Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat

<p>Abstract</p> <p>Background</p> <p>Neuroinflammation following acute brain trauma is considered to play a prominent role in both the pathological and reconstructive response of the brain to injury. Here we characterize and contrast both an acute and delayed phase of inflammation following experimental penetrating ballistic brain injury (PBBI) in rats out to 7 days post-injury.</p> <p>Methods</p> <p>Quantitative real time PCR (QRT-PCR) was used to evaluate changes in inflammatory gene expression from the brain tissue of rats exposed to a unilateral frontal PBBI. Brain histopathology was assessed using hematoxylin and eosin (H&E), silver staining, and immunoreactivity for astrocytes (GFAP), microglia (OX-18) and the inflammatory proteins IL-1β and ICAM-1.</p> <p>Results</p> <p>Time course analysis of gene expression levels using QRT-PCR indicated a peak increase during the acute phase of the injury between 3–6 h for the cytokines TNF-α (8–11 fold), IL-1β (11–13 fold), and IL-6 (40–74 fold) as well as the cellular adhesion molecules VCAM (2–3 fold), ICAM-1 (7–15 fold), and E-selectin (11–13 fold). Consistent with the upregulation of pro-inflammatory genes, peripheral blood cell infiltration was a prominent post-injury event with peak levels of infiltrating neutrophils (24 h) and macrophages (72 h) observed throughout the core lesion. In regions of the forebrain immediately surrounding the lesion, strong immunoreactivity for activated astrocytes (GFAP) was observed as early as 6 h post-injury followed by prominent microglial reactivity (OX-18) at 72 h and resolution of both cell types in cortical brain regions by day 7. Delayed thalamic inflammation (remote from the primary lesion) was also observed as indicated by both microglial and astrocyte reactivity (72 h to 7 days) concomitant with the presence of fiber degeneration (silver staining).</p> <p>Conclusion</p> <p>In summary, PBBI induces both an acute and delayed neuroinflammatory response occurring in distinct brain regions, which may provide useful diagnostic information for the treatment of this type of brain injury.</p

NNZ-2566 treatment inhibits neuroinflammation and pro-inflammatory cytokine expression induced by experimental penetrating ballistic-like brain injury in rats

<p>Abstract</p> <p>Background</p> <p>Inflammatory cytokines play a crucial role in the pathophysiology of traumatic brain injury (TBI), exerting either deleterious effects on the progression of tissue damage or beneficial roles during recovery and repair. NNZ-2566, a synthetic analogue of the neuroprotective tripeptide Glypromate^®, has been shown to be neuroprotective in animal models of brain injury. The goal of this study was to determine the effects of NNZ-2566 on inflammatory cytokine expression and neuroinflammation induced by penetrating ballistic-like brain injury (PBBI) in rats.</p> <p>Methods</p> <p>NNZ-2566 or vehicle (saline) was administered intravenously as a bolus injection (10 mg/kg) at 30 min post-injury, immediately followed by a continuous infusion of NNZ-2566 (3 mg/kg/h), or equal volume of vehicle, for various durations. Inflammatory cytokine gene expression from the brain tissue of rats exposed to PBBI was evaluated using microarray, quantitative real time PCR (QRT-PCR), and enzyme-linked immunosorbent assay (ELISA) array. Histopathology of the injured brains was examined using hematoxylin and eosin (H&E) and immunocytochemistry of inflammatory cytokine IL-1β.</p> <p>Results</p> <p>NNZ-2566 treatment significantly reduced injury-mediated up-regulation of IL-1β, TNF-α, E-selectin and IL-6 mRNA during the acute injury phase. ELISA cytokine array showed that NZ-2566 treatment significantly reduced levels of the pro-inflammatory cytokines IL-1β, TNF-α and IFN-γ in the injured brain, but did not affect anti-inflammatory cytokine IL-6 levels.</p> <p>Conclusion</p> <p>Collectively, these results suggest that the neuroprotective effects of NNZ-2566 may, in part, be functionally attributed to the compound's ability to modulate expression of multiple neuroinflammatory mediators in the injured brain.</p

Representativeness of Eddy-Covariance flux footprints for areas surrounding AmeriFlux sites

Large datasets of greenhouse gas and energy surface-atmosphere fluxes measured with the eddy-covariance technique (e.g., FLUXNET2015, AmeriFlux BASE) are widely used to benchmark models and remote-sensing products. This study addresses one of the major challenges facing model-data integration: To what spatial extent do flux measurements taken at individual eddy-covariance sites reflect model- or satellite-based grid cells? We evaluate flux footprints—the temporally dynamic source areas that contribute to measured fluxes—and the representativeness of these footprints for target areas (e.g., within 250–3000 m radii around flux towers) that are often used in flux-data synthesis and modeling studies. We examine the land-cover composition and vegetation characteristics, represented here by the Enhanced Vegetation Index (EVI), in the flux footprints and target areas across 214 AmeriFlux sites, and evaluate potential biases as a consequence of the footprint-to-target-area mismatch. Monthly 80% footprint climatologies vary across sites and through time ranging four orders of magnitude from 103 to 107 m2 due to the measurement heights, underlying vegetation- and ground-surface characteristics, wind directions, and turbulent state of the atmosphere. Few eddy-covariance sites are located in a truly homogeneous landscape. Thus, the common model-data integration approaches that use a fixed-extent target area across sites introduce biases on the order of 4%–20% for EVI and 6%–20% for the dominant land cover percentage. These biases are site-specific functions of measurement heights, target area extents, and land-surface characteristics. We advocate that flux datasets need to be used with footprint awareness, especially in research and applications that benchmark against models and data products with explicit spatial information. We propose a simple representativeness index based on our evaluations that can be used as a guide to identify site-periods suitable for specific applications and to provide general guidance for data use

A comparative clinical study of Shatapatrayadi churna tablet and Patoladi yoga in the management of Amlapitta

Amlapitta is a very common disease caused by Vidagdha Pitta with features such as Amlodgara, Hrid Kantha Daha, and Avipaka. This is a burning problem of the society. Irregular and improper food habits, and busy stressful lifestyle is one of the main culprit. Amlapitta is the GI disorder described in Ayurvedic texts that closely resembles with Gastritis in modern science. In chronic stage, it may lead to ulcerative conditions. In this study, total 41 patients were registered and were randomly divided into two groups. In group A, Shatapatrayadi churna tablet and in group B Patoladi Yoga tablet were given for 1 month. The Nidana, signs, and symptoms were observed carefully to get idea about the Samprapti of the disease. The effect of Patoladi Yoga on Roga Bala is 65.79%, 62.11% on Agni Bala, and 63.35% on Deha and Chetasa bala. The overall relief was 63.75%. The effect of Shatapatrayadi tablet on Roga Bala was 71.94%, 73.15% on Agni Bala, and 77.68% on Deha and Chetas Bala. The overall relief was 74.25%

Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat-1

<p><b>Copyright information:</b></p><p>Taken from "Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat"</p><p>http://www.jneuroinflammation.com/content/4/1/17</p><p>Journal of Neuroinflammation 2007;4():17-17.</p><p>Published online 2 Jul 2007</p><p>PMCID:PMC1933533.</p><p></p>sculature surrounding the immediate lesion track (lower panel). Bar = 100 μ

Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat-0

<p><b>Copyright information:</b></p><p>Taken from "Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat"</p><p>http://www.jneuroinflammation.com/content/4/1/17</p><p>Journal of Neuroinflammation 2007;4():17-17.</p><p>Published online 2 Jul 2007</p><p>PMCID:PMC1933533.</p><p></p> (QRT-PCR). Data presented as mean ± standard deviation (n = 3/group). * P < 0.05 as compared to contralateral hemisphere

Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat-3

<p><b>Copyright information:</b></p><p>Taken from "Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat"</p><p>http://www.jneuroinflammation.com/content/4/1/17</p><p>Journal of Neuroinflammation 2007;4():17-17.</p><p>Published online 2 Jul 2007</p><p>PMCID:PMC1933533.</p><p></p>roglial cells (OX-18 immunoreactivity) and reactive astrogliosis (GFAP immunoreactivity) surrounding the primary lesion site. Bar = 100 μm

Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat-2

<p><b>Copyright information:</b></p><p>Taken from "Acute and delayed neuroinflammatory response following experimental penetrating ballistic brain injury in the rat"</p><p>http://www.jneuroinflammation.com/content/4/1/17</p><p>Journal of Neuroinflammation 2007;4():17-17.</p><p>Published online 2 Jul 2007</p><p>PMCID:PMC1933533.</p><p></p>ymal invasion by 24 h and beyond (C, H&E) as compared to sham tissue (A, H&E). A dense array of large macrophage-like cells (white arrows) were prominent by 72 h, particularly along the immediate border of the PBBI lesion (D, H&E). By day 7 an intracranial cavity had formed surrounded by a dense cellular infiltrate (E, H&E) and large, highly ramified astrocytes (F, GFAP). Bar = 20 μm (A-D), 100 μm (E-F)