scholarly journals Changes in Cardiovascular Structure and Physiology Following Polystyrene Nanoparticle Exposure

2020 ◽  
Vol 3 ◽  
Author(s):  
Zachary Lett ◽  
Shelby Skidmore ◽  
Nathan Alves

Background  Microplastic (MP) pollution has been a growing concern in recent decades due to the proliferation and ease of manufacturing regarding plastics products.  Polystyrene (PS), being one the most abundant plastic polymers, is the subject of frequent studies due to its ubiquitous nature.  Trophic transfer, inhalation, and dermal exposure are all routes by which humans may be exposed to MPs every day.  There are undoubtedly more physiological consequences than we are currently aware of; however, many of these concerns are beginning to be better understood.    Their distribution throughout the body dictates the potential threats to human health.  The cardiovascular system is potentially the most susceptible, as it is the first medium the MPs are exposed to after entering the body.  Consequently, the cardiovascular system and thrombus generation is one such area where much recent attention has been allocated.    Project Methods  Data was gathered from a variety of well-established research articles to review the relationship between PS exposure and thrombus formation in vivo.  Additionally, this review looks at documented effects of MPs on platelet aggregation and discusses mechanisms through which these pathologies take place.    Results  PS plastics have varying impact on thrombus formation contingent upon both surface modifications and particle size.  Aminated PS appears to be the most potent regarding the generation of thrombi in vivo.  Literature on platelet aggregation is more consistent, with most studies revealing that carboxylated and aminated forms enhance aggregation while unmodified PS had insignificant effects.  Conclusion/Potential Impact  There is substantial ambiguity surrounding this field and more studies need to be conducted to reveal the full extent of pathologies caused by PS microplastics.  Most studies have been done with marine life, which may not accurately reflect MPs effects in humans.  Further research will allow us to begin developing viable solutions for those most susceptible to cardiovascular diseases. 

2013 ◽  
Vol 38 (3) ◽  
Author(s):  
Suelen Moraes de Lorenzo ◽  
Vitor Engrácia Valenti ◽  
Luiz Carlos de Abreu ◽  
Celso Ferreira ◽  
Carlos Bandeira de Mello Monteiro

The literature indicates stress as a response of the organism to a stimulation that requires enormous efforts to adapt to the changes in the environment and the body. When an individual is subjected to stress, the autonomic nervous system is triggered, the sympathetic pathway is activated, and the parasympathetic system is suppressed, which exerts several effects on the cardiovascular system and affects heart rate variability. This research aimed to conduct a literature review to find and analyze the studies that address clearly the implications of stress on heart rate variability. The methodology employed was an active search in the databases SciELO, PubMed and Lilacs. The results were five articles, most of which suggest a relationship between stress and heart rate variability. We observed that the majority of the studies indicated a strong association between stress and cardiac autonomic activity. The stress is present in the daily activities of the population, especially in labor. The subject is vast, however, were observed in the references the effects of stress on the body making it vulnerable to diseases. Thus, this information may contribute to the aid of preventive strategies against stress and diseases of the cardiovascular system.


1994 ◽  
Vol 71 (01) ◽  
pp. 095-102 ◽  
Author(s):  
Désiré Collen ◽  
Hua Rong Lu ◽  
Jean-Marie Stassen ◽  
Ingrid Vreys ◽  
Tsunehiro Yasuda ◽  
...  

SummaryCyclic Arg-Gly-Asp (RGD) containing synthetic peptides such as L-cysteine, N-(mercaptoacetyl)-D-tyrosyl-L-arginylglycyl-L-a-aspartyl-cyclic (1→5)-sulfide, 5-oxide (G4120) and acetyl-L-cysteinyl-L-asparaginyl-L-prolyl-L-arginyl-glycyl-L-α-aspartyl-[0-methyltyrosyl]-L-arginyl-L-cysteinamide, cyclic 1→9-sulfide (TP9201) bind with high affinity to the platelet GPIIb/IIIa receptor.The relationship between antithrombotic effect, ex vivo platelet aggregation and bleeding time prolongation with both agents was studied in hamsters with a standardized femoral vein endothelial cell injury predisposing to platelet-rich mural thrombosis, and in dogs with a carotid arterial eversion graft inserted in the femoral artery. Intravenous administration of G4120 in hamsters inhibited in vivo thrombus formation with a 50% inhibitory bolus dose (ID50) of approximately 20 μg/kg, ex vivo ADP-induccd platelet aggregation with ID50 of 10 μg/kg, and bolus injection of 1 mg/kg prolonged the bleeding time from 38 ± 9 to 1,100 ± 330 s. Administration of TP9201 in hamsters inhibited in vivo thrombus formation with ID50 of 30 μg/kg, ex vivo platelet aggregation with an ID50 of 50 μg/kg and bolus injection of 1 mg/kg did not prolong the template bleeding time. In the dog eversion graft model, infusion of 100 μg/kg of G4120 over 60 min did not fully inhibit platelet-mediated thrombotic occlusion but was associated with inhibition of ADP-induccd ex vivo platelet aggregation and with prolongation of the template bleeding time from 1.3 ± 0.4 to 12 ± 2 min. Infusion of 300 μg/kg of TP9201 over 60 min completely prevented thrombotic occlusion, inhibited ex vivo platelet aggregation, but was not associated with prolongation of the template bleeding time.TP9201, unlike G4120, inhibits in vivo platelet-mediated thrombus formation without associated prolongation of the template bleeding time.


2021 ◽  
pp. 097168582110159
Author(s):  
Sital Mohanty ◽  
Subhasis Sahoo ◽  
Pranay Kumar Swain

Science, technology and human values have been the subject of enquiry in the last few years for social scientists and eventually the relationship between science and gender is the subject of an ongoing debate. This is due to the event of globalization which led to the exponential growth of new technologies like assisted reproductive technology (ART). ART, one of the most iconic technological innovations of the twentieth century, has become increasingly a normal social fact of life. Since ART invades multiple human discourses—thereby transforming culture, society and politics—it is important what is sociological about ART as well as what is biological. This article argues in commendation of sociology of technology, which is alert to its democratic potential but does not concurrently conceal the historical and continuing role of technology in legitimizing gender discrimination. The article draws the empirical insights from local articulations (i.e., Odisha state in eastern India) for the understandings of motherhood, freedom and choice, reproductive right and rights over the body to which ART has contributed. Sociologically, the article has been supplemented within the broader perspectives of determinism, compatibilism alongside feminism.


2018 ◽  
Vol 115 (11) ◽  
pp. 1672-1679 ◽  
Author(s):  
Qi Ma ◽  
Weilin Zhang ◽  
Chongzhuo Zhu ◽  
Junling Liu ◽  
Quan Chen

Abstract Aims AKT kinase is vital for regulating signal transduction in platelet aggregation. We previously found that mitochondrial protein FUNDC2 mediates phosphoinositide 3-kinase (PI3K)/phosphatidylinositol-3,4,5-trisphosphate (PIP3)-dependent AKT phosphorylation and regulates platelet apoptosis. The aim of this study was to evaluate the role of FUNDC2 in platelet activation and aggregation. Methods and results We demonstrated that FUNDC2 deficiency diminished platelet aggregation in response to a variety of agonists, including adenosine 5′-diphosphate (ADP), collagen, ristocetin/VWF, and thrombin. Consistently, in vivo assays of tail bleeding and thrombus formation showed that FUNDC2-knockout mice displayed deficiency in haemostasis and thrombosis. Mechanistically, FUNDC2 deficiency impairs the phosphorylation of AKT and downstream GSK-3β in a PI3K-dependent manner. Moreover, cGMP also plays an important role in FUNDC2/AKT-mediated platelet activation. This FUNDC2/AKT/GSK-3β/cGMP axis also regulates clot retraction of platelet-rich plasma. Conclusion FUNDC2 positively regulates platelet functions via AKT/GSK-3β/cGMP signalling pathways, which provides new insight for platelet-related diseases.


Blood ◽  
1998 ◽  
Vol 91 (5) ◽  
pp. 1582-1589
Author(s):  
Mei-Chi Chang ◽  
Hui-Kuan Lin ◽  
Hui-Chin Peng ◽  
Tur-Fu Huang

A potent platelet glycoprotein Ib (GPIb) antagonist, crotalin, with a molecular weight of 30 kD was purified from the snake venom ofCrotalus atrox. Crotalin specifically and dose dependently inhibited aggregation of human washed platelets induced by ristocetin with IC50 of 2.4 μg/mL (83 nmol/L). It was also active in inhibiting ristocetin-induced platelet aggregation of platelet-rich plasma (IC50, 6.3 μg/mL). 125I-crotalin bound to human platelets in a saturable and dose-dependent manner with a kd value of 3.2 ± 0.1 × 10−7 mol/L, and its binding site was estimated to be 58,632 ± 3,152 per platelet. Its binding was specifically inhibited by a monoclonal antibody, AP1 raised against platelet GPIb. Crotalin significantly prolonged the latent period in triggering platelet aggregation caused by low concentration of thrombin (0.03 U/mL), and inhibited thromboxane B2formation of platelets stimulated either by ristocetin plus von Willebrand factor (vWF), or by thrombin (0.03 U/mL). When crotalin was intravenously (IV) administered to mice at 100 to 300 μg/kg, a dose-dependent prolongation on tail bleeding time was observed. The duration of crotalin in prolonging tail bleeding time lasted for 4 hours as crotalin was given at 300 μg/kg. In addition, its in vivo antithrombotic activity was evidenced by prolonging the latent period in inducing platelet-rich thrombus formation by irradiating the mesenteric venules of the fluorescein sodium-treated mice. When administered IV at 100 to 300 μg/kg, crotalin dose dependently prolonged the time lapse in inducing platelet-rich thrombus formation. In conclusion, crotalin specifically inhibited vWF-induced platelet agglutination in the presence of ristocetin because crotalin selectively bound to platelet surface receptor-glycoprotein Ib, resulting in the blockade of the interaction of vWF with platelet membrane GPIb. In addition, crotalin is a potent antithrombotic agent because it pronouncedly blocked platelet plug formation in vivo.


Blood ◽  
1998 ◽  
Vol 91 (5) ◽  
pp. 1582-1589 ◽  
Author(s):  
Mei-Chi Chang ◽  
Hui-Kuan Lin ◽  
Hui-Chin Peng ◽  
Tur-Fu Huang

AbstractA potent platelet glycoprotein Ib (GPIb) antagonist, crotalin, with a molecular weight of 30 kD was purified from the snake venom ofCrotalus atrox. Crotalin specifically and dose dependently inhibited aggregation of human washed platelets induced by ristocetin with IC50 of 2.4 μg/mL (83 nmol/L). It was also active in inhibiting ristocetin-induced platelet aggregation of platelet-rich plasma (IC50, 6.3 μg/mL). 125I-crotalin bound to human platelets in a saturable and dose-dependent manner with a kd value of 3.2 ± 0.1 × 10−7 mol/L, and its binding site was estimated to be 58,632 ± 3,152 per platelet. Its binding was specifically inhibited by a monoclonal antibody, AP1 raised against platelet GPIb. Crotalin significantly prolonged the latent period in triggering platelet aggregation caused by low concentration of thrombin (0.03 U/mL), and inhibited thromboxane B2formation of platelets stimulated either by ristocetin plus von Willebrand factor (vWF), or by thrombin (0.03 U/mL). When crotalin was intravenously (IV) administered to mice at 100 to 300 μg/kg, a dose-dependent prolongation on tail bleeding time was observed. The duration of crotalin in prolonging tail bleeding time lasted for 4 hours as crotalin was given at 300 μg/kg. In addition, its in vivo antithrombotic activity was evidenced by prolonging the latent period in inducing platelet-rich thrombus formation by irradiating the mesenteric venules of the fluorescein sodium-treated mice. When administered IV at 100 to 300 μg/kg, crotalin dose dependently prolonged the time lapse in inducing platelet-rich thrombus formation. In conclusion, crotalin specifically inhibited vWF-induced platelet agglutination in the presence of ristocetin because crotalin selectively bound to platelet surface receptor-glycoprotein Ib, resulting in the blockade of the interaction of vWF with platelet membrane GPIb. In addition, crotalin is a potent antithrombotic agent because it pronouncedly blocked platelet plug formation in vivo.


Author(s):  
Donald W. Winnicott

In this paper on psycho-somatic disorders, Winnicott begins by acknowledging the vastness of the subject. Psycho-somatic disorder merges into the universal problem of the healthy interaction between the psyche and the soma—that is, between the personality of an individual and the body in which the person lives. The relationship between body and mind, role of early development and stages of emotional development are also discussed.


Polymers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 1712
Author(s):  
Miran Hannah Choi ◽  
Alexandra Blanco ◽  
Samuel Stealey ◽  
Xin Duan ◽  
Natasha Case ◽  
...  

Platelet-rich plasma (PRP) is an autologous blood product that contains a variety of growth factors (GFs) that are released upon platelet activation. Despite some therapeutic potential of PRP in vitro, in vivo data are not convincing. Bolus injection of PRP is cleared rapidly from the body diminishing its therapeutic efficacy. This highlights a need for a delivery vehicle for a sustained release of PRP to improve its therapeutic effect. In this study, we used microfluidics to fabricate biodegradable PRP-loaded polyethylene glycol (PEG) microspheres. PRP was incorporated into the microspheres as a lyophilized PRP powder either as is (powder PRP) or first solubilized and pre-clotted to remove clots (liquid PRP). A high PRP loading of 10% w/v was achieved for both PRP preparations. We characterized the properties of the resulting PRP-loaded PEG microspheres including swelling, modulus, degradation, and protein release as a function of PRP loading and preparation. Overall, loading powder PRP into the PEG microspheres significantly affected the properties of microspheres, with the most pronounced effect noted in degradation. We further determined that microsphere degradation in the presence of powder PRP was affected by platelet aggregation and clotting. Platelet aggregation did not prevent but prolonged sustained PRP release from the microspheres. The delivery system developed and characterized herein could be useful for the loading and releasing of PRP to promote tissue regeneration and wound healing or to suppress tissue degeneration in osteoarthritis, and intervertebral disc degeneration.


Zootaxa ◽  
2012 ◽  
Vol 3556 (1) ◽  
pp. 80 ◽  
Author(s):  
MING LI ◽  
WEIDONG LI ◽  
XIANPING GE ◽  
CHONG WANG ◽  
LIN ZHANG ◽  
...  

The peritrich Epistylis unioi Gong, 1986 was collected from fry of Pelteobagrus fulvidraco during parasite surveys at Hon-ghu Lake Fish Hatchery, Hubei Province, central China in May 2010 and redescribed. Some revisions were done basedon live, silver-impregnated, and SEM specimens. The zooid is elongated and somewhat vase-like in shape, measuring56–88 × 22–38 µm in vivo. A single contractile vacuole is apically located slightly below the peristome disc. The macro-nucleus is horseshoe-shaped, always transversely situated at the foreside of the body. Haplokinety (H) and polykinety (Po)complete one and one-half circuits on the peristome before entering the infundibulum, with a distal kinetal fragment pres-ent at the distal end. Silverline system consists of 37–45 pellicular striations between peristome and aboral trochal band(TB), and of 26–33 between TB and scopula. Colony is asymmetrically and dichotomously branched, usually with onlytwo levels of branches. In addition, the telotrochs of E. unioi were also observed and its structures were described herein.Besides, obvious skin lesions caused by the ringlike base of E. unioi were detected and the relationship between these epizooites and their hosts was briefly discussed as well.


Sign in / Sign up

Export Citation Format

Share Document