0083, respectively). Univariate Cox regression analyses identified posttreatment maximum standardized uptake value ( cutoff 2.5) as the only preoperative prognostic factor ( P = .0071).

Conclusion: Posttreatment positron emission tomography with fludeoxyglucose F 18 reliably predicted histologic response and postoperative survival in advanced esophageal squamous cell carcinoma. This tool could potentially be used to tailor optimal treatment according to individual responses.”
“Opioid mechanisms are

involved in the control of water selleck compound and NaCl intake and opioid receptors are present in the lateral parabrachial nucleus (LPBN), a site of important inhibitory mechanisms related to the control of sodium appetite. Therefore, in the present study we investigated the effects of opioid receptor activation in the LPBN on 0.3 M NaCl and water intake in rats. Male Holtzman rats

with stainless steel cannulas implanted bilaterally in the LPBN were used. In normohydrated and satiated rats, bilateral injections of the opioid receptor agonist beta-endorphin (2 nmol/0.2 mu l) into the LPBN induced 0.3 M NaCl (17.8 +/- 5.9 vs. saline: 0.9 +/- 0.5 ml/240 min) and water intake (11.4 +/- 3.0 vs. saline: 1.0 +/- 0.4 ml/240 min) in a two-bottle test. Bilateral injections of the opioid antagonist naloxone (100 nmol/0.2 mu l) into the LPBN abolished sodium and water intake induced by 13-endorphin into the LPBN and also reduced 0.3 M NaCl intake (12.8 +/- 1.5 vs. vehicle: 22.4 Metabolism inhibitor +/- 3.1 ml/180 min) induced by 24 h of sodium depletion (produced by the treatment with the diuretic furosemide s.c.+sodium deficient food for 24 h). Bilateral injections of 13-endorphin into the LPBN in satiated rats produced no effect on water or 2% sucrose intake

when water alone or simultaneously with 2% sucrose was offered to the animals. The results show that opioid receptor activation in the LPBN induces hypertonic sodium intake in satiated and normohydrated VX-661 cost rats, an effect not due to general ingestive behavior facilitation. In addition, sodium depletion induced 0.3 M NaCl intake also partially depends on opioid receptor activation in the LPBN. The results suggest that deactivation of inhibitory mechanisms by opioid receptor activation in the LPBN releases sodium intake if excitatory signals were activated (sodium depletion) or not. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“In vitro, nitric oxide (NO) inhibits the firing rate of magnocellular neurosecretory cells (MNCs) of hypothalamic supraoptic and paraventricular nuclei and this effect has been attributed to GABAergic activation. However, little is known about the direct effects of NO in MNCs. We used the patch-clamp technique to verify the effect Of L-arginine, a precursor for NO synthesis, and N-omega-nitro-L-arginine methyl ester hydrochloride (L-NAME), an inhibitor of NOS, on spontaneous electrical activity of MNCs after glutamatergic and GABAergic blockade in Wistar rat brain slices.