scholarly journals The 3-step Greek protocol of neck skin rejuvenation inspired by a case of pseudoxanthoma elasticum: combination of laser skin resurfacing, collagen booster and PRP

2021 ◽  
Vol 5 (3) ◽  
pp. 66-73
Author(s):  
Emmanouil Dimonitsas
Keyword(s):  
Skin Biopsy ◽  
Platelet Rich Plasma ◽  
Genetic Disorder ◽  
Pseudoxanthoma Elasticum ◽  
Treatment Session ◽  
Elastic Fibers ◽  
Type I ◽  
Skin Resurfacing ◽  
Physiological Ageing ◽  
The Aesthetic

Aim: The physiological ageing process causes significant changes in the extracellular matrix (ECM) of the neck skin, which are the first signs of ageing witness for women. We are inspired by a young woman, who suffers from a rare genetic disorder called pseudoxanthoma elasticum (PXE), which manifests irregular, thickened, fragmented and haphazardly orientated elastic fibers. We herein present a combination of three different therapies (laser skin resurfacing, type I horse collagen boosters and platelet rich plasma)as an approach to ameliorate neck skin sagging. Methods: A 28-year-old Roma woman with a clinically diagnosed PXE, verified by ophthalmologic evidence and skin biopsy, underwent 3 sessions of this combined protocol every 3 weeks. One month after the last treatment session, a new biopsy was taken. During this period, the patient was encouraged for daily topical application of collagen mousse and vitamin C combined with sun block SPF50, along with limited exposure to sunlight. Results: Clinical assessment supported by photographic documentation was performed at each session. Severe changes in hydration and tightening of the neck skin were obvious 3 weeks after the second session, although the verification of the results was substantiated with the pathology of the post treatment skin biopsy obtained 1 month following the completion of the protocol. The elastic fibers in the mid-dermis were dense, non-fragmented and parallel oriented. The aesthetic performance was evident until the final follow-up visit. Conclusions: Nowadays, the primary goal of aesthetic medical research is oriented to the dermis bio-reconstruction, where specific treatments try to improve the dermis quality from the inside to repair imperfections of skin ageing. The key of success is attributed to the best possible treatment combination capable of fibroblast stimulation.

scholarly journals Histopathology of Pseudoxanthoma Elasticum and Related Disorders: Histological Hallmarks and Diagnostic Clues

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Mohammad J. Hosen ◽  
Anouck Lamoen ◽  
Anne De Paepe ◽  
Olivier M. Vanakker
Keyword(s):  
Differential Diagnosis ◽  
Skin Biopsy ◽  
Clinical Diagnosis ◽  
Molecular Analysis ◽  
Pseudoxanthoma Elasticum ◽  
Elastic Fibers ◽  
Causal Gene ◽  
Ectopic Mineralization ◽  
Golden Standard ◽  
Histological Characteristics

Among ectopic mineralization disorders, pseudoxanthoma elasticum (PXE)—a rare genodermatosis associated with ocular and cardiovascular manifestations—is considered a paradigm disease. The symptoms of PXE are the result of mineralization and fragmentation of elastic fibers, the exact pathophysiology of which is incompletely understood. Though molecular analysis of the causal gene,ABCC6, has a high mutation uptake, a skin biopsy has until now been considered the golden standard to confirm the clinical diagnosis. Although the histological hallmarks of PXE are rather specific, several other diseases—particularly those affecting the skin—can present with clinical and/or histological characteristics identical to or highly resemblant of PXE. In this paper, we will summarize the histopathological features of PXE together with those of disorders that are most frequently considered in the differential diagnosis of PXE.

Fibrillar type I collagens enhance platelet-dependent thrombin generation via glycoprotein VI with direct support of α2β1 but not αIIbβ3 integrin

2005 ◽  
Vol 94 (07) ◽  
pp. 107-114 ◽  
Author(s):  
Christelle Lecut ◽  
Martine Jandrot-Perrus ◽  
Marion A. H. Feijge ◽  
Judith M. E. M. Cosemans ◽  
Johan W. M. Heemskerk
Keyword(s):  
Thrombin Generation ◽  
Type I Collagen ◽  
Platelet Rich Plasma ◽  
Procoagulant Activity ◽  
Type I ◽  
Platelet Surface ◽  
Glycoprotein Vi ◽  
Collagen Receptors ◽  
Fibrillar Collagens

SummaryThe role of collagens and collagen receptors was investigated in stimulating platelet-dependent thrombin generation. Fibrillar type-I collagens, including collagen from human heart, were most potent in enhancing thrombin generation, in a way dependent on exposure of phosphatidylserine (PS) at the platelet surface. Soluble, non-fibrillar type-I collagen required pre-activation of integrin α2β1 with Mn2+ for enhancement of thrombin generation. With all preparations, blocking of glycoprotein VI (GPVI) with 9O12 antibody abrogated the collagen-enhanced thrombin generation, regardless of the α2β1 activation state. Blockade of α2β1 alone or antagonism of autocrine thromboxane A2 and ADP were less effective. Blockade of αIIbβ3 with abciximab suppressed thrombin generation in platelet-rich plasma, but this did not abolish the enhancing effect of collagens. The high activity of type-I fibrillar collagens in stimulating GPVI-dependent procoagulant activity was confirmed in whole-blood flow studies, showing that these collagens induced relatively high expression of PS. Together, these results indicate that: i) fibrillar type-I collagen greatly enhances thrombin generation, ii) GPVI-induced platelet activation is principally responsible for the procoagulant activity of fibrillar and non-fibrillar collagens, iii) α2β1 and signaling via autocrine mediators facilitate and amplify this GPVI activity, and iv) αIIbβ3 is not directly involved in the collagen effect.

Elastin exhibits a distinctive temporal and spatial pattern of distribution in the developing chick limb in association with the establishment of the cartilaginous skeleton

1994 ◽  
Vol 107 (9) ◽  
pp. 2623-2634 ◽  
Author(s):  
J.M. Hurle ◽  
G. Corson ◽  
K. Daniels ◽  
R.S. Reiter ◽  
L.Y. Sakai ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Spatial Pattern ◽  
Elastic Fiber ◽  
Spatial Location ◽  
Limb Bud ◽  
Confocal Laser ◽  
Elastic Fibers ◽  
Type I ◽  
Temporal And Spatial

In this work we have analyzed the presence of elastic components in the extracellular matrices of the developing chick leg bud. The distributions of elastin and fibrillin were studied immunohistochemically in whole-mount preparations using confocal laser microscopy. The association of these constituents of the elastic matrix with other components of the extracellular matrix was also studied, using several additional antibodies. Our results reveal the transient presence of an elastin-rich scaffold of extracellular matrix fibrillar material in association with the establishment of the cartilaginous skeleton of the leg bud. The scaffold consisted of elastin-positive fibers extending from the ectodermal surface of the limb to the central cartilage-forming regions and between adjacent cartilages. Fibrillin immunolabeling was negative in this fibrillar scaffold while other components of the extracellular matrix including: tenascin, laminin and collagens type I, type III and type VI; appeared codistributed with elastin in some regions of the scaffold. Progressive changes in the spatial pattern of distribution of the elastin-positive scaffold were detected in explant cultures in which one expects a modification in the mechanical stresses of the tissues related to growth. A scaffold of elastin comparable to that found in vivo was also observed in high-density micromass cultures of isolated limb mesodermal cells. In this case the elastic fibers are observed filling the spaces located between the cartilaginous nodules. The fibers become reoriented and attach to the ectodermal basal surface when an ectodermal fragment is located at the top of the growing micromass. Our results suggest that the formation of the cartilaginous skeleton of the limb involves the segregation of the undifferentiated limb mesenchyme into chondrogenic and elastogenic cell lineages. Further, a role for the elastic fiber scaffold in coordinating the size and the spatial location of the cartilaginous skeletal elements within the limb bud is also suggested from our observations.

Wound-healing effects of human dermal components with gelatin dressing

2017 ◽  
Vol 32 (6) ◽  
pp. 716-724 ◽  
Author(s):  
Hyun-Jun Jang ◽  
Yu-mi Kim ◽  
Bo-Young Yoo ◽  
Young-Kwon Seo
Keyword(s):  
Wound Healing ◽  
Normal Skin ◽  
Treated Group ◽  
Collagen Type I ◽  
Skin Wound ◽  
Blue Staining ◽  
Elastic Fibers ◽  
Type I ◽  
Initial Area

There have been numerous investigations regarding various types of dressings and artificial dermis of solid form, yet limited research and development on paste types, such as hydrogels with dermal powder, have ensued. In this study, we compared the in vivo wound healing effects of gelatin paste containing dermal powder to a collagen type I/chondroitin 6-sulfate (coll/chondroitin) sponge and gelatin alone, after 48 days post grafting, in a skin wound rat model. In the dermis powder/gelatin paste-treated group, wound area contraction was minimized 50%, while in the gelatin and coll/chondroitin sponge groups, the initial area contracted 83–85% and 79–85%, respectively. Histological analysis revealed the wounds treated with dermal powder/gelatin were associated with many fibroblasts, which infiltrated the wound bed, as well as thick collagen bundles that were arranged in dendritic arrays, resembling normal skin. Furthermore, in contrast to the gelatin- and coll/chondroitin sponge-treated groups, the powder/gelatin paste-treated wounds exhibited an abundance of elastic fibers (Victoria blue staining) and extensive formation of blood vessels around the dermis (CD31 staining). Therefore, the dermis powder/gelatin paste not only renders convenience to users but also has prominent wound-healing effects on full-thickness wounds.

scholarly journals Inhibition of platelet function by A02131-1, a novel inhibitor of cGMP- specific phosphodiesterase, in vitro and in vivo

Blood ◽  
1996 ◽  
Vol 87 (9) ◽  
pp. 3758-3767 ◽  
Author(s):  
SM Yu ◽  
SY Tsai ◽  
SC Kuo ◽  
JT Ou
Keyword(s):  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Atp Release ◽  
Camp Level ◽  
Cgmp Level ◽  
Prostaglandin D2 ◽  
Type I ◽  
Type V

The effect of A02131–1 [3-(5′-hydroxymethyl-2′-furyl)-1-benzyl thieno (3,2-c)pyrazole], a cGMP-specific phosphodiesterase (PDE) inhibitor, on platelet function was investigated. The compound was found to inhibit the aggregation of and adenosine triphosphate (ATP) release from human platelet-rich plasma and washed platelets that were induced by aggregation inducing drugs such as arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), adenosine diphosphate (ADP) and A23187, and the inhibitory effect was concentration-dependent. A02131–1 also disaggregated the performed platelet aggregates induced by these inducers. Thromboxane B2 (TXB2) formations caused by collagen, PAF, ADP, and A23187 were inhibited by A02131–1 at concentrations that did not affect the AA-induced formation of TXB2 and prostaglandin D2 (PGD2). A02131–1 suppressed both the generation of inositol 1,4,5- triphosphate (IP3) and the increase of intracellular Ca2+ concentration stimulated by these aggregation inducers. A02131–1 was shown to increase the cAMP and cGMP levels in platelets and the extent was found to be dependent on concentration as well as time. A02131–1 increased the cAMP level much more slowly than the cGMP level. Activities of adenylate cyclase, guanylate cyclase, and PDEs (type I and III) were not altered by A02131–1. However, the activity of cGMP-specific PDE (type V) was inhibited by A02131–1. The antiplatelet aggregation activity and the effect on raising cAMP level of A02131–1 were both potentiated by prostaglandin E1 (PGE1). In the mouse tail bleeding test, A02131–1 was clearly shown to be more effective than dipyridamole in prolonging the tail bleeding time of conscious mice. These data indicate that A02131–1 is a cGMP-specific PDE (type V) inhibitor in human platelets.

scholarly journals Moyamoya syndrome associated with neurofibromatosis type I in a pediatric patient

2011 ◽  
Vol 129 (2) ◽  
pp. 110-112 ◽  
Author(s):  
Luiz Guilherme Darrigo Júnior ◽  
Elvis Terci Valera ◽  
André de Aboim Machado ◽  
Antonio Carlos dos Santos ◽  
Carlos Alberto Scrideli ◽  
...  
Keyword(s):  
Moyamoya Disease ◽  
Autosomal Dominant ◽  
Genetic Disorder ◽  
Neurofibromatosis Type ◽  
Type I ◽  
Moyamoya Syndrome ◽  
Radiological Findings ◽  
Convulsive Seizures ◽  
Age Range

CONTEXT: Neurofibromatosis type 1 (NF-1) is the most prevalent autosomal dominant genetic disorder among humans. Moyamoya disease is a cerebral vasculopathy that is only rarely observed in association with NF-1, particularly in the pediatric age range. The present study reports an occurrence of this association in an infant. CASE REPORT: An eight-month-old female presented convulsive seizures with clonic movements. The patient suffered an ischemic stroke with hemiparesis. Magnetic resonance imaging revealed radiological findings compatible with moyamoya disease. The diagnosis of NF-1 was made at the age of 20 months. CONCLUSION: Despite the rarity of this association in childhood, children with focal neurological symptoms and a diagnosis of NF-1 deserve to be investigated for moyamoya syndrome.

scholarly journals Human USP18 deficiency underlies type 1 interferonopathy leading to severe pseudo-TORCH syndrome

2016 ◽  
Vol 213 (7) ◽  
pp. 1163-1174 ◽  
Author(s):  
Marije E.C. Meuwissen ◽  
Rachel Schot ◽  
Sofija Buta ◽  
Grétel Oudesluijs ◽  
Sigrid Tinschert ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Genetic Disorders ◽  
Genetic Disorder ◽  
Congenital Infection ◽  
Infectious Agent ◽  
Negative Regulator ◽  
Type I ◽  
Loss Of Function

Pseudo-TORCH syndrome (PTS) is characterized by microcephaly, enlarged ventricles, cerebral calcification, and, occasionally, by systemic features at birth resembling the sequelae of congenital infection but in the absence of an infectious agent. Genetic defects resulting in activation of type 1 interferon (IFN) responses have been documented to cause Aicardi-Goutières syndrome, which is a cause of PTS. Ubiquitin-specific peptidase 18 (USP18) is a key negative regulator of type I IFN signaling. In this study, we identified loss-of-function recessive mutations of USP18 in five PTS patients from two unrelated families. Ex vivo brain autopsy material demonstrated innate immune inflammation with calcification and polymicrogyria. In vitro, patient fibroblasts displayed severely enhanced IFN-induced inflammation, which was completely rescued by lentiviral transduction of USP18. These findings add USP18 deficiency to the list of genetic disorders collectively termed type I interferonopathies. Moreover, USP18 deficiency represents the first genetic disorder of PTS caused by dysregulation of the response to type I IFNs. Therapeutically, this places USP18 as a promising target not only for genetic but also acquired IFN-mediated CNS disorders.

scholarly journals Human platelet-rich plasma improves the nesting and differentiation of human chondrocytes cultured in stabilized porous chitosan scaffolds

2017 ◽  
Vol 8 ◽  
pp. 204173141769754 ◽  
Author(s):  
Maria Sancho-Tello ◽  
Sara Martorell ◽  
Manuel Mata Roig ◽  
Lara Milián ◽  
MA Gámiz-González ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Articular Chondrocytes ◽  
Platelet Rich Plasma ◽  
Cartilage Regeneration ◽  
Cell Number ◽  
Type I ◽  
Type Ii ◽  
Cell Counts ◽  
Porous Chitosan ◽  
Chitosan Scaffolds

The clinical management of large-size cartilage lesions is difficult due to the limited regenerative ability of the cartilage. Different biomaterials have been used to develop tissue engineering substitutes for cartilage repair, including chitosan alone or in combination with growth factors to improve its chondrogenic properties. The main objective of this investigation was to evaluate the benefits of combining activated platelet-rich plasma with a stabilized porous chitosan scaffold for cartilage regeneration. To achieve this purpose, stabilized porous chitosan scaffolds were prepared using freeze gelation and combined with activated platelet-rich plasma. Human primary articular chondrocytes were isolated and cultured in stabilized porous chitosan scaffolds with and without combination to activated platelet-rich plasma. Scanning electron microscopy was used for the morphological characterization of the resulting scaffolds. Cell counts were performed in hematoxylin and eosin–stained sections, and type I and II collagen expression was evaluated using immunohistochemistry. Significant increase in cell number in activated platelet-rich plasma/stabilized porous chitosan was found compared with stabilized porous chitosan scaffolds. Chondrocytes grown on stabilized porous chitosan expressed high levels of type I collagen but type II was not detectable, whereas cells grown on activated platelet rich plasma/stabilized porous chitosan scaffolds expressed high levels of type II collagen and type I was almost undetectable. In summary, activated platelet-rich plasma increases nesting and induces the differentiation of chondrocytes cultured on stabilized porous chitosan scaffolds.

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