The abundance of an invasive freshwater snail Tarebia granifera (Lamarck, 1822) in the Nseleni River,South Africa

The invasive freshwater snail Tarebia granifera (Lamarck, 1822) was first reported in South Africa in 1999 and it has become widespread across the country, with some evidence to suggest that it reduces benthic macroinvertebrate biodiversity. The current study aimed to identify the primary abiotic drivers behind abundance patterns of T. granifera, by comparing the current abundance of the snail in three different regions, and at three depths, of the highly modified Nseleni River in KwaZulu-Natal, South Africa. Tarebia granifera was well established throughout the Nseleni River system, with an overall preference for shallow waters and seasonal temporal patterns of abundance. Although it is uncertain what the ecological impacts of the snail in this system are, its high abundances suggest that it should be controlled where possible and prevented from invading other systems in the region.     

Reliability and detecting change following short-term creatine supplementation: comparison of two-component body composition methods

The purpose of the present study was twofold: firstly, to assess the reliability of various body composition methods, and secondly, to determine the ability of the methods to estimate changes in fat-free mass (FFM) following creatine (Cr) supplementation. Fifty-five healthy male athletes (weight 78.3 +/- 10.3 kg, age 21 +/- 1 years) gave informed consent to participate in this study. Subjects' FFM was estimated by hydrostatic weighing (HW), air-displacement plethysmography (ADP), bioelectrical impedance analysis (BIA), near-infrared spectroscopy (NIR), and anthropometric measurements (ANTHRO). Measurements were taken on 2 occasions separated by 7 days to assess the reliability of the methods. Following this, 30 subjects returned to the laboratory for an additional test day following 7 days of Cr supplementation (20 g.d(-1) Cr + 140 g.d(-1) dextrose) to assess each method's ability to detect acute changes in FFM. In terms of reliability, we found excellent test-retest correlations for all 5 methods, ranging from 0.983 to 0.998 (p < 0.001). The mean biases for the 5 methods were close to 0 (range -0.1 to 0.3 kg) and their 95% limits of agreement (LOAs) were within acceptable limits (HW = -1.1 to 1.7 kg; ADP = -1.1 to 1.2 kg; BIA = -1.0 to 1.0 kg; NIR = -1.4 to 1.4 kg); however, the 95% LOAs were slightly wider for ANTHRO (-2.4 to 2.6 kg). Following Cr supplementation there was a significant increase in body mass (from 77.9 +/- 10.1 kg to 78.9 +/- 10.3 kg, p = 0.000). In addition, all 5 body composition techniques detected the change in FFM to a similar degree (mean change: HW = 0.9 +/- 0.6 kg; ADP = 0.9 +/- 0.6 kg; BIA = 0.9 +/- 0.6 kg; NIR = 0.8 +/- 0.5 kg; ANTHRO = 1.0 +/- 0.7 kg; intraclass correlation coefficient = 0.962). We conclude that between-day differences in FFM estimation were within acceptable limits, with the possible exception of ANTHRO. In addition, all 5 methods provided similar measures of FFM change during acute Cr supplementation.     

Digit ratio (2D:4D) and performance in male surfers

The relative length of the second and fourth digits (2D:4D) is thought to be negatively related to prenatal testosterone and positively related to prenatal estrogen. Low 2D:4D has been linked to various measures of performance in a range of sports (e.g., soccer, rugby). In this study, we consider the relationship between 2D:4D and performance among male surfers. Our sample comprised 46 competitors in the Men's 5-star Professional World Qualifying Series surfing competition in Newquay, United Kingdom, in 2009. Three experienced surfing coaches rated the participants for overall surfing ability. The coach's ratings were significantly correlated with one another and an overall measure of surfing performance was obtained by calculating the mean of the 3 ratings. In addition, the final placing of the Newquay competition was used as an additional performance measure. Mean 2D:4D (SD) was as follows: right 0.994 (0.023) and left 0.976 (0.028). We found that right 2D:4D (but not left 2D:4D or right-left 2D:4D) was significantly negatively correlated with coaches' ratings (r(s) = 0.58) and the competition result (r(s) = 0.30). It appears that in line with other sports that low right 2D:4D (high prenatal testosterone and low prenatal estrogen) correlates to high surfing ability in men.     

Characterizing the normal proteome of human ciliary body

Background

The ciliary body is the circumferential muscular tissue located just behind the iris in the anterior chamber of the eye. It plays a pivotal role in the production of aqueous humor, maintenance of the lens zonules and accommodation by changing the shape of the crystalline lens. The ciliary body is the major target of drugs against glaucoma as its inhibition leads to a drop in intraocular pressure. A molecular study of the ciliary body could provide a better understanding about the pathophysiological processes that occur in glaucoma. Thus far, no large-scale proteomic investigation has been reported for the human ciliary body.

Results

In this study, we have carried out an in-depth LC-MS/MS-based proteomic analysis of normal human ciliary body and have identified 2,815 proteins. We identified a number of proteins that were previously not described in the ciliary body including importin 5 (IPO5), atlastin-2 (ATL2), B-cell receptor associated protein 29 (BCAP29), basigin (BSG), calpain-1 (CAPN1), copine 6 (CPNE6), fibulin 1 (FBLN1) and galectin 1 (LGALS1). We compared the plasma proteome with the ciliary body proteome and found that the large majority of proteins in the ciliary body were also detectable in the plasma while 896 proteins were unique to the ciliary body. We also classified proteins using pathway enrichment analysis and found most of proteins associated with ubiquitin pathway, EIF2 signaling, glycolysis and gluconeogenesis.

Conclusions

More than 95% of the identified proteins have not been previously described in the ciliary body proteome. This is the largest catalogue of proteins reported thus far in the ciliary body that should provide new insights into our understanding of the factors involved in maintaining the secretion of aqueous humor. The identification of these proteins will aid in understanding various eye diseases of the anterior segment such as glaucoma and presbyopia.     

FE65 as a link between VLDLR and APP to regulate their trafficking and processing

Background

Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) have been linked to familial Parkinson??s disease, but the underlying pathogenic mechanism remains unclear. We previously reported that loss of PINK1 impairs mitochondrial respiratory activity in mouse brains.

Results

In this study, we investigate how loss of PINK1 impairs mitochondrial respiration using cultured primary fibroblasts and neurons. We found that intact mitochondria in PINK1?/? cells recapitulate the respiratory defect in isolated mitochondria from PINK1?/? mouse brains, suggesting that these PINK1?/? cells are a valid experimental system to study the underlying mechanisms. Enzymatic activities of the electron transport system complexes are normal in PINK1?/? cells, but mitochondrial transmembrane potential is reduced. Interestingly, the opening of the mitochondrial permeability transition pore (mPTP) is increased in PINK1?/? cells, and this genotypic difference between PINK1?/? and control cells is eliminated by agonists or inhibitors of the mPTP. Furthermore, inhibition of mPTP opening rescues the defects in transmembrane potential and respiration in PINK1?/? cells. Consistent with our earlier findings in mouse brains, mitochondrial morphology is similar between PINK1?/? and wild-type cells, indicating that the observed mitochondrial functional defects are not due to morphological changes. Following FCCP treatment, calcium increases in the cytosol are higher in PINK1?/? compared to wild-type cells, suggesting that intra-mitochondrial calcium concentration is higher in the absence of PINK1.

Conclusions

Our findings show that loss of PINK1 causes selective increases in mPTP opening and mitochondrial calcium, and that the excessive mPTP opening may underlie the mitochondrial functional defects observed in PINK1?/? cells.