This paper presents analytical solutions for the effect of squeeze film damping on a MEMS torsion mirror. Both the Fourier series solution and the double sine series solution are derived for the linearized Reynold equation which is obtained under the assumption of small displacements. Analytical formulae for the squeeze film pressure variation and the squeeze film damping torque on the torsion mirror are derived. They are functions of the rotation angle and the angular velocity of the mirror. On the other hand, to verify the analytical modeling, the implicit finite difference method is applied to solve the nonlinear isothermal Reynold equation, and thus numerically determine the squeeze film damping torque on the mirror. The damping torques based on both the analytical modeling and the numerical modeling are then used in the equation of motion of the torsion mirror which is solved by the Runge-Kutta numerical method. We find that the dynamic angular response of the mirror based on the analytical damping model matches very well with that based on the numerical damping model. We also perform experimental measurements and obtain results which are consistent with those obtained from the analytical and numerical damping models. Although the analytical damping model is derived under the assumption of harmonic response of the torsion mirror, it is shown that with the air spring effect neglected, this damping model is still valid for the case of nonharmonic response. The dependence of the damping torque on the ambient pressure is also considered and found to be insignificant in a certain regime of the ambient pressure. Finally, the convergence of the series solutions is discussed, and an approximate one term formula is presented for the squeeze film damping torque on the torsion mirror.

BackgroundPatient identification within and between health services is an operational challenge in many resource-limited settings. When following HIV risk groups for service provision and in the context of vaccine trials, patient misidentification can harm patient care and bias trial outcomes. Electronic fingerprinting has been proposed to identify patients over time and link patient data between health services. The objective of this study was to determine 1) the feasibility of implementing an electronic-fingerprint linked data capture system in Zambia and 2) the acceptability of this system among a key HIV risk group: female sex workers (FSWs).MethodsWorking with Biometrac, a US-based company providing biometric-linked healthcare platforms, an electronic fingerprint-linked data capture system was developed for use by field recruiters among Zambian FSWs. We evaluated the technical feasibility of the system for use in the field in Zambia and conducted a pilot study to determine the acceptability of the system, as well as barriers to uptake, among FSWs.ResultsWe found that implementation of an electronic fingerprint-linked patient tracking and data collection system was feasible in this relatively resource-limited setting (false fingerprint matching rate of 1/1000 and false rejection rate of <1/10,000) and was acceptable among FSWs in a clinic setting (2 % refusals). However, our data indicate that less than half of FSWs are comfortable providing an electronic fingerprint when recruited while they are working. The most common reasons cited for not providing a fingerprint (lack of privacy/confidentiality issues while at work, typically at bars or lodges) could be addressed by recruiting women during less busy hours, in their own homes, in the presence of “Queen Mothers” (FSW organizers), or in the presence of a FSW that has already been fingerprinted.ConclusionsOur findings have major implications for key population research and improved health services provision. However, more work needs to be done to increase the acceptability of the electronic fingerprint-linked data capture system during field recruitment. This study indicated several potential avenues that will be explored to increase acceptability.

Compared with laboratory environments, complex natural environments promote brain cell proliferation and neurogenesis. Predators are one important feature of many natural environments, but, in the laboratory, predatory stimuli tend to inhibit brain cell proliferation. Often, laboratory predatory stimuli also elevate plasma glucocorticoids, which can then reduce brain cell proliferation. However, it is unknown how natural predators affect cell proliferation or whether glucocorticoids mediate the neurogenic response to natural predators. We examined brain cell proliferation in six populations of the electric fish, Brachyhypopomus occidentalis, exposed to three forms of predator stimuli: (i) natural variation in the density of predatory catfish; (ii) tail injury, presumably from predation attempts; and (iii) the acute stress of capture. Populations with higher predation pressure had lower density of proliferating (PCNAþ) cells, and fish with injured tails had lower proliferating cell density than those with intact tails. However, plasma cortisol did not vary at the population level according to predation pressure or at the individual level according to tail injury. Capture stress significantly increased cortisol, but only marginally decreased cell proliferation. Thus, it appears that the presence of natural predators inhibits brain cell proliferation, but not via mechanisms that depend on changes in basal cortisol levels. This study is the first demonstration of predator-induced alteration of brain cell proliferation in a free-living vertebrate.

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