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PubMed1999

Electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry.

The basic principles and recent advances in electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry are reviewed. A brief history of electrospray ionization is provided, along with a complete technical description of the technique, electrospray ionization variations, and advantages. Next, the fundamental principles of Fourier transform ion cyclotron resonance mass spectrometry are covered, including ion cyclotron motion, ion cyclotron resonance excitation, and image current detection. Instrumentation and methods used to couple these techniques are then described. Topics include ion source configuration, ion transport through a strong magnetic field gradient, and ion trapping methods. The article concludes with selected applications that highlight the strengths of electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry.

Animals↗
PubMed2005

Ionizing radiation activates late herpes simplex virus 1 promoters via the p38 pathway in tumors treated with oncolytic viruses.

Ionizing radiation potentiates the oncolytic activity of attenuated herpes simplex viruses in tumors exposed to irradiation at specific time intervals by inducing higher virus yields. Cell culture studies have shown that an attenuated virus lacking the viral gamma(1)34.5 genes underproduces late proteins whose synthesis depends on sustained synthesis of viral DNA. Here we report that ionizing radiation enhances gene expression from late viral promoters in transduced cells in the absence of other viral gene products. Consistent with this result, we show that in tumors infected with the attenuated virus, ionizing radiation increases 13.6-fold above baseline the gene expression from a late viral promoter as early as 2 hours after virus infection, an interval too short to account for viral DNA synthesis. The radiation-dependent up-regulation of late viral genes is mediated by the p38 pathway, inasmuch as the enhancement is abolished by p38 inhibitors or a p38 dominant-negative construct. The p38 pathway is not essential for wild-type virus gene expression. The results suggest that ionizing radiation up-regulates late promoters active in the course of viral DNA synthesis and provide a rationale for use of radiation to up-regulate cytotoxic genes introduced into tumor cells by viral vectors for cytoreductive therapy.

Animals↗
PubMedDate not supplied

Effect of ionizing radiation on partial seizures attributable to malignant cerebral tumors.

Empirical evidence in the clinical literature suggests that ionizing radiation influences human epileptic behavior. A group of patients with tumor-associated epilepsy, biopsy-proven malignancy, and primary antineoplastic treatment with ionizing radiation was selected to evaluate this observation. The antiepileptic effect of ionizing radiation was examined in 9 patients presenting with malignant cerebral tumor and medically refractory partial seizures during at least 2 months. Tissue diagnosis was obtained by stereotactic biopsy without further surgery. Histological categories included anaplastic astrocytoma (5 cases), glioblastoma (2), lymphoma (1), and metastatic non-small cell carcinoma of the lung (1). All patients had medically refractory simple partial seizures with or without secondary generalization with frequencies of 3/week to 8/day for 2-7 months before completion of therapy. Fractionated radiation therapy by parallel opposed fields was delivered with a cumulative dose range of 3,000-6,600 cGy. One patient also had 125I brachytherapy with implant removal after 6 months. Five patients had a seizure-free outcome for periods lasting 2-12 months, whereas the remainder experienced a reduction in frequency of greater than 75% during a follow-up period of 3 months to 6 years. One patient with a glioblastoma remained seizure-free for 3 months and experienced 2 generalized seizures during tumor progression and clinical deterioration but otherwise remained under good anticonvulsant control until his death after 1 year. This review of cases of partial seizures attributable to an unresected malignant cerebral tumor indicates that ionizing radiation may have a favorable effect upon medically refractory partial seizures with significant reduction or elimination of seizures. Moreover, the effect lasts beyond the immediate and early postradiation period. The therapy may thus also lessen the propensity for cerebral tissue towards later epileptogenicity that gives rise to a partial seizure disorder.

Adolescent↗
PubMed1987

Depressor effects of ionized calcium infusion in essential hypertension.

The circulatory effects of an acute increase in serum ionized calcium were assessed in 27 patients with mild to moderate hypertension. Following a control period of fifteen minutes with confirmed circulatory variables, 1,375 mg calcium gluconate was infused over three minutes. Systemic mean arterial blood pressure and heart rate were recorded before, at one-minute intervals during, and for five minutes following the infusion. There was a brief increase of serum ionized calcium concentration (from 1.28 +/- 0.06 mmol/liter to 1.42 +/- 0.07 mmol/liter; p less than 0.001) maximum by one minute after infusion with return toward control by a further four minutes. This was accompanied by a significantly decreased mean arterial blood pressure (from 117 +/- 8 mmHg to 110 +/- 9 mmHg at three minutes; p less than 0.05) and heart rate (from 70 +/- 11 min-1 to 63 +/- 10 min-1 at three minutes; p less than 0.01). There was a significant correlation between the change in ionized calcium and that of the systemic arterial blood pressure (r = 0.68; p less than 0.01). No major side effects were recorded. The blood pressure reduction may theoretically be related to increased membrane stabilization of vascular smooth muscle cells, the acute increase in extracellular ionized calcium impairing calcium ions influx.

Adult↗
PubMed1984

Ionization with diclofenac sodium in rheumatic disorders: a double-blind placebo-controlled trial.

A double-blind randomized study was performed to compare ionization with diclofenac sodium (150 mg) and ionization with saline solution in two groups of patients with scapulo-humeral periarthritis or elbow epicondylitis. The subjects of both groups were treated with 20 ionization sessions each lasting 30 minutes during a 1-month period. There was a significantly greater improvement in pain at rest, pain on pressure, pain on movement and joint swelling in the eleven patients treated with diclofenac compared with the thirteen placebo-treated patients, but no significant differences between the two treatments as regards functional impairment. However, placebo treatment produced a slight but significant improvement in pain on pressure, pain on movement and functional impairment. Further studies are needed to assess the relative role of the current and of autosuggestion in saline ionization response since both have well-known therapeutic effects on chronic rheumatic pain.

Adult↗
PubMedDate not supplied

Caspase-3 is dually regulated by apoptogenic factors mitochondrial release and by SAPK/JNK metabolic pathway in leukemic cells exposed to etoposide-ionizing radiation combined treatment.

Ionizing radiation induces a series of multiple intracellular events which can lead to activation of caspases, cytoplasmic proteases involved in the occurrence of apoptosis. The response of leukemic cells to ionizing radiation is amplified when they have been pre-treated with the anticancer drug etoposide, therefore the aim of this work has been to establish the lowest etoposide concentration combined with the lowest ionizing radiation dose to obtain the best antineoplastic response. Two leukemic cell lines, HL-60 and Jurkat, employed in this study demonstrated different sensitivities to ionizing radiation and to etoposide treatment, with Jurkat T cells requiring a higher dose (1 microM) to display cell cycle perturbation and apoptotic DNA damage similar to those seen in HL-60. We hypothesize that this kind of response could be mediated by mitochondrial release of apoptogenic factors and by SAPK/JNK metabolic pathway activation, both leading to caspase-3 cleavage. All in all these results provide insight into the sensitivity or resistance of leukemic cells to antineoplastic agents and identify molecular targets for rational therapeutic intervention strategies.

Antineoplastic Agents, Phytogenic↗
PubMed2002

Identification of essential ionizable groups and evaluation of subsite affinities in the active site of beta-D-glucosidase F1 from a Streptomyces sp.

Partial amino acid sequences, the essential ionizable groups directly involved in catalytic reaction, and the subsite structure of beta-D-glucosidase purified from a Streptomyces sp. were investigated in order to analyze the reaction mechanism. On the basis of the partial amino acid sequences, the enzyme seemed to belong to the family 1 of beta-glucosidase in the classification of glycosyl hydrolases by Henrissat (1991). Dependence of the V and Km values on pH, when the substrate concentration was sufficiently lower than Km, gave the values of 4.1 and 7.2 for the ionization constants, pKe1 and pKe2 of essential ionizable groups 1 and 2 of the free enzyme, respectively. When the dielectric constant of the reaction mixture was decreased in the presence of 10% methanol, the pKe1 and pKe2, values shifted to higher, to +0.60 and +0.35 pH unit, respectively. The findings supported the notion that the essential ionizable groups of the enzyme were a carboxylate group (-COO-, the group 1) and a carboxyl group (-COOH, the group 2). The subsite affinities Ai's in the active site were evaluated on the basis of the rate parameters of laminarioligosaccharides. Subsites 1 and 2 having positive Ai values (A1 was 1.10 kcal/mol and A2 was 4.98 kcal/mol) were considered to probably facilitate the binding of the substrate to the active site. However, the subsites 3 and 4 showed negative Ai values (A3 was -0.21 kcal/mol and A4 was -2.8 kcal/mol).

Algorithms↗
PubMed2005

Ionizing radiation and chronic lymphocytic leukemia.

The U.S. government recently implemented rules for awarding compensation to individuals with cancer who were exposed to ionizing radiation while working in the nuclear weapons complex. Under these rules, chronic lymphocytic leukemia (CLL) is considered to be a nonradiogenic form of cancer. In other words, workers who develop CLL automatically have their compensation claim rejected because the compensation rules hold that the risk of radiation-induced CLL is zero. In this article we review molecular, clinical, and epidemiologic evidence regarding the radiogenicity of CLL. We note that current understanding of radiation-induced tumorigenesis and the etiology of lymphatic neoplasia provides a strong mechanistic basis for expecting that ionizing radiation exposure increases CLL risk. The clinical characteristics of CLL, including prolonged latency and morbidity periods and a low case fatality rate, make it relatively difficult to evaluate associations between ionizing radiation and CLL risk via epidemiologic methods. The epidemiologic evidence of association between external exposure to ionizing radiation and CLL is weak. However, epidemiologic findings are consistent with a hypothesis of elevated CLL mortality risk after a latency and morbidity period that spans several decades. Our findings in this review suggest that there is not a persuasive basis for the conclusion that CLL is a nonradiogenic form of cancer.

Eligibility Determination↗
PubMed1998

DNA-dependent protein kinase does not play a role in adaptive survival responses to ionizing radiation.

We previously demonstrated that exposure of certain human tumor cells to very low chronic doses of ionizing radiation led to their enhanced survival following exposure to subsequent high doses of radiation. Survival enhancement due to these adaptive survival responses (ASRs) ranged from 1.5-fold to 2.2-fold in many human tumor cells. Furthermore, we showed that ASRs result from altered G1 checkpoint regulation, possibly mediated by overexpression of cyclin D1, proliferating cell nuclear antigen (PCNA), and the X-ray induction of cyclin A. Because cyclin D1 and PCNA proteins are components of many DNA synthetic and repair processes in the cell, we tested the hypothesis that preexposure of cells to low doses of ionizing radiation enabled activation of the DNA repair machinery needed for survival recovery after high-dose radiation. We examined the role of DNA break repair in ASRs using murine cells deficient (i.e., severe combined immunodeficiency [SCID] cells) or proficient (i.e., parental mouse strain [CB-17] cells) in DNA-dependent protein kinase catalytic subunit (DNA-PKcs) expression and DNA double-strand break repair, DNA-PKcs is a nuclear serine/threonine protein kinase that is activated by DNA breaks and plays a key role in double-strand break repair. DNA-PKcs also phosphorylates several nuclear DNA-binding regulatory transcription factor proteins (e.g., Sp1 and p53), which suggests that DNA-PKcs may play a role in regulating transcription, replication, and recombination as well as DNA repair, after radiation. Therefore, we exposed confluent SCID or CB-17 cells to low priming doses of ionizing radiation (i.e., 5 cGy) and compared the survival responses of primed cells to those of unprimed cells after an equitoxic high-dose challenge. Low-dose-primed SCID or CB-17 cells demonstrated 2-fold enhanced survival after a high-dose challenge compared to that of unprimed control cells. These data suggest that expression of the catalytic subunit of DNA-PKcs (expressed in CB-17 not SCID cells) and the presence of active double-strand break repair processes (active in CB-17, deficient in SCID cells) do not play a major role in ASRs in mammalian cells. Furthermore, we present data that suggest that DNA-PKcs plays a role in the regulation of the G2/M cell cycle checkpoint following extremely high doses of ionizing radiation.

Adaptation, Physiological↗
PubMed2004

A non-lensed fiber-optic resonance-enhanced multiphoton ionization probe.

We have developed a miniature fiber-optic probe with no focusing optics for in situ analysis of volatile organic compounds (VOCs). The probe uses an optical fiber to transmit a laser pulse to a vapor sample causing it to ionize adjacent to the fiber tip through a resonance-enhanced multiphoton ionization (REMPI) process. The distal end of the optical fiber is contained co-axially within 2-mm-inner-diameter stainless steel tubing that serves as an electrode. The electrode is biased at a high positive potential to collect electrons. The current generated is shown to be proportional over about two orders of magnitude to the concentration of the species ionized. Visible wavelength REMPI spectroscopy is used to determine probe sensitivities of 20 ppb (benzene) and 43 ppb (toluene). Designing the probe without focusing optics specifies an achromatic ionization region constant in size and position as the laser wavelength is scanned, which simplifies data collection and reduction. Focusing achromatic systems are discussed and the potential signal improvement is estimated.

Journal Article↗
PubMedDate not supplied

Magnesium in disease: a review with special emphasis on the serum ionized magnesium.

This review deals with the six main clinical situations related to magnesium or one of its fractions, including ionized magnesium: renal disease, hypertension, pre-eclampsia, diabetes mellitus, cardiac disease, and the administration of therapeutic drugs. Issues addressed are the physiological role of magnesium, eventual changes in its levels, and how these best can be monitored. In renal disease mostly moderate hypermagnesemia is seen; measuring ionized magnesium offers minimal advantage. In hypertension magnesium might be lowered but its measurement does not seem relevant. In the prediction of severe pre-eclampsia, elevated ionized magnesium concentration may play a role, but no unequivocal picture emerges. Low magnesium in blood may be cause for, or consequence of, diabetes mellitus. No special fraction clearly indicates magnesium deficiency leading to insulin resistance. Cardiac diseases are related to diminished magnesium levels. During myocardial infarction, serum magnesium drops. Total magnesium concentration in cardiac cells can be predicted from levels in sublingual or skeletal muscle cells. Most therapeutic drugs (diuretics, chemotherapeutics, immunosuppressive agents, antibiotics) cause hypomagnesemia due to increased urinary loss. It is concluded that most of the clinical situations studied show hypomagnesemia due to renal loss, with exception of renal disease. Keeping in mind that only 1% of the total body magnesium pool is extracellular, no simple measurement of the real intracellular situation has emerged; measuring ionized magnesium in serum has little added value at present.

Diabetes Mellitus↗
PubMedDate not supplied

Non-ionizing electromagnetic radiation: a study of carcinogenic and cancer treatment potential.

Non-ionizing electromagnetic radiation (NIEMR), particularly the magnetic field component, has been implicated in the development of human neoplasia. Research suggests that if these fields are part of the carcinogenic pathway, they may act as a promoter or in the progression of established cancer. Active progression of cancer cells by NIEMR negate the possible early detection of clinically silent neoplasms. We have observed the effect of non-ionizing electromagnetic fields on an established breast carcinoma cell line MCF-7, and found no stimulation of growth when exposed to a low-frequency magnetic field. The same magnetic field has been used as an adjuvant to anti-neoplastic chemotherapeutic agents. The results of this study have shown an improvement in the neoplastic cell kill by antineoplastic chemotherapy when coupled with a low frequency magnetic field. Non-ionizing electromagnetic radiation may be involved in the carcinogenic process; however, the answer to this question awaits further studies. We are exploring new methods of cancer treatment using non-ionizing electromagnetic radiation.

Animals↗
PubMed2002

Effects of combined photodynamic therapy and ionizing radiation on human glioma spheroids.

The effects of combined photodynamic therapy (PDT) and ionizing radiation are studied in a human glioma spheroid model. The degree of interaction between the two modalities depends in a complex manner on factors such as PDT irradiation fluence, fluence rate and dose of ionizing radiation. It is shown that gamma radiation and PDT interact in a synergistic manner only if both light fluence and gamma radiation dose exceed approximately 25 J cm(-2) and 8 Gy, respectively. Synergistic interactions are observed only for the lower fluence rate (25 mW cm(-2)) investigated. The degree of interaction appears to be independent of both sequence and the PDT or ionizing radiation time intervals investigated (1 and 24 h). Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assays show that low-fluence rate PDT is very efficient at inducing apoptotic cell death, whereas neither high-fluence rate PDT nor ionizing radiation produces significant apoptosis. Although the mechanisms remain to be elucidated, the data imply that the observed synergism is likely not due to gamma-induced cell cycle arrest or to PDT-induced inhibition of DNA repair.

Brain Neoplasms↗
PubMedDate not supplied

Counseling patients exposed to ionizing radiation during pregnancy.

Health physicists and knowledgeable clinicians have the responsibility to counsel women of reproductive age about the reproductive risks of ionizing radiation exposure before conception or during pregnancy. It is important to realize that lay individuals have many misconceptions about the reproductive risks of ionizing radiation. Many patients who have already had or will undergo some type of radiological test are apprehensive about the reproductive and developmental risks of diagnostic radiological procedures. Epidemiological studies and animal studies indicate that high exposures of ionizing radiation can cause miscarriage, congenital malformations, growth retardation, stillbirth, and cancer. With the exception of cancer, there are threshold exposures for those outcomes, with exposures below certain radiation doses not increasing the reproductive or developmental risks. The threshold exposure for birth defects at the most sensitive stage of development is 0.2 Gy, and the threshold for growth retardation and miscarriage is even higher. However, embryonic loss can occur from low exposures during the preimplantation and presomite stages of development ("the all or none period"). This is a stage when the embryo is more likely to die than survive malformed. The most sensitive period for the induction of mental retardation is from the 8th week to the 15th week of gestation. The threshold for deterministic effects increases after early organogenesis and also as the exposure is protracted, e.g., with radionuclides or multiple radiological procedures. Awareness that the threshold dose for developmental effects increases as the fetus develops complicates counseling because we do not have definitive data on threshold exposures at all stages of gestation. Ionizing radiation exposures prior to pregnancy represent a very low risk for the increased incidence of genetic disease in the offspring of the parents who have had radiation exposures to the ovary or testes. Counseling patients requires knowledge of embryology, genetics, radiation teratology, and the principles of teratology in order for the counselor to provide sympathetic, accurate, scholarly advice.

Abnormalities, Radiation-Induced↗
PubMed2000

Glucose-6-phosphate dehydrogenase and the oxidative pentose phosphate cycle protect cells against apoptosis induced by low doses of ionizing radiation.

The initial and rate-limiting enzyme of the oxidative pentose phosphate shunt, glucose-6-phosphate dehydrogenase (G6PD), is inhibited by NADPH and stimulated by NADP(+). Hence, under normal growth conditions, where NADPH levels exceed NADP(+) levels by as much as 100-fold, the activity of the pentose phosphate cycle is extremely low. However, during oxidant stress, pentose phosphate cycle activity can increase by as much as 200-fold over basal levels, to maintain the cytosolic reducing environment. G6PD-deficient (G6PD(-)) cell lines are sensitive to toxicity induced by chemical oxidants and ionizing radiation. Compared to wild-type CHO cells, enhanced sensitivity to ionizing radiation was observed for G6PD(-) cells exposed to single-dose or fractionated radiation. Fitting the single-dose radiation response data to the linear-quadratic model of radiation-induced cytotoxicity, we found that the G6PD(-) cells exhibited a significant enhancement in the alpha component of radiation-induced cell killing, while the values obtained for the beta component were similar in both the G6PD(-) and wild-type CHO cell lines. Here we report that the enhanced alpha component of radiation-induced cell killing is associated with a significant increase in the incidence of ionizing radiation-induced apoptosis in the G6PD(-) cells. These data suggest that G6PD and the oxidative pentose phosphate shunt protect cells from ionizing radiation-induced cell killing by limiting the incidence of radiation-induced apoptosis. The sensitivity to radiation-induced apoptosis was lost when the cDNA for wild-type G6PD was transfected into the G6PD(-) cell lines. Depleting GSH with l-BSO enhanced apoptosis of K1 cells while having no effect in the G6PD(-) cell line

Animals↗
PubMed2005

"Modeled microgravity" affects cell response to ionizing radiation and increases genomic damage.

The aim of this work was to assess whether "modeled microgravity" affects cell response to ionizing radiation, increasing the risk associated with radiation exposure. Lymphoblastoid TK6 cells were irradiated with various doses of gamma rays and incubated for 24 h in a modeled microgravity environment obtained by the Rotating Wall Vessel bioreactor. Cell survival, induction of apoptosis and cell cycle alteration were compared in cells irradiated and then incubated in 1g or modeled microgravity conditions. Modulation of genomic damage induced by ionizing radiation was evaluated on the basis of HPRT mutant frequency and the micronucleus assay. A significant reduction in apoptotic cells was observed in cells incubated in modeled microgravity after gamma irradiation compared with cells maintained in 1g. Moreover, in irradiated cells, fewer G2-phase cells were found in modeled microgravity than in 1g, whereas more G1-phase cells were observed in modeled microgravity than in 1g. Genomic damage induced by ionizing radiation, i.e. frequency of HPRT mutants and micronucleated cells, increased more in cultures incubated in modeled microgravity than in 1g. Our results indicate that modeled microgravity incubation after irradiation affects cell response to ionizing radiation, reducing the level of radiation-induced apoptosis. As a consequence, modeled microgravity increases the frequency of damaged cells that survive after irradiation.

Apoptosis↗
PubMedDate not supplied

[Occupational exposure to ionizing radiation and the occurrence of cataract].

Radiation cataract is one of ensuing effects of ionizing radiation, since its threshold dose under which it does not occur, and above which it shows dose dependency, has been observed. Clinical course of radiation cataract is identical for all the types of ionizing radiation and is very typical. Minimal dose for progressive cataract formation is determined by the type of radiation, i.e., its relative biological efficacy, dose, and the duration of the exposure period. Theoretically, threshold dose existence does not exclude the incidence of cataract formation under significantly smaller doses, as well. The aim of this study was to analyze the incidence of cataract formation among the medical staff professionally exposed to ionizing radiation. Neither of the diagnosed cataracts had typical morphology, nor was the correlation established between the dose, exposure time, and the cataract formation. All the diagnosed cataracts were described as premature, and therefore ionizing radiation was considered as a co-factor in premature cataract formation in the examined groups.

Adult↗
PubMed1988

Ionized calcium and acid-base status in arterial and venous whole blood during general anaesthesia.

Ionized calcium, pH, pCO2 and base excess (BE) have been measured in paired samples of anaerobically collected arterial (aB) and venous whole blood (vB) from patients under general anaesthesia and during recovery. A statistically significant decrease was found in the concentration of ionized calcium in anaerobic arterial and venous blood during induction of anaesthesia and during surgery partly due to variations in pH. Statistically significant correlations were found between logcCa2+ and pH (r = -0.67, p less than 0.001), and between cCa2+ and pCO2 (r = 0.66, p less than 0.001) in anaerobic arterial blood. The in vivo slope (dlogcCa2+/dpH) was found to be -0.15 +/- 0.08 and -0.14 +/- 0.06 for arterial and venous blood, respectively (mean +/- SE). The in vitro slope estimated by equilibrating arterial and venous serum at two pCO2 values was -0.22 +/- 0.03, and -0.21 +/- 0.03, respectively (mean +/- SE). Because of a considerable variability in slope we believe that the best clinical evaluation of ionized calcium is achieved by taking measurements from anaerobically collected whole blood. Interpolating or extrapolating ionized calcium to a standard pH of 7.40 on the basis of a standard slope may introduce unnecessary errors.

Acid-Base Equilibrium↗