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- Bachar-Wikstrom, E, et al.
(författare)
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Darier Disease - A Multi-organ Condition?
- 2021
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Ingår i: Acta dermato-venereologica. - : Medical Journals Sweden AB. - 1651-2057. ; 101:4, s. adv00430-
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Tidskriftsartikel (refereegranskat)
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- Jebril, W, et al.
(författare)
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Topical oxygen treatment relieves pain from hard-to-heal leg ulcers and improves healing: a case series
- 2022
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Ingår i: Journal of wound care. - : Mark Allen Group. - 0969-0700 .- 2052-2916. ; 31:1, s. 4-11
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Tidskriftsartikel (refereegranskat)abstract
- Managing painful hard-to-heal leg ulcers is challenging with current therapeutic options. Wounds are prone to being hypoxic, and the subsequent pain is often related to hypoxia. Hyperbaric oxygen therapy (HBOT) is used to treat hard-to-heal leg wounds by delivering 100% oxygen at a pressure 2–3 times higher than atmospheric pressure. Unfortunately, most patients cannot be offered HBOT because it is costly and needs to be applied at specialised centres. Therefore, topical continuous oxygen therapy (TCOT) is a novel alternative for continuous local oxygen delivery to wounds and is associated with improved wound healing; however, its effect on painful wounds is unknown. This retrospective study was conducted on 20 patients, of whom 17 had painful hard-to-heal leg ulcers. In 13 patients (76%) with painful ulcers, TCOT was associated with rapid and substantial pain alleviation. Also, eight (40%) of the patients' wounds healed entirely with TCOT. This study suggests that TCOT may represent a novel pain management device for hard-to-heal wounds.
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- Chen, CC, et al.
(författare)
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Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) activity is required for V(D)J recombination
- 2021
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 218:8
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Tidskriftsartikel (refereegranskat)abstract
- A whole-genome CRISPR/Cas9 screen identified ATP2A2, the gene encoding the Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) 2 protein, as being important for V(D)J recombination. SERCAs are ER transmembrane proteins that pump Ca2+ from the cytosol into the ER lumen to maintain the ER Ca2+ reservoir and regulate cytosolic Ca2+-dependent processes. In preB cells, loss of SERCA2 leads to reduced V(D)J recombination kinetics due to diminished RAG-mediated DNA cleavage. SERCA2 deficiency in B cells leads to increased expression of SERCA3, and combined loss of SERCA2 and SERCA3 results in decreased ER Ca2+ levels, increased cytosolic Ca2+ levels, reduction in RAG1 and RAG2 gene expression, and a profound block in V(D)J recombination. Mice with B cells deficient in SERCA2 and humans with Darier disease, caused by heterozygous ATP2A2 mutations, have reduced numbers of mature B cells. We conclude that SERCA proteins modulate intracellular Ca2+ levels to regulate RAG1 and RAG2 gene expression and V(D)J recombination and that defects in SERCA functions cause lymphopenia.
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| 18. |
- Curman, P, et al.
(författare)
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Amelanotic Melanoma Concealed by Psoriasis
- 2020
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Ingår i: Acta dermato-venereologica. - : Medical Journals Sweden AB. - 1651-2057. ; 100:36, s. adv00082-
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Tidskriftsartikel (refereegranskat)
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| 29. |
- Li, X, et al.
(författare)
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MicroRNA-132 promotes fibroblast migration via regulating RAS p21 protein activator 1 in skin wound healing
- 2017
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7:1, s. 7797-
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Tidskriftsartikel (refereegranskat)abstract
- MicroRNA (miR)-132 has been identified as a top up-regulated miRNA during skin wound healing and its inhibition impairs wound repair. In a human in vivo surgical wound model, we showed that miR-132 was induced in epidermal as well as in dermal wound–edge compartments during healing. Moreover, in a panel of cells isolated from human skin wounds, miR-132 was found highly expressed in human dermal fibroblasts (HDFs). In HDFs, miR-132 expression was upregulated by TGF-β1. By overexpression or inhibition of miR-132, we showed that miR-132 promoted HDF migration. Mechanistically, global transcriptome analysis revealed that RAS signaling pathway was regulated by miR-132 in HDFs. We found that RAS p21 protein activator 1 (RASA1), a known target of miR-132, was downregulated in HDFs upon miR-132 overexpression. Silencing of RASA1 phenocopied the pro-migratory effect of miR-132. Collectively, our study reveals an important role for miR-132 in HDFs during wound healing and indicates a therapeutic potential of miR-132 in hard-to-heal skin wounds.
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| 33. |
- Palin, L, et al.
(författare)
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Topical oxygen treatment relieves pain from hard-to-heal leg ulcers and improves healing: a case report
- 2021
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Ingår i: Journal of wound care. - : Mark Allen Group. - 0969-0700 .- 2052-2916. ; 30:3, s. 210-212
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Tidskriftsartikel (refereegranskat)abstract
- Pain from hard-to-heal wounds is common and challenging to manage with current therapies. Most hard-to-heal wounds show some degree of hypoxia that impairs healing and contributes to pain. Regular oxygen therapy is given in hyperbaric oxygen chambers and is costly, time-consuming and cannot be offered to most patients. Moreover, hyperbaric oxygen therapy (HBOT) only increases tissue oxygen for a short time and is given only for a few hours per week. Topical oxygen therapy (TOT) was introduced as an alternative and in this report we focus on topical continuous oxygen therapy (TCOT), which has been shown to be associated with healing of hard-to-heal ulcers. We report on a patient with type 1 diabetes with a painful hard-to-heal lower leg ulcer that failed to heal with standard wound dressings and that had insufficient response to pharmacological analgesia. The patient was on three different analgesics before treating the wound with TCOT. As the wound was considered hypoxic, due to longstanding diabetes and probable microangiopathy, TCOT was commenced. Within one week of treatment starting, the patient spontaneously ceased all his analgesics as he was free of pain; and after 2.5 months, the ulcer healed. The patient reported no adverse effects. In addition to promoting healing, TCOT may also be considered for its potential analgesic effects in hard-to-heal wound management.
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- Taddeo, EP, et al.
(författare)
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Mitochondrial Proton Leak Regulated by Cyclophilin D Elevates Insulin Secretion in Islets at Nonstimulatory Glucose Levels
- 2020
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 69:2, s. 131-145
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Tidskriftsartikel (refereegranskat)abstract
- Fasting hyperinsulinemia precedes the development of type 2 diabetes. However, it is unclear whether fasting insulin hypersecretion is a primary driver of insulin resistance or a consequence of the progressive increase in fasting glycemia induced by insulin resistance in the prediabetic state. Herein, we have discovered a mechanism that specifically regulates non–glucose-stimulated insulin secretion (NGSIS) in pancreatic islets that is activated by nonesterified free fatty acids, the major fuel used by β-cells during fasting. We show that the mitochondrial permeability transition pore regulator cyclophilin D (CypD) promotes NGSIS, but not glucose-stimulated insulin secretion, by increasing mitochondrial proton leak. Islets from prediabetic obese mice show significantly higher CypD-dependent proton leak and NGSIS compared with lean mice. Proton leak–mediated NGSIS is conserved in human islets and is stimulated by exposure to nonesterified free fatty acids at concentrations observed in obese subjects. Mechanistically, proton leak activates islet NGSIS independently of mitochondrial ATP synthesis but ultimately requires closure of the KATP channel. In summary, we have described a novel nonesterified free fatty acid–stimulated pathway that selectively drives pancreatic islet NGSIS, which may be therapeutically exploited as an alternative way to halt fasting hyperinsulinemia and the progression of type 2 diabetes.
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