Identification of Tsetse (Glossina spp.) using matrix-assisted laser desorption/ionisation time of flight mass spectrometry

Glossina (G.) spp. (Diptera: Glossinidae), known as tsetse flies, are vectors of African trypanosomes that cause sleeping sickness in humans and nagana in domestic livestock. Knowledge on tsetse distribution and accurate species identification help identify potential vector intervention sites. Morphological species identification of tsetse is challenging and sometimes not accurate. The matrix-assisted laser desorption/ionisation time of flight mass spectrometry (MALDI TOF MS) technique, already standardised for microbial identification, could become a standard method for tsetse fly diagnostics. Therefore, a unique spectra reference database was created for five lab-reared species of riverine-, savannah- and forest- type tsetse flies and incorporated with the commercial Biotyper 3.0 database. The standard formic acid/acetonitrile extraction of male and female whole insects and their body parts (head, thorax, abdomen, wings and legs) was used to obtain the flies' proteins. The computed composite correlation index and cluster analysis revealed the suitability of any tsetse body part for a rapid taxonomical identification. Phyloproteomic analysis revealed that the peak patterns of G. brevipalpis differed greatly from the other tsetse. This outcome was comparable to previous theories that they might be considered as a sister group to other tsetse spp. Freshly extracted samples were found to be matched at the species level. However, sex differentiation proved to be less reliable. Similarly processed samples of the common house fly Musca domestica (Diptera: Muscidae; strain: Lei) did not yield any match with the tsetse reference database. The inclusion of additional strains of morphologically defined wild caught flies of known origin and the availability of large-scale mass spectrometry data could facilitate rapid tsetse species identification in the futur

Understanding myopia: Pathogenesis and mechanisms

Myopia is a common refractive error, characterized by an excessive increase in axial length relative to the refractive power of the eye. Despite much research, the mechanisms underlying the development of myopia are unknown. A large body of work on animal models (such as chicks, guinea pigs, and monkeys) has been instrumental to our understanding of visually guided ocular growth, and potential mechanisms leading to myopia. These studies have shown that experimentally degrading the quality of the image formed on the retina by introducing translucent diffusers (i.e., form-deprivation), or altering the focal point of the image with respect to the retinal plane by imposing plus or minus lenses to the eyes (i.e., lens induced defocus) results in abnormal eye growth and development of reflective errors. Ocular changes in response to form-deprivation and lens induced defocus are primarily associated with changes in axial length (mainly due to changes in vitreous chamber depth) and choroidal thickness. These experimentally induced ocular changes quickly revert to normal upon removal of the imposed optical treatment. Physiological changes in retinal cells and neurotransmitters (such as dopamine), presence of ocular aberrations, altered accommodative response to visual stimuli, and even subtle variations in natural circadian rhythms of axial length may all influence ocular growth, and hence susceptibility to myopia. In fact, several optical interventions alter ocular aberrations, peripheral refraction, and the accommodative response of the eye in an attempt to arrest myopia development. Epidemiological studies have also linked excessive near work, better socioeconomic status, and urbanization to myopia, although the exact cause for these associations remain elusive. Based on decades of work on the effects of ambient lighting on refractive development in laboratory animals, recent clinical studies have revealed protective effects of greater outdoor exposures on development and progression of myopia in children. Experimental models continue to provide valuable information on the cellular and biochemical mechanisms of myopia.</p