Sperm detection in video frames of semen sample using morphology and effective ellipse detection method.

CASA (Computer assisted semen analysis) systems are designed to assist Andrologist labour. Most available CASA systems are not accurate or so expensive. Therefore labours use manual methods to provide parameters. Although some companies have achieved appropriate accuracy, they have not released their methods. So proposing methods in this area might be useful for groups who intend to design new CASA system. One of the parameters which these systems compute is sperm count. In this paper we introduce our algorithm which can count sperms with an acceptable accuracy. Sperm count or concentration is one determinant parameter in male fertility. Our program preprocesses the video frame or image of semen sample under the microscope recorded by camera, then use morphology and effective ellipse detection method techniques to segment sperms and then count appropriate sperms.

Seasonal study of aflatoxin M1 contamination in milk in five regions in Iran.

Between April 2003 and February 2004, 98 samples of raw milk were obtained from milk tanks in one dairy plant in each of five regions in Iran. These were chosen with mean distances apart of 400 km, whereby they have different ecologies (temperature, relative humidity, etc.) and different agricultural products were used for animal feeding. Samples (24-25 per season) were laboratory heat treated and were analyzed for aflatoxin M1 with a validated High Performance Liquid Chromatography (HPLC) system. The overall mean of all samples was 0.041-0.065 microg/L (95% confidence) and the adjusted mean based on statistical modification was 0.039 ppb: 61 samples had 0.000-0.050 microg/L, 29 samples were contaminated with 0.05-0.10 microg/L, and the remaining 8 samples had 0.1-0.39 microg/L. All of the samples were lower than Codex Alimentarius and FDA standards (0.5 microg/L). Levels of aflatoxin M1 were higher in winter and spring than in summer and autumn, but the differences were not statistically significant (P>0.07). However, the level of aflatoxin in milk from one region (Hamedan) was significantly lower (P<0.05) than in those of the other regions (Gorgan, Rasht, Shiraz, Tehran).

Preparation and evaluation of cosmetic patches containing lactic and glycolic acids.

BACKGROUND: Alpha-hydroxy acids such as glycolic acid (GA) and lactic acid (LA), are used in cosmetic patches. The important fact in cosmetic patches is its suitable adhesion and peel properties. AIM: The objective of this study was to prepare LA- and GA-containing cosmetic patches and evaluate in-vitro/in-vivo correlation of adhesion properties. METHODS: Pressure-sensitive adhesives with different concentrations of GA and LA were cast on a polyethylene terephthalate film. The patches were evaluated for peel adhesive strength. On the basis of in vitro adhesion properties the patches were selected for wear performance tests and skin irritation potential. RESULTS: The adhesion properties (adhesion to steel plate and skin) and cohesive strength tests indicated the substantial influence of GA and LA concentrations. Based on in vitro adhesion studies the patches containing 3% (w/w) GA were selected for in vivo studies. In vivo studies show that a formulation containing 3% GA displays good adhesion on the skin, but it leaves little residues on the skin. Skin Irritation studies on healthy human volunteers showed negligible erythema at the site of application after 48 h. CONCLUSION: The noninvasive patch test model was found useful for detecting irritant skin reactions to the cosmetic patch containing GA. Our results demonstrated a strong correlation between the adhesion to steel plate and adhesion to skin. But a weak correlation between the degree of adhesive residue on the skin in in vitro and in vivo tests was observed for the formulation containing 3% (w/w) GA.

Effect of galnon on induction of long-term potentiation in dentate gyrus of C57BL/6 mice.

The impairment of cognitive performance by galanin administration in rodents indicates a possible modulating effect of this neuropeptide on long-term potentiation (LTP) induction in the hippocampal formation. Galnon is a non-peptide, systemically active galanin receptor agonist which has been tested in feeding, seizure and forced swim task in in vivo rodent experimental models. Similarly to galanin (1-29) (i.c.v.), galnon (i.p.) has exhibited anticonvulsant effects in rats. We have investigated the effect of galnon on the synaptic transmission and plasticity in hippocampal dentate gyrus (DG) of C57Bl/6 mice and compared the galnon effects to the effect of galanin (1-29) and galmic, a non-peptide galanin receptor agonist. Similarly to galanin (1-29) and galmic, superfusion of galnon did not alter the input-output responses in DG. Administration of galnon (1 microM) significantly attenuated the LTP induction by 85.5 +/- 1% by 51 min after high frequency trains stimulation. This result was very similar to the effect of galanin (1-29) and galmic, which caused an 80 +/- 1.5% and 94 +/- 2% reduction in the level of field potentiation, respectively. The PPF responses, however, were not altered due to galnon superfusion which is in contrast to the effect of galanin (1-29) or galmic. In summary, these data indicate that the systemically active, non-peptide galanin receptor agonist, galnon can exert similar effects to galanin (1-29) in attenuation of DG LTP in mice.

Role of galanin receptor 1 and galanin receptor 2 activation in synaptic plasticity associated with 3',5'-cyclic AMP response element-binding protein phosphorylation in the dentate gyrus: studies with a galanin receptor 2 agonist and galanin receptor 1 knockout mice.

The neuropeptide galanin was shown to impair cognitive performance and reduce hippocampal CA1 long-term potentiation (LTP) in rodents. However, the contribution of the two main galanin receptors; GalR1 and GalR2, present in the hippocampus to these effects is not known. In the present study, we determined the protein expression levels of GalR1 and GalR2 in the mouse dentate gyrus (DG) and used galanin (2-11), a recently introduced GalR2 agonist, and GalR1 knockout mice to examine the contribution of GalR1 and GalR2 to the modulation of LTP and 3',5'-cyclic AMP response element-binding protein (CREB)-dependent signaling cascades. In the DG, 57+/-5% of the galanin binding sites were GalR2, and the remaining population corresponded to GalR1. In hippocampal slices, galanin (2-11) fully blocked the induction of DG LTP, whereas galanin (1-29), a high affinity agonist for both GalR1 and GalR2, strongly but not fully attenuated the late phase of LTP by 80+/-1.5%. Application of galanin (1-29) or galanin (2-11) after LTP induction caused a transient reduction in the maintenance phase of LTP, with the larger effect displayed by superfusion of galanin (2-11). The induction and maintenance of DG LTP was not altered in the GalR1 knockout mice. Superfusion of galanin (1-29) or galanin (2-11) blocked the LTP induction to the same degree indicating a role for GalR2 in the induction phase of DG LTP. Furthermore, we analyzed the effects of GalR1 and/or GalR2 activation on DG LTP-induced CREB phosphorylation, associated with the late transcriptional effects of LTP. In the lateral part of the granule cell layer, high-frequency trains stimulation caused a significant increase in the level of CREB phosphorylation, which was significantly reduced by application of either galanin (1-29) or galanin (2-11), indicating that both GalR1 and/or GalR2 can mediate some of their effects on LTP through inhibition of CREB-related signaling cascades.

Patterns of seizures, hippocampal injury and neurogenesis in three models of status epilepticus in galanin receptor type 1 (GalR1) knockout mice.

The neuropeptide galanin exhibits anticonvulsant effects in experimental epilepsy. Two galanin receptor subtypes, GalR1 and GalR2, are present in the brain. We examined the role of GalR1 in seizures by studying the susceptibility of GalR1 knockout (KO) mice to status epilepticus (SE) and accompanying neuronal injury. SE was induced in GalR1 KO and wild type (WT) mice by Li-pilocarpine, 60 min electrical perforant path stimulation (PPS), or systemic kainic acid (KA). Seizures were analyzed using Harmonie software. Cell injury was examined by FluoroJade B- and terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end labeling; neurogenesis was studied using bromodeoxyuridine labeling. Compared with WT littermates, GalR1 KO showed more severe seizures, more profound injury to the CA1 pyramidal cell layer, as well as injury to hilar interneurons and dentate granule cells upon Li-pilocarpine administration. PPS led to more severe seizures in KO, as compared with WT mice. No difference in the extent of neuronal degeneration was observed between the mice of two genotypes in CA1 pyramidal cell layer; however, in contrast to WT, GalR1 KO developed mild injury to hilar interneurons on the side of PPS. KA-induced seizures did not differ between GalR1 KO and WT animals, and led to no injury to the hippocampus in either of experimental group. No differences were found between KO and WT mice in both basal and seizure-induced neuronal progenitor proliferation in all seizure types. Li-pilocarpine led to more extensive glia proliferation in GalR1 KO than in WT, and in both mouse types in two other SE models. In conclusion, GalR1 mediate galanin protection from seizures and seizure-induced hippocampal injury in Li-pilocarpine and PPS models of limbic SE, but not under conditions of KA-induced seizures. The results justify the development and use of GalR1 agonists in the treatment of certain forms of epilepsy.

A role for protein kinase intracellular messengers in substance P- and nociceptor afferent-mediated excitation and expression of the transcription factor Fos in rat dorsal horn neurons in vitro.

Expression of the inducible transcription factor Fos in the spinal dorsal horn in vivo is associated with nociceptive afferent activation, but the underlying stimulation-transcription pathway is less clear. This in vitro spinal cord study concerns the role of protein kinase A and C second messengers in substance P receptor (NK1R)-mediated or nociceptive afferent-evoked neuronal excitation and Fos expression. Nociceptive afferent (dorsal root) stimulation of isolated spinal cords (10-14 day old rats) evoked a 'prolonged' excitatory polysynaptic potential (DR-EPSP) that was attenuated (P < 0.05) by: the protein kinase A inhibitor, Rp-cAMP; the protein kinase C inhibitor, bisindolymaleimide I; and the selective NK1R antagonist, GR82334. Neuronal excitations induced by the NK1R agonist [Sar9,Met(O2)11]-SP were attenuated by Rp-cAMP, bisindolymaleimide I and GR82334. Effects of the protein kinase A and C inhibitors on the DR-EPSP or the [Sar9,Met(O2)11]-SP-induced depolarization were nonadditive, suggesting convergence of these intracellular signalling pathways onto a common final target. Nociceptor afferent-induced Fos, detected by immunohistochemistry in superficial and deep dorsal horn laminae, was attenuated by Rp-cAMP, bisindolymaleimide I and GR82334. In spinal cords pretreated with TTX to eliminate indirect neuronal activation, [Sar9,Met(O2)11]-SP (1-20 microM) elicited a dose-related expression of Fos that was reduced by Rp-cAMP, bisindolymaleimide I and GR82334. The effects of these inhibitors were most pronounced in the deep laminae. These data support a causal relationship between protein kinase A- or C-dependent signal transduction, nociceptive afferent- or NK1R-induced neuronal excitation and Fos expression in dorsal horn. Implications for short- versus long-term modulation of nociceptive circuitry are discussed.