Tumour necrosis factor-α (TNF-α) in mycotic aborted placenta : an evaluation by Immunohistochemistry

The present study aims to study histopathological changes in the mycotic aborted and normal placenta of sheep ,in addition to study the levels of TNF-a in mycotic aborted and normal placenta by immunohistochimistry assay (IHC) Seventy five , samples of aborted placenta and twenty five of normal placenta were collected , during November 2017 to May 2018 from certain regions of AL-Najaf city .Placental samples were fixed in 10% neutral buffer formalin for 72 hrs for histopathological examination, paraffin embedded tissue belong to mycotic aborted and normal group were used for assessment of TNF alpha by immmunohistopathological study was carried out to determine TNF protein in the placenta sample. Histopathological examination showed suppurative necrotized placentitis, in addition to congestion of the blood vessels and fibrin deposition in the intera-villius space as well as calcium deposition in necrotized the necrotic area and fibrosis of stromal area in certain chorionic villi and sloughing and desquamation of syncytotrophoblast.Result of IHC of TNF alpha protein showed significant elevation in TNF alpha protein in inflammatory cell (macrophage) of aborted sheep placenta (increasing of intensity and score), while no changes could be observed for pro-inflammatory molecules in the control sample (normal delivery)

External Mass Transfer Processes During the Adsorption of Various Pollutants onto Activated Carbon

A wide range of experimental studies are reported for the adsorption of phenol and p-chlorophenol onto activated carbon - Type Filtrasorb 400 - in an agitated batch adsorber. A model has been used to determine the external mass transfer coefficient for the system and the effect of several experimental variables have been investigated: these include agitation, initial pollutant concentration, carbon mass, carbon particle size and solution temperature. The mass transfer coefficient has been correlated in terms of the dimensionless Sh/Sc0.33 against each variable. The Sherwood number, Sh = k(f)R/D(mol), relates the external mass transfer coefficient k(f) to particle radius, R, and molecular diffusivity, D(mol). The Schmidt number, Sc, is the ratio of kinematic viscosity, v, to molecular diffusivity. A few results are also reported for the adsorption of sodium dodecyl sulphate and mercuric ions onto activated carbon

Lactate, not glucose, up-regulates mitochondrial oxygen consumption both in sham and lateral fluid percussed rat brains

OBJECTIVE: Failure of energy metabolism after traumatic brain injury may be a major factor limiting outcome. Although glucose is the primary metabolic substrate in the healthy brain, the well documented surge in tissue lactate after traumatic brain injury suggests that lactate may provide an energy need that cannot be met by glucose. We hypothesized, therefore, that administration of lactate or the combination of lactate and supraphysiological oxygen may improve mitochondrial oxidative respiration in the brain after rat fluid percussion injury. We measured oxygen consumption (VO2) to determine what effects glucose, lactate, oxygen, and the combination of lactate and oxygen have on mitochondrial respiration in both injured and uninjured rat brain tissue. METHODS: Anesthetized Sprague-Dawley rats were intubated and ventilated with either 0.21 or 1.0 fraction of inspired oxygen (FIO2). Brain tissue from acute sham animals was subjected in vitro to 1.1 mM, 12 mM and 100 mM concentrations of glucose and L-lactate. In another group, injury (fluid percussion injury of 2.5 +/- 0.02 atmospheres) was induced over the left hemisphere. The VO2 of mug amounts of brain tissues were measured in a microrespirometry system (Cartesian diver). RESULTS: The VO2 was found to be independent of glucose concentrations, but dose-dependent for lactate. Moreover, the lactate dependent VO2s were all significantly higher than those generated by glucose. Injured rats on FIO2 0.21 had brain tissue VO2 rates that were significantly lower than those of shams or preinjury levels. In injured rats treated with FIO2 1.0, the reduction in VO2 levels was prevented. Injured rats that received an intravenous infusion of 100 mM lactate had VO2 rates that were significantly higher than those obtained with FIO2 1.0. Combined treatment further boosted the lactate generated VO2 rates by approximately 15%. CONCLUSION: Glucose sustains mitochondrial respiration at a low level "fixed" rate because, despite increasing its concentration nearly 100-fold, it cannot up-regulate VO2 after fluid percussion injury. Lactate produces a dose-dependent VO2 response, possibly enabling mitochondria to meet the increased energy needs of the injured brain

Basic fibroblast growth factor-enhanced neurogenesis contributes to cognitive recovery in rats following traumatic brain injury

Stem/progenitor cells reside throughout the adult CNS and are actively dividing in the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus. This neurogenic capacity of the SVZ and DG is enhanced following traumatic brain injury (TBI) suggesting that the adult brain has the inherent potential to restore populations lost to injury. This raises the possibility of developing strategies aimed at harnessing the neurogenic capacity of these regions to repair the damaged brain. One strategy is to enhance neurogenesis with mitogenic factors. As basic fibroblast growth factor (bFGF) is a potent stem cell mitogen, we set out to determine if an intraventricular administration of bFGF following TBI could affect the levels of injury-induced neurogenesis in the SVZ and DG, and the degree to which this is associated with cognitive recovery. Specifically, adult rats received a bFGF intraventricular infusion for 7 days immediately following TBI. BrdU was administered to animals daily at 2–7 days post-injury to label cell proliferation. At 1 or 4 weeks post-injury, brain sections were immunostained for BrdU and neuronal or astrocytic markers. We found that injured animals infused with bFGF exhibited significantly enhanced cell proliferation in the SVZ and the DG at 1 week post-TBI as compared to vehicle-infused animals. Moreover, following bFGF infusion, a greater number of the newly generated cells survived to 4 weeks post-injury, with the majority being neurons. Additionally, animals infused with bFGF showed significant cognitive improvement. Collectively, the current findings suggest that bFGF-enhanced neurogenesis contributes to cognitive recovery following TBI

Desensitization of α(2A)-adrenoceptor signalling by modest levels of adrenaline is facilitated by β(2)-adrenoceptor-dependent GRK3 up-regulation

1. Adrenaline (ADR) and noradrenaline (NA) can simultaneously activate inhibitory α(2)- and stimulatory β-adrenoceptors (AR). However, ADR and NA differ significantly in that ADR is a potent β(2)-AR agonist while NA is not. Only recently has the interaction resulting from the simultaneous activation of α(2)- and β(2)-AR been examined at the cellular level to determine the mechanisms of α(2)-AR regulation following concomitant activation of both α(2)- and β(2)-ARs by chronic ADR. 2. This study evaluates β(2)-AR regulation of α(2A)-AR signalling following chronic ADR (300 nM) and NA (1 and 30 μM) treatments of BE(2)-C human neuroblastoma cells that natively express both β(2)- and α(2A)-ARs. 3. Chronic (24 h) treatment with ADR (300 nM) desensitized the response to the α(2A)-AR agonist, brimonidine, in BE(2)-C cells. Addition of the β-AR antagonist, propranolol, blocked the ADR-induced α(2A)-AR desensitization. Unlike ADR, chronic NA (1 μM) treatment had no effect on the α(2A)-AR response. However if NA was increased to 30 μM for 24 h, α(2A)-AR desensitization was observed; this desensitization was partially reversed by propranolol. 4. Chronic ADR (300 nM) treatment reduced α(2A)-AR binding levels, contributing to the α(2A)-AR desensitization. This decrease was prevented by addition of propranolol during ADR treatment. Chronic NA (30 μM), like ADR, treatment lowered specific binding, whereas 1 μM NA treatment was without effect. 5. Chronic ADR treatment produced a significant increase in GRK3 levels and this was blocked by propranolol or GRK2/3 antisense DNA treatment. This antisense DNA, common to both GRK2 and GRK3, also blocked chronic ADR-induced α(2A)-AR desensitization and down-regulation. 6. Acute (1 h) ADR (300 nM) or NA treatment (1 μM) produced α(2A)-AR desensitization. The desensitization produced by acute treatment was β-AR independent, as it was not blocked by propranolol. 7. We conclude that chronic treatment with modest levels of ADR produces α(2A)-AR desensitization by mechanisms that involve up-regulation of GRK3 and down-regulation of α(2A)-AR levels through interactions with the β(2)-AR

The Effect of Epidermal Growth Factor in the Injured Brain after Trauma in Rats

Epidermal growth factor (EGF) is a known mitogen for neural stem and progenitor cells (NS/NPCs) in the central nervous system (CNS). In vitro, EGF maintains NS/NPCs in the proliferative state, whereas in the normal rodent brain it promotes their proliferation and migration in the subventricular zone (SVZ). Additionally, EGF administration can augment neuronal replacement in the ischemic-injured adult striatum. Recently we found that the SVZ and the hippocampus display an injury-induced proliferative response following traumatic brain injury (TBI) that is linked to increased EGF expression. As adult neurogenesis is associated with cognitive function, we hypothesized that post-TBI administration of EGF could affect neurogenesis and cognitive recovery. Adult rats were intraventricularly infused with EGF or vehicle for 7 days following TBI. 5-Bromo-2-deoxyuridine (BrdU) was administered to label proliferating cells and the animals were sacrificed at 1 or 4 weeks post-injury. Using immunohistochemistry and stereology, we found that at 1 week post-injury, compared to vehicle-infused animals EGF-infused animals had significantly more BrdU-positive cells in the SVZ and hippocampus concomitant with enhanced EGF receptor expression. At 4 weeks post-injury, the number of BrdU-positive cells in the hippocampus was similar in both groups, suggesting that EGF does not support long-term survival of newly generated cells. Furthermore, we found that the EGF-induced proliferative population differentiated preferentially toward astroglial phenotype. Nevertheless, animals treated with EGF showed significant improvement in cognitive function, which was accompanied by reduced hippocampal neuronal cell loss. Collectively, the data from this study demonstrate that EGF exerts a neuroprotective rather than neurogenic effect in protecting the brain from injury

FREQUENCY OF TRAUMAS IN LIBURNIAN POPULATION

<p><b>Copyright information:</b></p><p>Taken from "The presence of β-adrenoceptors sensitizes α-adrenoceptors to desensitization after chronic epinephrine treatment"</p><p>http://www.biomedcentral.com/1471-2210/7/16</p><p>BMC Pharmacology 2007;7():16-16.</p><p>Published online 20 Dec 2007</p><p>PMCID:PMC2234403.</p><p></p>o αand α) and αC4 (corresponding to α) gene products (Table 3). The reactions amplified fragments of the expected size from each set of primers. αC10/C4 primers amplified 233 bp products from SH-SY5Y mRNA that were sensitive to digestion by II (specific for the αproduct). Restriction digestion with XI of the 630 bp product of α 2C4 primer amplification gave three fragments of 271, 225 and 78 bp. All reactions were performed in the presence (+) or absence (-) of reverse transcriptase (RT) to rule out the possibility of DNA contamination. Lane M designates the 100 bp ladder; the 500 bp fragment is indicated by an arrow in each panel