Comparison of dichloran rose bengal chloramphenicol and Sabouraud dextrose agar with cycloheximide and chloramphenicol for airborne mold sampling

The more the mold species isolated on a culture medium, the more the sampling environment is represented accurately. According to the sampling purpose, it is crucial to use the best culture medium for mold. However, no study is available regarding the comparison of dichloran rose bengal chloramphenicol (DRBC) and Sabouraud dextrose agar with cycloheximide and chloramphenicol (SDA-CHX-CHL) culture media in terms of their application for airborne sampling, isolation, and identification of fungi. Airborne mold samples were impacted onto both DRBC and SDA-CHX-CHL, simultaneously using single-stage Andersen sampler. The limit of detection (LOD) value for airborne mold count was 7 CFU m^?3 (1 colony growth on the Petri dish). The total mold counts (TMC) ranged between <7 and 504 CFU m^?3 (med 56 CFU m^?3) and <7 and 1218 CFU m^?3 (med 259 CFU m^?3), collected on SDA-CHX-CHL and DRBC, respectively. Significantly higher TMC were observed on DRBC than on SDA regardless of the sampling environment (i.e, indoor or outdoor) (p < 0.05). Among the most predominant mold genera, observation frequencies of Penicillium spp. and Aspergillus spp. on both culture media were found to be more than 70%. Observation frequencies of Cladosporium spp., Alternaria spp., and yeast were found to be higher in samples collected on DRBC than those on SDA-CHX-CHL. Finally, DRBC was found to be superior to SDA in terms of both number of colonies and number of genera isolated from the air.     

Choline increases serum insulin in rat when injected intraperitoneally and augments basal and stimulated aceylcholine release from the rat minced pancreas in vitro.

Intraperitoneal injection of choline (30-90 mg.kg-1) produced a dose-dependent increase in serum insulin, glucose and choline levels in rats. The increase in serum insulin induced by choline (90 mg.kg-1) was blocked by pretreatment with the muscarinic acetylcholine receptor antagonists, atropine (2 mg.kg-1), pirenzepine (2 mg.kg-1) and 4-diphenylacetoxy-N-methylpiperidine (2 mg.kg-1) or the ganglionic nicotinic receptor antagonist, hexamethonium (15 mg.kg-1). The effect of choline on serum insulin and glucose was enhanced by oral glucose administration (3 g.kg-1). Choline administration was associated with a significant (P < 0.001) increase in the acetylcholine content of pancreatic tissue. Choline (10-130 microm) increased basal and stimulated acetylcholine release but failed to evoke insulin release from the minced pancreas at considerably higher concentrations (0.1-10 mm). Hemicholium-3, a choline uptake inhibitor, attenuated the increase in acetylcholine release induced by choline augmentation. Choline (1-32 mm) inhibited [3H]quinuclidinyl benzilate binding to the muscarinic receptors in the pancreatic homogenates. These data show that choline, a precursor of the neurotransmitter acetylcholine, increases serum insulin by indirectly stimulating peripheral acetylcholine receptors through the enhancement of acetylcholine synthesis and release.     

Internal loading of phosphorus from sediments of Lake Pontchartrain (Louisiana,USA) with implications for eutrophication

Diffusive flux of bioavailable soluble reactive phosphorus (SRP) across the sediment–water interface is one mechanism by which sediments can be a source of phosphorus to the water column in aquatic systems and contribute to primary productivity. This process is dependent on sediment biogeochemistry and SRP concentration gradients at the sediment–water interface. In systems subjected to episodic external pulses of nutrient-rich water, SRP concentration gradients can have potential implications for diffusive flux. In this study, we sought to investigate two hypotheses: (1) diffusive flux of SRP from sediments is a significant source of SRP in the annual budget for the oligohaline Lake Pontchartrain estuary and (2) under SRP-depleted water column conditions following large episodic, external pulses of nitrogen-rich Mississippi River water to the estuary, internal SRP loading by diffusive flux can regenerate SRP in the water column to previously observed levels rapidly. Our specific objectives were to: (i) determine sediment, water column, and phytoplankton characteristics at multiple locations in the estuary, (ii) measure rates of SRP diffusive flux from sediments using intact cores under aerobic and anaerobic incubations, (iii) estimate the potential for water column SRP regeneration by diffusive flux under SRP-depleted conditions using a simple model, and (iv) estimate the annual load of SRP from the sediments by diffusive flux. Results indicate that diffusive flux of SRP from Lake Pontchartrain sediments likely contributes ~30–44% of the annual SRP load to the estuary. Further, internal SRP loading by diffusion has the potential to regenerate SRP in SRP-depleted waters to previously observed concentrations in <60 days. Our findings suggest that a sequence of events is feasible where external pulses of nitrogen-rich water produce phosphorus-limited conditions, followed by an internal pulse of SRP from sediments to restore nitrogen-limited conditions. This internal SRP load may be an important contributor in promoting blooms of nitrogen-fixing harmful algae under summertime low-nutrient conditions.     

Lifelong Consumption of Sodium Selenite: Gender Differences on Blood–Brain Barrier Permeability in Convulsive,Hypoglycemic Rats

The aim of this study was to compare the effects of hypoglycemia and induced convulsions on the blood-brain barrier permeability in rats with or without lifelong administration of sodium selenite. There is a significant decrease of the blood-brain barrier permeability in three brain regions of convulsive, hypoglycemic male rats treated with sodium selenite when compared to sex-matched untreated rats (p<0.05), but the decrease was not significant in female rats (p>0.05). The blood-brain barrier permeability of the left and right hemispheres of untreated, moderately hypoglycemic convulsive rats of both genders was better than their untreated counterparts (p<0.05). Our results suggest that moderate hypoglycemia and lifelong treatment with sodium selenite have a protective effect against blood-brain barrier permeability during convulsions and that the effects of sodium selenite are gender-dependent.     

Antibacterial activity and phytochemical evidence for the plant origin of Turkish propolis from different regions

Honeybees collect propolis from practically any abundant plant source in the neighborhood of the hive, be it populus, eucalyptus, pine, sugarcane, cashew nut or orange trees. We have described that the origin plants of Turkish propolis are Populus sp., Eucalyptus sp. and Castanea sativa. In our previous study, propolis samples from Middle Anatolia displayed the typical pattern of “poplar” propolis: they contained pinobanksin, caffeic and ferulic acids and their esters. The propolis samples examined in this study were shown not to contain polar phenolics. The main components of Eucalyptus propolis were aromatic acids, mainly cinnamic acid and its esters, that are usually found in Eucalyptus species resins. The second distinct sample originated from West Anatolia. Although it contained low amounts of phenolic substances and aromatic acids, its main components were sugars and glycosides. The study revealed that there was no significant difference between propolis samples in antibacterial activity, however the yeasts were shown to be more sensitive to eucalyptus-propolis. Gram negative bacteria were susceptible to none of the samples tested.     

Elevated interleukin-12 and CXCL10 in subacute sclerosing panencephalitis

Immunosuppression associated with measles virus (MV) can be demonstrated by cytokine production failure in subacute sclerosing panencephalitis (SSPE) and may have implications on the pathogenesis of the disease. Cytokines (IL-12, IL-10, IL-4, IL-17, IL-18, IFN-alpha, IFN-gamma) and chemokines (CXCL8, CXCL10, CCL2 and CCL5) were measured in the cerebrospinal fluid (CSF) and serum samples from 60 patients with SSPE, 36 patients with infectious and/or inflammatory (IN) and 28 with other non-inflammatory (NIN) neurological diseases by ELISA. IL-12 p70+p40 was elevated in CSF and sera of SSPE when compared to the NIN group. However, the CSF levels of IL-12 p70 alone were not increased, indicating an increase of p40. The CSF of SSPE patients also showed relatively higher levels of IL-10 than that of the NIN group. CXCL10 levels in CSF were significantly higher in SSPE, whereas CXCL8 was increased in sera compared to NIN. No difference was detected in IFN-gamma, IFN-alpha, IL-17, IL-18, IL-4 or CCL2 and CCL5 levels. These results demonstrate that immune response against MV in SSPE may be impaired, although some T cell/Th1 inducing stimulations are present.     

Field assessment in land of origin of host specificity,infestation rate and impact of <Emphasis Type="Italic">Ceratapion basicorne</Emphasis> a prospective biological control agent of yellow starthistle

Yellow starthistle, Centaurea solstitialis (Asteraceae), is an important invasive alien weed in the western United States. Currently established biological control agents attack only the capitula (flowerheads), and are not effectively controlling the plant in much of its range. The geographic center of diversity for the plant appears to be in Turkey, but no agents have been introduced from this country. Ceratapion basicorne (Coleoptera: Apionidae) is common in Central Turkey, attacking 25–100% of yellow starthistle plants. In a field experiment, Ceratapion spp. attacked 90% of yellow starthistle plants and 88% of milk thistle plants (Silybum marianum) but not seven other plant species, including artichoke and safflower. We suspect that a different species of insect attacked milk thistle, but they emerged before the plants were sampled. Laboratory tests showed that C. basicorne does not oviposit in milk thistle. Ceratapion basicorne appears to be more host specific than was suggested by previous studies of a population in Italy (Clement etal. 1989. Ann. Entomol. Soc. Am. 82: 741–747). The insect is gregarious, and the number of larvae per plant was positively correlated to root diameter. The level of damage to individual plants was positively correlated to the proportion of plants attacked, indicating aggregation both among plants and within plants. Field data did not show any impact of the insect on plant size or number of capitula, but germination rate of seeds produced by infested plants was 15% lower than for uninfested plants at two of three sites studied.     

Reactive oxygen species are required for hyperoxia-induced Bax activation and cell death in alveolar epithelial cells

Exposure of animals to hyperoxia results in respiratory failure and death within 72 h. Histologic evaluation of the lungs of these animals demonstrates epithelial apoptosis and necrosis. Although the generation of reactive oxygen species (ROS) is widely thought to be responsible for the cell death observed following exposure to hyperoxia, it is not clear whether they act upstream of activation of the cell death pathway or whether they are generated as a result of mitochondrial membrane permeabilization and caspase activation. We hypothesized that the generation of ROS was required for hyperoxia-induced cell death upstream of Bax activation. In primary rat alveolar epithelial cells, we found that exposure to hyperoxia resulted in the generation of ROS that was completely prevented by the administration of the combined superoxide dismutase/catalase mimetic EUK-134 (Eukarion, Inc., Bedford, MA). Exposure to hyperoxia resulted in the activation of Bax at the mitochondrial membrane, cytochrome c release, and cell death. The administration of EUK-134 prevented Bax activation, cytochrome c release, and cell death. In a mouse lung epithelial cell line (MLE-12), the overexpression of Bcl-XL protected cells against hyperoxia by preventing the activation of Bax at the mitochondrial membrane. We conclude that exposure to hyperoxia results in Bax activation at the mitochondrial membrane and subsequent cytochrome c release. Bax activation at the mitochondrial membrane requires the generation of ROS and can be prevented by the overexpression of Bcl-XL.