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R C Jones

Publications and source records attributed to R C Jones.

At least 55 records · Page 3Linked to original sources

Relationship between motility and oxygen consumption of sperm from the cauda epididymides of the rat.

The oxygen consumption of rat sperm was low (2.7 microL O2 10(8) sperm(-1) h(-1)) in caudal epididymal semen (CES) when stimulation of motility was avoided. The addition of 1 microL of Krebs Ringer phosphate buffer (KRP) to 40 microL of CES (CES:KRP = 40:1) did not activate motility, but stimulated oxygen consumption 2-fold. Inclusion of 1-5 mM glucose, acetate, pyruvate or lactate in the KRP further stimulated respiration rate (up to 4.3-fold) without activating motility, but respiration was reduced when 2-deoxyglucose replaced energy substrates. Inclusion of dibutyryl cAMP (1 mM) activated sperm motility in all samples and stimulated oxygen consumption 2.9-fold. Dilution of CES at the ratio of CES:KRP = 40:1000 also activated sperm motility and stimulated respiration rate 2.9-fold. The combined effect of dibutyryl cAMP and glucose in stimulating respiration was greater than their individual effects. However, the response to cAMP or substrates was not altered by incubation in KRP containing either 0 or 0.5 mM Ca2+. It was concluded that the motility and metabolism of rat epididymal sperm are suppressed in vivo. Respiration can be stimulated by a small (1.025-fold) dilution and further stimulated by the inclusion of energy substrate, without activating motility. However, a larger dilution or inclusion of cAMP activated motility and simultaneously stimulated metabolism, with exogenous substrate being required to stimulate respiration to the maximum rate. This suggests that prior to activation, the rate of oxygen consumption and sperm motility are not coupled.

Acetates↗

The ultrastructure and metabolism of ejaculated tammar wallaby sperm are impaired by swim-up procedures when compared with sperm from the cauda epididymidis.

The metabolism, rate of intracellular accumulation of sugars, motility and ultrastructure of ejaculated tammar sperm were impaired by swim-up into artificial media, particularly when the cells were subsequently exposed to N-acetyl-D-glucosamine (NAG). The inclusion of hyaluronate, serum albumin, catalase or Desferal in swim-up media helped prevent deterioration of sperm motility, but failed to prevent detrimental NAG-induced metabolic and ultrastructural changes. However, the sperm were unavoidably diluted during swim-up into artificial media and their behavioural properties were modified by dilution. Thus, sperm collected from the cauda epididymidis were immotile and their rate of oxygen uptake was low in undiluted caudal epididymal semen (CES). Nevertheless, these sperm were viable, and vigorous motility was induced by 5- to 50-fold dilution in Krebs-Ringer phosphate (KRP). Sperm respiration also dramatically increased with moderate dilution (5- or 15-fold) in KRP, but decreased again at higher rates (50-fold). This suggested that motility and the metabolic properties of tammar sperm are modified both by dilution and on leaving the suppressing conditions of the epididymis. Diluted tammar epididymal sperm also displayed a Pasteur effect, but rapidly lost capacity for motility in an oxygen-depleted atmosphere. It was concluded that swim-up procedures compromise ejaculated tammar sperm by promoting dilution-induced changes. This may alter the permeability of the membrane with loss of the enzymes that process the ammonia generated during the metabolism of NAG in seminal plasma. Subsequent exposure to NAG further promotes ultrastructural damage culminating in loss of viability.

Acetylglucosamine↗

The role of Na+-H+ exchange in fluid and solute transport in the rat efferent ducts.

In vivo microperfusion techniques were used to investigate the role of Na+-H+ exchange in the efferent ducts of the rat. Individual efferent ducts were perfused with a Krebs-Ringer bicarbonate solution (KRB) containing 0, 1, 3, 5 or 7.5 mM amiloride. Concentrations of 1-5 mM amiloride inhibited fluid reabsorption from the efferent ducts in a linear dose-dependent manner with an apparent Km of 3 mM. Inhibition was maximal at 5 mM with reabsorption reduced by about 70 %. The effects of amiloride were completely reversible and there was little effect of amiloride on luminal osmolality and concentrations of Na+, Cl- or K+. It is concluded that Na+-H+ exchange is one of the principal mechanisms responsible for fluid and electrolyte reabsorption in the efferent ducts and offers a means by which the efferent ducts are able to achieve flow-dependent, autoregulated fluid reabsorption.

Amiloride↗

Tumor-associated antigen TA-90 immune complex assay predicts subclinical metastasis and survival for patients with early stage melanoma.

BACKGROUND: TA-90 is a tumor-associated antigen first identified in the urine and sera of patients with metastatic melanoma. In the early stages of disease, TA-90 is present in circulating immune complexes (ICs) that may be detected with an antigen specific enzyme-linked immunosorbent assay (ELISA). In this study, the authors evaluated the efficacy of the TA-90 IC assay in detecting subclinical metastasis of early stage melanoma and predicting the survival of patients with this disease. METHODS: Archival sera were collected preoperatively from 114 patients who underwent wide excision with or without regional lymphadenectomy in the treatment of clinical Stage I melanoma. Sera were analyzed for TA-90 IC in a blinded fashion, and results were correlated with the patient's clinical course as determined by database and chart review. Subclinical metastases were considered present at the time of surgery if the lymphadenectomy specimen was pathologically positive and/or the patient subsequently developed recurrence. RESULTS: The TA-90 IC assay predicted subclinical metastasis in 43 of 56 patients (P < 0.0001), with 14 false-positive and 13 false-negative results. Sensitivity and specificity for the detection of occult metastasis were 77% and 76%, respectively. Positive and negative predictive values were 75% and 77%, respectively. Fifteen of 18 tumor positive regional lymph node basins (83%) and 34 of 46 recurrences (74%) were accurately predicted when considered independently (P < 0.004). Preoperative TA-90 IC status was also highly correlated with survival: 5-year overall and disease free survival rates were 63% and 46%, respectively, for the TA-90 IC positive group, compared with 88% and 82%, respectively, for the TA-90 IC negative group (P=0.0001). A multivariate analysis with standard prognostic variables identified preoperative TA-90 IC status as a strong, independent prognostic factor for both overall and disease free survival. CONCLUSIONS: To the authors' knowledge, TA-90 is the first tumor marker that accurately predicts subclinical metastatic disease and survival for patients with early stage melanoma. For this reason, the TA-90 IC assay has the potential to improve dramatically the prognostic evaluation of patients with this disease. Its role in postoperative risk stratification and early detection of recurrence is being evaluated in a prospective study.

Adult↗

Tamoxifen induces selective membrane association of protein kinase C epsilon in MCF-7 human breast cancer cells.

Tamoxifen, a synthetic antiestrogen, is known for its antitumoral action in vivo; however, it is well accepted that many tamoxifen effects are elicited via estrogen receptor-independent routes. Previously, we reported that tamoxifen induces PKC translocation in fibroblasts. In the present study, we investigated the influence of tamoxifen, and several triphenylethylene derivatives, on protein kinase C (PKC) in MCF-7 human breast cancer cells. As measured by Western blot analysis, tamoxifen elicited isozyme-specific membrane association of PKC-epsilon, which was time-dependent (as early as 5 min post-treatment) and dose-dependent (5.0-20 microM). Tamoxifen did not influence translocation of alpha, beta, gamma, delta or zeta PKC isoforms. Structure-activity relationship studies demonstrated chemical requirements for PKC-epsilon translocation, with tamoxifen, 3-OH-tamoxifen and clomiphene being active. Compounds without the basic amino side chain, such as triphenylethylene, or minus a phenyl group, such as N,N-dimethyl-2-[(4-phenylmethyl)phenoxy]ethanamine, were not active. In vitro cell growth assays showed a correlation between agent-induced PKC-epsilon translocation and inhibition of cell growth. Exposure of cells to clomiphene resulted in apoptosis. Since PKC-epsilon has been associated with cell differentiation and cellular growth-related processes, the antiproliferative influence of tamoxifen on MCF-7 cells may be related to the interaction with PKC-epsilon.

Antineoplastic Agents, Hormonal↗

The specificity of peptides bound to human histocompatibility leukocyte antigen (HLA)-B27 influences the prevalence of arthritis in HLA-B27 transgenic rats.

Human histocompatibility leukocyte antigen B27 is highly associated with the rheumatic diseases termed spondyloarthropathies, but the mechanism is not known. B27 transgenic rats develop a spontaneous disease resembling the human spondyloarthropathies that includes arthritis and colitis. To investigate whether this disease requires the binding of specific peptides to B27, we made a minigene construct in which a peptide from influenza nucleoprotein, NP383-391 (SRYWAIRTR), which binds B27 with high affinity, is targeted directly to the ER by the signal peptide of the adenovirus E3/gp19 protein. Rats transgenic for this minigene, NP1, were made and bred with B27 rats. The production of the NP383-391 peptide in B27(+)NP1(+) rats was confirmed immunologically and by mass spectrometry. The NP1 product displaced approximately 90% of the 3H-Arg-labeled endogenous peptide fraction in B27(+)NP1(+) spleen cells. Male B27(+)NP1(+) rats had a significantly reduced prevalence of arthritis, compared with B27(+)NP- males or B27(+) males with a control construct, NP2, whereas colitis was not significantly affected by the NP1 transgene. These findings support the hypothesis that B27-related arthritis requires binding of a specific peptide or set of peptides to B27, and they demonstrate a method for efficient transgenic targeting of peptides to the ER.

Amino Acid Sequence↗

Sustained pulmonary hypertension and right ventricular hypertrophy after chronic hypoxia in mice with congenital deficiency of nitric oxide synthase 3.

Chronic hypoxia induces pulmonary hypertension and right ventricular (RV) hypertrophy. Nitric oxide (NO) has been proposed to modulate the pulmonary vascular response to hypoxia. We investigated the effects of congenital deficiency of endothelial NO synthase (NOS3) on the pulmonary vascular responses to breathing 11% oxygen for 3-6 wk. After 3 wk of hypoxia, RV systolic pressure was greater in NOS3-deficient than in wild-type mice (35+/-2 vs 28+/-1 mmHg, x+/-SE, P < 0.001). Pulmonary artery pressure (PPA) and incremental total pulmonary vascular resistance (RPI) were greater in NOS3-deficient than in wild-type mice (PPA 22+/-1 vs 19+/-1 mmHg, P < 0.05 and RPI 92+/-11 vs 55+/-5 mmHg.min.gram.ml-1, P < 0.05). Morphometry revealed that the proportion of muscularized small pulmonary vessels was almost fourfold greater in NOS3-deficient mice than in wild-type mice. After 6 wk of hypoxia, the increase of RV free wall thickness, measured by transesophageal echocardiography, and of RV weight/body weight ratio were more marked in NOS3-deficient mice than in wild-type mice (RV wall thickness 0.67+/-0.05 vs 0.48+/-0.02 mm, P < 0.01 and RV weight/body weight ratio 2.1+/-0.2 vs 1.6+/-0.1 mg. gram-1, P < 0.05). RV hypertrophy produced by chronic hypoxia was prevented by breathing 20 parts per million NO in both genotypes of mice. These results suggest that congenital NOS3 deficiency enhances hypoxic pulmonary vascular remodeling and hypertension, and RV hypertrophy, and that NO production by NOS3 is vital to counterbalance pulmonary vasoconstriction caused by chronic hypoxic stress.

Animals↗

Ratio of IgG:IgM antibodies to sialyl Lewis(x) and GM3 correlates with tumor growth after immunization with melanoma-cell vaccine with different adjuvants in mice.

Human melanoma cells (from biopsies and culture) express sialyl-Lewis(x) and sialyl Lewis(a), the ligands for ECAM. These ligands may facilitate tumor progression and metastasis in human cancers. To test whether the antibodies to these ligands inhibit tumor progression, IgG and IgM responses to sLe(x) and sLe(a) were induced in C57BL/6j mice (n = 76) by immunization with human melanoma cells, with or without adjuvants (BCG, MPL, KLH). Control mice were treated with saline or BCG. Tumor growth and antigen expression were monitored after challenge with B16 mouse melanoma cells expressing sLe(x), sLe(a) and the ganglioside GM3. Tumor growth was reduced in mice immunized with BCG alone or cells with BCG or MPL, while tumors in mice receiving cells without adjuvants grew larger than in the control. Augmentation of IgM titers to sLe(x) and GM3 after immunization with BCG, or with cells with BCG or MPL correlated with retarded tumor growth, while increased IgG titers to sLe(x) significantly correlated with aggressive tumor growth in mice immunized with cells without adjuvants. SLe(x), sLe(a) and GM3 were expressed in tumors from mice treated with saline or BCG. SLe(x) expression, in particular, was lost in tumors growing in mice immunized with cells with or without adjuvants. Anti-sLe(x) antibodies may promote or prevent tumor growth by antigenic modulation or by cytotoxic killing of tumor cells. Since early anti-sLe(x) IgM correlated with tumor regression, in contrast to anti-sLe(x) IgG, it may serve as a potential early endpoint for the effectiveness of melanoma vaccines expressing the antigens.

Animals↗

The metabolic properties of spermatozoa from the epididymis of the tammar wallaby, Macropus eugenii.

The utilization of various substrates by sperm from the cauda epididymidis of the tammar was examined because the major naturally occurring sugar in the semen of this species is N-acetyl-D-glucosamine (NAG) and not furctose, as in eutherian mammals. The sperm displayed a high level of endogenous respiration that supported motility for relatively prolonged periods of time in vitro. They also metabolised exogenous 14C-labelled glucose, NAG, sucrose, and acetate through glycolytic and/or oxidative processes to produce lactate and 14CO2 at varying rates. The rate of uptake of NAG by tammar sperm was about four times greater than that of other substrates. Glucose and/or NAG stimulated the rate of oxygen consumption by about 20%, but acetate stimulated oxygen consumption by more than 40%. The most striking findings were that NAG almost completely inhibited the oxidation of glucose and sucrose by the sperm and depressed the uptake of glucose, 3-O-methylglucose, and sucrose. Acetate oxidation also was inhibited by NAG, but only by about 50%. Tammar sperm generated substantial amounts of free glucose during incubation with NAG, but this and the inhibitory effects of NAG on glucose oxidation were not mimicked by rat sperm. It is proposed that tammar sperm fail to oxidise glucose in the presence of NAG because of the rapid cellular uptake of NAG relative to glucose. Also, the intracellular glucose and acetate liberated from NAG would compete with exogenous glucose for processing in the Embden-meyerhof and tricarboxylic acid (TCA) cycle pathways. It is also suggested that tammar sperm oxidise sucrose after extracellular hydrolysis into its glucose and fructose components. The biological implications of these metabolic and transport properties of tammar sperm have as yet to be determined.

Acetates↗

Cyclic-GMP-binding, cyclic-GMP-specific phosphodiesterase (PDE5) gene expression is regulated during rat pulmonary development.

Increased nitric oxide (NO) production plays a critical role in the mammalian pulmonary vascular adaptation to extrauterine life. NO activates soluble guanylate cyclase, increasing intracellular cGMP concentrations, thereby inducing relaxation of vascular smooth muscle. cGMP is inactivated by cyclic nucleotide phosphodiesterases (PDEs). One PDE isozyme, PDE5, specifically hydrolyzes cGMP, is abundant in lung tissues, and modifies the pulmonary vasodilatory response to exogenous NO. To investigate the regulation of PDE5 gene expression during pulmonary development, PDE5 mRNA levels, as well as cGMP-metabolizing PDE enzyme activity, were measured in the lungs of perinatal and adult rats. RNA blot hybridization revealed that PDE5 mRNA was detectable in fetal lung tissue as early as 18.5 d of the 22-d term gestation and reached maximal levels in neonatal lungs. mRNA levels in adult rat lungs were 3-4-fold less than the levels measured in lungs of 1- and 8-d-old rats. Pulmonary cGMP hydrolytic activity in 1-d-old animals was 30-fold greater than the cGMP hydrolytic activity of adult rat lungs. Zaprinast, a specific PDE5 antagonist, inhibited 52 and 56% of cGMP hydrolytic activity in lungs of 1- and 8-d-old rats, respectively, but only 18% of the activity in adult lungs. In situ hybridization revealed that PDE5 mRNA transcripts were present in the vascular smooth muscle cells of neonatal and adult lungs. PDE5 mRNA was also detected in the alveolar walls of neonatal rat lungs. These results demonstrate that the gene encoding PDE5 is abundantly expressed in the lungs of perinatal rats, and is available to participate in the mammalian pulmonary vascular transition to extrauterine life. Extravascular PDE5 gene expression in neonatal lungs suggests a potentially important nonvascular role for this enzyme during pulmonary development.

3',5'-Cyclic-GMP Phosphodiesterases↗

Fluid and electrolyte reabsorption in the ductuli efferentes testis.

The efferent ducts of mammals are a series of ducts that are arranged in parallel and reabsorb most of the fluid released with spermatozoa from the testis. This function is essential for spermatogenesis, and for sperm maturation and storage in the epididymis. There is evidence for the involvement of three major transport processes in the bulk reabsorption of water and low molecular weight solutes from the ducts: active solute transport, passive (presumably paracellular) diffusion and fluid phase endocytosis. A small back-flux into the ducts via anion secretion also appears to occur. Control of fluid reabsorption by the efferent ducts is emerging as a complex process with multiple components. Reabsorption is flow dependent which provides local control of reabsorption with a rapid response to changes in luminal conditions. Sex steroids (oestrogen as well as androgen), but not mineralocorticosteroids, are involved in the chronic control of reabsorption in the ducts. Control of epithelial transport in the efferent ducts appears to be mediated by cAMP and probably other signal transduction systems.

Absorption↗

Evolution of the vertebrate epididymis.

This review examines the structure and function of the extratesticular sperm ducts of vertebrates in terms of their evolutionary development and adaptive significance. The primitive extratesticular duct system of Chondrichthyes is described as an example of the vertebrate archetype. Adaptations of the duct system in higher vertebrates have involved a loss of some structures and specialization of others. The duct system probably evolved as a homeostatic mechanism to facilitate fertilization and some embryological development under conditions protected from the external environment. However, it is argued that the ducts also play an important role in the competition between males to achieve paternity. In vertebrates that practise internal fertilization the ducts are involved in post-testicular maturation and storage of spermatozoa. The biological significance of post-testicular sperm maturation has not been resolved. By contrast, sperm storage is essential in most male vertebrates because of the slow rate of spermatogenesis, particularly in ectotherms. Sperm storage is also important in the competition between males for paternity as it enables a male to mate a 'partner' a number of times during an oestrus in order to reduce the prospect of being cuckolded by another male. The extent of sperm maturation and storage in the epididymis of particular vertebrates depends on the relative roles of the testis and its extragonadal ducts in the competition between males for paternity. These roles depend on a number of factors, including allometric limitations to testis size, metabolic rate and the development of endothermy, and the reproductive strategy of females of the species.

Animals↗

Immune responses in the epididymis: implications for immunocontraception.

In recent years the need to develop vaccines against a variety of sexually transmitted diseases, the desire to treat male infertility and interest in developing alternative contraceptive methods have focused research interest on the immunology of the male reproductive tract. This paper reviews the current state of knowledge of immunity in the male tract. Both physical and immune mechanisms that operate to maintain the blood-testis barrier are discussed with regard to (i) their importance in preventing autoimmune responses against spermatozoa and (ii) how these can be overcome to induce specific immunity in the testis and efferent ducts. The role of both the systemic and mucosal arms of the humoral immune response are discussed both in terms of immune-mediated infertility and the induction of specific immunity. Finally some novel approaches to elicit immunity in the male reproductive tract are discussed.

Animals↗

Remittances and inequality: a question of migration stage and geographic scale.

The impact of migrant remittances on the place of migrant origin is examined using data from a 1988 household study undertaken in central Zacatecas state, Mexico. The focus is on whether remittances tend to increase or to decrease income inequalities. "Interfamilial inequalities are found first to decrease and then to increase as a place's migration experience deepens. Throughout this experience, however, rural incomes improve relative to urban ones, since remittances are targeted to the predominantly rural areas of origin."

Americas↗

Intercondylar notch encroachment following anterior cruciate ligament reconstruction: a prospective study.

Intercondylar notch impingement is a recognized cause of graft failure following anterior cruciate ligament (ACL) reconstruction and typically is attributed to anterior tibial tunnel placement or inadequate notchplasty. This prospective study assessed the incidence and nature of notch regrowth following initial ACL reconstruction. The study population was comprised of 36 patients who underwent ACL reconstruction using a patellar tendon-bone autograft. A 3- to 5-mm notchplasty was performed in all patients, and an intraoperative radiograph was taken confirming proper tunnel placement. Magnetic resonance imaging (MRI) was performed the first week following surgery and again at 6 months. The MRIs were reviewed by two skeletal radiologists to evaluate postoperative notch and graft changes. Of the 36 study patients, 28 (78%) knees showed no evidence of graft impingement as defined by graft indentation and intra-substance edema. The MRIs of 8 (22%) patients showed evidence of graft impingement. Four patients had clinical signs of graft impingement, namely persistent effusion or lack of full extension. Arthroscopically, 3 of these patients demonstrated graft encroachment and impingement by fibrocartilage with areas of immature bone. These results indicate that graft impingement from regrowth of the notch is a clinically relevant phenomenon that could potentially result in late graft demise in the ACL-reconstructed knee.

Adult↗

Tamoxifen activates cellular phospholipase C and D and elicits protein kinase C translocation.

The antiestrogen tamoxifen is widely used for endocrine therapy of breast cancer; however, the mechanisms of estrogen receptor-independent interactions of tamoxifen remain ill defined. Here we examine the effect of tamoxifen on the initial steps of cell signal transduction. To this end, phospholipid metabolism and protein kinase C (PKC) translocation were assessed in CCD986SK human mammary fibroblasts treated with tamoxifen. The addition of tamoxifen resulted in dose-dependent and time-dependent increases in the cellular second messengers phosphatidate (PA) and diacylglycerol (DG). On addition of ethanol to the medium, tamoxifen induced the formation of phosphatidylethanol, demonstrating that tamoxifen activates phospholipase D (PLD). Cellular DG also increased in the presence of ethanol, showing that tamoxifen also activates phospholipase C (PLC). In cells prelabeled with choline and ethanolamine, tamoxifen caused increases in choline, phosphorylcholine, ethanolamine and phosphorylethanolamine. Structure-activity relationship studies for activation of PLD revealed that tamoxifen was the most effective, whereas 4-hydroxy tamoxifen was nearly devoid of activity. Phorbol diesters also activated PLD, but estrogen had no influence. Pretreatment of cells with phorbol dibutyrate (PKC down-regulation protocol) blocked phorbol diester- and tamoxifen-induced PLD activity. Exposure of cells to the PKC inhibitor GF 109203X diminished tamoxifen-induced PLD activity. Addition of tamoxifen to cultures elicited selective membrane association of PKC epsilon. We conclude that tamoxifen exerts considerable extra-nuclear influence at the transmembrane signaling level. These events may contribute to effects beyond the scope of estrogen receptor-dependent actions.

Antineoplastic Agents, Hormonal↗

A simplified intravenous glucose loading protocol for fluorine-18 fluorodeoxyglucose cardiac single-photon emission tomography.

The myocardial uptake of fluorine-18 fluorodeoxyglucose (FDG) has emerged as the most sensitive and specific technique for the assessment of myocardial viability. With the development of FDG single-photon emission tomography (SPET) and dual head coincidence imaging, a hindrance to the widespread clinical use of FDG cardiac imaging is the complexity of the preinjection glucose loading necessary for obtaining interpretable myocardial FDG scans. In a population of 209 patients undergoing dual-isotope single acquisition (DISA) FDG/sestamibi (MIBI) SPET, we describe the improvements in both image quality and time efficiency using a new short, simple glucose/insulin/potassium (GIK) infusion protocol prior to FDG injection as compared to a conventional oral glucose loading protocol. DISA FDG/MIBI SPET scans were performed in 111 nondiabetic patients after oral loading with 50 g of glucose (group 1). Ninety-eight consecutive nondiabetic patients were subsequently scanned following preparation with a fixed-concentration GIK infusion administered at a standardized rate (group 2). A three-point grading scale was used to assess image quality. The time to FDG injection following glucose administration was significantly shorter for the group 2 patients (39.9+/-15.6 min; range 20-105 min) than for the group 1 patients (99.5+/-30.3 min; range 56-270 min) (P<0.0001), representing a 1-h decrease in patient preparation time. More of the group 1 patients (n=30; 27%) required supplemental intravenous boluses of regular insulin than did the group 2 patients (n=13; 13%) (P<0.02). There were more excellent and good quality graded images using the GIK method (group 2) than the more traditional oral loading protocol (group 1) (P<0.02). Nine of 111 scans (8%) in group 1 were uninterpretable, whereas only one of 98 scans (1%) in group 2 was uninterpretable. Standardized infusion of a fixed concentration of GIK prior to FDG administration and continued during myocardial FDG uptake is an effective yet simple method of obtaining consistently good to excellent quality FDG SPET cardiac scans. It is preferable to conventional oral glucose loading due to decreased patient preparation time and improved image quality. The technique is safe and should improve both the clinical use and the cost-effectiveness of FDG SPET imaging for the identification of injured but viable myocardium.

Case-Control Studies↗