiology and Biochemistry 36, no. 3 (2015): 1101–15. http://dx.doi.org/10.1159/000430282.
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Aims: Cigarette smoke (CS) in active smokers and second-hand smoke exposure exacerbate respiratory disorders such as asthma and chronic bronchitis. While women are known to experience a more asthmatic response to CS than emphysema in men, there is limited information on the mechanisms of CS-induced airway dysfunction. We hypothesize that CS interferes with a normal (protective) bronchodilatory role of estrogens, thus worsening airway contractility. Methods: We tested effects of cigarette smoke extract (CSE) on 17β-estradiol (E2) signaling in enzymatically-dissociated bronchial airway smooth muscle (ASM) obtained from lung samples of non-smoking female patients undergoing thoracic surgery. Results: In fura-2 loaded ASM cells, CSE increased intracellular calcium ([Ca2+]i) responses to 10µM histamine. Acute exposure to physiological concentrations of E2 decreased [Ca2+]i responses. However, in 24h exposed CSE cells, although expression of estrogen receptors was increased, the effect of E2 on [Ca2+]i was blunted. Acute E2 exposure also decreased store-operated Ca2+ entry and inhibited stromal interaction molecule 1 (STIM1) phosphorylation: effects blunted by CSE. Acute exposure to E2 increased cAMP, but less so in 24h CSE-exposed cells. 24h CSE exposure increased S-nitrosylation of ERα. Furthermore, 24h CSE-exposed bronchial rings showed increased bronchoconstrictor agonist responses that were not reduced as effectively by E2 compared to non-CSE controls. Conclusion: These data suggest that CS induces dysregulation of estrogen signaling in ASM, which could contribute to increased airway contractility in women exposed to CS.
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Kipnis, Pavel A., Brennan J. Sullivan, and Shilpa D. Kadam. "Sex-Dependent Signaling Pathways Underlying Seizure Susceptibility and the Role of Chloride Cotransporters." Cells 8, no. 5 (May 13, 2019): 448. http://dx.doi.org/10.3390/cells8050448.
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Seizure incidence, severity, and antiseizure medication (ASM) efficacy varies between males and females. Differences in sex-dependent signaling pathways that determine network excitability may be responsible. The identification and validation of sex-dependent molecular mechanisms that influence seizure susceptibility is an emerging focus of neuroscience research. The electroneutral cation-chloride cotransporters (CCCs) of the SLC12A gene family utilize Na+-K+-ATPase generated electrochemical gradients to transport chloride into or out of neurons. CCCs regulate neuronal chloride gradients, cell volume, and have a strong influence over the electrical response to the inhibitory neurotransmitter GABA. Acquired or genetic causes of CCCs dysfunction have been linked to seizures during early postnatal development, epileptogenesis, and refractoriness to ASMs. A growing number of studies suggest that the developmental expression of CCCs, such as KCC2, is sex-dependent. This review will summarize the reports of sexual dimorphism in epileptology while focusing on the role of chloride cotransporters and their associated modulators that can influence seizure susceptibility.
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Wang, Xian Mei, Ti Deng, Ling Yan Liang, and Zhi Liang Wang. "A Novel Smart Household Control System by Computer Vision." Advanced Materials Research 179-180 (January 2011): 264–69. http://dx.doi.org/10.4028/www.scientific.net/amr.179-180.264.
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For the disable people or the aged people, they need extra help in their daily household life. Various modern devices have been developed to improve their living quality. These devices always have automatic functions which are considered crucial for their independent life. Different to the traditional automatic household appliance such as manually infrared remote-controller and automatic voice-operated switch, this paper presents a novel approach based on computer vision to realize intelligent household control. This proposed system uses Adaboost and ASM algorithm for face detection and feature point calibration. Based on the facial key points, the head postures and mouth states are calculated and then coded into a special data packet. Finally, the packet is sent by an infrared carrier to the intelligent appliance with infrared receiver to control their operation manner. By using computer vision technology with infrared communication, the system is especially effective for the disable people such as the upper-body paraplegic and the people with hand dysfunction.
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Soverini, Simona, Caterina De Benedittis, Manuela Mancini, Michela Rondoni, Cristina Papayannidis, Antonella Padella, Giorgina Specchia, et al. "Genome-Wide Molecular Portrait of Aggressive Systemic Mastocytosis and Mast Cell Leukemia Depicted By Whole Exome Sequencing and Copy Number Variation Analysis." Blood 126, no. 23 (December 3, 2015): 4085. http://dx.doi.org/10.1182/blood.v126.23.4085.4085.
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Abstract Background and Aims: The term Systemic Mastocytosis (SM) identifies a poorly understood group of rare and clinically heterogenous myeloproliferative neoplasms characterized by abnormal growth and activation of mast cells (MCs) and their precursors in the bone marrow and in various tissues and organs. Based on phenotype and extent of organ infiltration/dysfunction, a spectrum of disease variants can be recognized ranging from indolent SM (ISM) to aggressive SM (ASM) and mast cell leukemia (MCL). The fact that in all cases, including ISM who have a (near) normal life expectancy, neoplastic MCs display the same D816V KIT gene mutation points to additional mechanisms and molecular defects as responsible for ASM and MCL. So far, however, this issue has mainly been addressed with targeted resequencing studies of candidate gene panels. We thus decided to undertake an integrated molecular characterization study of ASM and MCL to identify novel, functionally relevant molecular lesions and/or clinically actionable signaling pathways. Methods: A discovery panel including 6 patients with ASM and 6 patients with MCL was studied using whole exome sequencing (WES) and copy number variation (CNV) analysis. WES (80x) was performed on a Hiseq 2500 (Illumina). CNV was done using Cytoscan HD Arrays (Affymetrix). Paired normal/MC DNA was analyzed in all but 2 archival MCL cases for whom germline DNA was not available. A validation panel of 30 ISM, 5 smoldering SM and 20 additional ASM was also included in this study. Results: In the discovery panel, WES identified a total of 1554 point mutations, small insertions and deletions. Seven hundred and eighty-five were non-silent mutations in 698 genes, with an average of 51 (range, 30-186) non-silent mutations per patient. Non-silent mutations included 354 missense mutations, 188 nonsense mutations, 145 frameshift insertions/deletions, 98 non-frameshift insertions/deletions. C to T transitions were by far the most frequent. Orthogonal validation estimated the accuracy of mutation calls at >95%. Interrogation of the COSMIC and OMIM databases revealed 42 known cancer genes. Among the missense mutations, 87 were predicted to have a high probability of being deleterious by Condel. MCL cases were found not to harbour a higher mutation load as compared to ASM cases. High resolution CN analysis showed that focal amplifications/deletions/loss-of-heterozygosity (LOH) were prevalent over arm-level alterations (found in 3 patients only). Genes were selected for further assessment when recurrently mutated in ≥2 patients or concurrently identified in WES and CNV analyses or previously associated with leukemogenesis or cancer pathogenesis. Among these, genes already reported to be affected by mutations in SM included TET2, NRAS, ASXL1, CBL, IDH1, SRSF2, SF3B1, RUNX1. We also identified genetic alterations in genes not previously implicated in SM pathogenesis including TP53BP1, RUNX3, NCOR2, CDC27, CCND3, EI24, MLL3, ARID1B, ARID3B, ARID4A, SETD1A, SETD1B, KDM1B, PRDM1, ATM, WRN. A long tail of infrequently mutated genes dominated, resulting in significant intertumoural heterogeneity. However, when genes were assigned to functional pathways to discern patterns of mutations across different patients, we found that PI3K/Akt and MAPK pathways, calcium pathway, chromatin modification, DNA methylation, and DNA damage repair were consistently affected (Figure 1). Further assessment of the mutation frequency of selected genes within each pathway and functional validation at the protein level are currently ongoing in the validation panel. Preliminary findings on a tumor suppressor selected among those identified by WES show transcript and/or protein downmodulation due to inactivating mutations, transcriptional silencing or enhanced degradation in 17/20 ASM. Detailed results will be presented at the meeting. Conclusions: WES and CNV analyses of ASM and MCL revealed a complex landscape, not unexpected when considering the clinical heterogeneity of these patients. Nonetheless, key pathways were found to be recurrently altered. Further investigation of selected candidate genes and pathways is warranted and will cast light on the cooperative genetic (and epigenetic?) events underlying the more aggressive forms of SM - paving the way to a better prognostic stratification and more effective treatment. <>This study was supported by ELN, AIL, AIRC, progetto Regione-Università 2010-12 (L. Bolondi), FP7 NGS-PTL project. Disclosures Soverini: Ariad: Consultancy; Bristol-Myers Squibb: Consultancy; Novartis: Consultancy. Valent:Novartis: Consultancy, Honoraria, Research Funding; Ariad: Honoraria, Research Funding; Bristol-Myers Squibb: Honoraria; Pfizer: Honoraria; Celgene: Honoraria. Cavo:Janssen-Cilag, Celgene, Amgen, BMS: Honoraria. Martinelli:Novartis: Consultancy, Speakers Bureau; BMS: Consultancy, Speakers Bureau; ROCHE: Consultancy; Pfizer: Consultancy; Ariad: Consultancy; AMGEN: Consultancy; MSD: Consultancy.
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Moonim, Mufaddel T., Thibaud Kossier, Jon van Der Walt, Bridget Wilkins, Claire N. Harrison, and Deepti H. Radia. "CD30/CD123 Expression in Systemic Mastocytosis Does Not Correlate with Aggressive Disease." Blood 120, no. 21 (November 16, 2012): 1746. http://dx.doi.org/10.1182/blood.v120.21.1746.1746.
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Abstract Abstract 1746 Introduction: Systemic Mastocytosis (SM) is a myeloproliferative neoplasm (MPN) with heterogeneous clinical manifestations and limited treatment options for patients with aggressive disease. The WHO Classification sub divides SM patients into Indolent (ISM: evidence of clonal mast cells in bone marrow), Smouldering (SSM: Trypstase > 200ng/ml;organomegaly without dysfunction; bone marrow mast cell burden > 30% ), Aggressive (ASM: organomegaly with laboratory evidence of dysfunction), Mast Cell Leukaemia (MCL; > 20% mast cells on aspirate and >10% on blood film) and Associated Haematological Non-Mast Cell Disorders (AHNMD). The c-kit mutation (D816V) is present in > 90% of SM patients. Tryptase levels reflect total mast cell burden. To date there is no discriminatory marker to allow for identification of SM patients with more aggressive disease. CD30 (Ki-I antigen) has been reported as a potential marker for mast cells in high grade mastocytosis (Sotlar et al, 2011).We present preliminary data on 43 SM patients seen at Guys and St Thomas' Hospitals NHS Foundation Trust looking at CD30 and CD123 expression with clinical correlates. Methodology: 43/58 SM patients who have a full set of clinical records and bone marrow trephine samples have been evaluated. Bone marrow trephine processing: fixation in a neutral buffered formalin < 24hours; EDTA decalcification for 48 hours;Immunochemistry on an automated immunostainer (Leica Bondmax)using standard protocols: CD 30 (Dako dilution 1:75, antigen retrieval ER2). CD123 (BD Sciences, Novacastra, dilution 1:400,antigen retrieval ER2). Bone Marrow trephine samples were reviewed by haematopathologists at diagnostic MDM. Disease bulk was estimated as a percentage of the trephine sample. Immunocytochemistry review of the CD30/CD123 was reviewed by a single haematopathologist for this study. Clinical information was reviewed for laboratory results, tryptase levels, clinical symptoms and SM diagnosis. Results: 43 patients: M:F(18:25). SM diagnoses: 26 ISM (60%), 2 SSM (5%),3 ASM (7% ), 12 AHNMD (28%). Data on 43 patients for CD30 expression and 40 for CD123 expression. Tryptase: 20 CD30(+) patients median 74.9ng/ml (range 16.6–285ng/ml): 23 CD 30(−) patients median 43.6ng/ml (range 15.1–386ng/ml). Conclusions: Our preliminary data on 43 patients with SM/ CD30/123 expression suggests: Disclosures: Harrison: Novartis: Honoraria, Research Funding, Speakers Bureau; YM Bioscience: Consultancy, Honoraria; Sanofi Aventis: Honoraria; Shire: Honoraria, Research Funding.
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Suleymanova, A. K., and I. A. Baranova. "Evaluation of the relationship between the parameters of peripheral skeletal and respiratory muscles in patients with chronic obstructive pulmonary disease." Terapevticheskii arkhiv 92, no. 3 (April 27, 2020): 36–41. http://dx.doi.org/10.26442/00403660.2020.03.000448.
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Chronic obstructive pulmonary disease (COPD) is a group of diseases with high levels of comorbidity. Pathological changes of peripheral skeletal and respiratory muscles in COPD patients, which are often underestimated, occupy a special place.
Aim. To study the relationship between functional and quantitative parameters of the peripheral (limb muscle) and respiratory muscles in COPD patients.
Materials and methods. 127 patients (98 men/29 women, mean age 67.68.2 years) were under observation without acute COPD. All COPD patients were classified according to GOLD (2019) into groups A, B, C, D. The algorithm of the European Working Group on Sarcopenia in Older People (EWGSOP2) was used to diagnose sarcopenia. The muscle mass was measured using dual energy X-ray absorptiometry (DXA) and the appendicular lean mass index (ASM) was estimated. Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) were measured by body plethysmograph MasterScreen Body. Quantitative assessment of thoracic muscle cross-sectional areas were performed using the CT scan using Vidar Dicom Viewer software.
Results. Sarcopenia was diagnosed in 43.3% of COPD patients. Respiratory muscle dysfunction was determined in 66.1% of patients with COPD, its probability increased in groups C and D in comparison with groups A and B [chance ratio 6.6 (95% confidence interval 2.915.0); p0.0001]. Correlations between the functional parameters of sarcopenia and respiratory muscle strength as well as between the mass of peripheral skeletal muscles and respiratory muscle area have been established according to the data of computerized tomography (р0.01). Sarcopenia as well as respiratory muscle dysfunction was observed more frequently in persons with severe and extremely severe airway obstruction and in patients with predominantly emphysematic COPD phenotype (p0.01).
Conclusion. Sarcopenia is a frequent comorbidity in COPD and its development is connected with the severity of the course of the main disease. Correlation between parameters of peripheral (limb muscle) and respiratory muscles in patients with COPD has been determined.
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Cooper, J., M. M. Mita, J. Curtright, A. Ricart, A. Mita, C. Takimoto, A. Tolcher, A. Dowlati, S. Flick, and K. P. Papadopoulos. "A phase I study examining weekly dosing and pharmacokinetics (PK) of a novel spectrum selective kinase inhibitor, XL999, in patients (pts) with advanced solid malignancies (ASM)." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 13024. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13024.
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13024 Background: XL999 is a small molecule inhibitor of multiple kinases involved in tumor cell growth, angiogenesis, and metastasis, including VEGFR2 (KDR), PDGFRα/β, FGFR1/3, FLT-3, and SRC. A phase I study of XL999 administered as a 4 hr infusion every 2 weeks in pts with ASM showed that the maximum tolerated dose (MTD) was 3.2 mg/kg and the plasma t1/2 was approximately 24 hrs. Three pts dosed at 0.2–1.6 mg/kg (anaplastic thyroid cancer [1], renal cell carcinoma [1], hepatic squamous cell carcinoma [1]) had partial responses and 9 pts had stable disease for 3 to 11 months. Based on these data, a weekly (wkly) dosing schedule with PK monitoring was explored. Methods: XL999 at 3.2 mg/kg was administered to pts as a 4 hr infusion on day (d) 1 and 8 with toxicity assessment. Pts received further doses of XL999 wkly in the absence of unacceptable toxicity, disease progression, or accumulation based on PK results. Results: Overall 15 pts were enrolled and 7 were initially dosed at 3.2 mg/kg. Two of these pts experienced severe drug related toxicities, including 1 pt with G3 fatigue who was able to continue wkly XL999 at 2.4 mg/kg and another pt who was discontinued after developing reversible cardiac dysfunction on d1. The next 8 pts were treated at 2.4 mg/kg and none of these has experienced any G2 or worse drug related adverse events. One asymptomatic pt with non-specific ECG changes after d1 was discontinued from study. Four of 11 evaluable pts had SD. In 7 evaluable pts treated at the 2.4 dose level, the mean Cmax was 519 ng/mL with moderate interpatient variability (coefficient of variation, CV) of 38%. Intrapatient variability in the Cmax values on d1 and d15 was moderate (≤3-fold); however, there was no evidence of drug accumulation on repeat dosing. Conclusions: XL999 administered wkly as a 4 hr infusion at a dose of 2.4 mg/kg appears to be well tolerated with no evidence of drug accumulation. The safety and PK data suggest that 2.4 mg/kg on a wkly schedule is appropriate for phase 2 studies. [Table: see text]
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Watkin, Hywel. "Segmental Dysfunction." Acupuncture in Medicine 17, no. 2 (December 1999): 118–23. http://dx.doi.org/10.1136/aim.17.2.118.
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Spinal segmental dysfunction, although used in clinical practice by medical acupuncturists, musculoskeletal physicians, physiotherapists and osteopaths, is not a concept which is familiar to the majority of medical practitioners. The concept implies that a problem in the function of a spinal segment may cause symptoms without necessarily being caused by physical pathology. Studies of the dysfunctional spinal segment have shown that physical stress, emotional stress and visceral disease all cause a reaction at the dysfunctional segment more easily than at normal segments. In the same way that individuals may have asymptomatic latent trigger points which may later become symptomatic, so individuals may have asymptomatic dysfunction which later becomes symptomatic under the influence of appropriate stimuli. There is some evidence that the clinical features of segmental dysfunction may be mediated by the sympathetic nervous system. The detection of segmental dysfunction is a clinical skill worth developing and the properties of the dysfunctional segment are worthy of further research.
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Huh, Sungchul, Jae Heun Chung, Han Jo Kwon, and Hyun-Yoon Ko. "Unilateral Diaphragm Paralysis Associated With Neurosyphilis: A Case Report." Annals of Rehabilitation Medicine 44, no. 4 (August 31, 2020): 338–41. http://dx.doi.org/10.5535/arm.19216.
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Diaphragm dysfunction can originate from various etiologies, and bilaterality of the dysfunction depends on the cause. Symptoms of diaphragm dysfunction vary depending on the degree of phrenic nerve denervation, spinal cord lesion, and involvement of the diaphragm. Several infectious diaphragmatic dysfunctions have been reported, including the human immunodeficiency virus, poliovirus, West Nile virus, and dengue virus. Here, we report a case of unilateral diaphragm paralysis in a 34-year-old man with neurosyphilis.
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Kuliński, Włodzisław. "Physical Procedure in Temporomandibular Joint Dysfunctions. Clinical Study." Acta Balneologica 64, no. 6 (2022): 495–502. http://dx.doi.org/10.36740/abal202206101.
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Aim: Temporomandibular joint dysfunction is a common and difficult clinical problem. To present the use of physical therapy in patients with temporomandibular joint dysfunctions. Materials and Methods: The paper presents the etiopathogenesis and clinical presentation of temporomandibular joint dysfunctions as well as patient cases and describes physical therapy in joint dysfunction, including the methods and equipment used to perform the procedures. Conclusion: The paper stresses the importance of physical therapy in the treatment of temporomandibular joint dysfunctions. Physical therapy is a crucial part of treatment in patients with temporomandibular joint dysfunctions.
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Schwaab, Juliana, Susanne Schnittger, Karl Sotlar, Christoph Walz, Alice Fabarius, Markus Pfirrmann, Alexander Kohlmann, et al. "Mutational Complexity Is Related To Disease Severity In Systemic Mastocytosis." Blood 122, no. 21 (November 15, 2013): 4094. http://dx.doi.org/10.1182/blood.v122.21.4094.4094.
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Abstract Systemic mastocytosis (SM) is a rare hematologic neoplasm characterized by abnormal accumulation of mast cells in various tissues, predominantly skin, bone marrow and visceral organs. The morphologic phenotype and extent of organ infiltration/dysfunction are basis for the subclassification of SM into indolent SM (ISM), smoldering SM (SSM), SM with associated hematologic non-mast cell disease (SM-AHNMD), aggressive SM (ASM) and mast cell leukemia (MCL). A somatic point mutation in the kinase domain of the receptor tyrosine kinase (TK) KIT at position 816 (KIT D816V) is present in >95% of patients and plays a central role in the pathogenesis and diagnosis of SM. To further explore mechanisms contributing to the clinical diversity of SM, we analyzed 39 KIT D816V mutated patients with different SM subtypes [ISM, n=10; SSM, n=2; ISM-AHNMD, n=5 (CMML, n=2; MDS/MPNu, n=3); ASM, n=1; ASM-AHNMD, n=14 (CMML, n= 5, MDS/MPNu, n=4, HES/CEL, n=2; AML, n=3); MCL, n=3; MCL-AHNMD n=4 (MDS/MPNu, n=2; HES/CEL, n=1; MDS, n=1)] for the presence of additional mutations. We applied next-generation sequencing to investigate ASXL1, CBL, IDH1/2, JAK2, KRAS, MLL-PTD, NPM1, NRAS, TP53, SRSF2, SF3B1, SETBP1, U2AF1 at mutational hotspot regions, and analyzed the complete coding regions of EZH2, ETV6, RUNX1, and TET2. Additional molecular aberrations were identified in 24/27 (89%) patients with advanced SM (SM-AHNMD, 5/5; ASM/MCL, 19/23) while only 3/12 (25%) ISM/SSM patients carried one additional mutation each (U2AF1, SETBP1, CBL) (p<0.001). In TET2, 9 missense, 4 nonsense, 13 frameshift mutations and one in-frame deletion as well as one splice site mutation were found in 15/39 (39%) patients. Ten of 15 (67%) patients carried more than one TET2 mutation. In SRSF2, missense mutations were identified in 14/39 (36%) patients which were clustered at codon 95 (P95H, n=9; P95L, n=2; P95R, n=2), with one additional mutation identified at codon 18 (V18L, n=1). In RUNX1, 10 mutations (9 missense mutations, 1 frameshift) were identified in 9/39 (23%) patients. Ten CBL mutations were identified in 8 patients (8 missense mutations, 1 duplication, 1 splice mutation) and 8 ASXL1 mutations were identified in 8 patients (7 frameshift and 1 nonsense mutation). In 13 patients, two (TET2, n=8; KRAS, n=1), three (CBL, n=2) or four mutations (TET2, n=2) were found in a single gene. Less frequently affected genes were KRAS (n=4), NRAS, JAK2, U2AF1 (n=2, each), EZH2, SETBP1, and ETV6 (n=1, each). No mutations were identified in MLL, IDH1, IDH2, NPM1, SF3B1 and TP53. In advanced SM, 21/27 patients (78%) carried ³3 mutations and 11/27 patients (41%) exhibited ³5 mutations. The median number of mutations was 4. The concurrent presence of KIT-TET2-SRSF2 (10/39, 26%), KIT-SRSF2-RUNX1 (7/39, 18%), KIT-TET2-CBL (5/39, 13%), KIT-SRSF2-ASXL1 (4/39, 10%) and KIT-TET2-ASXL1 (4/39, 10%) was strongly associated with (A)SM/MCL-AHNMD in 16/16 (100%) of patients (CMML, 7/16, 44%; MDS/MPNu, 6/16, 38%; HES/CEL, 3/16, 19%). Clinical follow-up was available for 38 patients. Six of 38 (16%) patients died, all of whom had at least one additional mutation with 5 patients positive for ³3 and 2 patients for ³5 mutations. The median survival of all 26 patients with at least one additional mutation was 12 months. In contrast, none of the 12 cases with KIT D816V mutation only died. This translated into a significant inferior survival (p=0.019) for patients with additional mutations (figure 1). We therefore conclude that, in addition to the multilineage involvement by KIT D816V, the presence of additional molecular aberrations is a new molecular feature that may contribute essentially to the abnormal phenotype and behaviour of neoplastic mast cells in advanced SM and thus to the clinical diversity and prognosis of advanced mast cell disorders. Disclosures: No relevant conflicts of interest to declare.
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Buden, R. P. "Thyroid Dysfunction in Patients with Liver Disease." Academia Journal of Medicine 2, no. 2 (July 24, 2019): 138–40. http://dx.doi.org/10.21276/ajm.2019.2.2.35.
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Dčttore, Davide, Helen Casale, and Antonella Montano. "Fattori cognitivi ed emotivi legati allo sviluppo del Disturbo Maschile dell'Erezione." RIVISTA DI SESSUOLOGIA CLINICA, no. 2 (December 2009): 21–48. http://dx.doi.org/10.3280/rsc2009-002002.
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- The aim of the present research is to investigate the relation between beliefs about sexuality, cognitive factors, emotional factors, and erectile dysfunction. 15 adult males (aged 29-66) with psychogenic erectile dysfunction were compared with 15 adult non-dysfunctional males (aged 29-71) with regard to their beliefs in sexual myths, their expectations, and their emotions during sexual activity. Erectile dysfunction was assessed by SDI (Sexual Dysfunction Interview) and measured by the International Index of Erectile Function (IIEF). Beliefs about sexuality, as well as cognitive and emotional factors of sexual function were measured respectively by Sexual Dysfunctional Beliefs Questionnaire (SDBQ) and Sexual Modes Questionnaire (SMQ). Results show in dysfunctional group an higher level of dysfunctional or irrational beliefs, of negative emotions and automatic thoughts during sexual activity. Beyond this, our data show high correlations between automatic thoughts and sexual functioning, and between worry and sexual functioning These results emphasize the role of cognitive-emotional processes on erectile dysfunction development and maintenance.
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Stankovic, Sasa, Mirjana Boskovic, Zorica Ajdukovic, Ljiljana Kesic, Ljiljana Aleksov, and Radivoje Radosavljevic. "Neurophysiological conception of pain in craniomandibular disfunction." Medical review 61, no. 9-10 (2008): 478–82. http://dx.doi.org/10.2298/mpns0810478s.
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Introduction. Ethiopathogenesis of dysfunction and pain in temporomandibular joints has been the subject of passionate discussions between supporters of purely mechanical conception and the ones who are supporters of psyhosomatic conception. The aim of the study: Relying on neurophysiological data, the authors are trying to reveal the main role of reticular mesencephalical formation in mechanisms which provoke craniomandibular dysfunctions and confront the influence of emotional factors from neocortex and painful stimuli from oral structures. Discussion. From dynamical point of view, not only the morphological aspects of teeth and arcades, but also sensitive-sensorial mechanisms connected to masticatory muscles, periodontal structures and oral structures, should be considered. The ideal bite and perfect morphology of tooth arcades are not enough for reconstitution of correct occlusion, if there are no neuromuscular system, temporomandibular joint, and especially central nervous system. Conclusion. The presence of pain is just one of the craniomandibular dysfunction symptoms, but if it is added to the other clinical signs and emotional or affect - provoking factor, it will provoke dysfunctional syndrome.
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Pavone, Carlo, Ninfa Giacalone, Marco Vella, Lidia Urso, Leila Zummo, and Brigida Fierro. "Relation between Sexual Dysfunctions and Epilepsy, Type of Epilepsy, Type of Antiepileptic Drugs: A Prospective Study." Urologia Journal 84, no. 2 (March 18, 2017): 88–92. http://dx.doi.org/10.5301/uro.5000222.
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Introduction The aim of this study was to evaluate the incidence of sexual dysfunctions in males with epilepsy, the type of epilepsy, the frequency of seizures, the type of antiepileptic drugs (AEDs), the serum hormonal profile and the presence of psychiatric comorbidity. Methods Sixty-one patients focused on type of epilepsy, frequency of seizures, AEDs, hormonal profile and presence of mood disorders. We excluded all patients with severe neurologic and psychiatric impairment and patient who were not able to fill questionnaires. Mean age was 31.2 years (range 18-50 years); 31 patients (50.8%) had an idiopathic generalised epilepsy and 30 (49.2%) a focal epilepsy; among them, latter 18 (60%) had probably symptomatic type and 12 (40%) symptomatic type. Sexual functions were evaluated by “International Inventory of Erectile Function” questionnaire. Results Out of 61 enrolled patients, 22 (36.7%) showed sexual dysfunctions: erectile dysfunctions in 14 (23%), orgasmic dysfunctions in (11.5%) and sexual drive dysfunctions in 12 (19.7%). Out of 61 patients, 36 were subjected to blood measurement of sexual hormones and 21 (58.3%) showed hormonal modifications. Conclusions Sexual dysfunction are present in 36.7% of enrolled males with epilepsy; there is any association between sexual dysfunctions and various AEDs in the treatment, except for carbamazepine (CBZ); there is not any association between sexual dysfunctions and frequency of seizures; hormonal changes are associated with sexual dysfunction in males with epilepsy treated with AEDs but not with the orgasmic dysfunction; there is not any association between hormonal changes and type of AEDs, except for CBZ; depression is associated with sexual dysfunctions.
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Можейко, М. П., С. А. Лихачев, and И. П. Марьенко. "Characteristics of the Effect of Optokinetic Stimulation on Maintaining the Balance Function in Patients with Vestibular Dysfunction of Various Genesis." Неврология и нейрохирургия. Восточная Европа, no. 1 (April 15, 2022): 7–16. http://dx.doi.org/10.34883/pi.2022.12.1.042.
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Цель. Оценить особенности влияния оптокинетической стимуляции на функцию равновесия у пациентов с вестибулярной дисфункцией в стадии субкомпенсации.Материалы и методы. Было обследовано 50 пациентов, из них 25 пациентов с центральным вестибулярным синдромом (ЦВС) при рассеянном склерозе (РС) (34±5,6 года), 25 пациентов (39±4,8 года) с периферическим вестибулярным синдромом (ПВС) при вестибулярном нейроните, доброкачественном позиционном пароксизмальном головокружении (ДППГ), болезни Меньера с жалобами на нарушение функции равновесия (ФР) и шаткость при ходьбе. Контрольная группа включала 25 здоровых испытуемых (31±6 лет). Всем обследованным для оценки ФР проводилось стабилометрическое исследование в стадии субкомпенсации. В исследовании использовался компьютерный стабилоанализатор «Стабилан-01-2» с БОС (производства ОАО «Ритм», Россия). Проводились тест Ромберга и тест «Оптокинетическая стимуляция» (ОКС).Результаты. Установлено достоверное изменение показателей КФР в тесте Ромберга со зрительным контролем у пациентов с ЦВС 75,4 [62,6; 83,08]% и ПВС 88,3 [84,03; 92,4]% по сравнению со здоровыми испытуемыми – 93,5 [89,4; 96,1]%. В группе испытуемых с ПВС при ОКС вниз достоверно увеличился показатель ССП ЦД до 8,3 [6,9; 11,7] мм/с (Т=35, Z=1,964, p<0,05), который прямо влияет на снижение показателя КФР до 75 [65; 83]% (T=63, Z=2,7, p<0,05) и демонстрирует напряжение некоторых звеньев статокинетической устойчивости (СКУ) для сохранения ФР. В группе испытуемых с ЦВС в стадии субкомпенсации установлено достоверное изменение всех показателей статокинезиограммы при ОКС во всех плоскостях, что ухудшает ФР до умеренной степени и указывает на зрительную стратегию замещения в сохранении ФР. Заключение. Результаты позволили выявить ведущие стратегии поддержания ФР у пациентов с ВД и на этой основе целесообразность использования методов медицинской реабилитации. Установлена зрительная стратегия замещения в поддержании ФР в группе с ЦВС, что подтверждено достоверными изменениями показателей статокинезиограммы при воздействии ОКС и указывает на значимость применения в медицинской реабилитации подходов для стимуляции проприоцептивной афферентации. В группе с ПВС не установлено зрительной зависимости, отмечена тенденция к изменению показателей статокинезиограммы, что отражает напряжение процессов, направленных на сохранение ФР и говорит о ведущей роли проприоцептивной стратегии в сохранении равновесия. Purpose. To evaluate the features of the effect of optokinetic stimulation on the balance function in patients with vestibular dysfunction from the subcompensation stage.Materials and methods. 50 patients examined, including 25 patients with central vestibular syndrome (CVS) in multiple sclerosis (MS) (34±5.6), 25 patients (39±4.8) with peripheral vestibular syndrome (PVS) with vestibular neuritis, benign positional paroxysmal vertigo (BPPV), Meniere’s disease with complaints of impaired balance function (BF) and unsteadiness in walking. The control group included 25 healthy subjects (31±6). All the examined patients underwent the stabilometric research in the subcompensation stage to assess BF. The computer stabiloanalyzer "Stabilan-01-2" with BOS (manufactured by JSC "Rhythm", Russia) used. The Romberg’s test and the "Optokinetic Stimulation" (OKS) test performed.Results. There was significant change in QBF indicators in the Romberg’s test with visual control, CVS 75.4 [62.6; 83.08]% and PVS 88.3 [84.03; 92.4]% compared with healthysubjects – 93.5 [89.4; 96.1]%. In the group with PVS, in OKS downwards, the ASM PC index significantly increased to 8.3 [6.9; 11.7] mm/s (T=35, Z=1.964, p<0.05), which directly affects the decrease in the QBF index to 75 [65; 83]% (T=63, Z=2.7, p<0.05). It demonstrates the stress of the static kinetic stability (SKS) to maintain the BF in stable level. In the group with CVS at the surcompensation stage, the significant change in all indicators of the statokinesiogram in OKS in all planes found, which worsens the BF to a moderate degree in general, which indicates for visual replacement strategy in maintaining the balance.Conclusion. The results help to identify the leading strategies for maintaining BF in patients with VD, and on this basis, the expediency of using medical rehabilitation methods. The visual replacement strategy established in maintaining BF in the group with CVS, which confirmed in significant changes in statokinesiogram indicators when exposed to OKS and indicates the importance of using approaches to stimulate proprioceptive afferentation in medical rehabilitation. In the group with PVS, no visual dependence established a tendency to change in the statokinesiogram indicators noted which reflects the tension of processes aimed at preserving BF and indicates the leading role of the proprioceptive strategy in maintaining balance.
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Brochini, Ana Paula Zanetti, Thiago Eiras Dela Coleta, Roberto Dela Coleta, Ana Lúcia Franco Micheloni, and Karina Eiras Dela Coleta Pizzol. "Are there evidences of correlation between temporomandibular dysfunction and orthodontic treatment?" Journal of Research in Dentistry 4, no. 3 (January 30, 2017): 95. http://dx.doi.org/10.19177/jrd.v4e3201695-99.
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Aim: The aim of this study was verifying, through literature review, whether there are evidences of correlation between temporomandibular dysfunctions and the orthodontic treatment.Material and Methods: Papers published from 1981 to 2015 were excluded and 41 articles and 06 books composed this review.Results: It is known that temporomandibular dysfunctions is a general term that represents signals and symptoms involving masticatory muscles, the temporomandibular joint and associated structures, and it is the main cause of pain from non-dental origin in the orofacial region, including head, face and other structures. Its etiology is multifactorial involving a large number of direct and indirect causes. Among them, the occlusion was already considered one of the main etiological factors for temporomandibular dysfunction. From epidemiological studies, it is known that signals and symptoms of temporomandibular dysfunction occur in healthy people, they are common in children and adolescents and tend to increase with age, particularly after adolescence, from 13 to 45 years old. The hypothesis for causality between orthodontics and temporomandibular dysfunction has led to legal problems for dentists and orthodontists. For these reasons, the interest on the relation among occlusal factors, orthodontic treatments and temporomandibular dysfunction has growth and several studies were carried out. Conclusions: We conclude that until this moment, it is not possible affirm that the orthodontic treatment could prevent, cure or cause temporomandibular dysfunction.
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Antonis, Theofilidis. "Dyslexia and Cerebral Dysfunction." Clinical Research and Clinical Trials 5, no. 1 (January 7, 2022): 01–03. http://dx.doi.org/10.31579/2693-4779/070.
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Children with slow visual-motor responses to visual-temporal response tests also have brain dysfunctions in the mobile and motor areas (6, 4). If the left parietal cortex does not participate in these dysfunctions, then this child will also have difficulties in reading. Furthermore, we could say that the brain dysfunctions that are detected by visual-motor tests and that the performance in them is low, are accompanied by difficulties in reading. Aim: In this study we want to show the function of the child's brain in dyslexia. Method: We followed the most up-to-date literature on the subject: neuropsychology and dyslexia. Conclusions: brain organization and its relationship to dyslexia is a major problem for Neuropsychology and Neurolinguistics.
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Siembida, Jakub, Piotr Frończuk, Justyna Morylowska-Topolska, Aleksandra Siek, and Hanna Karakuła-Juchnowicz. "An overlooked issue: sexual dysfunctions in men addicted to alcohol." Current Problems of Psychiatry 19, no. 2 (June 1, 2018): 112–24. http://dx.doi.org/10.2478/cpp-2018-0010.
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Abstract Introduction According to the data obtained in the EZOP Poland study (2015), the prevalence of alcohol dependence in lifetime in Poland amounts to about 2.2% of the population, entailing enormous social, family and personal harm, including health damage. It is estimated that about 72% of alcohol-dependent patients complain about one or more problems related to the sexual sphere, which may result from both the development of somatic complications in the course of alcohol dependence, and from psychiatric complications that themselves can lead to sexual dysfunction. There are reports and clinical observations indicating that the occurrence of sexual dysfunction (SD) can affect the shortening or interruption of the period of abstinence. Aim The aim of this work is to show sexual dysfunctions in alcohol-dependent men and to discuss the factors that may affect the occurrence of the above-mentioned dysfunctions. Material and methods The available literature was reviewed using Medline, Google Scholar and ScienceDirect browsers by entering the keywords: alcohol dependence, sexual dysfunction, comorbidity, alcohol-caused diseases and time descriptors: 1979-2016. Results • Alcohol dependence is associated with the occurrence of various types of sexual dysfunctions (SD). • The diagnosis of SD should take into account all possible causes that may lead to the development of SD in this group of patients, including the comorbidity of somatic diseases or the negative impact of drugs on sexual function. • Occurrence of SD is connected with a higher risk of abstinence interruption. • There is a need to carry out more research in order to better understand the relationship between alcohol dependence and the prevalence of sexual dysfunctions.
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Berková, Alena, Petr Vlček, Vladimír Červeňák, Jiří Dolina, Tamara Vystrčilová, Beata Hemmelová, and Zdeněk Chovanec. "Pelvic floor disorders of women from the point of coloproctologist‘s view." Gastroenterologie a hepatologie 76, no. 4 (August 31, 2022): 319–26. http://dx.doi.org/10.48095/ccgh2022319.
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Summary: Disorders of the pelvic floor and anorectal dysfunction are a major cause of discomfort for many women. As a result of shyness and embarrassment, women come for medical examination after a longer period of difficulties, mostly for progressive disorder of defecation and continence. Despite the low morbidity, anorectal dysfunctions have a very significant impact on patient’s quality of life and therefore diagnosis and subsequent treatment should be aimed at every possible cause. Gastroenterological examination can play an important part In primary detection, but also in the multidisciplinary diagnostic process of pelvic floor pathology. Likewise, coloproctology is an integral part of the diagnostic-therapeutic algorithm of pelvic dysfunctions. The aim of the article is to provide information on the pathophysiology, diagnosis and treatment of anorectal disorders from the perspective of coloproctology. Anorectal dysfunctions are a multidisciplinary problem, therefore, to achieve good treatment results, the cooperation of different specializations is essential. Key words: anorectal dysfunction – defecation – prolapse – rectocele – incontinence – rectopexy
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Ivanitska, Tetiana, and Olena Venger. "FEATURES OF SEXUAL DYSFUNCTIONS IN PATIENTS WITH NEUROTIC DISORDERS." Grail of Science, no. 20 (October 7, 2022): 155–59. http://dx.doi.org/10.36074/grail-of-science.30.09.2022.032.
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Deterioration of mental health is an extremely important risk factor for sexual dysfunction. The aim is to investigate sexual dysfunction in patients with neurotic mental disorders. Material. Peculiarities of sexual dysfunctions in 256 patients (120 men and 136 women) were analyzed. Research. Assessment of sexual dysfunctions was performed on the basis of individual interviews and questionnaires of each patient. Intimate disorders such as perversion, anorgasmia, deactualization, hypoaesthesia, hyperesthesia, decreased libido, alibidemia, decreased sexual activity, abstinence, decreased erection, premature ejaculation, and pain during sex were evaluated. Conclusions. The issue of sexual disorders in various forms of neurosis is an extremely relevant topic, as these disorders cause significant disharmony in different areas of life of patients. Not only does it not lose its relevance, but it is gaining more and more medical and social significance.
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Costa, Anna Maria Niccolai, Mauricio Silva de Lima, and Jair de Jesus Mari. "A systematic review on clinical management of antipsychotic-induced sexual dysfunction in schizophrenia." Sao Paulo Medical Journal 124, no. 5 (2006): 291–97. http://dx.doi.org/10.1590/s1516-31802006000500012.
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INTRODUCTION: Sexual dysfunction frequently occurs in patients with schizophrenia under antipsychotic therapy, and the presence of sexual side effects may affect compliance. The aim of this study was to review and describe clinical findings relating to the appropriate management of such dysfunctions. MATERIAL AND METHODS: The research was carried out through Medline (from 1966 to March 2005), PsycInfo (from 1974 to March 2005), and Cochrane Library (from 1965 to March 2005) and included any kind of study, from case reports to randomized trials. RESULTS: The most common sexual dysfunctions found in the literature were libido decrease, difficulties in achieving and maintaining erection, ejaculatory dysfunction, orgasmic dysfunction, and menstrual irregularities. Thirteen papers were found: eight of them were open-label studies, four were descriptions of cases, and only one was a randomized clinical trial. All of them were short-term and had small sample sizes. The agents used were: bromocriptine, cabergoline, cyproheptadine, amantadine, shakuyaku-kanzo-to, sildenafil and selegiline. DISCUSSION: There was no evidence that those agents had proper efficacy in treating the antipsychotic-induced sexual dysfunction. An algorithm for managing sexual dysfunction induced by antipsychotics is suggested as a support for clinical decisions. Since the outcome from schizophrenia treatment is strongly related to compliance with the antipsychotics, prevention of sexual dysfunction is better than its treatment, since there is a scarcity of data available regarding the efficacy of intervention to deal with these problems.
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M., Chaithra, Anitha G. S., and Savitha C. "A prospective study of thyroid dysfunction in dysfunctional uterine bleeding." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 8, no. 11 (October 23, 2019): 4387. http://dx.doi.org/10.18203/2320-1770.ijrcog20194861.
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Background: Dysfunctional uterine bleeding is abnormal uterine bleeding in the absence of any palpable pelvic pathology and demonstrable extra genital causes. Thyroid dysfunction is the systemic disease most often associated with abnormal uterine bleeding. Aim was to evaluate thyroid function test in women with DUB; to assess bleeding pattern in thyroid dysfunction.Methods: Prospective observational study was done in the department of obstetrics and gynaecology, Vanivilas hospital, Bangalore from august 2018 to July 2019. Pre structured and predesigned proforma filled. All routine blood investigations including serum T3, T4, TSH, USG were advised. These patients were categorized as euthyroid, subclinical hypothyroid, hypothyroid or hyperthyroid based on thyroid profile.Results: 0.5% belonged to the age group of 31-40 years, prevalence of subclinical hypothyroidism is 11%, there were 5.5% of cases of hypothyroidism and 1.5% case of hyperthyroidism.Conclusions: Thyroid screening must be done mandatory for all the cases of DUB and prompt response to treatment with thyroxine would avoid unnecessary surgeries, hormonal treatment, and associated comorbities.
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Lee, Kwang-Hyuk, and Leanne M. Williams. "Eye Movement Dysfunction as a Biological Marker of Risk for Schizophrenia." Australian & New Zealand Journal of Psychiatry 34, no. 1_suppl (February 2000): A91—A100. http://dx.doi.org/10.1177/000486740003401s14.
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Objective Our aim was to review smooth pursuit eye movement (SPEM) studies in schizophrenia and groups at high risk for schizophrenia, with a view to evaluating the utility of SPEM dysfunction as a biological marker of risk for schizophrenia. Method Smooth pursuit eye movement studies, related saccade function and the unresolved issues in this area of schizophrenia research were addressed. The different perspectives on the trait marker status of SPEM dysfunction, provided by both high-risk studies and related developmental research were considered. Attention was also given to the relationship between eye movement dysfunction and symptom profiles. Results Converging evidence points to the robust and specific nature of SPEM dysfunction in schizophrenia, and highlights the role of frontal lobe and a related network dysfunction. The vast majority of ‘high risk’ studies support the view that SPEM dysfunction is also genetically specific to schizophrenia, and is not simply due to the overt expression of this illness. Studies assessing SPEM in relation to symptomatology show an association with the Disorganisation syndrome in particular. Conclusions Evidence for the specificity of SPEM dysfunction to diagnosed schizophrenia, as well as to healthy individuals with a genetic vulnerability to schizophrenia, suggests that the SPEM task has efficacy as a test of gene carrier status in schizophrenia, and therefore as a trait marker of risk for schizophrenia. Future studies should seek to explore the relationships between SPEM and other eye movement dysfunctions (antisaccades, express saccades), in view of evidence that some of these dysfunctions also show specificity for schizophrenia.