CDIA™ Tetrodotoxin Colloidal Gold Test Cassette (DTSJYJ123)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
25T
Sample
Tissue, puffer fish
Intended Use
CDIA™ Tetrodotoxin Colloidal Gold Test Cassette is a lateral flow chromatographic immunoassay for the detection of TTX in samples.
Storage
The kit can be stored at room temperature (4-30°C). The test kit is stable through the expiration date (12 months). DO NOT FREEZE. Do not store the test kit in directsunlight.
Sensitivity
Tissue, puffer fish…………………………… 12.5ppm(µg/g)
General Description
Tetrodotoxin (TTX) is a powerful neurotoxin, which is tolerance to heat, salt and cooking. Minimum lethal dose for human is about 0.5mg/60 kg of body weight, the toxicity is 1000 times great than the sodium cyanide. Every year many people are ill due to improper eating or eating puffer fish. Therefore, it is significant to accurate detection of tetrodotoxin in puffer fish in order to prevention and control of tetrodotoxin poisoning.
Compared to the traditional method, the developed colloidal gold nanoparticle probe for the immunoassay is rapid and accuracy, and the detection can be finished in several minutes.

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References


Non-genomic action of vitamin D3 on N-methyl-D-aspartate and kainate receptor-mediated actions in juvenile gonadotrophin-releasing hormone neurons

REPRODUCTION FERTILITY AND DEVELOPMENT

Authors: Bhattarai, Pravin; Bhattarai, Janardhan P.; Kim, Min Sun; Han, Seong Kyu

Vitamin D is a versatile signalling molecule that plays a critical role in calcium homeostasis. There are several studies showing the genomic action of vitamin D in the control of reproduction; however, the quick non-genomic action of vitamin D at the hypothalamic level is not well understood. Therefore, to investigate the effect of vitamin D on juvenile gonadotrophin-releasing hormone (GnRH) neurons, excitatory neurotransmitter receptor agonists N-methyl-D-aspartate (NMDA, 30M) and kainate (10M) were applied in the absence or in the presence of vitamin D3 (VitaD3, 10nM). The NMDA-mediated responses were decreased by VitaD3 in the absence and in the presence of tetrodotoxin (TTX), a sodium-channel blocker, with the mean relative inward current being 0.56 +/- 0.07 and 0.66 +/- 0.07 (P<0.05), respectively. In addition, VitaD3 induced a decrease in the frequency of gamma-aminobutyric acid mediated (GABAergic) spontaneous postsynaptic currents and spontaneous postsynaptic currents induced by NMDA application with a mean relative frequency of 0.595 +/- 0.07 and 0.56 +/- 0.09, respectively. Further, VitaD3 decreased the kainate-induced inward currents in the absence and in the presence of TTX with a relative inward current of 0.64 +/- 0.06 and 0.68 +/- 0.06, respectively (P<0.05). These results suggest that VitaD3 has a non-genomic action and partially inhibits the NMDA and kainate receptor-mediated actions of GnRH neurons, suggesting that VitaD3 may regulate the hypothalamic-pituitary-gonadal (HPG) axis at the time of pubertal development.

Xenin Augments Duodenal Anion Secretion via Activation of Afferent Neural Pathways

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS

Authors: Kaji, Izumi; Akiba, Yasutada; Kato, Ikuo; Maruta, Koji; Kuwahara, Atsukazu; Kaunitz, Jonathan D.

Xenin-25, a neurotensin (NT)-related anorexigenic gut hormone generated mostly in the duodenal mucosa, is believed to increase the rate of duodenal ion secretion, because xenin-induced diarrhea is not present after Roux-en-Y gastric bypass surgery. Because the local effects of xenin on duodenal ion secretion have remained uninvestigated, we thus examined the neural pathways underlying xenin-induced duodenal anion secretion. Intravenous infusion of xenin-8, a bioactive C-terminal fragment of xenin-25, dose dependently increased the rate of duodenal HCO (3) (-) secretion in perfused duodenal loops of anesthetized rats. Xenin was immunolocalized to a subset of enteroendocrine cells in the rat duodenum. The mRNA of the xenin/NT receptor 1 (NTS1) was predominantly expressed in the enteric plexus, nodose and dorsal root ganglia, and in the lamina propria rather than in the epithelium. The serosal application of xenin-8 or xenin-25 rapidly and transiently increased short-circuit current in Ussing-chambered mucosa-submucosa preparations in a concentration-dependent manner in the duodenum and jejunum, but less so in the ileum and colon. The selective antagonist for NTS1, substance P (SP) receptor (NK1), or 5-hydroxytryptamine (5-HT) (3), but not NTS2, inhibited the responses to xenin. Xenin-evoked Cl-secretion was reduced by tetrodotoxin (TTX) or capsaicin-pretreatment, and abolished by the inhibitor of TTX-resistant sodiumchannel Nav1.8 in combination with TTX, suggesting that peripheral xenin augments duodenal HCO3- and Cl- secretion through NTS1 activation on intrinsic and extrinsic afferent nerves, followed by release of SP and 5-HT. Afferent nerve activation by postprandial, peripherally released xeninmay account for its secretory effects in the duodenum.

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