Differential expression of the calcium-sensing receptor in the ischemic and border zones after transient focal cerebral ischemia in rats.

G-protein-coupled calcium-sensing receptor (CaSR) has been recently recognized as an important modulator of diverse cellular functions, beyond the regulation of systemic calcium homeostasis. To identify whether CaSR is involved in the pathophysiology of stroke, we studied the spatiotemporal regulation of CaSR protein expression in rats undergoing transient focal cerebral ischemia, which was induced by middle cerebral artery occlusion. We observed very weak or negligible immunoreactivity for CaSR in the striatum of sham-operated rats, as well as in the contralateral striatum of ischemic rats after reperfusion.

Overexpression of class III beta tubulin and amplified HER2 gene predict good response to paclitaxel and trastuzumab therapy.

Through this study, we aimed to validate several biomarkers that have been known to possibly predict the outcomes of the trastuzumab and paclitaxel (TP). Human epidermal growth factor 2 (HER2) positive metastatic breast cancer (MBC) patients who had been treated with TP in single institute from 2006 to 2009 were included in this study. For procured formalin fixed paraffin embedded tumor tissues, HER2 amplification index (AI) and polymorphisms of the immunoglobulin G fragment C receptors (FCGR) were assessed as biomarkers to the trastuzumab and expression of class III beta tubulin (bTubIII) was evaluated as a predictive factor to the paclitaxel.

5-hydroxy-L-tryptophan Suppressed Food Intake in Rats Despite an Increase in the Arcuate NPY Expression.

This study was conducted to define the underlying mechanism of hypophagia induced by increased central serotonergic action. Rats received 3 daily injections of 5-hydroxy-L-tryptophan (5-HTP), a serotonin precursor, at a dose of 100 mg/kg/10 ml saline at 1 h before lights off. A significant suppression in food intake was observed shortly after the 5-HTP injection and persisted during 3 daily 5-HTP injections.

Enhanced expression of the sweet taste receptors and alpha-gustducin in reactive astrocytes of the rat hippocampus following ischemic injury.

The heterodimeric sweet taste receptors, T1R2 and T1R3, have recently been proposed to be associated with the brain glucose sensor. To identify whether sweet taste signaling is regulated in response to an ischemic injury inducing acute impairment of glucose metabolism, we investigated the spatiotemporal expression of the sweet taste receptors and their associated taste-specific G-protein α-gustducin in the rat hippocampus after ischemia. The expression profiles of both receptor subunits and α-gustducin shared overlapping expression patterns in sham-operated and ischemic hippocampi.

Leptin blocks the fasting-induced increase of pERK1/2 in the paraventricular nucleus of rats.

This study was conducted to define molecular mechanisms by which food deprivation increases phosphorylated extracellular signal-regulated protein kinase (pERK1/2) in the hypothalamic paraventricular nucleus of rats. pERK1/2 immunoreactivity (-ir) is markedly increased in the paraventricular nucleus by 48h of food deprivation. Treatment with RU486, glucocorticoid antagonists, during food deprivation did not affect the fasting-induced increase of pERK1/2-ir in the paraventricular nucleus, but intracerebroventricular (icv) leptin blocked the increase of pERK1/2-ir by food deprivation.

Capsaicin receptors are colocalized with sweet/bitter receptors in the taste sensing cells of circumvallate papillae.

We examined co-localization of vanilloid receptor (VR1) with sweet receptors T1R2, T1R3, or bitter receptor T2R6 in taste receptor cells of rat circumvallate papillae. Tissue sections of rat circumvallate papillae were doubly reacted with anti-VR1 antibodies and anti-T1R2, anti-T1R3 or anti-T2R6 antibodies, using double-immunofluorescence histochemistry technique. Localizations of VR1, T1Rs and T2R6 in the vallate taste cells containing α-gustducin were also examined.

Proteomic analysis of lithium-induced gene expression in the rat hypothalamus.

The hypothalamic proteomes were analyzed 1 and 6 hr after an intraperitoneal injection of lithium chloride or sodium chloride (0.15 M, 12 ml/kg). Results showed that expression of 14 and 32 proteomes was increased consistently by 1 hr and 6 hr of lithium treatment, respectively.

Intra-oral pre-treatment with capsaicin increases consumption of sweet solutions in rats.

Sprague-Dawley rats received preference tests for sucrose or saccharin daily following oral treatment with 0.02% capsaicin. Consumed sweet solutions and preference scores increased in capsaicin-treated rats, compared to control rats on the second to fifth exposure period for sucrose and all exposure periods for saccharin.

Histamine H1 receptor induces cytosolic calcium increase and aquaporin translocation in human salivary gland cells.

One of the common side effects of antihistamine medicines is xerostomia (dry mouth). The current consensus is that antihistamine-induced xerostomia comes from an antimuscarinic effect. Although the effect of antihistamines on salivary secretion is both obvious and significant, the cellular mechanism whereby this happens is still unclear because of the lack of knowledge of histamine signaling in human salivary glands.

Involvement of apoptosis and calcium mobilization in tetrahydrobiopterin-induced dopaminergic cell death.

Parkinson's disease is a neurodegenerative disorder associated with selective loss of the dopaminergic neurons in the substantia nigra. We have previously shown that tetrahydrobiopterin (BH4), the obligatory cofactor for dopamine synthesis, exerts selective toxicity on dopamine-producing cells. In the present study we determined, both in vitro and in vivo, whether the cell death induced by this endogenous molecule involves apoptosis, resembling that which occurs in Parkinson's disease.

Lectin-induced apoptosis of mature olfactory receptor cells.

Previous studies showed that uptake of the lectin conjugate, wheat germ agglutinin-horseradish peroxidase (WGA-HRP) by olfactory receptor cells results in a thinning of the olfactory epithelium (OE) and increased turnover of globose basal cells. To ascertain the cell-type lost as well as the time course and mechanism of the loss, the current study measured changes in the number of dendritic knobs, olfactory marker protein (OMP) expression and assessed TUNEL labeling as an indicator of apoptosis. Electron microscopic analysis of the number of dendritic knobs showed that the largest reduction occurred at 1 week after intranasal irrigation with WGA-HRP.