Brain edema can be classified into three categories: vasogenic, cytotoxic, and interstitial. The mechanism of edema is thought to be different in each type. The authors studied the movement of water molecules in each type of white matter edema in a rat model by using diffusion-weighted magnetic resonance imaging. Conventional T2-weighted imaging did not allow distinction between the three types of white matter edema; the three types of edema were, however, distinguished by using diffusion-weighted imaging. The apparent diffusion coefficient (ADC) of water was different in each type of edema. Water molecules in cytotoxic edema induced by triethyl-tin intoxication showed a smaller and less anisotropic ADC than in normal white matter. In contrast, water in vasogenic edema induced by cold injury had a larger and more anisotropic ADC than in normal white matter. Water in interstitial edema due to kaolin-induced hydrocephalus had an anisotropic and very large ADC.

Animals↗

PubMedDate not supplied

Mapping of cerebral metabolites in rats by 1H magnetic resonance spectroscopic imaging. Distribution of metabolites in normal brain and postmortem changes.

The goal of this study was to examine metabolic differences between cortex and basal ganglia in normal rat brain and to determine postmortem changes using in vivo 1H magnetic resonance spectroscopic imaging at 300 MHz. The resonances observed were: choline, creatine + phosphocreatine, N-acetyl aspartate (NAA), lactate (Lac), and three small resonances in the amino acid region which included resonances from aspartate + NAA (Asp), glutamine + NAA (Gln), and glutamate + GABA (Glu). A previously unassigned resonance was observed at 1.13 ppm in brain of rats anesthetized with pentobarbital. Spectroscopic images in normal brain demonstrated increased NAA and Gln and decreased Glu in cortex compared to basal ganglia. The major postmortem changes were an increase of Lac, Glu and Cho and a decrease of NAA and Asp. The rise in Lac was significantly higher in cortex than in basal ganglia.

Amino Acids↗

PubMedDate not supplied

Identification and quantification of p-hydroxyethylamphetamine as a novel metabolite of ethylamphetamine in rat by gas chromatography-mass spectrometry.

Ethylamphetamine and two major metabolites in urine, obtained after intraperitoneal administration of the drug to rats, have been isolated by gas chromatography-mass spectrometry. We have also synthesized an authentic sample of p-hydroxy-N-ethylamphetamine by a simple method. In rat, the metabolic pathway of ethylamphetamine is similar to that of amphetamine and methylamphetamine according to quantitative analysis of the major metabolites using a selected ion monitoring (SIM) method.

Amphetamine↗

PubMedDate not supplied

IP-10, apoptotic genes, and calcineurin subtype messenger RNA kinetics occurring in rat renal isografts from brain-dead donors.

BACKGROUND: Brain death (BD) and following ischemia/reperfusion(I/R) injury has cardinal implications in kidney transplantation (Tx). We hypothesize that inflammation, apoptosis, and drug nephrotoxicity are central mechanisms leading to initial organ damage in transplantation from BD donors. In this study, the gene kinetics of a chemokine (IP-10), an apotosis-related gene, and of calcineurin (Cn) subtype were compared using kidney isografts from BD versus living donors. METHODS: Donors were intubated and mechanically ventilated for 6 hours. Grafts were harvested 6 hours after BD, and at 1, 6, and 24 hours and 5 days after engraftment. Messenger RNA (mRNA) expression was assessed using real-time reverse transcriptase-polymerase chain reaction. RESULTS: Gene expression of IP-10 was up-regulated only among BD donor kidneys, particularly following I/R injury. These changes recovered to baseline levels thereafter. Bcl-2 was suppressed within 6 hours of BD and 1 hour after engraftment. In contrast, Bax in kidneys from BD donors was significantly up-regulated at 6 hours after engraftment. These changes were minimal in the controls. Cn Aalpha and Abeta were decreased in kidneys from BD donors before and within 1 hour after engraftment. However, these differences became insignificant thereafter. CONCLUSIONS: Marked up-regulation of IP-10 may predict the initial graft injury and the onset of delayed graft function. Apoptotic gene changes may lead kidney grafts to a preapoptotic condition and up-regulate renal toxicity caused by Cn inhibitors. This initial antigen-independent donor circumstance may be one risk factor for chronic rejection.

Animals↗

PubMedDate not supplied

The differential ACTH responses to combined dexamethasone/CRH administration in major depressive and dysthymic disorders.

In a preliminary study, we performed the combined dexamethasone/CRH test on patients with major depressive and dysthymic disorders as well as healthy controls. The ACTH response was significantly enhanced in the major depression group compared to the control group and tended to be heightened compared to the dysthymia group. The cortisol response was not significantly different among the three groups. We assume that major depression and dysthymia are neuroendocrinologically distinct disorders, although whether the difference is quantitative or qualitative remains to be examined.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Psychological, autonomic and neuroendocrine responses to acute stressors in the combined dexamethasone/CRH test: a study in healthy subjects.

The combined dexamethasone/CRH test (DEX/CRH test) is reported to produce augmented ACTH and cortisol responses in various psychiatric disorders as well as in some non-psychiatric conditions. To examine whether stress affects the outcome of DEX/CRH test, two stress groups in a repeated measures design were compared to an age-matched control group with regard to the psychological, autonomic and neuroendocrine responses after the combined dexamethasone and CRH challenge. Cold pressor (4 degrees C, total 10 min) produced stronger subjective distress than mental arithmetic (15 min). Cold exposure, but not the mental test, elevated systolic and diastolic blood pressure, whereas the mental test increased pulse rate and skin conductance level more markedly than cold exposure. Neither stressor produced a significantly enhanced response of ACTH and cortisol in DEX/CRH test, and there was no correlation between psychological and neuroendocrine responses. These findings suggest that different stressors induce different patterns of sympathetic activation and that acute stress is unlikely to affect the results of DEX/CRH test.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Rapid diagnosis of donor and renal allograft infection using a polymerase chain reaction technique.

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Adolescent↗

PubMedDate not supplied

Analysis of synergism between stem cell factor and granulocyte-macrophage colony-stimulating factor on human megakaryoblastic cells: an increase in tyrosine phosphorylation of 145 kDa subunit of c-kit in two-factor combination.

In normal hematopoiesis, stem cell factor (SCF) stimulates survival, proliferation and differentiation of hematopoietic progenitors. Although SCF acts synergistically with a variety of cytokines, the mechanism of growth factor-cooperation remains to be determined. To analyze the synergism between SCF and granulocyte-macrophage colony-stimulating factor (GM-CSF), we established a new megakaryoblastic cell line, HML-2, by culture in the presence of both SCF and GM-CSF. While SCF alone or GM-CSF alone supported modest cell growth, SCF and GM-CSF together induced substantial growth of this cell line. SCF alone tyrosine-phosphorylated several bands including the 145 kDa subunit of c-kit. GM-CSF alone did not cause the tyrosine phosphorylation of the 145 kDa subunit, but markedly up-regulated the expression of the 145 kDa subunit of c-kit. The combination of SCF and GM-CSF resulted in a synergistic increase in tyrosine phosphorylation of the 145 kDa subunit of c-kit. Several proliferation inhibitors which removed the two-factor interaction on the growth of the HML-2 cells down-regulated the 145 kDa subunit of c-kit. Thus, a synergistic increase in tyrosine phosphorylation of the 145 kDa subunit of c-kit may be one possible mechanism underlying the cooperation of SCF and GM-CSF on the HML-2 cell growth.

Blotting, Western↗

PubMedDate not supplied

Clinofibrate therapy raises high-density lipoprotein levels and lowers atherogenic index in diabetes mellitus patients.

The effects of clinofibrate on serum lipoprotein concentrations, lecithin cholesterol acyl transferase activity and atherogenic index were studied in 10 diabetes mellitus patients. The patients comprised five with well-controlled non-insulin-dependent diabetes, and five with poorly controlled insulin-dependent diabetes; six non-insulin-dependent diabetics acted as placebo controls. No adverse side-effects were reported and there were no significant changes in total cholesterol, triglyceride or high-density lipoprotein 3-cholesterol concentrations following 600 mg/kg clinofibrate treatment for 4 weeks in either insulin-dependent or non-insulin-dependent diabetics. High-density lipoprotein-cholesterol concentrations and lecithin cholesterol acyl transferase activity were significantly (P less than 0.05) increased by clinofibrate treatment in insulin-dependent and non-insulin-dependent diabetics and high-density lipoprotein 2-cholesterol concentrations were significantly (P less than 0.05) increased by clinofibrate in insulin-dependent diabetics. The atherogenic index was significantly (P less than 0.01) reduced in non-insulin-dependent diabetics. It is suggested that the enhanced plasma lecithin cholesterol acyl transferase activity following clinofibrate therapy is the result of increased high-density lipoprotein-cholesterol and high-density lipoprotein 2-cholesterol concentrations and may play a central role in the efficacy of clinofibrate.

Adult↗

PubMedDate not supplied

Influence of prostaglandin E1 on heavy proteinuria in slightly azotaemic diabetics.

Treatment of non-insulin-dependent diabetes mellitus patients with nephropathy of the nephrotic type using 40 micrograms prostaglandin E1 given intravenously twice daily for 4 weeks reduced the urinary protein concentration. Prostaglandin E1 also increased the total serum protein and serum albumin concentrations, and reduced creatinine clearance and plasma renin activity following frusemide loading. Treatment with the prostaglandin did not, however, significantly affect the blood urea nitrogen and the serum creatinine concentration. It is concluded that prostaglandin E1 has overt effects on diabetic nephropathy.

Aged↗