Consensus Recommendation for Mouse Models of Ocular Hypertension to Study Aqueous Humor Outflow and Its Mechanisms.

Due to their similarities in anatomy, physiology, and pharmacology to humans, mice are a valuable model system to study the generation and mechanisms modulating conventional outflow resistance and thus intraocular pressure. In addition, mouse models are critical for understanding the complex nature of conventional outflow homeostasis and dysfunction that results in ocular hypertension. In this review, we describe a set of minimum acceptable standards for developing, characterizing, and utilizing mouse models of open-angle ocular hypertension. We expect that this set of standard practices will increase scientific rigor when using mouse models and will better enable researchers to replicate and build upon previous findings

Consensus recommendation for mouse models of ocular hypertension to study aqueous humor outflow and its mechanisms

Due to their similarities in anatomy, physiology, and pharmacology to humans, mice are a valuable model system to study the generation and mechanisms modulating conventional outflow resistance and thus intraocular pressure. In addition, mouse models are critical for understanding the complex nature of conventional outflow homeostasis and dysfunction that results in ocular hypertension. In this review, we describe a set of minimum acceptable standards for developing, characterizing, and utilizing mouse models of open-angle ocular hypertension. We expect that this set of standard practices will increase scientific rigor when using mouse models and will better enable researchers to replicate and build upon previous findings

Optimization of process parameters for slow pyrolysis of neem press seed cake for liquid and char production

Slow pyrolysis of neem press seed cake (NPSC) was carried out in a fixed bed batch reactor to study the effects of temperature, retention time, and nitrogen (N 2 ) flow rate on liquid and char yields. Response surface methodology (RSM) based on Box-Behnken design was used to determine the optimum operating conditions to maximize the liquid yield. The highest liquid yield of 52.1 wt% was obtained at 512.5 °C, after 60 min using 0.5 L/min N 2 flow rate. Scanning electron microscopy (SEM), elemental analysis, bomb calorimeter, Fourier transform infrared (FT-IR) spectroscopy, X-ray powder diffraction techniques and gas chromatography-mass spectrometry (GC-MS) were used to determine the physicochemical properties of NPSC and char, and chemical properties of liquid. GC-MS analysis showed that the bio-oil was rich in 9-octadecenamide, 2-propenyl decanoate, heptadecanenitrile, and oleanitrile. The higher heating value of the bio-oil and NPSC were 32.8 and 16.05 MJ/kg, respectively at 575 °C. The FT-IR results showed a decrease in the number of O-H (hydroxyl), C-H (alkanes), C=O (esters), -C-H (alkanes), and C-O (primary alcohol) groups in NPSC with increasing pyrolysis temperature

The Canonical Wnt Signaling Pathway Inhibits the Glucocorticoid Receptor Signaling Pathway in the Trabecular Meshwork

Glucocorticoid-induced glaucoma is a secondary open-angle glaucoma. About 40% of the general population may develop elevated intraocular pressure on prolonged glucocorticoid treatment secondary to damages in the trabecular meshwork (TM), a tissue that regulates intraocular pressure. Therefore, identifying the key molecules responsible for glucocorticoid-induced ocular hypertension is crucial. In this study, Dickkopf-related protein 1 (Dkk1), a canonical Wnt signaling inhibitor, was found to be elevated in the aqueous humor and TM of glaucoma patients. At the signaling level, Dkk1 enhanced glucocorticoid receptor (GR) signaling, whereas Dkk1 knockdown or Wnt signaling activators decreased GR signaling in human TM cells as indicated by luciferase assays. Similarly, activation of the GR signaling inhibited Wnt signaling. At the protein level, glucocorticoid-induced extracellular matrix was inhibited by Wnt activation using Wnt activators or Dkk1 knockdown in primary human TM cells. In contrast, inhibition of canonical Wnt signaling by β-catenin knockdown increased glucocorticoid-induced extracellular matrix proteins. At the physiological level, adenovirus-mediated Wnt3a expression decreased glucocorticoid-induced ocular hypertension in mouse eyes. In summary, Wnt and GR signaling inhibit each other in the TM, and canonical Wnt signaling activators may prevent the adverse effect of glucocorticoids in the eye