Juncao grass (Cenchrus fungigraminus Z.X. Lin, D.M. Lin, and S.R. Lan) is a recently developed C4 forage which has been introduced to several tropical countries supported by different aid programs. However, there is no information on the potential of forage production, nutritive value, and agronomic characteristics of this new species to support management recommendations. This research aimed to compare two cultivars of Juncao to Guatemala (Tripsacum andersonii J.R. Gray) and Elephant grass [Cenchrus purpureus (Schumach.) Morrone cv. Napier] in relation to annual forage production and nutritive value subjected to different pre-harvest canopy heights. The trial was designed using randomised blocks (n = 3) in a split-plot arrangement where pre-harvesting canopy heights (0.5, 1.0, 1.5, and 2.0 m) composed the main plots and forage species/cultivars (n = 4) as the subplots. The annual forage accumulation of Juncao green and purple was approximately double that of Elephant and Guatemala grass when averaged across 2 years, while crude protein and metabolisable energy concentration was similar to Elephant and higher than Guatemala grass. Juncao green and purple cultivars should be harvested between 1 and 2 m of pre-harvest canopy height, with shorter pre-harvest targets favouring nutritional value and taller targets promoting greater biomass production per harvest, although no increments in annual forage accumulation were observed when pre-harvesting canopy height was over 1 m. The high forage production of Juncao grass, combined with its nutritional value comparable to other tropical forage, indicates substantial potential for its adoption in cut-and-carry systems in the wet tropics.

The caveolin (Cav) family of proteins comprises key constituents of caveolar structures in cell membranes, which are involved in receptor-independent endocytosis and cellular signalling pathways. Three isoforms of caveolin viz. cav-1, cav-2 and cav-3 encoded by CAV1, CAV2 and CAV3 genes respectively, have been reported to be expressed in various tissues. Genetic polymorphism in CAV has been identified as associated with the development of pathological changes in the cardiovascular system, chronic kidney disease as well as neurodegenerative diseases of the brain and retina such as Alzheimer's disease, Parkinson's disease and glaucoma. In this study, we investigate and characterise various polymorphisms associated with CAV1, CAV2 and CAV3 by using a combination of in silico algorithms such as SIFT, Polyphen 2.0, I-Mutant, PROVEAN, PANTHER, SNP&Go, PhD-SNP, MutPred and SNPEffects. Three-dimensional comparative modelling was performed using Phyre2 server, ab initio modelling, using the I-TASSER and RaptorX program. The predicted models were evaluated using Ramachandran plot to establish the accuracy of the models generated. The resulting mutant and wild type proteins obtained were energy minimized in Swiss Deep Viewer and evaluated. The study has identified two of the non-synonymous single nucleotide polymorphism (nsSNP) in CAV3 gene that may have a damaging effect on the protein stability. The surface residues in the wild type and mutant forms highlight different accessible surface area (ASA) of amino acid residues in the corresponding proteins. Our analysis predicted that none of the known nsSNPs have a negative effect on the CAV1 and CAV2 protein structures. Phylogenetic analysis using ConSurf further identified that most of the disease-associated nsSNPs were within the conserved regions in human cav3.

Background: Retinal ganglion cell (RGC) degeneration is a major feature of glaucoma pathology. Neuroprotective approaches that delay or halt the progression of RGC loss are needed to prevent vision loss which can occur even after conventional medical or surgical treatments to lower intraocular pressure.

Objective: The aim of this review was to examine the progress in genetics and cellular mechanisms associated with endoplasmic reticulum (ER) stress, RGC dysfunction and cell death pathways in glaucoma.

Materials and Methods: Here, we review the involvement of neurotrophins like brain derived neurotrophic factor (BDNF) and its high affinity receptor tropomyosin receptor kinase (TrkB) in glaucoma. The role of ER stress markers in human and animal retinas in health and disease conditions is also discussed. Further, we analysed the literature highlighting genetic linkage in the context of primary open angle glaucoma and suggested mechanistic insights into potential therapeutic options relevant to glaucoma management.

Results: The literature review of the neurobiology underlying neurotrophin pathways, ER stress and gene associations provide critical insights into association of RGCs death in glaucoma. Alteration in signalling pathway is associated with increased risk of misfolded protein aggregation in ER promoting RGC apoptosis. Several genes that are linked with neurotrophin signalling pathways have been reported to be associated with glaucoma pathology.

Conclusion: Understanding genetic heterogeneity and involvement of neurotrophin biology in glaucoma could help to understand the complex pathophysiology of glaucoma. Identification of novel molecular targets will be critical for drug development and provide neuroprotection to the RGCs and optic nerve.

PURPOSE. To investigate whether the brain-derived neurotrophic factor (BDNF) Val66Met genotype is associated with the rate of progression of open-angle glaucoma (OAG).

METHODS. In this retrospective cohort study, 148 OAG patients (292 eyes) were enrolled with a median follow-up period of 5.3 (range, 1.1–8.6) years. All participants had undergone regular clinical examinations by using spectral-domain optical coherence tomography (SD-OCT) scans and Humphrey (SITA) visual field tests. BDNF Val66Met polymorphisms were genotyped in all participants. Longitudinal visual field and retinal nerve fiber layer (RNFL) changes were compared between Met carriers (n = 68, 135 eyes) and Val homozygotes (n = 80, 157 eyes) by using the generalized estimating equations (GEE) model and Kaplan-Meier survival analysis.

RESULTS. There was no significant difference in mean rates of progression for the two genotypes. However, there was a significant association between the Val66Met genotypes and slower OAG progression, as suggested by a higher rate of global RNFL loss in Val/Val homozygotes (P = 0.008) in the long-term survival analysis. The effect demonstrated a degree of sex specificity, with the significant difference present only in females (P = 0.016) but not males. Similar sexual dimorphism was presented in superior (P = 0.005 in females, P = 0.38 in males) and inferior (P = 0.004 in females, P = 0.41 in males) RNFL loss. No significant difference was observed in visual field parameters.

CONCLUSIONS. Our results suggested that carriage of Met allele reduces the rate of long-term OAG progression. However, the fact that this effect is observed only in females indicates BDNF Val66Met influences the progression rate of OAG in a sex-specific manner.