SciCombinator

Discover the most talked about and latest scientific content & concepts.

Journal: Journal of biological regulators and homeostatic agents

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Stigmata are one of the most ancient and fascinating mysteries of the Christian religion. The word “stigmata” derives by the Greek “stigma”, that means sign, mark. Classically, stigmata are the sores inflicted on Jesus Christ during his passion and crucifixion. Today, the term stigmatized has been extended to designate several cases of individuals, who show skin sores similar to those of Christ. The Authors report a brief history of stigmata, trying to give an explanation to such a fascinating phenomenon.

Concepts: Religion, Christianity, Jesus, Christ, New Testament, Good Friday, Crucifixion of Jesus, Saint Peter

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Collagen Matrix (CM) 10826 is a nanostructured bi-layered collagen membrane obtained from type I and III porcine collagen, which in vitro has shown to have the potential to be a substitute and/or stimulant for soft oral tissue regeneration. The objective of this study was to evaluate the in vivo potential and safety of this membrane for soft tissue regeneration in the early stage of wound healing. Two soft tissue wounds (test and control) were created on the back skin of 5 rabbits (female New Zealand White Rabbits specific pathogen free). All wounds were protected by a special poly-tetra-fluoro-ethylene (PTFE) healing camera. On each rabbit on the test side CM-10826 was used, while on the control side conventional treatment (an autologous pedicle graft) was performed. The healing process was observed clinically after 2 and 6 days, and Magnetic Resonance Imaging (MRI) was performed after this period. After 7 days, animals were sacrificed and specimens were analyzed with light optic microscopy (LM), Transmission Electron Microscopy (TEM) and Scanning Electron Microscopy (SEM). These in vivo trials on rabbits confirmed that CM-10826 is well tolerated, without signs of histological inflammatory reaction and proved to be able to accelerate the spontaneous repair of the skin defect taken as the control. The light-optic and ultra-microscopy of serial biopsies showed that the new matrix is biocompatible and is able to function as a scaffold inducing soft tissue regeneration. In conclusion this study demonstrates that CM-10826 promote early soft tissue regeneration and suggests it is a potential constituent for human autologous keratinocytes seeded derma bioequivalent. It protects the wound from injuries and bacterial contamination accelerating healing process. As a clinical relevance, we consider that the quality of life of patients will be improved avoiding the use of major autologous grafts, reducing the hospitalization time and morbidity.

Concepts: Electron, Wound healing, Collagen, Healing, Magnetic resonance imaging, Wound, Transmission electron microscopy, Scanning electron microscope

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This study aimed to explore the protective effect of Lycium barbarum polysaccharides (LBPs) against hyperlipidemia and lipid-induced renal injury in a rat model. Male Sprague-Dawley rats (n=30) were randomly divided into three equal groups: a control group (fed a regular diet) and two experimental groups (fed a high-fat diet). By feeding rats a high-fat diet for 12 weeks, an animal model of hyperlipidemia was established, after which one experimental group received oral LBPs at a dose of 300 mg/kg per day. Blood lipids, renal function, and urinary proteins were measured after 12 weeks. Changes in renal pathology and expression levels of sterol regulatory element binding transcription factor 1 (SREBP-1), interleukin-6 (IL- 6), tumor necrosis factor-alpha (TNF-α), AMP-activated protein kinase (AMPK) were determined. Rats with hyperlipidemia induced by a high-fat diet showed increases in blood lipids and blood urea nitrogen, serum creatinine, and urinary protein, as well as increases in renal levels of SREBP-1, TNF-α, and IL-6 and decreases in renal levels of adiponectin and AMPK. Administration of LBPs restored blood lipid, blood urea nitrogen, serum creatinine, and urinary protein levels, downregulated renal levels of SREBP-1, TNF-α, and IL-6, and upregulated renal levels of adiponectin and AMPK. These results indicate that LBPs may mediate lipid metabolism, enhance anti-inflammatory responses, and ameliorate renal injury caused by lipid metabolism disorders in a rat model of hyperlipidemia.

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In order to study the mechanism of the effect of progesterone receptor on the growth of primary uterine leiomyoma cells, the primary cells were extracted from uterine leiomyoma cells and identified by immunohistochemistry (IHC). Mitochondrial progesterone receptor-positive [PR-M(+)], mitochondrial progesterone receptor-negative [PR-M(-)], progesterone receptor A (PR-A) and progesterone receptor B (PR-B) were screened by Western blotting. Different concentrations of Mifepristone (MIF), a progesterone receptor antagonist, were used to interfere with PR-M(+) and PR-M(-) cell lines, respectively. Proliferation and apoptosis of PR-M(+) and PR-M(-) cell lines were detected by tetramethylazolyl blue method and flow cytometry, respectively. The expression of Caspase-3 and B-cell lymphoma 2 (Bcl-2) protein was detected by Western blotting. The results showed that the growth of PR-M(+) and PR-M(-) uterine leiomyoma cells was inhibited with the increase of MIF concentration. Furthermore, the proliferation inhibition rate and apoptosis rate were gradually increased. However, the expression of Caspase-3 protein on progesterone receptor M increased, while the expression of Bcl-2 decreased. Moreover, progesterone could induce progesterone receptor M to up-regulate apoptotic protein Caspase-3 and down-regulate anti-apoptotic protein Bcl-2, thus it could inhibit the apoptosis of primary cultured uterine leiomyoma cells and promote the proliferation of leiomyoma cells.

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Magnetic Resonance (MR) is a non-invasive modality of choice for the evaluation of brain morphology, with superior performance as compared to other techniques. However, MR images are typically assessed qualitatively, thus relying on the experience of the involved radiologist. This may lead to errors of interpretation in the presence of subtle alterations and does not exploit the full potential of this technique as a quantitative diagnostic tool. To this end Magnetic Resonance Relaxometry (MRR), which is able to quantitively characterize the tissues under investigation through their relaxation rates, seems extremely promising. Many studies assessed the feasibility of relaxometry as a diagnostic tool in human brain disorders, with the most promising results obtained in the evaluation of neurodegenerative diseases and in the oncologic field. However, despite such extensive literature in human medicine, due to the lack of standardized protocols and the need of high-field MRI scanners, to date few studies have been performed on companion animals. In this work, first we describe relaxometry applications in human neuropathology and their possible extension to companion animals both in the experimental and clinical fields. Then, we present two experiments performed on a typical standard clinical scanner operating at 0.25 T to show that, despite the low field intensity, this technique may be promising even in the clinical setup. We tested the relaxometry protocol in a phantom study and then applied it to a real clinical case study. The results showed that this protocol used on a phantom led to a higher contrast, as compared to the standard approach. Furthermore, when applied to a real case study, this protocol revealed brain lesions undetected by the standard technique which were confirmed by a histopathological examination. These preliminary results are encouraging and support the development of this approach as an advanced diagnostic tool even in a clinical setting where low field MRI scanners are typically employed.

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Osteoarthritis (OA) is a chronic rheumatic disease characterized by joint cartilage wear and loss of normal function. Clodronate (CLO) is a first-generation non-nitrogen-containing bisphosphonate that exerts anti-inflammatory and analgesic and modulatory effects on bone and cartilage metabolism. To date, few clinical studies have evaluated the effect of CLO in OA. Current evidence suggests that CLO may represent a new type of analgesic drug as it reduces pain in bone diseases characterized by edema such as Complex Regional Pain Syndrone type-1 and vertebral fractures. Thanks to its anti-inflammatory and analgesic effects, CLO has been shown to afford benefit in knee OA, erosive OA of the hand, painful knee hip prosthesis and veterinary practice. Transforming growth factor β1 has also been found to play an important role in the pathogenesis of OA. The present review article examines recent evidence on the potential use of CLO in the treatment of OA.

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Orthodontic tooth movement determines a biological response of all the tissues surrounding the teeth to which force is applied. The aim of this study is to evaluate which ideal orthodontic force, at the biological level, arouses an acute inflammatory response on periodontal tissues, and the duration of the force in order to establish an ideal experimental model of dental movement. The periodontal ligament and the alveolar bone change abruptly due to the biochemical adaptive response, resulting in a re-organization of the intracellular and the extracellular matrix. There is a modification of the local vascularization which stimulates a cascade production, synthesis and the release of arachidonic acid, metabolites, proteins, such as cytokines, and growth factors. Every dentist can control and should know the above-mentioned mechanism. Moreover, the production of proteins by modulating the direction and the intensity of the force can be changed but, above all, the duration.

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Aconitine (ACO), the main active component in Aconitum carmichaelii Debeaux (family: Ranunculaceae), has high cardiotoxicity, however the mechanisms of this effect remain unclear. Paeoniflorin (PF), the main chemical ingredient in herbaceous peony, can protect the heart from damage through antioxidant, vasodilatory and other effects. In this study, we focused on the mechanism by which PF reduces ACO cardiotoxicity. We selected H9c2 cells as the experimental model. MTT assay, Western blot analysis and real-time PCR were used to measure cell proliferation, apoptosis, ion channels and oxidative stress. Cell proliferation was significantly increased, the Bcl-2/Bax ratio and p53 level were upregulated, and Caspase-3 was slightly reduced in the ACO+PF group compared with the ACO group. SCN5A mRNA expression was significantly increased in the ACO+PF group compared with the ACO group, while RyR2 and Cx43 mRNA expression was decreased. Compared with the ACO group, the ACO+PF group showed marked decreases in extracellular lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA), while there was no difference in intracellular superoxide dismutase (SOD). The above data demonstrate that the cardiotoxicity of ACO in H9c2 cells was significantly decreased by PF.

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Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and β, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17β, or with testosterone replacement treatment). Freund’s complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and β protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and β in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER β.

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Transforming growth factor-beta (TGF-β) functions in fibrogenesis as a profibrotic mediator, regulating cell proliferation, migration, apoptosis and collagen production of fibroblasts. microRNA-155 (miR-155), the expression of which has been related to bleomycin-induced idiopathic pulmonary fibrosis, has been involved in TGF-β induced epithelial-mesenchymal transition. Here, we found that miR-155 expression was decreased in human pulmonary fibroblasts by TGF-β treatment. We overexpressed miR-155 in fibroblasts to investigate the functional impact of miR-155 on TGF-β-induced fibrotic phenotype of fibroblasts. It is suggested that miR-155 overexpression attenuated the stimulatory effect of TGF-β on fibroblast proliferation, migration and collagen synthesis, by evidence from assessment of cell cycle, viability, apoptosis, migration and collagen content. Furthermore, quantitative measurement showed that SMAD1 gene expression was decreased following miR-155 inhibition, thereby demonstrating an indirect miRNA-SMAD interaction that links miR-155 to TGF-β signaling. Our work helped uncover an miRNA-mediated mechanism of fibroblast response to TGF-β. Moreover, it will help to achieve a better understanding of the regulatory roles of miR-155 in fibrogenesis.