N-terminal pro-brain natriuretic peptide predicts hospitalization for ischemic stroke in Japanese hemodialysis patients

Clinical and Experimental Nephrology - The association between N-terminal pro-brain natriuretic peptide (NT-proBNP) and stroke in Japanese hemodialysis (HD) outpatients is unclear. Therefore, in...     

A case of recurrent biliary cystadenocarcinoma successfully treated with 5FU/CDDP systemic chemotherapy]

We report a case of biliary cystadenocarcinoma which recurred 41 months postoperatively. A 60-year-old woman was admitted for further examination of multiple metastatic tumors and a large amount of ascites. Systemic administration of 5FU and CDDP caused her CEA level to decrease gradually and abdominal computed tomography revealed considerable reduction of the metastatic tumors and ascites. Since her general condition had improved, chemotherapy was continued in the outpatient clinic.     

Activation of protein kinase C and nicotinamide adenine dinucleotide phosphate oxidase in leukocytes of spontaneously hypertensive rats.

The involvement of oxidative stress in polymorphonuclear leukocytes (PMN) in the pathogenesis of hypertension remains to be elucidated. We analyzed the generation of reactive oxygen species (ROS) by the circulating and peritoneally infiltrating PMN from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Flow cytometric analysis revealed that ROS generation by PMN from SHR was higher than that from WKY before (at 6 weeks of age) and after (at 16 weeks of age) the onset of hypertension. In vivo, ROS generation by PMN from SHR, but not that by PMN from WKY, was significantly suppressed by 10-week treatment with 50 mg/kg/day carvedilol, and this treatment did not affect blood pressure. Western blotting analysis revealed that protein kinase C alpha (PKCalpha), but not PKCbetaI or betaII, was activated more strongly in PMN from SHR than in PMN from WKY. Furthermore, expression of p47phox of nicotinamide adenine dinucleotide phosphate oxidase, but not of p67phox, in PMN from SHR was higher than that in PMN from WKY. These results suggest that ROS generation by PMN is principally enhanced in SHR through activation of PKCalpha and p47phox.     

Strain difference in tolerance to low-temperature treatment of fertilized mouse oocytes

Background and Aims:  The aim of this study was to determine which mouse strains exhibit tolerance to cooling when fertilized oocytes have been stored at 4°C.
Methods:  In-vitro -fertilization-derived oocytes of eight mouse strains were incubated at 4°C in 20 mmol/L Hepes-potassium modified simplex optimized medium (KSOM) medium for 0, 24, 48, 60 or 72 h, and then returned to normal culture conditions at 37°C in KSOM medium. The rates of development of cultured oocytes into blastocysts and cell numbers of blastocysts were examined. In some cases, a Comet assay was carried out to evaluate DNA damage. In addition, the effects of β-mercaptoethanol on the development of the 4°C-treated oocytes were assessed.
Results:  Of the eight strains tested, BDF1, B6C3F1 and FVB/N strains exhibited relatively higher degrees of tolerance to 4°C treatment and approximately 90%, 83% and 78% of oocytes treated at 4°C for 48 h developed to morphologically normal blastocysts, respectively. Comet assay revealed no clear DNA damage in oocytes treated at 4°C. Treatment with β-mercaptoethanol failed to improve the in vitro survival rate of low-temperature-treated oocytes.
Conclusion:  Strain differences were observed in tolerance to cooling treatment when fertilized oocytes were temporarily treated with 4°C, although the reasons for this remain unclear. (Reprod Med Biol 2006; 5 : 43–50)     

Different postnatal development of cells expressing mRNA encoding neurotensin receptor.

In situ hybridization histochemistry revealed three different ontogenetic patterns of localized expression of the high-affinity type of neurotensin receptor mRNA in the developing rat brain: one comprises sites which showed transient expression of neurotensin receptor mRNA during the first postnatal week, the expression greatly decreasing thereafter (type I); another comprises sites at which there is a gradual increase in neurotensin receptor mRNA after birth, as there is in cell number and intensity, with advancing age, followed by a plateau (type II); the third comprises sites at which there is much expression of neurotensin receptor mRNA already at birth, and a slight decrease thereafter (type III). The cerebral cortex, except retrosplenial and entorhinal cortices, and the anterior dorsal thalamic nucleus exhibit the type I pattern, while the horizontal and vertical limbs of the diagonal band of Broca, magnocellular preoptic nucleus, substantia innominata, ventral part of the suprachiasmatic nucleus, medial habenular nucleus, ventral tegmental area and substantia nigra pars compacta exhibit the type II pattern. The tenia tecta, retrosplenial and entorhinal cortices exhibit the type III pattern. One of the most striking findings in this study was that the entire neocortex and most of the limbic cortex exhibit the type I pattern, i.e. neurotensin receptor mRNA is expressed transiently long before a neuronal network is established there. This suggests that neurotensin plays an important role in cortical development, other than its reported transmitter-like role in the adult.     

Proliferation of Hepatocytes and Attenuation from Carbon Tetrachloride Hepatotoxicity by Gadolinium Chloride in Rats

Abstract: Intravenous injection of gadolinium chloride (GdCl₃) at a dose of 10 mg/kg caused an increase in proliferating cell nuclear antigen labeling index and the grade of pyronin positivity (RNA level) in rat liver. In CCl₄-exposed rats, pretreatment with GdCl₃ also showed a preventive effect of the liver injury both biochemically and histologically. Moreover, the proliferative action preceded the attenuative effect of the liver injury. Results suggest that GdCl₃ induces hepatocyte proliferation, and this action of GdCl₃ may modify the development of CCl₄-induced liver injury.     

Dopaminergic transmission in the hypothalamic arcuate nucleus to produce acupuncture analgesia in correlation with the pituitary gland

Acupuncture analgesia (AA) caused by low frequency stimulation of the acupuncture point (AP) was abolished by hypophysectomy and adrenalectomy. Termination of the AA producing pathway from the AP to the pituitary gland was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with AA was in the posterior HARN (P-HARN). AA in the hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during acupuncture stimulation, were both restored by intraperitoneal microinjection of 0.5 mg/kg morphine or 0.1 micrograms beta-endorphin into the P-HARN during acupuncture stimulation. Of the analgesia produced by dopamine or beta-endorphin injected into the P-HARN, that caused by beta-endorphin disappeared after denervation of the M-HARN. The P-HARN neurons that responded to acupuncture stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-endorphin. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-endorphin might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy.     

Changes of Electroencephalographic Bicoherence during Isoflurane Anesthesia Combined with Epidural Anesthesia

Background: The authors previously reported that, during isoflurane anesthesia, electroencephalographic bicoherence values changed in a fairly restricted region of frequency versus frequency space. The aim of the current study was to clarify the relation between electroencephalographic bicoherence and the isoflurane concentration.

Methods: Thirty elective abdominal surgery patients (male and female, aged 34-77 yr, American Society of Anesthesiologists physical status I-II) were enrolled. After electroencephalogram recording with patients in an awake state, anesthesia was induced with 3 mg/kg thiopental and maintained with oxygen and isoflurane. Continuous epidural anesthesia with 80-100 mg/kg 1% lidocaine was also administered. Using software they developed, the authors continuously recorded the FP1-A1 lead of the electroencephalographic signal and expired isoflurane concentration to an IBM-PC compatible computer. After confirming the steady state of each isoflurane (end-tidal concentration at 0.3, 0.5, 0.7, 0.9, 1.1, 1.3, and 1.5%), electroencephalographic bicoherence values were calculated.

Results: In a light anesthetic state, electroencephalographic bicoherence values were low (generally <= 15.0%). At increased concentrations of isoflurane, two peaks of electroencephalographic bicoherence emerged along the diagonal line (f1 = f2). The peak emerged at around 4.0 Hz and grew higher as isoflurane concentration increased until it reached a plateau (43.8 +/- 3.5%, mean +/- SD) at isoflurane 0.9%. The other peak, at about 10.0 Hz, also became significantly higher and reached a plateau (32.6 +/- 9.2%) at isoflurane 0.9%; at isoflurane 1.3%, however, this peak slightly decreased.