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Search Results: 1 - 10 of 472886 matches for " William A Banks "
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Pseudacteon Obtusus (Diptera: Phoridae)Attacking Solenopsis Invicta(Hymenoptera: Formicidae) in Brazil
David F. Williams,William A. Banks
Psyche , 1987, DOI: 10.1155/1987/85157
Convolutions with probability distributions, zeros of L-functions, and the least quadratic nonresidue
William D. Banks,Konstantin A. Makarov
Mathematics , 2014,
Abstract: Let $d$ be a probability distribution. Under certain mild conditions we show that $$ \lim_{x\to\infty}x\sum_{n=1}^\infty \frac{d^{*n}(x)}{n}=1,\qquad\text{where}\quad d^{*n}:=\underbrace{\,d*d*\cdots*d\,}_{n\text{ times}}. $$ For a compactly supported distribution $d$, we show that if $c>0$ is a given constant and the function $f(k):=\widehat d(k)-1$ does not vanish on the line $\{k\in{\mathbb C}:\Im\,k=-c\}$, where $\widehat d$ is the Fourier transform of $d$, then one has the asymptotic expansion $$ \sum_{n=1}^\infty\frac{d^{*n}(x)}{n}=\frac{1}{x}\bigg(1+\sum_k m(k) e^{-ikx}+O(e^{-c x})\bigg)\qquad (x\to +\infty), $$ where the sum is taken over those zeros $k$ of $f$ that lie in the strip $\{k\in{\mathbb C}:-c<\Im\,k<0\}$, $m(k)$ is the multiplicity of any such zero, and the implied constant depends only on $c$. For a given distribution $d$ of this type, we briefly describe the location of the zeros $k$ of $f$ in the lower half-plane $\{k\in{\mathbb C}:\Im\,k<0\}$. For an odd prime $p$, let $n_0(p)$ be the least natural number such that $(n|p)=-1$, where $(\cdot|p)$ is the Legendre symbol. As an application of our work on probability distributions, in this paper we generalize a well known result of Heath-Brown concerning the behavior of the Dirichlet $L$-function $L(s,(\cdot|p))$ under the assumption that the Burgess bound $n_0(p)\ll p^{1/(4\sqrt{e})+\epsilon}$ cannot be improved.
Lipopolysaccharide-enhanced transcellular transport of HIV-1 across the blood-brain barrier is mediated by luminal microvessel IL-6 and GM-CSF
Shinya Dohgu, Melissa A Fleegal-DeMotta, William A Banks
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-167
Abstract: Human immunodeficiency virus type 1 (HIV-1) infection induces neurological dysfunctions known as the AIDS-dementia complex or HIV-associated dementia (HAD). Although highly active antiretroviral therapy (HAART) and combination antiretroviral therapy (cART) have dramatically decreased the incidence and severity of HAD, the prevalence of HAD, including minor cognitive and motor disorders, is increasing with the longer lifespan of HIV patients [1]. Most antiretroviral drugs comprising HAART have a restricted entry into the brain because of blood-brain barrier (BBB) efflux transporters so that the brain serves as a reservoir for HIV-1 [2] and a source for viral escape [3]. Therefore, HIV-1 in the brain can contribute to the incidence and development of HIV-associated neurological impairment in HIV-1 patients both prior to and after treatment with HAART/cART.HIV-1 can enter the brain by two routes: the passage of cell-free virus by an adsorptive endocytosis-like mechanism [4-7] and trafficking of HIV-1-infected immune cells across the BBB [8]. HIV-1 infection of brain endothelial cells (BECs) is not a productive infection [9] and penetration of HIV-1 is independent of the CD4 receptor [10]. At the early stage, HIV-1 enters the brain through an intact, normally functioning BBB [11]. At later stages of infection, elevated levels of proinflammatory cytokines/chemokines in the blood of patients with AIDS [12-14] are likely associated with the increase in HIV-1 infiltration [15-17], while HIV-1 gp120 and Tat induce the disruption of tight junctions in BECs [17-20].As reported by Brenchley et al. and confirmed by others, plasma levels of lipopolysaccharide (LPS), a Gram-negative bacterial endotoxin, are higher in chronic HIV-infected patients with HAART than in the uninfected [3,21]. Bacterial infection in HIV patients influences the severity and rate of disease progression [22]. Peripheral LPS induces various inflammatory and immunological reactions including the production o
Brain microvascular pericytes are immunoactive in culture: cytokine, chemokine, nitric oxide, and LRP-1 expression in response to lipopolysaccharide
Andrej Kovac, Michelle A Erickson, William A Banks
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-139
Abstract: Supernatants were collected from primary cultures of mouse brain pericytes. Release of nitric oxide (NO) was measured by the Griess reaction and the level of S-nitrosylation of pericyte proteins measured with a modified "biotin-switch" method. Specific mitogen-activated protein kinase (MAPK) pathway inhibitors were used to determine involvement of these pathways on NO production. Cytokines and chemokines were analyzed by multianalyte technology. The expression of both subunits of LRP-1 was analyzed by western blot.Lipopolysaccharide (LPS) induced release of NO by pericytes in a dose-dependent manner that was mediated through MAPK pathways. Nitrative stress resulted in S-nitrosylation of cellular proteins. Eighteen of twenty-three cytokines measured were released constitutively by pericytes or with stimulation by LPS, including interleukin (IL)-12, IL-13, IL-9, IL-10, granulocyte-colony stimulating factor, granulocyte macrophage-colony stimulating factor, eotaxin, chemokine (C-C motif) ligand (CCL)-3, and CCL-4. Pericyte expressions of both subunits of LRP-1 were upregulated by LPS.Our results show that cultured mouse brain microvascular pericytes secrete cytokines, chemokines, and nitric oxide and respond to the innate immune system stimulator LPS. These immune properties of pericytes are likely important in their communication within the neurovascular unit and provide a mechanism by which they participate in neuroinflammatory processes in brain infections and neurodegenerative diseases.The blood-brain barrier (BBB) is a selective barrier that is created by the endothelial cells in cerebral microvessels. Endothelial cells and supporting cells such as astrocytes, pericytes, neurons, and perivascular microglia are organized together to form the "neurovascular unit" which is essential for induction, function, and support of the BBB [1]. In contrast to the considerable knowledge characterizing the crosstalk among brain endothelial cells, astrocytes, and microglia within
Forest Response to the US 1990 Clean Air Act: The Southern Spruce-Fir Ecosystem  [PDF]
Stephen A. Banks
American Journal of Plant Sciences (AJPS) , 2014, DOI: 10.4236/ajps.2014.53050

The history of the Black Mountains in North Carolina and the southern Spruce-Fir ecosystem has been fraught with widespread forest decline since the mid 1960’s. Balsam Woolly Adelgid attacks and acidic deposition were two of the most recognized causes of decline. Uncertainty arose about the future of these forests, and projections were made regarding the endangerment or extinction of the endemic Fraser fir ([Pursh] Poiret). This study analyzed data sets from a permanent plot network in the Black Mountains dating 1985, 2002, and 2012. Indications that the Fraser fir population is stabilizing from a “boom-bust” cycle of population growth and has entered the stem exclusion stage of forest stand development are evident. Fir live stem density increased more than 250% from 1985 to 2002, and then declined 40% by 2012 at the highest elevations in the forest. Overall, fir appeared to be more impacted on western facing slopes than eastern ones. The population of red spruce experienced a steady decrease in live stem counts, but an increase in live basal area through all years, and at all elevation classes (1675 m, 1830 m, and 1980 m), indicating a normal progression through stand development. Red spruce was also most negatively impacted on western facing slopes. Live stem density was significantly higher (P < 0.001) than eastern plots, but live basal area was similar between the two aspects. Atmospheric deposition concentrations of the four main acidic molecules at Mt. Mitchell all peaked in 1998, but decreased by 2012. These reductions, occurring shortly after tightened regulations in the 1990 amendments to the Clean Air Act may have potential implications for increased forest resilience.

Pharmacokinetics and modeling of immune cell trafficking: quantifying differential influences of target tissues versus lymphocytes in SJL and lipopolysaccharide-treated mice
Banks William A,Niehoff Michael L,Ponzio Nicholas M,Erickson Michelle A
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-231
Abstract: Background Immune cell trafficking into the CNS and other tissues plays important roles in health and disease. Rapid quantitative methods are not available that could be used to study many of the dynamic aspects of immune cell-tissue interactions. Methods We used pharmacokinetics and modeling to quantify and characterize the trafficking of radioactively labeled lymphocytes into brain and peripheral tissues. We used variance from two-way ANOVAs with 2 × 2 experimental designs to model the relative influences of lymphocytes and target tissues in trafficking. Results We found that in male CD-1 mice, about 1 in 5,000 intravenously injected lymphocytes entered each gram of brain. Uptake by brain was 2 to 3 times higher in na ve SJL females, but uptake by spleen and clearance from blood was lower, demonstrating a dichotomy in immune cell distribution. Treatment of CD-1 mice with lipopolysaccharide (LPS) increased immune cell uptake into brain but decreased uptake by spleen and axillary nodes. Conclusions Differences in brain uptake and in uptake by spleen between SJL and CD-1 mice were primarily determined by lymphocytes, whereas differences in uptake with LPS were primarily determined by lymphocytes for the brain but by the tissues for the spleen and the axillary lymph node. These results show that immune cells normally enter the CNS and that tissues and immune cells interact in ways that can be quantified by pharmacokinetic models.
Soluble Interleukin-6 Receptor Induces Motor Stereotypies and Co-Localizes with Gp130 in Regions Linked to Cortico-Striato-Thalamo-Cortical Circuits
Ankur Patel, Youhua Zhu, Eldo V. Kuzhikandathil, William A. Banks, Allan Siegel, Steven S. Zalcman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041623
Abstract: Soluble cytokine receptors are normal constituents of body fluids that regulate peripheral cytokine and lymphoid activity and whose levels are increased in states of immune activation. Soluble interleukin-6 receptor (sIL-6R) levels positively correlate with disease progression in some autoimmune conditions and psychiatric disorders. Particularly strong links between levels of sIL-6R and the severity of psychotic symptoms occur in schizophrenia, raising the possibility that sIL-6R is involved in this disease. However, there is no evidence that peripheral sIL-6R induces relevant behavioral disturbances. We showed that single subcutaneous injections of sIL-6R (0–1 μg), stimulated novelty stress-induced exploratory motor behaviors in male Balb/c mice within 20–40-min of injection. A progressive increase in vertical stereotypies was observed 40–80 min post injection, persisting for the remainder of the test session. Paralleling these stimulant-like effects, sIL-6R pre-treatment significantly enhanced stereotypy scores following challenge with GBR 12909. We found that peripherally administered sIL-6R crossed the blood-brain barrier, localizing in brain regions associated with cortico-striatal-thalamo-cortical (CSTC) circuits, which are putative neuroanatomical substrates of disorders associated with repetitive stereotypies. Peripherally administered sIL-6R co-localized with gp130, a transmembrane protein involved in IL-6 trans-signaling, in the nucleus accumbens, caudate-putamen, motor and infralimbic cortices, and thalamic nuclei, but not with gp130 in the ventral tegmental area, substantia nigra, or sensorimotor cortex,. The results suggest that peripheral sIL-6R can act as a neuroimmune messenger, crossing the blood brain barrier (BBB) to selectively target CSTC circuits rich in IL-6 trans-signaling protein, and inducing repetitive stereotypies. As such sIL-6R may represent a novel therapeutic agent for relevant psychiatric disorders.
Human Immunodeficiency Virus-1 Uses the Mannose-6-Phosphate Receptor to Cross the Blood-Brain Barrier
Shinya Dohgu, Jan S. Ryerse, Sandra M. Robinson, William A. Banks
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039565
Abstract: HIV-1 circulates both as free virus and within immune cells, with the level of free virus being predictive of clinical course. Both forms of HIV-1 cross the blood-brain barrier (BBB) and much progress has been made in understanding the mechanisms by which infected immune cells cross the blood-brain barrier BBB. How HIV-1 as free virus crosses the BBB is less clear as brain endothelial cells are CD4 and galactosylceramide negative. Here, we found that HIV-1 can use the mannose-6 phosphate receptor (M6PR) to cross the BBB. Brain perfusion studies showed that HIV-1 crossed the BBB of all brain regions consistent with the uniform distribution of M6PR. Ultrastructural studies showed HIV-1 crossed by a transcytotic pathway consistent with transport by M6PR. An in vitro model of the BBB was used to show that transport of HIV-1 was inhibited by mannose, mannan, and mannose-6 phosphate and that enzymatic removal of high mannose oligosaccharide residues from HIV-1 reduced transport. Wheatgerm agglutinin and protamine sulfate, substances known to greatly increase transcytosis of HIV-1 across the BBB in vivo, were shown to be active in the in vitro model and to act through a mannose-dependent mechanism. Transport was also cAMP and calcium-dependent, the latter suggesting that the cation-dependent member of the M6PR family mediates HIV-1 transport across the BBB. We conclude that M6PR is an important receptor used by HIV-1 to cross the BBB.
Susceptibility of juvenile and adult blood–brain barrier to endothelin-1: regulation of P-glycoprotein and breast cancer resistance protein expression and transport activity
Harati Rania,Villégier Anne-Sophie,Banks William A,Mabondzo Aloise
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-273
Abstract: Background P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) play a critical role in keeping neurotoxic substances from entering the brain. We and others have previously reported an impact of inflammation on the regulation of adult blood–brain barrier (BBB) efflux transporters. However, studies in children have not been done. From the pediatric clinical perspective, it is important to understand how the central nervous system (CNS) and BBB drug efflux transporters differ in childhood from those of adults under normal and inflammatory conditions. Therefore, we examined and compared the regulation of P-gp and BCRP expression and transport activity in young and adult BBB and investigated the molecular mechanisms underlying inflammatory responses. Methods Rats at postnatal day (P) P21 and P84, corresponding to the juvenile and adult stages of human brain maturation, respectively, were treated with endothelin-1 (ET-1) given by the intracerebroventricular (icv) route. Twenty-four hours later, we measured P-gp and BCRP protein expression in isolated brain capillary by immunoblotting as well as by transport activity in vivo by measuring the unbound drug partitioning coefficient of the brain (Kp,uu,brain) of known efflux transporter substrates administered intravenously. Glial activation was measured by immunohistochemistry. The release of cytokines/chemokines (interleukins-1α, 1-β (IL-1β), -6 (IL-6), -10 (IL-10), monocyte chemoattractant protein (MCP-1/CCL2), fractalkine and tissue inhibitor of metalloproteinases-1 (TIMP-1)) were simultaneously measured in brain and serum samples using the Agilent Technology cytokine microarray. Results We found that juvenile and adult BBBs exhibited similar P-gp and BCRP transport activities in the normal physiological conditions. However, long-term exposure of the juvenile brain to low-dose of ET-1 did not change BBB P-gp transport activity but tended to decrease BCRP transport activity in the juvenile brain, while a significant increase of the activity of both transporters was evidenced at the BBB in the adult brain. Moreover, juvenile and adult brain showed differences in their expression profiles of cytokines and chemokines mediated by ET-1. Conclusions BBB transporter activity during neuroinflammation differs between the juvenile and adult brains. These findings emphasize the importance of considering differential P-gp and BCRP transport regulation mechanisms between adult and juvenile BBB in the context of neuroinflammation.
Zeta functions and asymptotic additive bases with some unusual sets of primes
William D. Banks
Mathematics , 2015,
Abstract: Fix $\delta\in(0,1]$, $\sigma_0\in[0,1)$ and a real-valued function $\varepsilon(x)$ for which $\limsup_{x\to\infty}\varepsilon(x)\le 0$. For every set of primes ${\mathcal P}$ whose counting function $\pi_{\mathcal P}(x)$ satisfies an estimate of the form $$\pi_{\mathcal P}(x)=\delta\,\pi(x)+O\bigl(x^{\sigma_0+\varepsilon(x)}\bigr),$$ we define a zeta function $\zeta_{\mathcal P}(s)$ that is closely related to the Riemann zeta function $\zeta(s)$. For $\sigma_0\le\frac12$, we show that the Riemann hypothesis is equivalent to the non-vanishing of $\zeta_{\mathcal P}(s)$ in the region $\{\sigma>\frac12\}$. For every set of primes ${\mathcal P}$ that contains the prime $2$ and whose counting function satisfies an estimate of the form $$\pi_{\mathcal P}(x)=\delta\,\pi(x)+O\bigl((\log\log x)^{\varepsilon(x)}\bigr),$$ we show that ${\mathcal P}$ is an asymptotic additive basis for ${\mathbb N}$, i.e., for some integer $h=h({\mathcal P})>0$ the sumset $h{\mathcal P}$ contains all but finitely many natural numbers. For example, an asymptotic additive basis for ${\mathbb N}$ is provided by the set $$ \{2,547,1229,1993,2749,3581,4421,5281\ldots\}, $$ which consists of $2$ and every hundredth prime thereafter.
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