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PubMed1993

Tricarboxylic acid cycle activity in postischemic rat hearts.

BACKGROUND: Although myocardial oxidative tricarboxylic acid (TCA) cycle activity and contractile function are closely linked in normal cardiac muscle, their relation during postischemic reperfusion, when contractility often is reduced, is not well defined. METHODS AND RESULTS: To test the hypothesis that oxidative TCA cycle flux is reduced in reperfused myocardium with persistent contractile dysfunction, TCA cycle flux was measured by analyzing the time course of sequential myocardial glutamate labeling during 13C-labeled substrate infusion with 13C nuclear magnetic resonance spectroscopy in beating isolated rat hearts at 37 degrees C. Total TCA cycle flux, indexed by both empirical and mathematical modeling analyses of the 13C data, was not reduced but rather increased in hearts reperfused after 17-20 minutes of ischemia (left ventricular pressure, 73 +/- 5% of preischemic values) compared with flux in developed pressure-matched controls (e.g., total flux, 2.5 +/- 0.4 versus 1.6 +/- 0.1 mumol.min-1.g wet wt-1, respectively; p < 0.01). No TCA cycle activity was detectable by 13C nuclear magnetic resonance in hearts reperfused after 40-45 minutes of ischemia, which lacked contractile recovery and had ultrastructural evidence of irreversible injury. CONCLUSIONS: These results suggest that TCA cycle activity is not persistently decreased in dysfunctional reperfused myocardium after a brief ischemic episode and therefore cannot account for the reduced contractile function at that time.

Animals↗
PubMed2005

Postpartum resumption of ovarian cycling activity in first-calf suckled beef cows exposed to familiar or unfamiliar bulls.

The objective of this experiment was to determine if the proportion of first-calf suckled beef cows that resumed ovulatory cycles and the interval to resumption of ovarian cycling activity differ after exposure to either "unfamiliar" bulls or cows on d 35 postpartum, after exposure to either "familiar" bulls or cows for the first 30-32 d after calving. Fifty AngusxHereford cows were stratified by calving date, calf BW, and calf sex by d 3 postpartum, and assigned to be exposed to familiar epididectomized bulls (BEF; n=25) or familiar mature ovariectomized (OVX) cows (CEF; n=25). On d 35 after calving, 12 BEF cows were assigned to be exposed to unfamiliar bulls (BEU); likewise, 12 CEF cows were assigned to be exposed to unfamiliar OVX cows (CEU). Cows were in their treatments for either 95 d (BEF and CEF) or 60 d (BEU and CEU) during the experiment. Blood samples were collected every third d from the beginning to the end of the experiment. A rise in progesterone concentration of >0.5ng/mL in consecutive samples was used as the criterion for resumption of ovulatory cycles. Exposing cows to bulls on d 5 after calving and then switching a subset of these cows to be exposed to unfamiliar bulls 30-32 d later did not (P>0.10) alter: (1) the proportion of cows that resumed cycling activity; and (2) postpartum interval to resumption of ovarian cycling activity compared to cows exposed to familiar bulls. However, 32% more (P<0.05) cows exposed to bulls (BEF and BEU) resumed cycling activity by approximately 14.8 d before cows that were exposed to OVX cows (CEF and CEU). We conclude that the familiarity of first-calf cows to either bulls or ovariectomized cows, did not affect the postpartum occurrence of cycling activity or the interval from calving to resumption of ovulatory cycles. However, bull exposure, whether familiar or unfamiliar, stimulates first-calf cows to resume ovulatory cycles sooner after calving than if they are not exposed to bulls.

Animals↗
PubMed2001

Keratins and the keratinocyte activation cycle.

In wound healing and many pathologic conditions, keratinocytes become activated: they turn into migratory, hyperproliferative cells that produce and secrete extracellular matrix components and signaling polypeptides. At the same time, their cytoskeleton is also altered by the production of specific keratin proteins. These changes are orchestrated by growth factors, chemokines, and cytokines produced by keratinocytes and other cutaneous cell types. The responding intracellular signaling pathways activate transcription factors that regulate expression of keratin genes. Analysis of these processes led us to propose the existence of a keratinocyte activation cycle, in which the cells first become activated by the release of IL-1. Subsequently, they maintain the activated state by autocrine production of proinflammatory and proliferative signals. Keratins K6 and K16 are markers of the active state. Signals from the lymphocytes, in the form of Interferon-gamma, induce the expression of K17 and make keratinocytes contractile. This enables the keratinocytes to shrink the provisional fibronectin-rich basement membrane. Signals from the fibroblasts, in the form of TGF-beta, induce the expression of K5 and K14, revert the keratinocytes to the healthy basal phenotype, and thus complete the activation cycle.

Humans↗
PubMed1976

Sensitivity to radiation and cycle-active drugs as a function of stem cell compartment repletion.

We have studied the sensitivity of normal mouse hemopoietic tissue to radiation and cycle-active drugs in relation to stem cell compartment repletion. Recovery of erythropoiesis in endogenous spleen colonies, blood reticulocytes, and 30-day survivals were determined in mice after an initial large dose of partial-body irradiation. We found that the normal stem cell compartment is more sensitive to cycle-independent modes of therapy, like radiation and cyclophosphamide, than it is to cycle-active agents like cytosine arabinoside and methotrexate. The depleted stem cell compartment exhibits marked sensitivity to cycle-independent agents but less to cycle-active agents, which, however, suppress its recovery more than they do the normal. The overshoot phase of recovery is relatively resistant to either cycle-independent or cycle-active agents. A reticulocytosis following a reticulocytopenia signals the overshoot phase of stem cell compartment recovery and relatively increased resistance. These findings may prove useful in designing chemotherapy regimens and in anticipating marrow recovery in planning for supportive care in patients with neoplastic disease.

Animals↗
PubMed2005

Luteinizing hormone-releasing hormone fusion protein vaccines block estrous cycle activity in beef heifers.

Two LHRH fusion proteins, thioredoxin and ovalbumin, each containing seven LHRH inserts were tested for their ability to inhibit estrous cycle activity. The objective was to evaluate immune and biological responses from alternating the two fusion proteins in an immunization schedule. One hundred ten heifers were divided equally into 11 groups. Two control groups consisted of either spayed or intact, untreated heifers. Heifers in the other nine groups were immunized on wk 0, 4, and 9. Treatments were immunizations of the same protein throughout or alternating the proteins in different booster sequences. Blood was collected weekly for 22 wk, and serum was assayed for concentrations of progesterone and titers of anti-LHRH. At slaughter, reproductive tracts were removed from each heifer and weighed. Heifers with >or=1 ng/mL of progesterone were considered to have a functional corpus luteum and thus to have estrous cycle activity. All LHRH-immunized groups of heifers had a smaller (P < 0.05) proportion of heifers showing estrous cycle activity after 6 wk than the intact, untreated control group. There was no difference in number of heifers cycling between the immunized groups and the spayed heifers during wk 9 to 22. Anti-LHRH did not differ among immunized groups during wk 1 to 9. Starting at wk 10 and continuing through the conclusion of the study, there was an overall difference among treatment groups for anti-LHRH (P < 0.05). Uterine weights differed among treatments (P < 0.05), with intact control animals having heavier uteri than all other groups (P < 0.05). Uterine weights were negatively correlated with maximum LHRH antibody binding (r = -0.44). In summary, the LHRH fusion proteins were as effective as surgical spaying in suppression of estrous cycle activity, but alternating the two proteins in an immunization schedule did not enhance the immunological or biological effectiveness of the vaccine.

Animals↗
PubMed1996

Uncoupling of contractile function from mitochondrial TCA cycle activity and MVO2 during reperfusion of ischemic hearts.

In this study we determined whether contractile function becomes uncoupled during reperfusion of ischemic hearts from mitochondrial tricarboxylic acid (TCA) cycle activity or myocardial O2 consumption (MVO2). Isolated working rat hearts perfused with buffer containing 1.2 mM palmitate and 11 mM glucose were subjected to 30 min of global ischemia followed by 60 min of aerobic reperfusion. During reperfusion, cardiac work recovered to 26.5 +/- 5.4% (n = 29) of preischemic levels, even though TCA cycle activity, fatty acid beta-oxidation, glucose oxidation, glycolysis, and MVO2 rapidly recovered. As a result, the efficiency of coupling between cardiac work and TCA cycle activity and between cardiac work and mitochondrial respiration decreased during reperfusion. In contrast, coupling of TCA cycle activity to MVO2 during reperfusion recovered to preischemic values. Addition of 1 mM dichloroacetate at reperfusion resulted in a significant increase in both cardiac work and cardiac efficiency during reperfusion. This was associated with a significant decrease in H+ production due to an improved balance between glycolysis and glucose oxidation. These data demonstrate that mitochondrial function and overall myocardial ATP production quickly recover in rat hearts after a 30-min period of global ischemia. However, mitochondrial ATP production is not efficiently translated into mechanical work during reperfusion. This may be due to an imbalance between glycolysis and glucose oxidation, resulting in an increase in H+ production and a decrease in cardiac efficiency.

Adenosine Triphosphate↗
PubMed2004

Rest-activity cycles in childhood and adolescent depression.

OBJECTIVE: To quantify circadian rhythms in rest-activity cycles in depressed children and adolescents. METHOD: Rest-activity cycles were evaluated by actigraphy over five consecutive 24-hour periods in 100 children and adolescents, including 59 outpatients with major depressive disorder (MDD) and 41 healthy normal controls. Total activity, total light exposure, and time spent in light at more than 1,000 lux were averaged over the recording period for each participant. Time series analysis was used to determine the amplitude and period length of circadian rhythms in rest-activity. RESULTS: Overall, adolescents with MDD had lower activity levels, damped circadian amplitude, and lower light exposure and spent less time in bright light than healthy controls. Among children, those with MDD showed lower light exposure and spent less time in bright light, but only depressed girls showed damped circadian amplitude. The sex differences were substantially greater in the MDD group than in the normal control group. CONCLUSIONS: These results confirm damped circadian rhythms in children and adolescents with MDD and highlight the influence of gender and age on these measures.

Activity Cycles↗
PubMed1997

A schizophrenic patient with an arrhythmic circadian rest-activity cycle.

A haloperidol-treated patient with chronic schizophrenia had a near-arrhythmic circadian rest-activity cycle, whereas rhythms of 6-sulphatoxy-melatonin and core body temperature were of normal amplitude and phase-advanced. Sleep electroencephalography measured throughout a 31-h 'constant-bedrest' protocol revealed a phase-delayed sleep-wake propensity cycle, low sleep continuity (ultradian 'bouts'), and very little slow-wave sleep and slow-wave activity (0.75-4.5 Hz). Switching treatment to the atypical neuroleptic clozapine improved both the circadian organization of the rest-activity cycle and the patient's clinical state. This observation can be conceptualized in terms of the two-process model of sleep regulation. High-dose haloperidol treatment may have lowered the circadian alertness threshold, whereas clozapine augmented circadian amplitude (perhaps through its high affinity to dopamine D4 and serotonin 5HT7 receptors in the suprachiasmatic nuclei). Measurement of the circadian rest-activity cycle may be a useful non-invasive method to follow functional consequences of neuroleptic treatment.

Adult↗
PubMed1994

Insulin stimulates glycolysis and pentose cycle activity in bovine microvascular endothelial cells.

Glucose metabolism via the pentose cycle, glycolysis and the Krebs cycle was quantified in bovine microvascular endothelial cells. The major measured end-product of glucose was L-lactate, with relatively small amounts of glucose carbons converted to CO2 and pyruvate. The pentose cycle accounted for less than 4% of the glucose utilized. About 60-70% of the metabolized glucose carbons could not be accounted for by lactate, pyruvate and CO2. Insulin stimulated glycolysis and pentose cycle activity, but had no effect on glucose oxidation via the Krebs cycle. As the pentose cycle is a major source of NADPH which is required for the synthesis of nitric oxide (the endothelium relaxing factor), insulin may play a role in regulating NO generation in endothelial cells by modulating the pentose cycle activity.

Animals↗
PubMed1972

Interrelationship and control of glucose metabolism and lipogenesis in isolated fat-cells. Control of pentose phosphate-cycle activity by cellular requirement for reduced nicotinamide adenine dinucleotide phosphate.

By using inhibitors and stimulators of different metabolic pathways the interdependence of the pentose phosphate cycle and lipogenesis in isolated fat-cells was studied. Rotenone, which is known to inhibit electron transport in the respiratory chain, blocked glucose breakdown at the site of pyruvate dehydrogenase. Consequently, because of the lack of acetyl-CoA, fatty acid synthesis was almost abolished. A concomitant decrease in pentose phosphate-cycle activity was observed. Phenazine methosulphate stimulated pentose phosphate-cycle activity about five- to ten-fold without a considerable effect on fatty acid synthesis. The influence of rotenone on both the pentose phosphate cycle and lipogenesis could be overcome by addition of phenazine methosulphate, indicating that rotenone has no direct effect on these pathways. The decreased rate of the pentose phosphate cycle in the presence of rotenone therefore has to be considered as a consequence of decreased fatty acid synthesis. The rate of glucose catabolism via the pentose phosphate cycle in adipocytes appears to be determined by the requirement of NADPH for lipogenesis. Treatment of cells with 6-aminonicotinamide caused an accumulation of 6-phosphogluconate, indicating an inhibition of 6-phosphogluconate dehydrogenase. The rate of glucose metabolism via the pentose phosphate cycle as well as the rate of fatty acid synthesis, however, was not affected by 6-aminonicotinamide treatment and could still be stimulated by addition of insulin. Since even in cells from starved animals, in which the pentose phosphate-cycle activity is extremely low, no accumulation of 6-phosphogluconate was observed, it is concluded that the control of this pathway is achieved by the rate of regeneration of NADP at the site of glucose 6-phosphate dehydrogenase.

Adipose Tissue↗
PubMed2005

Cardiomyocyte cell cycle activation ameliorates fibrosis in the atrium.

MHC-TGFcys33ser transgenic mice have elevated levels of active transforming growth factor (TGF)-beta1 in the myocardium. Previous studies have shown that these animals develop atrial, but not ventricular, fibrosis. Here we show that atrial fibrosis was accompanied with cardiomyocyte apoptosis. Although similar levels of cardiomyocyte apoptosis were present in the right and left atria of MHC-TGFcys33ser hearts, the extent of fibrosis was more pronounced in the right atrium. Thus, additional factors influence the degree of atrial fibrosis in this model. Tritiated thymidine incorporation studies revealed cardiomyocyte cell cycle activity in left atrial cardiomyocytes, but not in right atrial cardiomyocytes. These observations suggested that cardiomyocyte cell cycle activation ameliorated the severity of atrial fibrosis. To directly test this hypothesis, MHC-TGFcys33ser mice were crossed with MHC-cycD2 mice (which have constitutive cardiomyocyte cell cycle activity in the right atrium). Mice inheriting both transgenes exhibited right atrial cardiomyocyte cell cycle activity and a concomitant reduction in the severity of right atrial fibrosis, despite the presence of a similar level of cardiomyocyte apoptosis as was observed in mice inheriting the MHC-TGFcys33ser transgene alone. These data support the notion that cardiomyocyte cell cycle induction can antagonize fibrosis in the myocardium.

Animals↗
PubMed1976

Physiology and metabolism of pathogenic neisseria: tricarboxylic acid cycle activity in Neisseria gonorrhoeae.

Tricarboyxlic acid cycle activity was examined in Neisseria gonorrhoeae CS-7. The catabolism of glucose in N. gonorrheae by a combination of the Entner-Doudoroff and pentose phosphate pathways resulted in the accumulation of acetate, which was not further catabolized until the glucose was depleted or growth became limiting. Radiorespirometric studies revealed that the label in the 1 position of acetate was converted to CO2 at twice the rate of the label in the 2 position, indicating the presence of a tricarboxylic acid cycle. Growth on glucose markedly reduced the levels of all tricarboxylic acid cycle enzymes except citrate synthase (EC 4.1.3.7). Extracts of glucose-grown cells contained detectable levels of all tricarboxylic acid cycle enzymes except aconitase (EC 4.2.1.3), isocitrate dehydrogenase (EC 1.1.1.42), and a pyridine nucleotide-dependent malate dehydrogenase (EC 1.1.1.37). Extracts of cells capable of oxidizing acetate lacked only the pyridine nucleotide-dependent malate dehydrogenase. In lieu of this enzyem, a particulate pyridine nucleotide-independent malate oxidase (EC 1.1.3.3) was present. This enzyme required flavin adenine dinucleotide for activity and appeared to be associated with the electron transport chain. Radiorespirometric studies utilizing labeled glutamate demonstrated that a portion of the tricarboxylic acid cycle functioned during glucose catabolism. In spite of the presence of all tricarboxylic acid cycle enzymes, N. gonorrhoeae CS-7 was unable to grow in medium supplemented with cycle intermediates.

Acetates↗
PubMed2006

Connecting cell-cycle activation to neurodegeneration in Drosophila.

Studies in cell-culture systems and in postmortem tissue from human disease have suggested a connection between cell-cycle activation and neurodegeneration. The fruit fly Drosophila melanogaster has recently emerged as a powerful model system in which to model neurodegenerative diseases. Here we review work in the fly that has begun to address some of the important questions regarding the relationship between cell-cycle activation and neurodegeneration in vivo, including recent data implicating cell-cycle activation as a downstream effector of tau-induced neurodegeneration. We suggest how powerful research tools in Drosophila might be utilized to approach fundamental questions that remain.

Animals↗
PubMed1996

Suppression of TCA cycle activity in the cardiac muscle cell by hydroperoxide-induced oxidant stress.

Excess H2O2 contributes to myocardial reperfusion injury. We detail the effect of H2O2-induced oxidant stress on the tricarboxylic acid (TCA) cycle in isolated heart muscle cells. Cardiomyocyte exposure to bolus H2O2 ( > 50 microM) acutely suppressed TCA cycle activity. Loss of cardiomyocyte TCA cycle function on cellular H2O2 exposure was supported by the rapid in situ inactivation of aconitase along with cardiomyocyte membrane peroxidation. Without peroxidation, the loss of aconitase catalysis was itself sufficient to jeopardize TCA cycle activity. Only H2O2 dismutation completely preserved both cardiomyocyte aconitase activity and TCA cycle flux during H2O2 overload. Restoration of aconitase catalysis after alleviation of the oxidant insult was prohibited by cell-permeable metal chelators, and TCA cycle flux could not be reestablished in peroxidized cells, even if aconitase activity had recovered. The characteristics of aconitase inactivation-reactivation observed are consistent with adverse redox changes to the enzyme's (Fe-S) cluster. These data demonstrate that specific aspects of the TCA cycle in heart muscle are sensitive to H2O2-induced oxidative stress and identify a peroxidative component of the injury process.

Acetate-CoA Ligase↗
PubMed2002

Volitional lifestyle in healthy elderly: its relevance to rest-activity cycle, nocturnal sleep, and daytime napping.

Sleep-related problems are prevalent among the aged. The present study examined the influence of a mentally active or "volitional" lifestyle on the rest-activity cycle, nocturnal sleep, and daytime napping in the healthy elderly. 14 aged individuals with a high Volitional lifestyle (M = 74.1 yr. old) and 14 with a Low Volitional lifestyle (M = 73.0 yr. old) were screened by questionnaires including the Philadelphia Geriatric Center Morale scale and the Self-confidence scale. Their activity levels were monitored by a wrist actigraph system for 14 consecutive days. They were also asked to record daily sleep logs. The total times of nocturnal sleep and daytime napping did not differ between the groups. However, the acrophases of circadian (tau = 24 hr.) and circasemidian (tau = 12 hr.) activity cycles were more advanced in the Low Volitional group. In addition, the High Volitional group took a daytime nap with a better timing than did the Low Volitional group: the former started a nap during the phase in which their activity level was going down, whereas the latter when their activity level was going up. These results suggest that high volitional lifestyle may be related to better rest-activity cycle in the healthy elderly.

Aged↗
PubMed1997

Evidence that cutaneous carcinogen-initiated epithelial cells from mice are quiescent rather than actively cycling.

The basal layer of the epidermis and hair follicles is composed of actively cycling, transit-amplifying cells and quiescent cells including stem cells. To determine which population is the target of carcinogenic chemicals, we treated CD-1 female mice topically with 5-fluorouracil (5-FU), an agent known to kill cycling but not quiescent cells, to probe the origin of the neoplastic lesions. We first determined that 5-FU kills cycling cells in the epidermis. Treatment of mice at 59 days of age (when in anagen 1) with topical 5-FU delayed hair regrowth by 10 days compared to vehicle-treated controls, suggesting that 5-FU killed the cells in anagen. Moreover, 5-FU suppressed the usual hyperplastic response of the epidermal cells to treatment with 12-O-tetradecanoylphorbol-13-acetate. 5-FU reduced the number of epidermal basal cells counted in cross-sections of skin and suppressed DNA synthesis. Approximately 50% of mice treated with 5-FU developed, within 1 week of treatment, a sloughing of the epidermis persisting for 3 weeks, followed by complete healing. Despite the evidence of cell killing in the epidermis and lower hair follicles, in a carcinogenesis experiment where 5-FU or vehicle was applied following tumor initiation with 7,12-dimethylbenz[a]anthracene, the papilloma and carcinoma responses were virtually identical whether or not the mice were treated with 5-FU, suggesting that the tumors arose from quiescent, rather than actively cycling, epidermal cells. When 5-FU was applied before initiation, the papilloma but not the carcinoma responses were slightly but significantly reduced relative to controls. These results are consistent with the hypothesis that the quiescent rather than the rapidly proliferating cells are the targets of tumor initiation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Decline in long-term circadian rest-activity cycle organization in a patient with dementia.

Continuous measurement of the circadian rest-activity cycle for 598 days in a demented patient with probable Alzheimer's disease revealed slow progressive changes in temporal organization until death. Circadian and sleep analysis of the actigraphic data provided objective documentation of the gradual insertion of wakefulness into rest and rest into wake periods. Pacing, a nonphotic zeitgeber strengthening, led to improved synchronization of the rest-activity cycle.

Aged↗