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Economic Indicators of the College Station-Bryan MSA, April 2024 ���
No full textMonthly economic report for the College Station-Bryan MSA.The Business-Cycle Index increased 0.2% from January to February 2024. The local unemployment rate for February 2024 was 3.1%, unchanged from the previous month. February���s local nonfarm employment increased by 0.2% from January 2024. Inflation-adjusted taxable sales were down by almost 1% from January 2024 to February 2024. Inflation-adjusted quarterly wage payments were down by 1.6% in the third quarter of 2023 compared to the previous quarter. College Station - Bryan ranks ninthth-lowest in overall Regional Price Parity and in Regional Housing Price Parity among eleven selected college towns
The Effects of Airflow as a Stressor of E. coli Strains and Its Impact on Survival Mechanisms Triggered
No full textUnderstanding how bacteria respond to ventilated environments is a crucial concept, especially when considering accurate airflow modeling and detection limits. To properly design facilities for aseptic conditions, we must minimize the parameters for pathogenic bacteria to thrive. Identifying how pathogenic bacteria continue to survive, particularly due to their multi-drug resistance characteristics, is necessary for designing sterile environments and minimizing pathogen exposure. A conserved characteristic among bacterial organisms is their ability to maintain intracellular homeostasis for survival and growth in hostile environments, mechanosensitive (MS) channels are one of the characteristics that guide this phenomenon. Interestingly, during extreme stress, bacteria will forgo favorable homeostasis to execute fast-acting survival strategies. The physiological sensors, such as MS channels, that trigger this survival mechanism is not clearly understood and leaves a gap between how bacteria translate physical stress to an intracellular response. Here we study the role of mechanosensitive ion channels that are potentially triggered by aerosolization. We hypothesize that change in antimicrobial uptake is affected by aerosolization stress. Bacteria regulate their defense mechanisms against antimicrobials which leads to varying susceptibility. Based on this information we hypothesize that aerosolization stress affects the antimicrobial resistance defense mechanisms of Escherichia coli (E. coli). Here we analyze the culturability and quantification of five different E. coli mechanosensitive channels knockout strains and compare antibiotic susceptibility in stressed and unstressed airflow conditions. As a result of this study, we can identify how defensive mechanisms of resistant bacteria are triggered for their survival in built environments. By changing ventilation airflow velocity, observing the change in antibiotic response, we show how pathogenic bacteria respond to ventilated environments through mechanosensitive ion channels
Role of NCK2 Signaling and Mechanical Forces in Endothelial Dysfunction and Atherosclerosis
No full textA better understanding of endothelial dysfunction holds promise for more effective interventions for atherosclerosis prevention and treatment. Endothelial dysfunction resulting from metabolic imbalance in combination with abnormal mechanotransduction drives atherosclerosis. Current therapies for atherosclerosis rely on reducing cholesterol and inflammation but do not preserve or restore endothelial homeostasis. Development of improved therapies requires, therefore, a better understanding of mechanisms underpinning endothelial dysfunction. To bridge this gap in knowledge, we examined key pathways modulating the endothelial and arterial phenotype in proatherogenic mouse models.
Our first study explored endothelial signaling by the non-catalytic region of the tyrosine kinase (NCK) family of adaptors, consisting of NCK1 and NCK2, which are involved in cardiovascular development and postnatal angiogenesis. We showed stage- and sex-dependent effects of endothelial NCK2 signaling on arterial wall inflammation and atherosclerosis development. Male and female Nck1-null atheroprone (APOE-deficient) mice enabling inducible, endothelial-specific Nck2 inactivation were fed a high fat diet for 8 or 16 weeks to model atherosclerosis initiation and progression, respectively. At advanced stages of disease, plaque size and severity of atherosclerotic lesions were reduced, only in males, by abrogation of endothelial NCK2 signaling. Markers of vascular inflammation were reduced by endothelial NCK2 deficiency in both males and females during atherosclerosis progression. Collectively, these results demonstrate stage- and sex-dependent modulation of atherosclerosis development by endothelial NCK2 signaling.
Our second study aimed to decouple the effect of disturbed blood flow from arterial wall stiffening in the endothelial mechanical phenotype. We induced acute or chronic disturbed blood flow via partial ligation (PCL) of the left carotid in male and female mice. To modulate arterial wall stiffness, mice experiencing chronic disturbed blood flow were also affixed with osmotic minipumps delivering saline or 150 mg/kg/day of ��-aminopropionitrile (BAPN), an inhibitor of the collagen crosslinking enzymes of the lysyl oxidase family. Two days (acute) or two weeks (chronic) after induction of disturbed blood flow by PCL, we determined the elastic moduli of the endothelium and subendothelial matrix of carotid preparations en face using atomic force microscopy. We found that preventing stiffening of the arterial wall by BAPN treatment increases endothelial and subendothelial compliance, a finding with potential therapeutic implications in atherosclerosis
Evaluation of the Effects of Printing Parameters and New Bioink Composition on Green Bioprinted Constructs
Get PDFBioprinting is an additive manufacturing process capable of fabricating bioprinted constructs containing cells via layer-by-layer deposition of bioink. Bioink contains the cells using during bioprinting, and may contain additional materials to promote cell adhesion, cell viability, structural integrity, and/or shape fidelity of bioprinted constructs. While bioprinting using mammalian cells has been extensively studied, less research has been conducted regarding bioprinting using photosynthetic cells, also known as green bioprinting. Potential benefits of green bioprinting include production and easy harvesting of metabolites for use in the pharmaceutical, cosmetic, and food industries. Constructs fabricated using green bioprinting have also been shown to remove metal from water, and green bioprinted constructs are capable of providing oxygen to mammalian cells in order to supplement tissue engineering research.
Despite potential benefits, more research is required to determine the optimal printing parameters for green bioprinting. In order to be functional, bioprinted constructs must have high cell viability post bioprinting. Research was conducted to test the effects of variable extrusion pressures and needle diameters on Chlamydomonas reinhardtii algae cell viability in green bioprinted constructs. It was determined that increasing extrusion pressure and decreasing needle diameter decreased the cell viability in green bioprinted constructs.
Additionally, in currently published literature, only two bioinks have been used for green bioprinting applications. These bioinks, alginate:methylcellulose and alginate:agarose:methylcellulose, promote high photosynthetic cell viability. However, the bioinks do not have sufficient physical properties to bioprint constructs with high shape fidelity. A new bioink, alginate:methylcellulose:GelMA, was synthesized to improve the shape fidelity of green bioprinted constructs while maintaining high cell viability. Constructs bioprinted with alginate:methylcellulose:GelMA bioink were tested for Chlamydomonas reinhardtii algae cell viability and shape fidelity of the bioprinted constructs. Rheological analysis was also performed of a sample of unprinted alginate:methylcellulose:GelMA bioink to determine if the viscosity of the bioink is suitable for use with bioprinting. It was determined that alginate:methylcellulose:GelMA bioink has suitable viscosity, and can be used to bioprint green constructs with high cell viability and shape fidelity
VOF with Center of Mass and Lagrangian Particles (VCLP) - A Surface Tracking and Advection Method for Fluids
No full textThis dissertation presents a novel surface tracking, and advection algorithm for incompressible fluid flows in two and three dimensions. This method based on the volume-of-fluid (VOF) method, is named VOF-with-center-of-mass-and-Lagrangian-particles (VCLP), and it uses spatially and temporally localized Lagrangian particles (LPs) inside a finite volume framework. The fluid surface is recaptured and reconstructed piecewise using the mean slope, mean curvature, and
fluid estimated using new methods from the local spatial distribution of the volume fluid fraction values. The reconstructed surfaces are either a finite plane or part of a spherical surface, in 3D and line segments or circular arcs, in 2D. The fluid mass inside each cell is discretized spatially by LPs and distributed as blue noise. LPs are then advected cell by cell with a choice of two different advection schemes in time using interpolated velocity and approximated acceleration fields. VCLP continuously tracks the center of mass of the fluid parcels in the Lagrangian way and this helps to reduce the errors due to numerical acceleration resulting from lack of information to reconstruct the interface accurately. LPs enable VCLP to work with structured and unstructured grids in two and three dimensions and might work for Courant���Friedrichs���Lewy numbers larger than one. LPs exist only inside a single fluid cell at a given time-step, allowing it to work without constraints on domain size and storage memory, unlike standard Lagrangian methods. LPs make it easy to adjust
computational accuracy vs. speed by only changing the number of LPs. VCLP���s performance is evaluated using standard benchmark tests such as translation, rotation, single vortex, deformation, and Zalesk���s tests from the literature. VCLP is applied to TSUNAMI2D, a 2D Navier-Stokes model to simulate the dam-break problem and breaking waves
Effects of Prenatal Testosterone Treatment on Puberty, Reproductive Cyclicity, and Responsiveness of the Neuroendocrine Axis to Steroid Feedback Mechanisms in First-Generation Ewes: A Model for Polycystic Ovary Syndrome
No full textPolycystic ovary syndrome is the leading cause of anovulatory infertility in women of reproductive age, characterized by anovulation, polycystic ovarian morphology, and hyperandrogenism. It is a multifactorial disease impacted by environmental, lifestyle, genetic, and epigenic influences. Obesity can increase the severity and development of PCOS phenotype. Prenatal testosterone exposure can alter the developmental trajectory to cause reprogramming of key processes that may lead to onset of PCOS in adulthood. We hypothesized that prenatal exposure to testosterone (T) excess would 1) advance time of puberty attainment and disrupt progesterone cycles; 2) reduce the responsiveness of the neuroendocrine axis to estradiol positive feedback; 3) disrupt periovulatory LH surge dynamics; and 4) reduce neuroendocrine sensitivity to progesterone negative feedback during the mid-luteal phase in first generation ewes. Our results indicate that while prenatal T treatment combined with postnatal excessive weight gain did not alter age at puberty, it exacerbated the reproductive defects seen during the first breeding season (early adulthood) and further deteriorated reproductive cyclicity in the second breeding season (adulthood). In addition, the estradiol positive feedback mechanism was impaired in both T maintenance (prenatally exposed to T excess and postnatally fed 100% of NRC requirements) and T overfed females (prenatally T treated and postnatally fed 130% of NRC requirements), through a delayed LH surge and reduced LH surge amplitude, which can have detrimental effects on ovulation and subsequent fertility. Key features of the preovulatory LH surge were altered, with no further amplification of postnatal overfeeding observed. Lastly, responsiveness to progesterone negative feedback was reduced in prenatal T maintenance fed ewes and amplified in T overfed ewes, through an observed increase of LH pulse amplitude, peak, and pulse frequency. These data herein support our previous findings that prenatal T treatment in female sheep results in neuroendocrine dysfunction and periovulatory disruptions, and that the shorter T treatment window of gestational day 60-90 is sufficient to program these effects. Moreover, postnatal overfeeding had varying effects on these neuroendocrine disruptions and provides valuable insight into the effects of obesity on PCOS pathogenesis in women
