Impacts of bioreactor operating parameters on removal efficiency, biodegradation rate, molecular distribution, and toxicity of commercial naphthenic acids.

Effects of naphthenic acids (NAs) concentration (50-200 mg NA L; 35-140 mg TOC L) and loading rate (1.4-1249 mg NA L h; 1-874 mg TOC L h) on removal efficiency, removal rate, and molecular distribution of NAs, and effluent toxicity were evaluated for biodegradation of commercial NAs mixture in circulating packed bed bioreactors (CPBBs). Increase of NAs concentration and loading rate (shorter residence times) increased the removal rate, while removal efficiency initially declined and then stabilized.

Acceleration of skin wound healing by low-dose indirect ionizing radiation in male rats.

A recent hypothesis has revealed that low-dose irradiation (LDI) with ionizing radiation might have a promoting effect on fracture healing. The aim of this study was to investigate the influence of direct (electron beam) and indirect (gamma-ray) low-dose ionizing irradiations on the wound healing process in male rats. In 72 male rats, a full-thickness wound was incised.

Comparative Evaluation of Tacrolimus Versus Interferon Alpha-2b Eye Drops in the Treatment of Vernal Keratoconjunctivitis: A Randomized, Double-Masked Study.

Purpose: Vernal keratoconjunctivitis (VKC) is a bilateral, chronic, external ocular inflammatory disorder that mainly affects patients in their first or second decade. This study was designed to compare tacrolimus and interferon alpha-2b (IFN alpha-2b) eye drops in the treatment of VKC.

Methods: In this randomized, double-masked clinical trial, 40 consecutive patients with VKC were sent to a referral eye hospital in a tropical region southeast of Iran.

Deletion of the GluRδ2 Receptor in the Hotfoot Mouse Mutant Causes Granule Cell Loss, Delayed Purkinje Cell Death, and Reductions in Purkinje Cell Dendritic Tree Area.

Recent studies have found that in the cerebellum, the δ2 glutamate receptor (GluRδ2) plays a key role in regulating the differentiation of parallel fiber-Purkinje synapses and mediating key physiological functions in the granule cell-Purkinje cell circuit. In the hotfoot mutant or GluRδ2 knockout mice, the absence of GluRδ2 expression results in impaired motor-related tasks, ataxia, and disruption of long-term depression at parallel fiber-Purkinje cell synapses. The goal of this study was to determine the long-term consequences of deletion of GluRδ2 expression in the hotfoot mutant (GluRδ2 ) on Purkinje and granule cell survival and Purkinje cell dendritic differentiation.

Intravitreal autologous plasmin prepared by urokinase for vitreolysis: a pilot study.

Purpose: To evaluate the effects of intravitreal autologous plasmin injection (IVAP) on vitreoretinal diseases and vitreolysis.

Methods: In this interventional, prospective, case series pilot study, 8 eyes were assigned to IVAP. Plasminogen as centrifuged from the patients' plasma was converted to plasmin by adding urokinase.

Changes in the Distribution of the α 3 Na(+)/K(+) ATPase Subunit in Heterozygous Lurcher Purkinje Cells as a Genetic Model of Chronic Depolarization during Development.

A common assumption of excitotoxic mechanisms in the nervous system is that the ionic imbalance resulting from overstimulation of glutamate receptors and increased Na(+) and Ca(++) influx overwhelms cellular energy metabolic systems leading to cell death. The goal of this study was to examine how a chronic Na(+) channel leak current in developing Purkinje cells in the heterozygous Lurcher mutant (+/Lc) affects the expression and distribution of the α 3 subunit of the Na(+)/K(+) ATPase pump, a key component of the homeostasis system that maintains ionic equilibrium in neurons. The expression pattern of the catalytic α 3 Na(+)/K(+) ATPase subunit was analyzed by immunohistochemistry, histochemistry, and Western Blots in wild type (WT) and +/Lc cerebella at postnatal days P10, P15, and P25 to determine if there are changes in the distribution of active Na(+)/K(+) ATPase subunits in degenerating Purkinje cells.

Enhanced survival of wild-type and Lurcher Purkinje cells in vitro following inhibition of conventional PKCs or stress-activated MAP kinase pathways.

Recent studies using both dissociated and organotypic cell cultures have shown that heterozygous Lurcher (Lc/+) Purkinje cells (PCs) grown in vitro share many of the same survival and morphological characteristics as Lc/+ PCs in vivo. We have used this established tissue culture system as a valuable model for studying cell death mechanisms in a relatively simple system where neurodegeneration is induced by a constitutive cation leak mediated by the Lurcher mutation in the δ2 glutamate receptor (GluRδ2). In this study, Ca(++) imaging and immunocytochemistry studies indicate that intracellular levels of Ca(++) are chronically increased in Lc/+ PCs and the concentration and/or distribution of the conventional PKCγ isoform is altered in degenerating Lc/+ PCs.

Herbs in dentistry.

Herbs have been used for centuries to prevent and control disease. Herbal extracts are effective because they interact with specific chemical receptors within the body and are in a pharmacodynamic sense, drugs themselves. By using herbal medicines, patients have averted the many side effects that generally come with traditional medicines, but this does not mean that side effects do not occur.

Stimulation of the endometrium with high-grade blastocyst culture supernatant (SEHB) can improve pregnancy outcome for couples undergoing intracytoplasmic sperm injection (ICSI): a randomized clinical trial.

Purpose: To evaluate the impact of stimulating the endometrium with high-grade blastocyst culture supernatant (SEHB) perfusion before blastocyst transfer (BT) on implantation rate, pregnancy rate, and pregnancy outcome in ICSI cycles.

Materials And Methods: Ninety-four infertile couples who were referred to the Valiasr department of Imam Hospital complex between January 2010 and March 2011 enrolled in this randomized clinical trial. They were randomly divided into only BT or SEHB groups.

Death and survival of heterozygous Lurcher Purkinje cells in vitro.

The differentiation and survival of heterozygous Lurcher (+/Lc) Purkinje cells in vitro was examined as a model system for studying how chronic ionic stress affects neuronal differentiation and survival. The Lurcher mutation in the delta2 glutamate receptor (GluRdelta2) converts an orphan receptor into a membrane channel that constitutively passes an inward cation current. In the GluRdelta2(+/Lc) mutant, Purkinje cell dendritic differentiation is disrupted and the cells degenerate following the first week of postnatal development.

Effects of rivastigmine on memory and cognition in multiple sclerosis.

Background: Cognitive dysfunction is one of the common clinical symptoms in multiple sclerosis (MS), but there is no effective treatment for it.

Objective: The aim of this study was to evaluate the effect of rivastigmine in treating memory and cognitive dysfunction in MS.

Methods: A single-center double-blind placebo-controlled randomized clinical trial conducted from October 2005 to February 2007.

Specific JNK inhibition by D-JNKI1 protects Purkinje cells from cell death in Lurcher mutant mouse.

In the Lurcher mutant mouse (+/Lc), Purkinje cells (PCs) selectively die due to the mutation that converts alanine to threonine in the glutamate ionotropic receptor GRID 2, thus resulting in a constitutively leaky cation channel. This intrinsic cell death determines a target-dependent cell death of granule cells and olivary neurons and cerebellum cytoarchitecture is severely disrupted in the adult Lurcher mutant. Although the +/Lc mutant has been widely characterized, less is known about the molecules involved in +/Lc PC death.

Cell loss in the inferior olive of the staggerer mutant mouse is an indirect effect of the gene.

Staggerer (sg) is an autosomal recessive mutation in mouse that causes severe cerebellar atrophy. In this mutant, the Purkinje cell (PC) number is reduced by about 75% and the remaining Purkinje cells have a reduced dendritic arbor and an ectopic location. Previous analysis of staggerer chimeras has demonstrated that the Purkinje cell phenotypes are all direct consequences of the cell-autonomous action of the staggerer gene.

BCL-2 counteracts Doppel-induced apoptosis of prion-protein-deficient Purkinje cells in the Ngsk Prnp(0/0) mouse.

The pro-apoptotic factor BAX has recently been shown to contribute to Purkinje cell (PC) apoptosis induced by the neurotoxic prion-like protein Doppel (Dpl) in the prion-protein-deficient Ngsk Prnp(0/0) (NP(0/0)) mouse. In view of cellular prion protein (PrP(c)) ability to counteract Dpl neurotoxicity and favor neuronal survival like BCL-2, we investigated the effects of the anti-apoptotic factor BCL-2 on Dpl neurotoxicity by studying the progression of PC death in aging NP(0/0)-Hu-bcl-2 double mutant mice overexpressing human BCL-2 (Hu-bcl-2). Quantitative analysis showed that significantly more PCs survived in NP(0/0)-Hu-bcl-2 double mutants compared with the NP(0/0) mutants.

BAX contributes to Doppel-induced apoptosis of prion-protein-deficient Purkinje cells.

Research efforts to deduce the function of the prion protein (PrPc) in knock-out mouse mutants have revealed that large deletions in the PrPc genome result in the ectopic neuronal expression of the prion-like protein Doppel (Dpl). In our analysis of one such line of mutant mice, Ngsk Prnp0/0 (NP0/0), we demonstrate that the ectopic expression of Dpl in brain neurons induces significant levels of cerebellar Purkinje cell (PC) death as early as six months after birth. To investigate the involvement of the mitochondrial proapoptotic factor BAX in the Dpl-induced apoptosis of PCs, we have analyzed the progression of PC death in aging NP0/0:Bax-/- double knockout mutants.

Complement activation in very early Alzheimer disease.

The activation of the classical complement (C)-system in early-stage Alzheimer disease (AD) and nondemented aging was examined with immunohistochemistry in subjects assessed by the Clinical Dementia Rating (CDR). Activation (staining for C3 and C4 fragments) was found in all brains with amyloid deposits, including all nondemented (CDR 0) cases, with either small numbers of diffuse plaques or with sufficient plaques and tangles to indicate preclinical AD. Staining for C3 and C4 increased in parallel with plaque density in very mild to severe clinical AD.

Cell number in the inferior olive of nervous and leaner mutant mice.

Naturally occurring cell death is an important feature of neuronal network development: the absence of adequate postsynaptic target neurons during a critical period may result in the death of presynaptic neurons, the degree of death varying inversely with the size of the target population. Studies of mouse mutants with abnormal cerebellar development provide support for this neuron/target relationship in circuits within the CNS. In the present study we analysed the inferior olivary cell population in two cerebellar mutant mice, nervous (nr/nr) and leaner (Cacna1ala/la).

Cerebellar Purkinje cell loss in aging Hu-Bcl-2 transgenic mice.

The number of cerebellar Purkinje cells is increased by over 40% in young transgenic mice that overexpress a human Bcl-2 transgene (Hu-Bcl-2). To determine whether the Bcl-2-mediated rescue of Purkinje cells persists through life, the numbers of Purkinje cells were estimated in 6-, 12-, 18-, and 24-month-old Hu-Bcl-2 transgenic mice and age-matched controls. In addition, the expression of four markers for Purkinje cell differentiation, calbindin (CaBP), the 67-kDa isoform of glutamic acid decarboxylase (GAD67), gamma-aminobutyric acid transaminase (GABA-T), and the NMDA-R1 receptor subtype (NMDA-NR1) was analyzed in 6-month-old Hu-Bcl-2 transgenics and controls to determine whether overexpression of Bcl-2 and rescue from naturally occurring cell death affects the normal differentiation of Purkinje cells.

Estradiol (E2) enhances neurite outgrowth by repressing glial fibrillary acidic protein expression and reorganizing laminin.

Neuronal remodeling in response to deafferenting lesions in the brain can be enhanced by estradiol (E2). Astrocytes are among the targets of E2 in complex interactions with neurons and may support or inhibit neuronal remodeling. In ovariectomized female rats given entorhinal cortex lesions, E2 replacement inhibited the increase of glial fibrillary acidic protein (GFAP) protein.

Electrophysiological and morphological changes in striatal spiny neurons in R6/2 Huntington's disease transgenic mice.

We examined passive and active membrane properties and synaptic responses of medium-sized spiny striatal neurons in brain slices from presymptomatic (approximately 40 days of age) and symptomatic (approximately 90 days of age) R6/2 transgenics, a mouse model of Huntington's disease (HD) and their age-matched wild-type (WT) controls. This transgenic expresses exon 1 of the human HD gene with approximately 150 CAG repeats and displays a progressive behavioral phenotype associated with numerous neuronal alterations. Intracellular recordings were obtained using standard techniques from R6/2 and age-matched WT mice.

Progressive atrophy of cerebellar Purkinje cell dendrites during aging of the heterozygous staggerer mouse (Rora(+/sg)).

Staggerer (Rora(sg/sg)) is an autosomal mutation in an orphan nuclear hormone receptor gene, RORalpha, that acts intrinsically within the Purkinje cells and causes dysgenesis of the cerebellar cortex. Purkinje cell number is severely reduced, and the surviving cells are small with poorly developed dendrites. In contrast, the cytoarchitecture of the cerebellar cortex of the heterozygous staggerer (Rora(+/sg)) appears to be normal.

Decrease in striatal enkephalin mRNA in mouse models of Huntington's disease.

Huntington's disease is a devastating progressive neurodegenerative illness characterized by massive neuronal loss in the striatum. It is caused by the presence of an expanded CAG repeat in the gene encoding huntingtin, a protein of unknown function. We have examined the expression of neurotransmitters and other antigens present in striatal neurons with immunohistochemistry, and the level of expression of mRNAs encoding enkephalin, substance P, and glutamic acid decarboxylases with quantitative in situ hybridization histochemistry, in the striatum of two mouse models of Huntington's disease: transgenic animals expressing exon 1 of the human huntingtin gene with 144 CAG repeats and "knock-in" mice containing a chimeric mouse/human exon 1 with 71 or 94 CAG repeats inserted by homologous targeting.

Enhanced sensitivity to N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease.

We used two mouse models of Huntington's disease (HD) to examine changes in glutamate receptor sensitivity and striatal electrophysiology. One model, a transgenic, consisted of mice expressing exon 1 of the human HD gene and carrying 141-157 CAG repeat sequences (R6/2 line). The second model, a CAG repeat "knockin," consisted of mice with different lengths of CAG repeats (CAG71 and CAG94 repeats).

Overexpression of a Hu-bcl-2 transgene in Lurcher mutant mice delays Purkinje cell death.

Cerebellar Purkinje cells in the heterozygous Lurcher mutant undergo cell autonomous degeneration beginning in the second week of postnatal development and becoming almost total around 30-45 days. The Lurcher mutation was recently identified as gain-of-function defect in the delta 2 glutamate receptor causing a constitutive current leak, suggesting that +/Lc Purkinje cells die by an excitotoxic mechanism. In previous studies we have shown that overexpression of bcl-2, a key regulator of cell death, in the heterozygous Lurcher mutant does not prevent +/Lc Purkinje cell death.