Shaping and transporting diamagnetic sessile drops

Electromagnetic fields are commonly used to control small quantities of fluids in microfluidics and digital microfluidics. Magnetic control techniques are less well studied than their electric counterparts, with only a few investigations into liquid diamagnetism. The ratio of magnetic to surface energy (magnetic Bond number B m) is an order of magnitude smaller for diamagnetic drops (B m ≈-0.3 at 1.2 T applied field) than for paramagnetic drops (B m ≈ 9.0 at 1.2 T applied field). This weaker interaction between the magnetic field and the diamagnetic drop has led to the phenomenon being overlooked in digital microfluidics. Here, we investigate shaping and transport of diamagnetic drops using magnetostatic fields. Our findings highlight how diamagnetic fluids can be used as a novel tool in the toolbox of microfluidics and digital microfluidics

A Single 10-Minute Vape Exposure Alters Ventilation in Adult Rats

E-cigarettes, also known as electronic nicotine delivery systems (ENDS), are an alternative to the traditional cigarette. ENDS function using a heating device (e.g. “vape pen”, such as JUUL) to heat liquids containing nicotine and other chemicals. Recent research in humans and animal models suggests that acute exposure (5 to 60 minutes) to e-cigarette vapor increases airway resistance and proinflammatory cytokine presence in lung tissue. These acute effects may lead to long term functional changes in the lung and tissue changes at the respiratory membrane. PURPOSE: The purpose of this study was to investigate the effects of an acute 10-minute e-cigarette vapor exposure on lung function and proinflammatory cytokine expression, specifically IL-1β in adult rats. METHODS: Adult male Long Evans rats (n=18) were randomly assigned to either the experimental vapor exposure group or the control air group. The vapor exposure group (n=9) was exposed once to 5% nicotine vapor for 10 minutes using whole-body exposure chambers. The air group (n=9) were placed in a chamber, but only exposed to room air. Ventilation recordings were completed the day before exposure (pre) and immediately after vapor or air exposure (post) using unrestrained whole-body plethysmography. Tidal volume/100g, breathing frequency, and minute ventilation/100g were assessed. Blood was collected at the end of the post-treatment day for all animals and processed to serum. Serum cotinine (a nicotine metabolite) and proinflammatory cytokine IL-1β were measured using enzyme linked immunosorbent assays (ELISA). RESULTS: The presence of cotinine was confirmed in the serum collected from the vapor exposed group (89.16 ± 31.16 ng/mL) compared to the air control group (0.054 ± 0.051 ng/mL). Baseline ventilation data (pre-) and post-treatment were compared between air and vapor exposed groups across three different parameters: tidal volume/100g, frequency, and minute ventilation/100g. These parameters were compared resulting in three distinct 2x2 (time x treatment) Mixed Model ANOVAs. A main effect of time (pre-treatment vs. post-treatment) on frequency (p = 0.036) and minute ventilation (p = 0.006) was observed. The main effect of time on breathing frequency was not due to the treatment group (p = 0.906). The minute ventilation for the vapor exposed group decreased from pre-treatment (83.2 ± 16.8 mL/min/100g) to post-treatment (59.5 ± 8.75 mL/min/100g; p = 0.007), while the minute ventilation of the air control group remained relatively constant pre-treatment (72.1 ± 8.6 mL/min/100g) to post-treatment (73.1 ± 15.1 mL/min/100g; p = 0.76). And while a main effect of time on tidal volume was not significant, there is a trend of a decrease in tidal volume for the vapor exposed group from pre- to post-treatment. There was no significant difference (unpaired student’s t-test, p = 0.44) in circulating proinflammatory IL-1β cytokine levels in the serum between the vapor exposed group (4.96 ± 5.98 pg/mL) and air group (8.05 ± 9.98 pg/mL). CONCLUSIONS: After an acute 10-minute e-cigarette vapor exposure, respiratory function was altered in that minute ventilation and possibly tidal volume were decreased in rats exposed to vape. Circulating levels of proinflammatory cytokine IL-1β did not differ between exposure groups. Taken together these results suggest that even a single bout of e-cigarette vapor exposure results in functional changes in the adult lungs. Future studies will investigate the duration of this functional change and additional cytokine presence

Field-induced shaping of sessile paramagnetic drops

We use the electromagnetic stress tensor to describe the elongation of paramagnetic drops in uniform magnetic fields. This approach implies a linear relationship between the shape of the drops and the square of the applied field, which we confirm experimentally. We show that this effect scales with the volume and susceptibility of the drops. By using this unified electromagnetic approach, we highlight the potential applications of combining electric and magnetic techniques for controlled shaping of drops in liquid displays, liquid lenses, and chemical mixing of drops in microfluidics

Seven Day E-cigarette Vapor Exposure Does Not Modify Ventilation Patterns in Long-Evans Rats

Electronic nicotine delivery systems or e-cigarettes are devices used to deliver aerosolized liquids often containing nicotine and other chemicals. These devices were originally created as a way to assist with smoking cessation in adults; however, use of these devices is increasing in adolescent and young adult populations. The long and short term effects of vaping are still under active investigation. PURPOSE: The purpose of this study was to investigate the effects of 7 days of e-cigarette vapor exposure in adult rats on lung function and lung tissue inflammatory cytokine expression, specifically IL-1. METHODS: Using random assignment, 10 adult male long-evans rats were assigned to vape (experimental) or air (control) groups. The animals were exposed to either air (n = 4) or 5% nicotine vapor (n=6) using a whole-body exposure chamber, twice a day for ten minutes for seven consecutive days. Ventilation recordings were completed on day 0 (before exposure) and day 8 (after exposure) using unrestrained whole-body plethysmography. Minute ventilation, tidal volume, and breathing frequency were assessed. Blood was collected on day 8 to look for the presence of cotinine (a nicotine metabolite). Whole lung tissue was also collected on day 8 for inflammatory cytokine assay, IL-1 ELISA. RESULTS: Cotinine was found to be present in the serum samples of the vape groups (86.6 ng/ml +/- 1.0 ng/mL) but not the air groups (0.0 ng/mL) confirming drug exposure. Baseline ventilation data collected on day 0 and post-exposure ventilation data collected on day 8 were compared between air and vape groups across three different parameters: minute ventilation, frequency, and tidal volume. These parameters were compared resulting in three distinct two-way ANOVAs comparing the variables time and treatment. No significant difference was found among any of the comparisons (p \u3e 0.05 for all). Similarly, no difference in lung inflammatory cytokine IL-1 was observed in the lung tissue of the air (85.6 pg/mL +/- 10.2 pg/mL) or vape (82.7 pg/mL +/- 14.9 pg/mL) exposure groups (p \u3e 0.05, t-test). CONCLUSIONS: In this study, 7 days of e-cigarette vapor exposure did not affect ventilation parameters or increase the presence of inflammatory cytokine, IL-1, in whole lung tissue. Limitations to this study include a small sample size (n = 10) and unreliable negative-pressure which were used to produce the vapor for the e-cigarette exposure. Future studies will modify the vape exposure system and include a larger sample size

Effects of 14 Day E-Cigarette Exposure on Ventilation and Circulating Pro-Inflammatory Cytokines in Adolescent Rats

Electronic nicotine delivery systems or e-cigarettes are devices used to deliver vaporized liquids often containing nicotine and other chemicals. These devices were originally created as a way to assist with smoking cessation in adults; however, use of these devices is increasing in adolescent and young adult populations. Recent research suggests that exposure to the chemicals in e-cigarette vapor may cause harm to adolescent lung tissue and promote a proinflammatory immune response in the lungs. These molecular changes may lead to functional changes in terms of lung volumes or gas exchange at the respiratory membrane. PURPOSE: The purpose of this study was to investigate the effects of 14 days of e-cigarette vapor exposure in adolescent rats on lung function and lung tissue proinflammatory cytokine expression, specifically IL-1β. METHODS: Using random assignment, 20 adolescent male Long Evans rats were assigned to vape (experimental) or air (control) groups. The animals were exposed to either air (n = 10) or 5% nicotine vapor (n=10) using a whole-body exposure chamber, once a day for ten minutes for fourteen consecutive days. Ventilation recordings were completed on day 0 (before exposure) and day 15 (after exposure) using unrestrained whole-body plethysmography. Minute ventilation/100g, tidal volume/100g, and breathing frequency were assessed. Blood was collected on day 15 and processed to serum. Serum samples were analyzed for circulating levels of the nicotine metabolite, cotinine, and the proinflammatory cytokine, IL-1β, using enzyme linked immunosorbent assays (ELISA). RESULTS: Cotinine was found to be present in the serum samples of the vape groups (20.71 ng/ml +/- 6.875 ng/mL) but not the air groups (0.007 +/- 0.019 ng/mL) confirming nicotine and vapor exposure. Baseline ventilation data collected on day 0 and post-exposure ventilation data collected on day 15 were compared between air and vape groups across three different parameters: minute ventilation/100g , frequency, and tidal volume/100 g. These parameters were compared resulting in three distinct 2x2 (time x treatment) Mixed Model ANOVAs. Between baseline and post-treatment measurements, for both groups, there was a significant decrease in values in minute ventilation (F(1,15) = 5.647, p = 0.0312) and tidal volume (F(1,15) = 12.38, p = 0.0031). Between treatment groups there was also a significant difference in minute ventilation (F(1,15) = 7.979, p = 0.0128) and frequency (F(1,15) = 11.35, p = 0.0042). There was also significantly lower levels observed in the inflammatory cytokine IL-1β (p \u3c 0.0136) for the vape group (22.13 +/- 19.96 pg/mL) in comparison to the air group (3.28 +/- 3.52 pg/mL). CONCLUSIONS: Following 14 days of e-cigarette vapor exposure, ventilation patterns were altered in the vapor exposed animals, specifically decreasing tidal volume and minute ventilation. Additionally, in these same vapor exposed animals, circulating levels of the pro-inflammatory cytokine, IL-1ꞵ, was decreased suggesting dysregulation of immune pathways. Taken together these results suggest that the use of e-cigarettes may lead to both functional and molecular changes in adolescent lungs, interfering with pulmonary function and affecting one’s quality of life

Neuronal pentraxins mediate synaptic refinement in the developing visual system

Peer reviewedPublisher PD

Pharmacological evaluation of novel bioisosteres of an adamantanyl benzamide P2X7 receptor antagonist

Adamantanyl benzamide 1 was identified as a potent P2X7R antagonist but failed to progress further due to poor metabolic stability. We describe the synthesis and SAR of a series of bioisosteres of benzamide 1 to explore improvements in the pharmacological properties of this lead. Initial efforts investigated a series of heteroaromatic bioisosteres, which demonstrated improved physicochemical properties but reduced P2X7R antagonism. Installation of bioisosteric fluorine on the adamantane bridgeheads was well tolerated and led to a series of bioisosteres with improved physicochemical properties and metabolic stability. Trifluorinated benzamide 34 demonstrated optimal physicochemical parameters, superior metabolic stability (ten times longer than lead benzamide 1), and an improved physicokinetic profile and proved effective in the presence of several known P2X7R polymorphisms

Toll-like receptor signaling adapter proteins govern spread of neuropathic pain and recovery following nerve injury in male mice.

BackgroundSpinal Toll-like receptors (TLRs) and signaling intermediaries have been implicated in persistent pain states. We examined the roles of two major TLR signaling pathways and selected TLRs in a mononeuropathic allodynia.MethodsL5 spinal nerve ligation (SNL) was performed in wild type (WT, C57BL/6) male and female mice and in male Tlr2-/-Tlr3-/-, Tlr4-/-, Tlr5-/-, Myd88-/-, Triflps2, Myd88/Triflps2, Tnf-/-, and Ifnar1-/- mice. We also examined L5 ligation in Tlr4-/- female mice. We examined tactile allodynia using von Frey hairs. Iba-1 (microglia) and GFAP (astrocytes) were assessed in spinal cords by immunostaining. Tactile thresholds were analyzed by 1- and 2-way ANOVA and the Bonferroni post hoc test was used.ResultsIn WT male and female mice, SNL lesions resulted in a persistent and robust ipsilateral, tactile allodynia. In males with TLR2, 3, 4, or 5 deficiencies, tactile allodynia was significantly, but incompletely, reversed (approximately 50%) as compared to WT. This effect was not seen in female Tlr4-/- mice. Increases in ipsilateral lumbar Iba-1 and GFAP were seen in mutant and WT mice. Mice deficient in MyD88, or MyD88 and TRIF, showed an approximately 50% reduction in withdrawal thresholds and reduced ipsilateral Iba-1. In contrast, TRIF and interferon receptor null mice developed a profound ipsilateral and contralateral tactile allodynia. In lumbar sections of the spinal cords, we observed a greater increase in Iba-1 immunoreactivity in the TRIF-signaling deficient mice as compared to WT, but no significant increase in GFAP. Removing MyD88 abrogated the contralateral allodynia in the TRIF signaling-deficient mice. Conversely, IFNβ, released downstream to TRIF signaling, administered intrathecally, temporarily reversed the tactile allodynia.ConclusionsThese observations suggest a critical role for the MyD88 pathway in initiating neuropathic pain, but a distinct role for the TRIF pathway and interferon in regulating neuropathic pain phenotypes in male mice

Religious Identity, Religious Attendance, and Parental Control

Using a national sample of adolescents aged 10–18 years and their parents (N = 5,117), this article examines whether parental religious identity and religious participation are associated with the ways in which parents control their children. We hypothesize that both religious orthodoxy and weekly religious attendance are related to heightened levels of three elements of parental control: monitoring activities, normative regulations, and network closure. Results indicate that an orthodox religious identity for Catholic and Protestant parents and higher levels of religious attendance for parents as a whole are associated with increases in monitoring activities and normative regulations of American adolescents