The value of a fabric-coated self-expanding stent in iliac arterial occlusions or aneurysms--the primary and long-term results

The present study focused on the role of catecholaminergic neurons and estrogens on the release of gonadotropins I and II in immature and early vitellogenic female rainbow trout. The ovariectomy-induced increase of GtH I blood levels (from about 10 to 15 ng/ml) was prevented in vitellogenic fish by E2 supplementation. E2 implantation of immature fish decreased blood GtH I levels (from about 6 to 1 ng/ml). Blood levels of GtH II were low (about 0.5 ng/ml) and not altered by ovariectomy and E2 treatment. These data demonstrate that estrogens exert a negative feedback on the release of GtH I in trout. A treatment with alpha-methyl-p-tyrosine (MPT), an inhibitor of catecholamine synthesis, increased blood GtH II levels of sham-operated vitellogenic fish and ovariectomized fish implanted with E2, but had no effects in ovariectomized fish. MPT did not modify blood GtH I levels in any experimental group. A treatment of E2-implanted immature or vitellogenic fish with the dopamine antagonist pimozide also increased blood GtH II levels, but did not significantly change blood GtH I levels. These data demonstrate that release of GtH II, but not of GtH I, depends on an E2-activated DA inhibitory tone.     

The effect of melperon on ocular readaptation time, as assessed by a new recording technique

A new simplified technique recording readaptation time after photo stress, RAT, is described. The psychometric properties in terms of internal consistency and retest reliability were tested, and the effect on RAT after intake of melperon at two different dose levels was investigated and correlated to blood plasma levels. The results show that there was a satisfactory consistency of RAT at each occasion but stability over a 1 month period could not be demonstrated. Significantly dose-dependent changes were recorded after intake of melperon but the prolongation of RAT was not significantly correlated to blood plasma levels.     

Increase in resting levels of superoxide anion in the whole blood of uremic patients on chronic hemodialysis

Recently, we developed a new method to measure the resting level of superoxide anion in whole blood using an ultrasensitive chemiluminescence analyzer and lucigenin amplification. The advantage of this method is that the assay system can be performed in the absence of leukocyte isolation and stimulant administration. In this study, we applied this method to measure the blood resting levels of superoxide anion in 104 uremic patients on chronic hemodialysis (CHD) and 98 sex- and age-matched healthy controls to clarify the influence of HD on blood levels of superoxide anion. Simultaneously, the plasma levels of copper, zinc superoxide dismutase (Cu,Zn-SOD), glutathion peroxidase (GPX), myeloperoxidase (MPO) and lactoferrin (Lacto-F) were measured. The results showed that the basal blood levels of superoxide anion, Cu,Zn-SOD, and MPO in CHD patients were significantly greater than those of healthy controls. However, there was no difference in the basal plasma levels of Lacto-F and GPX between CHD patients and healthy controls. One session of HD further increased the blood levels of superoxide anion, MPO, Lacto-F and Cu,Zn-SOD but not GPX. These results suggest that the blood levels of superoxide anion are higher in CHD patients and further increase after one session of HD. This mechanism should be studied further.     

The importance of lead pollution for pregnant women and the newborn in the Ruhr area. II. Communication (author's transl)

Systematic measurements of blood lead levels in 315 mature and immature neonates and 198 mothers show that at least 40% of statistical variance in blood lead levels depends on lead immission at the mother's place of residence. Almost identical blood lead levels are found in identical and non-identical twins. These investigations demonstrate the value of a biological lead monitoring system. On this basis blood lead levels in areas not covered by the present study can be prognosticated.     

Circulating plasma prekallikrein and tissue kallikrein in normotensive and hypertensive humans: effects of angiotensin II infusion

Kinins lower blood pressure but the stimuli leading to kinin generation and their origin are less well known. We administered angiotensin II in graded infusion doses to patients with primary hypertension and normotensive controls to study the effects of on circulating kallikreins. Angiotensin II infusion did not significantly alter plasma prekallikrein or tissue kallikrein levels and the plasma levels and their changes did not correlate with blood pressure levels or changes. In the normotensive group prekallikrein levels and renin activity correlated negatively with urinary sodium and chloride excretion during basal conditions and partially during the infusion. U-tissue kallikrein concentration increased in the normotensive group. Thus, acute elevation of blood pressure induced by angiotensin II does not activate the circulating kallikrein-kinin systems. Data rather indicate that the circulating kallikrein-kinin systems may be related to alterations in volume and sodium balance and that these mechanisms may be altered in primary hypertension.     

Primary Sj?gren''s syndrome presenting as autonomic neuropathy. Case report

A study conducted at P.G.I., Chandigarh to find out the effect of spinal anaesthesia on arterial blood gases, blood glucose, and pyruvate-lactate during spinal anaesthesia. All patients received night sedation of oral diazepam in dose of 0.2 mg/kg body weight. No narcotic/antisialogogue premedication was given to any patient. All patients received spinal anaesthesia with 5% lignocaine (hyperbaric), in lateral position. All patients received normal saline intravenously as a maintenance fluid. Blood samples for the measurement of blood pyruvate, lactate levels and arterial blood gas analysis were collected preoperatively, 10 minutes after the administration of spinal anaesthesia after fixation of drug, and half hour after the end of operative procedure. Even though there was continued rise in blood sugar levels intraoperatively, which persisted in postoperative period, the values were within normal clinical range. Blood lactate levels and blood pyruvate levels remained unchanged. Hypocapnoea observed intra-operatively in our report is attributed to hyperventilation. There was 12.44% fall in bicarbonate level. (P > .001) which even though statistically significant did not alter the pH. We conclude that spinal anaesthesia up to T8 level does not affect the metabolic processes.     

An epidemiological study of the haemostatic and other effects of oral contraceptives

Factors V, VII and VIII (each determined by biological assay), fibrinogen, platelet count and adhesiveness, and fibrinolytic activity were measured in 234 white pre-menopausal women, of whom 57 (24%) were on oral contraceptives and 177 (76%) were not. Cholesterol, triglyceride and blood pressure levels were also recorded. In 20 of the women on oral contraceptives, and in an age-matched group of 20 who were not, prothrombin, factor X, antithrombin III and alpha 2-macroglobulin levels were determined, and factors VII and VIII were also measured immunologically. For the majority of the variables studied, the differences between those using and not using oral contraceptives were greater in younger than older women; in the case of factor VII (biological assay) and fibrinogen, the differences between the regression slopes on age were statistically significant, and mean values were substantially higher in those on oral contraceptives. There was also a significant difference between regression slopes on age for cholesterol. Mean levels of prothrombin, factors VII (immunological assay) and X, triglycerides and blood pressure were significantly higher, and mean levels of antithrombin III significantly lower, in those on oral contraceptives compared with those not. Overall, fibrinolytic activity was significantly higher in the women on oral contraceptives; this difference was, however, almost entirely due to the greatly increased fibrinolytic activity of the non-smokers on oral contraceptives, activity in the smokers on oral contraceptives being similar to that of the women not on these preparations. There were no significant differences in mean platelet count or adhesiveness, or in haemoglobin, packed cell volume, uric acid and blood sugar levels. Among the women on oral contraceptives, there was a significant negative correlation between factor VIII and fibrinolytic activity; this was largely due to five women all of blood groups A and B, in whom, besides high factor-VIII levels and poor fibrinolytic activity, other variables (e.g. fibrinogen) were raised in a direction that might be expected to favour thrombogenesis. It is possible that it is those women whose fibrinolytic activity does not increase in order to compensate for the effects of oral contraceptives on clotting factors, lipids and blood pressure, who are at special risk of thromboembolic episodes. The differential effects of oral contraceptives by age must be borne in mind in evaluating the effects of these preparations on the haemostatic and lipid systems.     

Mechanisms by which Hange-shashin-to reduces prostaglandin E2 levels

To determine the mechanisms by which Hange-shashin-to (TJ-14) reduces prostaglandin E2 (PGE2) levels, the effects on blood corticosterone levels were examined in vivo and the effects on cyclooxygenase (COX) activity in vitro assessed. TJ-14, orally administered to rats at dose levels between 125 and 1000 mg/kg, caused a dose-dependent increase in blood corticosterone levels. We also showed that Glycyrrhizae Radix and Ginseng Radix, constituents of TJ-14, are involved in the increase in blood corticosterone. The activity of COX-1 was not inhibited by TJ-14 even at a dose of 1000 microg/ml, while COX-2 was inhibited at dose levels between 10 and 1000 microg/ml. The constituents Scutellariae Radix, Glycyrrhizae Radix and Coptidis Rhizoma were believed to be involved in COX-2 inhibition. These results suggest that the effect of TJ-14 in decreasing PGE2 is partially mediated by corticosterone and inhibition of COX-2.     

Renin and aldosterone suppression in the antihypertensive action of clonidine

In 18 hypertensive patients receiving a constant (100 mEq/day) sodium diet, treatment with clonidine (0.3 mg/day for 5 days) decreased blood pressure in 11 patients with high and normal renin levels and 7 with low renin levels. The high and normal renin group had early and rapid reductions in blood pressure and plasma renin activity. In contrast, the low renin group had a more gradual hypotensive response and only a small absolute decrease in plasma renin. For all patients, pretreatment renin levels were related to the initial decrease in blood pressure but not to the reductions measured after 5 days. Thus, two mechanisms of action of clonidine are possible, one related to acute inhibition of the renin-angiotensin system in patients with high and normal renin levels and another that is independent of renin mechanisms and occurs in all hypertensive patients. In six additional patients with high renin levels induced by prior sodium depletion (10 mEq/day sodium diet), clonidine did not reduce blood pressure or renin, thus indicating that the suppressive action of this agent on renin pressor mechanisms occurs only in patients whose elevated renin levels are intrinsic to hypertension and unrelated to sodium depletion. Of the 18 patients receiving a normal sodium diet, 13 were classified as responding to treatment (decrease in both systolic and diastolic pressures of at least 10%). The five nonresponders had greater weight gain and higher values for aldosterone excretion. For all patients, there was a significant correlation between decrements in blood pressure and in aldosterone, suggesting that the countervailing effects of fluid accumulation on blood pressure in nonresponding patients resulted from a failure of aldosterone to be suppressed. Changes in aldosterone, in turn, correlated significantly with changes in renin. Thus, the antirenin effect of clonidine enhances its antihypertensive action not only by acutely ablating renin-angiotensin pressor mechanisms, but also by inhibiting aldosterone production and thereby minimizing longer-term reactive volume retention during treatment.     

Reduction of blood glucose levels in chronically ill Type 2 diabetics by brief biofeedback-assisted relaxation training.

21 chronically ill Type 2 diabetics with multiple symptomatology and poor prognosis, who had been admitted to a rehabilitation hospital, were randomly assigned to 1 of 3 treatment conditions: (1) biofeedback-relaxation (BR), (2) nondirective patient-centered insight therapy (IT), or (3) no-treatment control (NT). Results indicate that BR was effective in reducing Ss' intra-session blood glucose levels. IT and NT (simple feedback of blood glucose levels) were not generally effective in reducing these levels, although much variability occurred. Decreases in blood glucose were noted in IT Ss depending on whether they reported reduction in anxiety by talking about their problems. By the 3rd weekly session, IT Ss were not different than BR Ss in blood glucose reduction. A suggestion of inter-session generalization occurred in BR Ss. All 8 Ss who completed questionnaires at 3-mo follow-up reported that they had their diabetes under control. It is suggested that behavioral techniques that affect emotional states may be useful adjuncts to the medical management of Type 2 diabetes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in proliferating cell nuclear antigen, a protein involved in DNA repair, in vulnerable hippocampal neurons following global cerebral ischemia

Increasing evidence indicates that early low-level lead (Pb) exposure produces enduring cognitive impairment in children, underscoring the need to develop improved therapeutic intervention. Although chelating agents have been shown to effectively reduce body Pb levels, it is not yet known whether this treatment ameliorates Pb-induced cognitive dysfunction. Clinical research in this area is hampered by the need to rely on reductions in blood Pb levels as the index of treatment efficacy, despite the fact that brain Pb level is the exposure parameter of greatest relevance to neurocognitive outcomes. The present studies were designed to provide information that will aid future research in this area in both human and animal models. The objectives of these studies were (1) to evaluate the efficacy of different doses and durations of succimer (meso-2,3-dimercaptosuccinic acid; DMSA) chelation for reducing brain and blood Pb levels and (2) to determine the extent to which blood Pb can serve as a surrogate of brain Pb following chelation. Long-Evans hooded rats were exposed to Pb from birth until day 31 (Study 1) or day 40 (Study 2) of life, followed by oral treatment with a vehicle or one of two succimer regimens for a duration of either 7 or 21 days. Results indicated that 7 days of succimer treatment produced a 1.5- to 2.5-fold greater reduction of Pb in blood than in brain, relative to time-matched vehicle groups. Prolonged treatment (21) days did not further reduce blood Pb levels (relative to 7-day succimer treatment), but did produce further reductions in brain Pb level compared to time-matched vehicle groups. Thus, chelation-mediated reductions in brain Pb did not parallel reductions in blood Pb over the course of treatment. While the relevance of these data to humans may be confounded by anatomical and physiological differences between rodents and primates, as well as differences in the metabolism of succimer (DMSA), they suggest that clinical studies should exercise caution when using blood Pb as an index of the efficacy of chelation treatment for reducing brain Pb levels.     

Maintenance of low screen filtration pressure in blood stored in a new liquid medium: BAGPM

Formation of microaggregates in blood stored in conventional media is reflected by rapidly rising screen filtration pressure (SFP). We show that the BAGPM (bicarbonate, adenine, glucose, phosphate, and mannitol) blood preservation system maintains SFP at near normal levels throughout the storage period of 42 days. Whenever the SFP had a tendency to rise in BAGPM blood, filtration through a routine in-line blood filter reverted SFP back to baseline levels. Blood from the same donors stored in citrate-phosphate-dextrose (CPD) adenine had a rapidly rising SFP by 7 to 14 days of storage. Filtration through the routine blood filter had no effect on the SFP of blood stored in CPD-adenine, CPD, or ACD. BAGPM not only maintains adequate levels of ATP and 2,3-diphosphoglyceric acid (2,3-DPG) during full 42 days of storage but also offers a unique system in which microparticulate material is prevented from forming, with maintenance of low SFP, perhaps because of its low leukocyte, platelet, and fibrinogen content.     

Estrogen and sequential movement.

Normal movement depends in part on the brain's ability to produce and use dopamine, which regulates basal ganglia function. Behavioral, neuroanatomical, and neurophysiological data suggest that the basal ganglia are critical for the performance of sequential movement. Dopaminergic function is modulated by estrogen in animals and in humans. To test the hypothesis that estrogen modulates sequential movement, this study measured the reaction time (RT) and movement time (MT) of 15 women and 10 men in a choice RT task with sequential responses. Higher levels of estradiol in women's blood were associated with faster total movement time (RT plus MT). Testosterone levels in women's blood were not associated with keypressing performance. Hormone levels in men's blood were unrelated to keypressing performance. These results suggest that women's motor performance was affected by hormone levels, and that estrogen may interact with dopaminergic function in women. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Glucose loading and dehydration in the camel

Five female bedouin camels were subjected to large infusions of glucose, both when water was readily available and following 10 days of water deprivation. When the camels were hydrated the extra glucose was readily given off in the urine with only a slight increase in blood levels. Following dehydration, the blood glucose levels increased greatly while the urinary excretion was limited. Dehydration led to decreased blood insulin levels, while glucose infusion led to increased levels. The data show that the acclimatization of the camel to dehydration is not only a question of long-term adaption to desert conditions but that even following acute nonphysiological stress, i.e., glucosuria, excess loss of body water was prevented.     

Predictive neural networks for learning the time course of blood glucose levels from the complex interaction of counterregulatory hormones

Diabetes mellitus is a widespread disease associated with an impaired hormonal regulation of normal blood glucose levels. Patients with insulin-dependent diabetes mellitus (IDDM) who practice conventional insulin therapy are at risk of developing hypoglycemia (low levels of blood glucose), which can lead to severe dysfunction of the central nervous system. In large retrospective studies, up to approximately 4% of deaths of patients with IDDM have been attributed to hypoglycemia (Cryer, Fisher, & Shamoon, 1994; Tunbridge, 1981; Deckert, Poulson, & Larsen, 1978). Thus, a better understanding of the complex hormonal interaction preventing hypoglycemia is crucial for treatment. Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. By simulating the deficiency of single hormonal factors in this regulatory network, we found that the predictive impact of glucagon, epinephrine, and growth hormone secretion, but not of cortisol and norepinephrine, were dominant in restoring normal levels of blood glucose following hypoglycemia.     

Progesterone reduces sympathetic tone without changing blood pressure or fluid balance in men

There is scant information on the effects of progesterone on circulation. Changes in catecholamine levels, blood pressure and transcapillary fluid balance were measured in 12 men before and during administration of natural progesterone (Utrogestan). Before administration, systolic blood pressure was significantly correlated with venous adrenaline (r = 0.67, p = 0.01). There was a significant decrease (p = 0.004) in venous noradrenaline during progesterone administration, and systolic blood pressure was significantly correlated with the arteriovenous difference for noradrenaline (r = 0.66, p = 0.02). Serum progesterone, which attained levels similar to those found in women during the luteal phase, did not significantly alter blood pressure, body weight or intra- to extravascular fluid shift. It is concluded that progesterone may have a direct action by increasing the uptake of noradrenaline from the synaptic cleft or by decreasing the nerve firing rate. Interestingly, the pretreatment finding of a significant correlation between blood pressure and adrenaline was less evident during progesterone administration.     

Diurnal variation and effects of feeding on blood glucose in the giant tiger prawn, Penaeus monodon

Previous studies on crustacea have demonstrated significant diurnal rhythms in blood glucose. However, glucose concentration in the blood of food-deprived Penaeus monodon, held in indoor or outdoor tanks, did not exhibit a diurnal rhythm under photoperiods of 8 h light and 16 h darkness (8L: 16D) or under a 13.5L: 9.5D photoperiod, with simulated or natural full moon conditions. Prawns held on photoperiods of constant light, 20L : 4D, 16L : 8D, 12L : 12D, 8L : 16D, 4L : 20D, or continuous darkness did not have significantly different mean blood glucose levels. Mean blood glucose levels varied between 0.77 and 1.39 mmol/L, depending on conditions. Pronounced and significant increases in blood glucose levels occurred within 20 min of feeding, with peak levels after 100 min. The rise in blood glucose level observed after feeding was independent of the eyestalks, and hence putative crustacean hyperglycaemic hormone, and was not from endogenous carbohydrate stores. Under appropriately controlled conditions, blood glucose concentrations can be used as an index of nutritional status in penaeid prawns.     

Studies of the oxidation of ethanol to acetaldehyde by oxyhemoglobin using fluorigenic high-performance liquid chromatography

We noted a rise in acetaldehyde levels in clinical samples of venous whole blood containing ethanol that did not occur in samples from teetotalers. Experiments were performed to define the mechanism involved in acetaldehyde production. The addition of 0.10% ethanol to whole blood produced an immediate increase in acetaldehyde due to acetaldehyde in the stock solution followed by a subsequent increase that became statistically significant by 48 hr. Separation of blood into components documented that the increase in acetaldehyde was associated with the red cell but not plasma fraction. Incubation of isolated hemoglobin with ethanol produced a rise in acetaldehyde levels. Incubation of oxygenated whole blood with ethanol produced a linear increase in acetaldehyde, whereas nitrogen-exposed blood produced no increase. The rise of acetaldehyde in the presence of ethanol was dependent on the concentration of oxygenated hemoglobin A0. Addition of inhibitors of catalase, alcohol dehydrogenase, and glycolytic enzymes (aminotriazole, azide, pyrazole, sodium fluoride, sodium citrate, and iodoacetate) did not inhibit the rise of acetaldehyde, but addition of the hemoglobin ligand cyanide abolished the rise in acetaldehyde. Kinetic analysis with oxygenated whole blood plus inhibitors revealed a Km of 2.5 mM and Vmax of 1.42 microM/min. We conclude that oxyhemoglobin contributes to the metabolism of ethanol to acetaldehyde. These findings may explain in part the high levels of acetaldehyde found in red cells compared with plasma. The results also have implications for the optimum storage of blood samples for acetaldehyde analysis.     

Hemolytic uremic syndrome as a clinical manifestation of oxidative stress

An examination was made of seventeen children having various stages of the hemolytic uremic syndrome: Stage 1 is the period of an expanded clinical picture of the disease, the patients' condition is grave (anuria, azotemia, severe hemolytic anemia and thrombocytopenia); Stage 2 is the period of recovery. The plasma levels of malonic dialdehyde, dienic conjugates, alpha-tocopherol at the first stage of the disease were considerably higher than the control ones, on recovery there were their reductions though their levels remained higher than the normal levels. The levels of malonic dialdehyde in the red blood cell membranes in ill children were also much higher than those in healthy donors, but at the second stage they decreased, but remained high. The activity of superoxide dismutase in the red blood cells of ill children in the acute period of the disease did not significantly differ from that of donors. At the second stage of the disease there was a significant fall in the activity of red blood cell superoxide dismutase. The activity of catalase in the red blood cells of ill children was thrice higher than in the controls; however, this index decreased during treatment and at the second stage it did not differ from that in the controls. There were no significant differences in the activity of red blood cell superoxide dismutase in donors and ill children. Mechanisms responsible for abnormal plasma and red blood cell peroxidation are considered in the hemolytic uremic syndrome. It is concluded that free radical reactions play a substantial role in the pathogenesis of this abnormality.