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Calcineurin (PPP3CB) adjusts angiotensin II-dependent vascular renovating through potentiating EGFR signalling in these animals.
3 ± 19.0 vs. 605.9 ± 18.6 µm; P 0.05). Conclusions The relative significant thinning of the anterior sclera along the inferior meridian with increasing degree of myopia compared with the other three meridians indicates the potential role of AST, especially in the inferior meridian, to act as a marker for myopia progression.Purpose We developed a combined biomechanical and hemodynamic model of the human eye to estimate blood flow and oxygen concentration within the lamina cribrosa (LC) and rank the factors that influence LC oxygen concentration. Methods We generated 5000 finite-element eye models with detailed microcapillary networks of the LC and computed the oxygen concentration of the lamina retinal ganglion cell axons. For each model, we varied the intraocular pressure (IOP) from 10 mm Hg to 55 mm Hg in 5-mm Hg increments, the cerebrospinal fluid pressure (13 ± 2 mm Hg), cup depth (0.2 ± 0.1 mm), scleral stiffness (±20% of the mean values), LC stiffness (0.41 ± 0.2 MPa), LC radius (1.2 ± 0.12 mm), average LC pore size (5400 ± 2400 µm2), the microcapillary arrangement (radial, isotropic, or circumferential), and perfusion pressure (50 ± 9 mm Hg). Blood flow was assumed to originate from the LC periphery and drain via the central retinal vein. Finally, we performed linear regressions to rank the influence of each factor on the LC tissue oxygen concentration. Results LC radius and perfusion pressure were the most important factors in influencing the oxygen concentration of the LC. IOP was another important parameter, and eyes with higher IOP had higher compressive strain and slightly lower oxygen concentration. In general, superior-inferior regions of the LC had significantly lower oxygen concentration than the nasal-temporal regions, resulting in an hourglass pattern of oxygen deficiency. Conclusions To the best of our knowledge, this study is the first to implement a comprehensive hemodynamical model of the eye that accounts for the biomechanical forces and morphological parameters of the LC. The results provide further insight into the possible relationship of biomechanical and vascular pathways leading to ischemia-induced optic neuropathy.Purpose Neurons carry electrical signals and communicate via electrical activities. The therapeutic potential of electrical stimulation (ES) for the nervous system, including the retina, through improvement of cell survival and function has been noted. Here we investigated the neuroprotective and regenerative potential of ES in a mouse model of inherited retinal degeneration. selleck kinase inhibitor Methods Rhodopsin-deficient (Rho-/-) mice received one or two sessions of transpalpebral ES or sham treatments for 7 consecutive days. Intraperitoneal injection of 5-ethynyl-2'-deoxyuridine was used to label proliferating cells. Weekly electroretinograms were performed to monitor retinal function. Retinal morphology, photoreceptor survival, and regeneration were evaluated in vivo using immunohistochemistry and genetic fate-mapping techniques. Müller cell (MC) cultures were employed to further define the optimal conditions of ES application. Results Noninvasive transpalpebral ES in Rho-/- mice improved photoreceptor survival and electroretinography function in vivo. ES also triggered residential retinal progenitor-like cells such as MCs to reenter the cell cycle, possibly producing new photoreceptors, as shown by immunohistochemistry and genetic fate-mapping techniques. ES directly stimulated cell proliferation and the expression of progenitor cell markers in MC cultures, at least partially through bFGF signaling. Conclusions Our study showed that transpalpebral ES improved photoreceptor survival and retinal function and induced the proliferation, probably photoreceptor regeneration, of MCs; this occurs via stimulation of the bFGF pathways. These results suggest the exciting possibility of applying noninvasive ES as a versatile tool for preventing photoreceptor loss and mobilizing endogenous progenitors for reversing vision loss in patients with photoreceptor degeneration.BACKGROUND Diet plays an important role in kidney stone formation. Several individual components have been associated with the risk of kidney stone formation, but there is limited evidence regarding the role of healthful dietary patterns. OBJECTIVE To prospectively study the association between adherence to the Mediterranean diet and the risk of incident kidney stones. METHODS We conducted a longitudinal study using 3 different cohorts the Health Professionals Follow-up Study (n = 42,902 men), the Nurses' Health Study I (n = 59,994 women), and the Nurses' Health Study II (n = 90,631 women). We assessed diet every 4 y using an FFQ and calculated adherence to a Mediterranean diet using the alternate Mediterranean diet score (aMED). A subgroup of 6077 participants provided ≥1 24-h urine sample, and urinary solute excretion was analyzed. We used Cox proportional hazards regression to examine the independent association between the aMED and incidence of kidney stones, adjusting for potential confounders. We used adjusted linear regression models to study the relation between aMED and urine composition. RESULTS During 3,316,633 person-years of follow-up, 6576 cases of incident kidney stones were identified. For participants in the highest aMED score category, the risk of developing a kidney stone was between 13% and 41% lower compared with participants in the lowest score (pooled HR 0.72, 95% CI 0.59, 0.87; P value for trend less then 0.001). A higher aMED score was associated with higher urinary citrate, magnesium, oxalate, phosphate, uric acid, volume, and pH, and lower urinary sodium, resulting in lower supersaturation for calcium oxalate, calcium phosphate, and uric acid. CONCLUSION Adherence to a Mediterranean diet is associated with a lower risk of developing a kidney stone. Copyright © The Author(s) 2020.Brown adipose tissue (BAT) has long been described according to its histological features as a multilocular, lipid-containing tissue, light brown in color, that is also responsive to the cold and found especially in hibernating mammals and human infants. Its presence in both hibernators and human infants, combined with its function as a heat-generating organ, raised many questions about its role in humans. Early characterizations of the tissue in humans focused on its progressive atrophy with age and its apparent importance for cold-exposed workers. However, the use of positron emission tomography (PET) with the glucose tracer [18F]fluorodeoxyglucose ([18F]FDG) made it possible to begin characterizing the possible function of BAT in adult humans, and whether it could play a role in the prevention or treatment of obesity and type 2 diabetes (T2D). This review focuses on the in vivo functional characterization of human BAT, the methodological approaches applied to examine these features and addresses critical gaps that remain in moving the field forward.
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