7 research outputs found
Study of the duration of the post-covid effects and associated risks among doctors
Research to investigate the duration of symptoms following COVID and danger indicators associated with them among recovered individuals. Given the widespread impact of COVID-19, understanding these aspects is crucial for effective management and support for those affected. Researchers conducted phone interviews with 186 healthcare professionals who were COVID-19-recovered.To evaluate the association between pre-existing conditions, demographic variables, and the probability of enduring long-term COVID-19 effects, logistic regression (LR) analysis was used. Analysis of the data revealed that a significant proportion of individuals experienced multiple acute post-COVID symptoms, with exhaustion being the most commonly reported (44,1 %). Risk factors for prolonged post-COVID symptoms were identified through logistical regression analysis, with female sex and pre-existing medical conditions being associated with increased odds ratios (OR) (OR, 2, 18; 96 % CI, 1,09-4,78; p-value 0,031, OR 2,78; 94 % CI, 1,26-6,07). This study highlights the frequency of both transient and chronic symptoms of COVID-19 among medical doctors who have recovered from the disease. The findings suggest that female sex and pre-existing medical conditions are significant risk factors for experiencing prolonged post-COVID effects.
E2F1 Hinders Skin Wound Healing by Repressing Vascular Endothelial Growth Factor (VEGF) Expression, Neovascularization, and Macrophage Recruitment.
Refractory surface of wound and dermal chronic ulcer are largely attributed to poor neovascularization. We have previously shown that E2F1 suppresses VEGF expression in the ischemic heart, and that genetic deletion of E2F1 leads to better cardiac recovery. However, whether E2F1 has a role in dermal wound healing is currently not known.Skin wounds were surgically induced in E2F1-null (E2F1-/-) mice and WT littermates. E2F1-/- displayed an accelerated wound healing including wound closure, dermal thickening and collagen deposition, which was associated with an increased endothelial cell proliferation and greater vessel density in the border zone of the wound. Furthermore, more macrophages were recruited to the skin lesions and the level of VEGF expression was markedly higher in E2F1-/- than in WT mice.E2F1 hinders skin wound healing by suppressing VEGF expression, neovascularization, and macrophage recruitment. Strategies that target E2F1 may enhance wound healing
E2F1-deficiency accelerates wound healing.
(A) Representative skin wounds in WT and E2F1–/– mice at serial time points post- surgery. (B) Quantifications of the wound healing rates (percent wound closure). *p<0.05 vs. WT at same time points. N.S., not significant; n = 10 per group.</p
The dermal thickness and collagen amount are greater in E2F1<sup>–/–</sup> mice than in WT mice.
Wound tissues were isolated at day 7 post-surgery and analyzed histologically. (A-B) H.E. and (C) Masson’s trichrome staining. Both entire wound (A) and wound border zone (B-C) are shown. Arrowheads indicate edges of wound granulation tissue. Double-headed arrow bars indicate the distance between the leading edges of wounded epidermis. (D) Quantifications of Epithelial gap (left panel), dermal thickness (middle panel), and collagen deposition (right panel). **p*p<0.05; n = 10 per group.</p
VEGF-A level is significantly higher in the wound of E2F1<sup>–/–</sup> mice than in WT mice.
Wound tissues were isolated at day 7 post-surgery. (A) Immumohistochemical staining of VEGF (brown), 20X original magnification (left panels), the inlets were enlarged (right panels). (B) VEGF mRNA expression was analyzed by qRT-PCR and normalized to the level of GAPDH. (C) Representatives of Western blotting (upper panel) and quantification of VEGF protein levels (lower panel). Protein levels were quantified densitometrically and normalized to tubulin levels. **p<0.01; n = 5.</p
More infiltrating macrophages are found in the wound of E2F1<sup>–/–</sup> mice than in WT mice.
At day 7 post-surgery, the wound skin tissues were analyzed immunochemically and by qRT-PCR. Shown are representative staining (left and middle panels) (original magnification, X400; 0.06 mm2/field) and quantifications (right panels) of the cells stained positive for CD68 (A), MPO (B) and CD3 (C). (D) The expression levels of M1 and M2 macrophage marker genes in the wounded skin tissues of WT and E2F1–/– mice were analyzed by qRT-PCR. **p<0.01. n.s., not significant; n = 10 per group.</p
E2F1-deficiency enhances vessel growth in the border area of the skin wound.
At day 7 post-surgery, Lectin was i.v. injected 10 min before euthanasia to identify vasculature; subsequent analyses were performed in sections of wound skin and quantified at the border zone of wounds. (A) Functional vessels were identified by staining with anti-lectin antibodies (red) (left and middle panels, scale bar = 50mm) and quantified (right panel). (B) Proliferation cells were identified by staining for BrdU (green) (left and middle panels) and quantified (right panel). (C) Proliferating ECs (yellow) were identified by co-staining for BrdU (green) and lectin (red) (left and middle panels, scale bar = 50 mm) and quantified as the number of lectin+BrdU+ vessels per mm2 (right panel); nuclei were stained with DAPI (blue). **p<0.01; n = 10 per group.</p
