Cal Poly Microgrid Fixed PV Array

The Mechanical Engineering Department at California Polytechnic State University of San Luis Obispo would like an adjustable, fixed angle solar panel mount to help educate students on basic solar energy principles. Our team has developed a unique sawhorse design utilizing ideation techniques and design selection tools. The selected design allows for multiple panel adjustability and control of both azimuth and tilt angle. Safety concerns are addressed with action plans to mitigate risk. Concept prototypes to justify gearbox functionality and subsystem cohesion was utilized to reduce manufacturing issues. Manufacturing began in March 2020 and proceed through until the end of the month. The manufacturing of the mount was halted due to COVID-19, forcing the design to end strictly in a what-if manufacturing procedure to allow the construction of it to be done in future time

Major histocompatibility (B) complex control of the growth pattern of v-src DNA-induced primary tumors

Observations that the major histocompatibility (B) complex is a determinant of the growth pattern of Rous sarcoma virus (RSV)-induced tumors raised the question as to whether control is exerted at the level of a v-src-determined, i.e., transformation-specific, function. To investigate this point, the tumor size scores and tumor profile indices of v-src-induced tumors were compared in two lines of chickens congenic for B complex genotypes. The finding that the growth patterns of tumors, induced by v-src DNA inoculation at 6 weeks posthatch, differ in these two lines establishes that the B complex exerts control over tumor growth at the level of a v-src-determined function. The potential importance of this control, in terms of the naturally occurring case of an avian sarcoma virus infection, is suggested by the observation that the patterns of tumor growth in a given congenic line are similar whether the tumors are induced by v-src DNA or by RSV

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Cell culture and reagents Human neonatal foreskin keratinocyte cultures were initiated and propagated in MCDB153 complete medium, as previously describe

Electrophysiological assessment and pharmacological treatment of blast-induced tinnitus.

Tinnitus, the phantom perception of sound, often occurs as a clinical sequela of auditory traumas. In an effort to develop an objective test and therapeutic approach for tinnitus, the present study was performed in blast-exposed rats and focused on measurements of auditory brainstem responses (ABRs), prepulse inhibition of the acoustic startle response, and presynaptic ribbon densities on cochlear inner hair cells (IHCs). Although the exact mechanism is unknown, the "central gain theory" posits that tinnitus is a perceptual indicator of abnormal increases in the gain (or neural amplification) of the central auditory system to compensate for peripheral loss of sensory input from the cochlea. Our data from vehicle-treated rats supports this rationale; namely, blast-induced cochlear synaptopathy correlated with imbalanced elevations in the ratio of centrally-derived ABR wave V amplitudes to peripherally-derived wave I amplitudes, resulting in behavioral evidence of tinnitus. Logistic regression modeling demonstrated that the ABR wave V/I amplitude ratio served as a reliable metric for objectively identifying tinnitus. Furthermore, histopathological examinations in blast-exposed rats revealed tinnitus-related changes in the expression patterns of key plasticity factors in the central auditory pathway, including chronic loss of Arc/Arg3.1 mobilization. Using a formulation of N-acetylcysteine (NAC) and disodium 2,4-disulfophenyl-N-tert-butylnitrone (HPN-07) as a therapeutic for addressing blast-induced neurodegeneration, we measured a significant treatment effect on preservation or restoration of IHC ribbon synapses, normalization of ABR wave V/I amplitude ratios, and reduced behavioral evidence of tinnitus in blast-exposed rats, all of which accorded with mitigated histopathological evidence of tinnitus-related neuropathy and maladaptive neuroplasticity

Effects of Antioxidant Treatment on Blast-Induced Brain Injury

<div><p>Blast-induced traumatic brain injury has dramatically increased in combat troops in today’s military operations. We previously reported that antioxidant treatment can provide protection to the peripheral auditory end organ, the cochlea. In the present study, we examined biomarker expression in the brains of rats at different time points (3 hours to 21 days) after three successive 14 psi blast overpressure exposures to evaluate antioxidant treatment effects on blast-induced brain injury. Rats in the treatment groups received a combination of antioxidants (2,4-disulfonyl α-phenyl tertiary butyl nitrone and N-acetylcysteine) one hour after blast exposure and then twice a day for the following two days. The biomarkers examined included an oxidative stress marker (4-hydroxy-2-nonenal, 4-HNE), an immediate early gene (c-fos), a neural injury marker (glial fibrillary acidic protein, GFAP) and two axonal injury markers [amyloid beta (A4) precursor protein, APP, and 68 kDa neurofilament, NF-68]. The results demonstrate that blast exposure induced or up-regulated the following: 4-HNE production in the dorsal hippocampus commissure and the forceps major corpus callosum near the lateral ventricle; c-fos and GFAP expression in most regions of the brain, including the retrosplenial cortex, the hippocampus, the cochlear nucleus, and the inferior colliculus; and NF-68 and APP expression in the hippocampus, the auditory cortex, and the medial geniculate nucleus (MGN). Antioxidant treatment reduced the following: 4-HNE in the hippocampus and the forceps major corpus callosum, c-fos expression in the retrosplenial cortex, GFAP expression in the dorsal cochlear nucleus (DCN), and APP and NF-68 expression in the hippocampus, auditory cortex, and MGN. This preliminary study indicates that antioxidant treatment may provide therapeutic protection to the central auditory pathway (the DCN and MGN) and the non-auditory central nervous system (hippocampus and retrosplenial cortex), suggesting that these compounds have the potential to simultaneously treat blast-induced injuries in the brain and auditory system.</p> </div

Examples of APP immunolabeling in the hippocampus of the NC (A), 24H-B (B) and 24H-B/T (C) groups.

<p>No positive APP staining was observed in the hippocampus of normal controls (A). Strong positive APP labeling was observed in the hippocampus of the 24H-B group (arrows in B). Decreased APP expression was observed in the hippocampus of the 24H-B/T group relative to the 24H-B group (arrows in C). APP-positive labeling in the hippocampus was quantified and statistically analyzed (D). Two to three hippocampal sections from each rat brain (6 rats in each group) were used in these analyses. Significantly increased APP expression was observed in the hippocampus of the 24H-B group compared to the NC group (<i>p</i> < 0.001). An antioxidant treatment effect was found at 24 hours after blast exposure (<i>p</i> < 0.001), however no significant difference was observed between the treated and untreated groups 7 days after blast exposure (7D-B v.s. 7D-B/T, all <i>p</i> > 0.05). Error bars represent standard error of the means. Scale bar = 10 µm in C for A-C. *** indicate <i>p</i> < 0.001.</p

A low magnification image of the DCN is shown in A.

<p>The DCN is divided into three parts (<i>dashed </i><i>lines</i> in A): <i>medial</i>, <i>middle</i>, and <i>lateral</i>. The <i>squares</i> in A indicate where images were collected for cell counting. Examples of GFAP staining (arrows in B-D) in the <i>middle</i> region of the DCN of the NC (B), 21D-B (C) and 21D-B/T (D) groups. ML, FCL, and DL in B demarcate the molecular layer, fusiform cell layer, and deep layer, respectively. Scale bar in A = 500 µm, in D = 200 µm in for B-D.</p