The development of an artificial neural network – genetic algorithm model (ANN-GA) for the adsorption and photocatalysis of methylene blue on a novel sulfur–nitrogen co-doped Fe2O3 nanostructure surface

In this study, a new sulfur–nitrogen co-doped Fe₂O₃ nanostructure was synthesized via a simple and efficient method and characterized via UV-Vis spectrophotometry, X-ray diffraction, field emission scanning electron microscopy, energy-dispersive X-ray spectroscopy, and Brunauer–Emmett–Teller surface area analysis. The as-synthesized nanoparticles showed high efficiency for the removal of methylene blue. The experimental conditions including the dose of the nanoparticle, the concentration of the dye, pH and the light dose were studied and optimized. The removal percentage was approximately 95% in a short time (5 min). A three-layer artificial neural network (ANN) model was proposed for predicting the efficiency of the dye removal. The network was trained using the obtained experimental data at optimum values. Some training functions were tested and their ability to predict different numbers of neurons was evaluated. The coefficient of determination (R-squared) and the mean squared error (MSE) were measured for comparison. In order to improve the accuracy of the prediction and to remove its dependency on the number of neurons, the ANN parameters were optimized using the genetic algorithm (GA). The final model results showed an acceptable agreement with experimental data. Furthermore, the relative importance of the dose of the nanoparticle, the concentration of the dye, and pH on the efficiency were obtained as 39%, 46%, and 15%, respectively. Moreover, interestingly, the obtained results showed that this newly synthesized nanoparticle has some photocatalytic properties with a band gap of 1.65 eV and therefore, it can be proposed as a low-cost visible light-driven photocatalyst for engineering applications.

In this research an S-N doped Fe₂O₃ nanostructure is synthesized and its adsorption ability and photocatalytic activity were evaluated. The optimum experimental conditions were obtained and an ANN-GA model was proposed for predicting experimental values.     

Sciatic nerve transection in neonatal rats induces apoptotic neuronal death in L5 dorsal root ganglion

Transection of a peripheral nerve in neonatal rats induces death of the axotomized neurons which may be due to either necrosis or apoptosis. In the present investigation, neuronal cell death in L5 dorsal root ganglion was evaluated after unilateral sciatic nerve transection in rats at 1, 3, 5, 7 and 10 days age. After 5 days, right (experimental) and left (control) dorsal root ganglia in all groups were removed, fixed, processed and embedded for either light or electron microscopy. Normal nucleoli were counted in paraffin embedded serial sections, and correction factors for split and multiple nucleoli were applied as well as the physical disector. The number of neurons in the right dorsal root ganglia, as compared with the controls, was significantly lower in all groups, and the percentage of the reduction at 1, 3, 5, 7 and 10 days was 32.4, 27.2, 23.8, 22.8 and 21.8% respectively. On the other hand, the results of neuronal counts using the disector method showed 34.0, 25.7, 20.2, 20.0 and 14.2% reduction in the number of neurons at 1, 3, 5, 7 and 10 days, respectively. The microscopic and ultrastructural results indicated that there were typical morphological changes similar to those of apoptosis, including condensed basophilic nuclei, formation of nuclear caps, cell shrinkage and apoptotic body formation. We concluded that there is an increase in apoptosis in dorsal root ganglia following sciatic nerve axotomy with the greatest neuronal loss on postnatal day 1.     

Response functions for computing absorbed dose to skeletal tissues from photon irradiation--an update

A comprehensive set of photon fluence-to-dose response functions (DRFs) is presented for two radiosensitive skeletal tissues-active and total shallow marrow-within 15 and 32 bone sites, respectively, of the ICRP reference adult male. The functions were developed using fractional skeletal masses and associated electron-absorbed fractions as reported for the UF hybrid adult male phantom, which in turn is based upon micro-CT images of trabecular spongiosa taken from a 40 year male cadaver. The new DRFs expand upon both the original set of seven functions produced in 1985, and a 2007 update calculated under the assumption of secondary electron escape from spongiosa. In this study, it is assumed that photon irradiation of the skeleton will yield charged particle equilibrium across all spongiosa regions at energies exceeding 200 keV. Kerma coefficients for active marrow, inactive marrow, trabecular bone and spongiosa at higher energies are calculated using the DRF algorithm setting the electron-absorbed fraction for self-irradiation to unity. By comparing kerma coefficients and DRF functions, dose enhancement factors and mass energy-absorption coefficient (MEAC) ratios for active marrow to spongiosa were derived. These MEAC ratios compared well with those provided by the NIST Physical Reference Data Library (mean difference of 0.8%), and the dose enhancement factors for active marrow compared favorably with values calculated in the well-known study published by King and Spiers (1985 Br. J. Radiol. 58 345-56) (mean absolute difference of 1.9 percentage points). Additionally, dose enhancement factors for active marrow were shown to correlate well with the shallow marrow volume fraction (R(2) = 0.91). Dose enhancement factors for the total shallow marrow were also calculated for 32 bone sites representing the first such derivation for this target tissue.     

An image-based skeletal model for the ICRP reference adult male-specific absorbed fractions for neutron-generated recoil protons

Recoiling hydrogen nuclei are a principle mechanism for energy deposition from incident neutrons. For neutrons incident on the human skeleton, the small sizes of two contrasting media (trabecular bone and marrow) present unique problems due to a lack of charged-particle (protons) equilibrium. Specific absorbed fractions have been computed for protons originating in the human skeletal tissues for use in computing neutron dose response functions. The proton specific absorbed fractions were computed using a pathlength-based range-energy calculation in trabecular skeletal samples of a 40 year old male cadaver.     

The Zebrafish fade out mutant: a novel genetic model for Hermansky-Pudlak syndrome

PURPOSE: To characterize retinal morphology and visual system function in the zebrafish mutant fade out (fad) and to establish the mutant as a lower vertebrate model for Hermansky-Pudlak syndrome (HPS). METHODS: Retinal morphology of fad larvae was examined between 3 and 9 days postfertilization (dpf) by standard histology, transmission electron microscopy, and immunohistochemistry examination. Apoptotic cells were visualized by TdT-mediated dUTP nick-end labeling (TUNEL) staining. Visual system function was probed by electroretinography and behavioral assessment by optokinetic response measurements. Blood clotting was evaluated by time to occlusion testing of blood vessels as an arterial thrombosis assay. The chromosomal location of fad was determined by simple sequence-length polymorphism mapping. Genomic fragments of candidate genes were cloned by standard molecular techniques and mapped to the zebrafish genome by radiation hybrid mapping. RESULTS: Mutant fad larvae are hypopigmented and show structural defects in the outer retina. Melanosomes of these larvae in the retinal pigment epithelium are hypopigmented, generally smaller, and progressively reduced in number compared to nonmutant larvae. Progressive microvilli protrusions into the photoreceptor cell layer are not detectable, and photoreceptor outer segments get shorter and are misaligned. Photoreceptors subsequently undergo apoptosis, with a peak of cell death at 6 dpf. Electrical responses of the retina and visual performance are severely reduced. Blood clotting is prolonged in mutant fad larvae. Genomic mapping of fad reveals distinct genomic positions of the mutant gene from known human HPS genes. CONCLUSIONS: The fad mutant shows syndromic defects in pigmentation, outer retinal structure and function, and blood clotting. This syndrome is characteristic of Hermansky-Pudlak syndrome (HPS), making fad a novel genetic model of HPS. The gene does not cosegregate with the known human HPS genes, suggesting a novel molecular cause of HPS.     

Infection of Anisakids Larvae in Long Tail Tuna (Thunnus tonggol) In North Persian Gulf

Background

The aim of this paper was to study the prevalence and intensity of Anisakids larvae in the long tail tuna fish captured from Iranian shores of Persian Gulf.

Methods

Different organs including skin, abdominal cavity, stomach and intestinal contents, stomach sub serous tissues, liver, spleen, gonads and 20 grams of muscles of 100 long tail tuna fish (Thannus tonggol) caught from waters of the north parts of Persian Gulf were searched for anisakid nematodes larvae. Twenty grams of around the body cavity muscles were digested in artificial gastric juice. Different organs and digested muscles were examined with naked eyes for the presence of anisakids larvae. The collected larvae were preserved in 70% alcohol containing 5% glycerin, and cleared in lactophenol for identification.

Results

Our findings revealed that 89% of fish harbored 3^rd stage larvae of Anisakis sp. of which 2% were infected with both Anisakis and Raphidascaris. All inspected organs except that of skin were found to be infected, while stomach sub serous tissues were the most infected organ (80%) followed by abdominal cavity (10%), liver (4%), testicle (3%), stomach contents and spleen (2%) and intestinal contents (1%). Intestine and abdominal cavity were the organs harbored Raphidascaris sp. Digested muscles were free of parasite. Mean intensity was low for both species and ranged between 1.5 for Raphidascaris sp. and 3.67 for Anisaki sp.

Conclusion

Anisakids larvae especially Anisakis are very prevalent in some fish including tunas of Persian Gulf, and consumption of infected fish if it is not properly cooked may lead to human anisakiasis.     

Active macrophage-associated TGF-beta co-localizes with type I procollagen gene expression in atherosclerotic human pulmonary arteries.

Vascular remodeling in adult atherosclerotic pulmonary arteries is characterized by discrete areas of neointimal smooth muscle cell extracellular matrix gene expression in close proximity to non-foamy macrophages, suggesting regulation by local macrophage-associated factors. The purpose of these studies was to begin addressing the role of putative macrophage-associated factors such as transforming growth factor-beta (TGF-beta), by determining the spatial relationship between TGF-beta and neointimal matrix gene expression in human atherosclerotic pulmonary arteries. For example, the participation of TGF-beta in vascular remodeling could be inferred by its colocalization with non-foamy macrophages in areas of active matrix synthesis. In situ hybridization and immunohistochemistry demonstrated focal neointimal procollagen gene expression in close association with non-foamy but not foamy macrophages. Immunohistochemistry with isoform-specific anti-TGF-beta antibodies demonstrated all three isoforms of TGF-beta associated with non-foamy macrophages, but foamy macrophages were not immunoreactive. Neointimal and medial smooth muscle cells stained lightly. In contrast, intense TGF-beta immunoreactivity was also associated with medial smooth muscle cells in normal nonremodeling vessels. Immunohistochemistry with antibodies specific for latent TGF-beta was similar to immunohistochemistry for mature TGF-beta in both remodeling and nonremodeling vessels. Finally, using an antibody specific for active TGF-beta 1, immunoreactivity was only seen in non-foamy neointimal macrophages but not in foamy macrophages or medial smooth muscle cells from hypertensive or normal vessels. These observations suggest non-foamy macrophages may participate in modulating matrix gene expression in atherosclerotic remodeling via a TGF-beta-dependent mechanism.