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At least 1,207 records · Page 67Linked to original sources

PubMed1985

Neurogenic bladder. New clinical finding in Legionnaires' disease.

Legionnaires' disease presents with a spectrum of organ involvement including pulmonary, hepatic, gastrointestinal, metabolic, and renal dysfunction. Known neurologic manifestations include hallucinations, delirium, cerebral and cerebellar disturbance, and encephalomyelitis. Clinical and subclinical peripheral neuropathy has been described. This report describes a 51-year-old man with legionnaires' disease complicated by cerebral and persistent cerebellar and brainstem dysfunction, without evidence of direct bacterial invasion of the nervous system. Of particular interest was the development of a flaccid neurogenic bladder, a clinical manifestation not previously described.

Bipolar Disorder↗

PubMed1979

Conduction velocity through the somesthetic pathway in chronic renal failure.

The latencies of evoked potentials recorded at different levels of the peripheral and central nervous system by median nerve stimulation were measured before and after dialysis, and compared with similar recordings in normal volunteers. Abnormally slow conduction velocity was more often found in proximal rather than in distal segments of the peripheral pathway in patients with chronic renal failure. This abnormality was not correlated with the presence of clinical signs of neuropathy or low values of motor conduction velocity, neither was it affected by dialysis. These findings support the hypothesis of peripheral nerve dysfunction secondary to metabolic derangement in uraemic patients.

Adult↗

PubMed1992

Increased brain concentrations of a neurotoxin, 3-hydroxykynurenine, in Huntington's disease.

Concentrations of the neurotoxic tryptophan metabolite, 3-hydroxykynurenine, were determined in brain tissue taken post-mortem from patients with Huntington's disease and Alzheimer's disease. 3-Hydroxykynurenine was substantially and significantly increased in all three brain areas studied in Huntington's disease, but not significantly increased in the cortex in Alzheimer's disease, when compared to matched controls. These results demonstrate a possible dysfunction of tryptophan metabolism, via the kynurenine pathway, in Huntington's disease.

Aged↗

PubMed1993

Effects of a new diphenylpiperazine calcium antagonist, KB-2796, on cerebral ischemic neuronal damage in rats.

1. The effects of KB-2796, a new diphenylpiperazine calcium antagonist, on the mitochondrial dysfunction and energy metabolism deficits were examined in the ischemic rat brain. 2. KB-2796 (30 mg/kg, p.o.), administered 60 min prior to decapitation, improved the reduced respiratory activity of mitochondria obtained from rat brain 5 min after decapitative ischemia. 3. KB-2796 (30 mg/kg, p.o.), administered 60 min prior to ischemic insult, improved both the reductions in pyruvate and ATP and prevented increases in the lactate/pyruvate ratio induced by 30-min forebrain ischemia in rats with 4-vessel occlusion (4-VO). 4. The effect of KB-2796 on local cerebral glucose utilization (LCGU) was examined by a quantitative autoradiographic 2-[14C]deoxyglucose method in normal and 4-VO rats. 5. Postischemic LCGU measured 24 hr after reperfusion in the forebrain, in particular in the cortex, thalamus, geniculate body, hippocampus, caudate-putamen, nucleus accumbens, colliculus, and corpus callosum, was below the normal control value. 6. KB-2796 (1 mg/kg, i.v.), administered 1 min prior to the injection of 2-[14C]deoxyglucose, improved the reductions in LCGU that were produced by cerebral ischemia in the cortex, thalamus, geniculate body, caudate-putamen, nucleus accumbens and substantia nigra, but did not affect LCGU in normal rats. 7. These findings suggest that KB-2796 minimized the deficits in brain energy metabolism produced by ischemia; this agent may therefore be a valuable therapeutic drug in cerebrovascular-related disorders.

Animals↗

PubMed1991

Determination of 3-hydroxykynurenine in human brain and plasma by high-performance liquid chromatography with electrochemical detection. Increased concentrations in hepatic encephalopathy.

A simple and specific method was developed for the determination of 3-hydroxykynurenine in brain tissue and blood plasma using high-performance liquid chromatography with electrochemical detection. This involved an extraction procedure using strong cation-exchange columns and also permitted the determination of 3-hydroxyanthranilic acid in brain tissue. The method was applied to the investigation of post mortem brain tissue from patients with hepatic encephalopathy. Cortical 3-hydroxykynurenine concentrations were substantially increased in such patients above control values, providing evidence for a dysfunction of tryptophan metabolism in this disease.

Brain↗

PubMedDate not supplied

Anesthesia for glucagonoma resection.

Anesthetic experience with three cases of the resection of glucagonoma, a rare tumor of alpha cells of pancreatic islets, is presented. Marked increases of blood glucagon and glucose levels, with the potential for clinically significant metabolic and myocardial dysfunction, did not occur during anesthesia and surgery. Associated tumors of other endocrine cell types also were absent in the three study patients. Strategies for anticipating and managing other perioperative problems associated with glucagonoma also are discussed.

Adult↗

PubMed2004

[Study and evaluation of patients with obliterating arteriopathy of the lower limbs: use of isokinetics to analyze muscular strength and fatigue].

OBJECTIVES: The aim of the study was to evaluate strength of the dorsal and plantar flexors in patients with obliterating arteriopathy of the lower limbs (stage 2) and to evaluate fatigue. POPULATION AND METHODS: The comparison was based on two groups of ten patients: one with obliterating arteriopathy, and the second with healthy limbs as a control group. Each group of patients underwent bilateral plantar flexion and dorsiflexion of the ankle on an isokinetic machine, with the following movements: three series of five movements at 120 degrees/s, then three series of three movements at 30 degrees/s in a concentric mode to evaluate strength. The exercise was repeated 20 times at 180 degrees/s to evaluate fatigue. The isokinetic parameters selected were the couple peak and ratio of workload to total weight of the patient. Tests controlled for cardiac frequency, as measured by electrocardiography, and blood pressure. RESULTS: Patients with obliterating arteriopathy of the lower limbs were generally weaker in global strength of plantar and dorsal flexors and had greater muscular fatigue than the control group (P < 0.05). CONCLUSION: Decreased performance in the leg muscles in patients with obliterating arteriopathy of the lower limbs is likely due to arterial deficit. Muscular metabolism anomalies such dysfunction of the terminal stages of the oxidative phosphorylation could also affect strength. Use of isokinetics represents an interesting possibility for treatment of patients with multiple cardiovascular abnormalities.

Adult↗

PubMed2006

1,1'-Xylyl bis-1,4,8,11-tetraaza cyclotetradecane: a new potential copper chelator agent for neuroprotection in Alzheimer's disease. Its comparative effects with clioquinol on rat brain copper distribution.

Dysfunction of copper metabolism leading to its excess or deficiency results in severe ailments. Recently, neurodegenerative disorders such as Alzheimer's disease have been associated with copper metabolism. Compounds having the ability to reduce copper levels in brain or to affect its distribution could have neuroprotective effects, mainly through a downregulation of the transcription of amyloid peptide precursor (APP). We report here the biological effect of compound 1,1'-xylyl bis-1,4,8,11-tetraaza cyclotetradecane, which specifically affects copper concentration in the brain cortex region. Its copper homeostatic activity is compared with that of clioquinol, a well-known drug, which has been recently reported as an active A beta-peptide clearance drug in vivo for Alzheimer's patients.

Alzheimer Disease↗

PubMed2006

Serum NTX is a practical marker for assessing antiresorptive therapy for glucocorticoid treated patients with chronic kidney disease.

INTRODUCTION: In chronic kidney disease (CKD) patients, serum concentration of type I collagen N-telopeptide (S-NTX) increases as renal function declines because of perturbed bone metabolism by renal dysfunction itself and impaired urinary excretion of NTX. Glucocorticoid (GC), which is often used for the treatment of kidney disease, may enhance bone resorption. We studied the bone resorption state in GC-treated CKD patients and the effects of bisphosphonate on S-NTX. METHODS: We measured S-NTX and creatinine clearance (Ccr) in 48 non-diabetic patients with declining renal function who had never received GC, vitamin D, calcium or bisphosphonate (reference group). Bone markers including S-NTX and BSAP (bone specific alkaline-phosphatase) in 144 patients receiving GC (prednisone equivalent of > or =2.5 mg/day) for more than 6 months (GC-treated group) were measured. We compared the GC-treated group to the reference group in a cross-sectional study. In a longitudinal study, we further followed 55 patients from the GC-treated group, whose Ccr was more than 60 mL/min (CKD stage 1 or 2) for 1 year after 2.5 mg/day of risedronate was commenced. RESULTS: In the reference group, S-NTX was correlated with Ccr (S-NTX = 456.6/Ccr + 4.5, r = 0.797, P < 0.0001). S-NTX values in the GC-treated group were higher than those found in the reference group at any Ccr. We defined the resorption index (RI) as a ratio of measured S-NTX to estimated NTX given by the correlation curve. Whereas BSAP did not change significantly, S-NTX decreased significantly by risedronate treatment. RI decreased from 1.59 (baseline) to 1.54, 1.25 (P < 0.01, versus baseline) and 1.23 (P < 0.01) at 1, 3 and 6 months after the start of therapy, respectively, which means that S-NTX values approached the correlation curve. Percent changes of S-NTX at 3 months were larger in patients with higher pretreatment S-NTX. CONCLUSION: Higher S-NTX in the GC-treated group suggests that bone resorption is enhanced by GC. In CKD patients with mild renal dysfunction, S-NTX is a practical and useful marker for monitoring bone resorption during GC treatment.

Adolescent↗

PubMedDate not supplied

Is there a role for copper in neurodegenerative diseases?

Copper is an essential metal in living organisms; thus, the maintenance of adequate copper levels is of vital importance and is highly regulated. Dysfunction of copper metabolism leading to its excess or deficiency results in severe ailments. Two examples of illnesses related to alterations in copper metabolism are Menkes and Wilson diseases. Several proteins are involved in the maintenance of copper homeostasis, including copper transporters and metal chaperones. In the last several years, the beta-amyloid-precursor protein (beta-APP) and the prion protein (PrP(C)), which are related to the neurodegenerative disorders Alzheimer and prion diseases respectively, have been associated with copper metabolism. Both proteins bind copper through copper-binding domains that also have been shown to reduce copper in vitro. Moreover, this ability to reduce copper is associated with a neuroprotective effect exerted by the copper-binding domain of both proteins against copper in vivo. In addition to a functional link between copper and beta-APP or PrP(C), evidence suggests that copper has a role in Alzheimer and prion diseases. Here, we review the evidence that supports both, the role of beta-APP and PrP(C), in copper metabolism and the putative role of copper in neurodegenerative diseases.

Amyloid beta-Peptides↗

PubMed2005

Methimazole-induced hypothyroidism paradoxically decreases homocysteine.

Clinical hypothyroidism is associated with hyperhomocysteinemia, whereas the opposite is seen in hyperthyroidism. The effects of mild thyroid dysfunction on homocysteine concentrations are not known. We performed the following study to investigate this. Total homocysteine, vitamins B6 and B12, folate, fibrinogen, plasminogen activator inhibitor type 1, and lipids were measured in 11 subjects at baseline and after methionine loading. Subjects began methimazole (MMI), 40 mg daily, and were restudied during 2 stages of hypothyroidism. Liothyronine was added and subjects were restudied once thyrotropin normalized. Methimazole was stopped and studies were repeated during 2 stages of hyperthyroidism. Data were analyzed using repeated-measures analysis of variance. Post-methionine homocysteine decreased in each hypothyroid study compared with baseline (28.8+/-10.7, 27.5+/-9.9 vs 34.4+/-9.2 micromol/L, respectively). In addition, both fasting and post-methionine homocysteine decreased in the euthyroid/MMI study arm compared with baseline despite equivalent thyrotropin values (fasting, 7.5+/-3.0 vs 8.8+/-3.5 micromol/L, P<.05; and post-methionine, 27.2+/-10.6 vs 34.4+/-9.2 micromol/L, P<.05, respectively). Fasting homocysteine decreased in the first hyperthyroidism study arm compared with baseline (6.6+/-2.3 vs 8.8+/-3.5 micromol/L, P<.05) and post-methionine homocysteine decreased in both hyperthyroid arms compared with baseline (25.2+/-8.1, 24.2+/-10 vs 34.4+/-9.2 micromol/L, P<.05 respectively). In conclusion, mild thyroid dysfunction changes homocysteine metabolism. Unexpectedly, our results suggest a homocysteine-lowering effect of MMI.

Adolescent↗

PubMed2005

Synergistic inhibition of respiration in brain mitochondria by nitric oxide and dihydroxyphenylacetic acid (DOPAC). Implications for Parkinson's disease.

The inhibition of mitochondrial respiration by nitric oxide (.NO) at cytochrome c oxidase level has been established as a physiological regulatory mechanism of mitochondrial function. Given, on the one hand, the potential involvement of .NO and dopamine metabolism in mitochondrial dysfunction associated with neurodegeneration and, on the other hand, the reported interaction of .NO with dihydroxyphenylacetic acid (DOPAC), a major mitochondrial-associated dopamine metabolite, we examined the combined effects of .NO and DOPAC on the respiratory chain of isolated rat brain mitochondria. Whereas dopamine or DOPAC induced no measurable effects on the mitochondrial respiration rate, a mixture of .NO with DOPAC inhibited the rate in a way stronger than that exerted by .NO. This effect was noticed with actively respiring (state 3) and resting (state 4) mitochondria. At variance with DOPAC, dopamine failed to potentiate .NO inhibitory effects. The inhibition was dependent on the concentration of both compounds, .NO and DOPAC, and exhibited characteristics similar to those exerted by .NO, namely: it was reversible and dependent on the concentration of oxygen. Analysis of respiratory enzymatic activities demonstrated a selective inhibition at the level of cytochrome c oxidase (complex IV). Insights into the chemical mechanisms underlying the inhibitory effect were inferred from experiments using metmyoglobin (a ligand for .NO and derived species, such as nitroxyl anion) and ferrocyanide (a reductant of .NO, producing nitroxyl anion). Whereas metmyoglobin decreased the inhibition, ferrocyanide potentiated the inhibition. Moreover, a mixture of ferrocyanide with .NO reproduced the effects exerted by the mixture of .NO with DOPAC. The results are consistent with the notion of a reaction of .NO with DOPAC producing a nitric oxide-derived compound(s), which inhibit O2 uptake at the cytochrome oxidase level. Although the mechanism in question remains to be clearly elucidated it is suggested that the .NO/DOPAC-dependent inhibition of cytochrome oxidase may involve nitroxyl anion. The significance of these observations for mitochondrial dysfunction inherent in Parkinson's disease is discussed.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2005

Serotonin-related gene expression in female monkeys with individual sensitivity to stress.

Female cynomolgus monkeys exhibit different degrees of reproductive dysfunction with moderate metabolic and psychosocial stress. In this study, the expression of four genes pivotal to serotonin neural function was assessed in monkeys previously categorized as highly stress resistant (n=3; normal menstrual cyclicity through two stress cycles), medium stress resistant (n=5; ovulatory in the first stress cycle but anovulatory in the second stress cycle), or low stress resistant (i.e. stress-sensitive; n=4; anovulatory as soon as stress is initiated). In situ hybridization and quantitative image analysis was used to measure mRNAs coding for SERT (serotonin transporter), 5HT1A autoreceptor, MAO-A and MAO-B (monoamine oxidases) at six levels of the dorsal raphe nucleus (DRN). Optical density (OD) and positive pixel area were measured with NIH Image software. In addition, serotonin neurons were immunostained and counted at three levels of the DRN. Finally, each animal was genotyped for the serotonin transporter long polymorphic region (5HTTLPR). Stress sensitive animals had lower expression of SERT mRNA in the caudal region of the DRN (P<0.04). SERT mRNA OD in the caudal DRN was positively correlated with serum progesterone during a pre-stress control cycle (P<0.0007). 5HT1A mRNA OD signal tended to decline in the stress-sensitive group, but statistical difference between averages was lacking in analysis of variance. However, 5HT1A mRNA signal was positively correlated with control cycle progesterone (P<0.009). There was significantly less MAO-A mRNA signal in the stress-sensitive group (P<0.007) and MAO-A OD was positively correlated with progesterone from a pre-stress control cycle (P<0.007). MAO-B mRNA exhibited a similar downward trend in the stress-sensitive group. MAO-B OD also correlated with control cycle progesterone (P<0.003). There were significantly fewer serotonin neurons in the stress-sensitive group. All animals contained only the long form of the 5HTTLPR. Thus, all serotonin-related mRNAs examined in the dorsal raphe to date were lower (SERT, MAO-A) or exhibited a lower trend (5HT1A, MAO-B) in the stress sensitive animals, which probably reflects the lower number of serotonin neurons present.

Amenorrhea↗

PubMed1995

Myocardial stunning: a therapeutic conundrum.

Dobutamine and pyruvate are two inotropic agents with different mechanisms of action. Although both agents alter postischemic myocardial dysfunction, their potential metabolic effects in the setting of in vivo myocardial stunning have not been addressed. In this study, the effects of dobutamine and pyruvate on systolic wall thickening, myocardial phosphorylation potential index, interstitial fluid adenosine level, and myocardial oxygen consumption in in vivo stunned porcine myocardium were assessed. Stunning was induced with a 10-minute occlusion of the left anterior descending coronary artery. After 30 minutes of reperfusion, pigs were treated with either intravenous dobutamine (10 micrograms/kg per minute) or intracoronary pyruvate (1 ml/min, 150 mmol/L solution, pH 7.4). Infusion of both agents resulted in a marked improvement in regional systolic wall thickening. The dobutamine effect, however, produced a marked increase in myocardial oxygen consumption and was associated with an increase in interstitial adenosine caused by myocardial de-energization, because the myocardial phosphorylation potential index ratio decreased from 0.17 +/- 0.02 to 0.09 +/- 0.02 (p < 0.05). In contrast, pyruvate enhanced myocardial energy status, because the myocardial phosphorylation potential index ratio increased from 0.20 +/- 0.03 to 0.55 +/- 0.08 (p < 0.01). These experimental findings suggest that under certain circumstances the use of beta-receptor agonists to treat myocardial stunning may be suboptimal, if not undesirable. Further investigation is warranted to determine the optimum therapy for the stunned heart.

Adenosine↗

PubMed1999

In vivo imaging of spontaneous ultraweak photon emission from a rat's brain correlated with cerebral energy metabolism and oxidative stress.

Living cells spontaneously emit ultraweak light during the process of metabolic reactions associated with the physiological state. The first demonstration of two-dimensional in vivo imaging of ultraweak photon emission from a rat's brain, using a highly sensitive photon counting apparatus, is reported in this paper. It was found that the emission intensity correlates with the electroencephalographic activity that was measured on the cortical surface and this intensity is associated with the cerebral blood flow and hyperoxia. To clarify the mechanism of photon emission, intensity changes from whole brain slices were examined under various conditions. The removal of glucose from the incubation medium suppressed the photon emission, and adding 50 mM potassium ions led to temporal enhancement of emission and subsequent depression. Rotenone (20 microM), an inhibitor of the mitochondrial electron transport chain, increased photon emission, indicating electron leakage from the respiratory chain. These results suggest that the photon emission from the brain slices originates from the energy metabolism of the inner mitochondrial respiratory chain through the production of reactive oxygen. Imaging of ultraweak photon emission from a brain constitutes a novel method, with the potential to extract pathophysiological information associated with neural metabolism and oxidative dysfunction of the neural cells.

Animals↗

PubMed2002

Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers synergistically increase coronary blood flow in canine ischemic myocardium: role of bradykinin.

OBJECTIVES: We examined whether the combination of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II receptor blocker (ARB) synergistically mediates coronary vasodilation and improves myocardial metabolic and contractile dysfunction in ischemic hearts. BACKGROUND: Either an ACE inhibitor or ARB mediates coronary vasodilation in ischemic hearts. METHODS: In dogs with myocardial ischemia, we infused an ACE inhibitor (temocaprilat, 10 microg/kg/min) or ARB (RNH-6270, 10 microg/kg/min) into the coronary artery. RESULTS: Perfusion pressure of the left anterior descending coronary artery was reduced from 104 +/- 8 to 42 +/- 2 mm Hg, so that coronary blood flow (CBF) decreased to one-third of the baseline value. Ten minutes after starting the infusion of temocaprilat, the cardiac bradykinin level increased (from 32 +/- 6 to 98 +/- 5 pg/ml). Coronary blood flow (29 +/- 2 to 44 +/- 3 ml/100 g/min) and the cardiac level of nitric oxide (NO) (7.8 +/- 1.9 to 17.5 +/- 3.2 microm) also increased, with these changes being attenuated by either N(omega)-nitro-L-arginine methyl ester or HOE140. RNH-6270 alone caused a modest increase in CBF (34 +/- 3 ml/100 g/min), with no increase in the cardiac NO or bradykinin levels. Both temocaprilat and RNH-6270 caused a further increase in both CBF (51 +/- 4 ml/100 g/min) and cardiac NO levels, without increasing the bradykinin level, and these changes were inhibited by HOE140. In the nonischemic heart, RNH-6270 augmented bradykinin-induced increases in CBF. CONCLUSIONS: The combination of an ACE inhibitor and ARB mediates greater increases in CBF and more potent cardioprotective effects through bradykinin-dependent mechanisms than either drug alone.

Angiotensin II↗

PubMed1991

Rheumatic manifestations of haemochromatosis.

Haemochromatosis (HC) is a group of phenotypically heterogeneous clinical syndromes, which may have a common molecular basis. Classical genetic haemochromatosis (GHC) is one of these syndromes and is a disorder of iron storage due to an increase in intestinal iron absorption, which results in progressive and massive iron deposition leading to fibrosis and organ malfunction. The liver, pancreas, heart and pituitary are commonly involved. There is a specific arthropathy and an association with osteoporosis. Clinically, the arthropathy may resemble rheumatoid arthritis, with acute attacks of inflammation associated with bilateral destruction of the metacarpophalangeal joints. However, bony joint swelling may occur, suggestive of osteoarthritis. Hip arthritis may be unduly severe and disabling. Haemochromatosis arthritis is composed of three radiographic categories: isolated chondrocalcinosis, hypertrophic osteoarthritis which is indistinguishable from pyrophosphate associated arthropathy, and disease specific changes such as subchondral radiolucency of the femoral head, hook-like osteophytes on the metacarpal heads and a degenerative predilection for the metacarpophalangeal joint rather than the scapholunate. The characteristic histological changes are: abnormal amounts of iron deposits, little or no signs of synovial inflammation and CPPD deposition. Subchondral radiolucency of the femoral head and atypical stripping of the cartilage from the subchondral bone are thought to be specific radiographic and histological changes of HC. The pathogenesis of HC arthritis has been associated with the presence of iron in joint tissue, a defect in cartilage metabolism and immunological dysfunction. Treatment has little effect on clinical, radiological or histological progression.

Arthritis↗

PubMed2003

Gastric mucosal-to-end-tidal PCO2 difference during major abdominal surgery: influence of the arterial-to-end-tidal PCO2 difference?

BACKGROUND AND OBJECTIVE: Because gastric mucosal PCO2 must be referenced to arterial values via a gastric-to-arterial PCO2 gap (Pg-aCO2), the gastric-to-end-tidal PCO2 difference (Pg-ETCO2) may be proposed as a surrogate method to monitor Pg-aCO2. However, the influence of arterial-to-end-tidal PCO2 (Pa-ETCO2) on its value remains unknown. Pa-ETCO2 may be enhanced by a low cardiac output and subsequent reduced perfusion of the lungs. This study was designed to compare such gaps observed during abdominal surgery in patients with or without preoperative cardiac dysfunction. METHODS: Haemodynamic, metabolic and tonometric variables were measured in seven patients with Crohn's disease and in five patients with chronic heart failure scheduled for abdominal surgery. Data were collected before skin incision (T0); at extractor placement (T1), 30 (T2) and 60 (T3) min later; at organ extraction (T4), 30 (T5) and 60 (T6) min later, and at the end of surgery (T7). RESULTS: Gradients appeared larger in the cardiac group. The difference was significant for Pg-ETCO2 during the whole study period, while it was only reached at T1-T2 for Pa-ETCO2 and at T5-T6 for Pg-aCO2. Gaps did not change significantly over the peroperative time points in either group. No major haemodynamic variations were registered in either group. CONCLUSIONS: In patients with preoperative chronic heart failure, Pg-ETCO2 remained constant throughout a major general surgical procedure and was only moderately influenced by the Pa-ETCO2 gap. In these patients, Pg-ETCO2 may be used as a reliable index of gastrointestinal perfusion after control of PaCO2.

Abdomen↗