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Remote camera-traps are commonly used to estimate the abundance, diversity, behavior and habitat use of wildlife in an inexpensive and nonintrusive manner. Because of the increasing use of remote-cameras in wildlife studies, students interested in wildlife biology should be exposed to the use of remote-cameras early in their academic careers. Although there is a rich literature on the use of remote-cameras in wildlife studies, few have provided meaningful examples within an academic course setting. Due to the time constraint of a typical semester, many laboratory exercises generate data sufficient for the activity but lack inference to actual wildlife populations. This article describes a series of laboratory exercises that are both useful to student learning and provide relevant biological data. Students use remote-cameras to measure diversity, diel behavior (i.e. over a 24-hour period) and the relative abundance of mammals in a biological corridor. Other abundance methods such as mark-recapture or random encounter models that require marked individuals and/or extensive temporal and spatial methodology are often not practical in a course framework. The approach described in this article teaches students about research design and local wildlife abundance and behavior, using simple methodologies employed over a three-lab period.

This paper describes a series of laboratory exercises for upper level biology courses, independent research and/or honors programs. Students sampled fish from a local water body with the assistance of a local fish and wildlife agency. Tissue samples from collected fish were utilized to obtain estimates of the stable isotopes delta[superscript 13]C and delta[superscript 15]N. An open-source mass balance model was utilized to estimate fish diets from isotope values. Isotopes were also used to measure trophic position (TP) and evaluate dietary niche overlap between native and introduced species. It was found that delta[superscript 15]N concentrations increased with each trophic level starting with benthic algae (lowest) to omnivores, then primary carnivores and ultimately piscivores (highest). Estimates of delta[superscript 13]C suggested all collected taxa utilized littoral habitats for feeding purposes. Native chain pickerel ("Esox niger") had the highest delta[superscript 15]N and TP estimates at 14.4 and 4.11, respectively. Nonnative largemouth bass ("Micropterus salmoides") delta[superscript 15]N and TP estimates were 13.56 and 3.86, respectively. Model estimates suggested that chain pickerel and largemouth bass diets were partitioned: pickerel consumed only fish and bass consumed principally invertebrates with some intermittent fish contributions. This lab helped integrate multiple disciplines, provide practical experience, and encourage critical-thinking skills while educating students about trophic ecology. (Contains 4 figures and 1 table.)

Sorsby fundus dystrophy (SFD) is an autosomal dominant macular dystrophy with an estimated prevalence of 1 in 220,000 and an onset of disease around the 4th to 6th decade of life. Similar to age-related macular degeneration (AMD), ophthalmoscopy reveals accumulation of protein/lipid deposits under the retinal pigment epithelium (RPE), referred to as drusen, in the eyes of patients with SFD. SFD is caused by variants in the gene for tissue inhibitor of metalloproteinases-3 (TIMP3), which has been found in drusen-like deposits of SFD patients. TIMP3 is constitutively expressed by RPE cells and, in healthy eyes, resides in Bruch's membrane. Most SFD-associated TIMP3 variants involve the gain or loss of a cysteine residue. This suggests the protein aberrantly forms intermolecular disulphide bonds, resulting in the formation of TIMP3 dimers. It has been demonstrated that SFD-associated TIMP3 variants are more resistant to turnover, which is thought to be a result of dimerisation and thought to explain the accumulation of TIMP3 in drusen-like deposits at the level of Bruch's membrane. An important function of TIMP3 within the outer retina is to regulate the thickness of Bruch's membrane. TIMP3 performs this function by inhibiting the activity of matrix metalloproteinases (MMPs), which have the function of catalysing breakdown of the extracellular matrix. TIMP3 has an additional function to inhibit vascular endothelial growth factor (VEGF) signalling and thereby to inhibit angiogenesis. However, it is unclear whether SFD-associated TIMP3 variant proteins retain these functions. In this review, we discuss the current understanding of the potential mechanisms underlying development of SFD and summarise all known SFD-associated TIMP3 variants. Cell culture models provide an invaluable way to study disease and identify potential treatments. These allow a greater understanding of RPE physiology and pathophysiology, including the ability to study the blood-retinal barrier as well as other RPE functions such as phagocytosis of photoreceptor outer segments. This review describes some examples of such recent in vitro studies and how they might provide new insights into degenerative diseases like SFD. Thus far, most studies on SFD have been performed using ARPE-19 cells or other, less suitable, cell-types. Now, induced pluripotent stem cell (iPSC) technologies allow the possibility to non-invasively collect somatic cells, such as dermal fibroblast cells and reprogram those to produce iPSCs. Subsequent differentiation of iPSCs can generate patient-derived RPE cells that carry the same disease-associated variant as RPE cells in the eyes of the patient. Use of these patient-derived RPE cells in novel cell culture systems should increase our understanding of how SFD and similar macular dystrophies develop., (Copyright © 2017 Elsevier Ltd. All rights reserved.)