Photon energy dependence of the sensitivity of radiochromic film and comparison with silver halide film and LiF TLDs used for brachytherapy dosimetry

There is a new radiochromic film, a highly uniform, thin (100-microns) detector whose sensitive layer (6 microns thick) changes from colorless to blue by dye polymerization without processing, upon exposure to ionizing radiation. Because the dose gradients around brachytherapy sources are steep, the high spatial resolution offered by film dosimetry is an advantage over other detectors such as thermoluminescent dosimeters (TLDs). This compares the photon energy dependence of the sensitivities of GafChromic film, silver halide verification film (Kodak X-Omat V Film), and lithium fluoride TLDs (Harshaw), over the photon energy range 28 keV to 1.7 MeV, which is of interest in brachytherapy. Sensitivity of the radiochromic film is observed to decrease by about 30% as effective photon energy decreases from 1710 keV (4-MV x rays) to 28 keV (60-kV x rays, 2-mm A1 filter). In contrast, the sensitivity of verification film increases by 980% and that of LiF TLDs increases by 41%. The variation of the sensitivity of radiochromic film with photon energy is considerably less than that for silver halide film and similar to that for LiF TLDs, but in the opposite direction. Radiochromic film, like LIF TLDs, does not exhibit the drastic sensitivity changes below 127 keV that silver halide film exhibits. Dose distribution in the immediate vicinity of a high activity (370 GBq) brachytherapy 192Ir source has been mapped using radiochromic film and is presented to illustrate the applicability of this new technology to brachytherapy dosimetry.     

Inhibition of interleukin-2 production by adherent cell factors from lepromatous leprosy patients.

Twenty-four hour supernatants (MoF) were obtained from monocyte rich 2 h adherent cells of 19 leprosy patients and four healthy contacts. MoF from borderline and lepromatous patients produced 52-61% inhibition of human interleukin-2 (IL-2) production by a PHA conditioned T cell line (Jurkat). Non-adherent cell supernatants and MoF from tuberculoid and healthy individuals had little effect on IL-2 production. The suppression effected by MoF was in the first 12 h of initiation of PHA stimulated Jurkat cell cultures. Suppressive MoF did not interfere with (1) IL-2 release, (2) IL-2 utilization by Con A-induced T cell blasts or (3) constitutive proliferation of Jurkat cells. Such MoF were released spontaneously from adherent cells of bacilliferous leprosy patients but required in vitro antigen triggering in long term treated lepromatous patients. It is possible that the unresponsiveness associated with lepromatous leprosy is related to the inhibition of IL-2 production by suppressive factors, thereby, preventing the further expansion of antigen reactive T cells.     

Interaction of polystyryl radical with copper(II) complexes

The polymerization of styrene initiated by 2,2′-azoisobutyronitrile (AIBN) was studied in N,N-dimethylformamide (DMF) solution at 60°C in the presence of tetrakis(N,N-dimethylformamide)copper(II) perchlorate, and also in the presence of its monoazido copper(II) complex [Cu(DMF)₃N₃]⁺. The monoazido complex in DMF was prepared in situ by mixing solid sodium azide with tetrakis(N,N-dimethylformamide)copper(II) perchlorate in a mole ratio of 1:1. The nature of the complex was established by Job's method. The equilibrium constant K for the reaction [Cu(DMF)₄]²⁺ + N ? [Cu(DMF)₃N₃]⁺ + DMF determined by the limiting logarithmic method was found to be 1,25 · 10⁴l · mol^?1. The presence of [Cu(DMF)₄]²⁺ ions in the polymerization systems caused retardation, but [Cu(DMF)₃N₃]⁺ ions produced well defined induction periods. The rate constants at 60°C for the interaction of polystyryl radical towards [Cu(DMF)₄]²⁺ and [Cu(DMF)₃N₃]⁺ ions were calculated to be 6,6 · 10² and 5,74 · 10⁴ l · mol^?1 · s^?1, respectively.     

Effect of lymphocyte mediators on macrophages in vitro. A correlation of morphological and cytochemical changes

Sephadex purified PPD and Con A induced mediator rich fractions (MRF) were applied to guinea-pig macrophages cultured in vitro. At varying times after the addition of the MRF, cells were removed from culture for morphological study and for cytochemical tests. Respiratory enzyme activity and lysosomal acid phos-phatase activity were estimated and the former was quantitated using an integrating microdensitometer. Early changes, 1 hr after MRF contact, were observed and subsequent alterations in activity up to 48 hr after the addition of MRF were also seen. These changes have been related to the inhibition of migration and subsequent `activation' of the macrophages which has been observed morphologically at times up to 3 weeks after MRF addition.

It is suggested that alterations in the cytochemistry of the macrophages after MRF contact could help explain changes in the behaviour of the cells under these experimental conditions.

     

Linkage analysis of SLE susceptibility: confirmation of SLER1 at 5p15.3

We detected a novel susceptibility gene, SLER1, for systemic lupus erythematosus (SLE) at 5p15.3.(1) This finding was based on a selected subgroup of SLE families, where two or more family members have had alleged rheumatoid arthritis (SLE-RA). The main objective of this study was to replicate the linkage at 5p15.3 based on an independent data set of 88 SLE-RA families. Heterogeneity in the genetic model led us to use a nonparametric allele-sharing method. Since our a priori hypothesis of linkage at 5p15.3 was fixed, we genotyped six markers at the linked region. Our new results replicate the initial linkage at 5p15.3 (Zlr=2.58, P<0.005, LOD=1.45). Moreover, evidence of linkage was sustained when analysis was restricted to the subset of SLE families who had 3 or more individuals with alleged RA (Zlr=3.32, P=0.008, LOD=2.40) The results of our previous findings, together with these new results, confirm the SLER1 linkage at 5p15.3. Our results also demonstrate the utility of clinically defined subgroup analysis for detecting susceptibility loci for complex genetic diseases, such as SLE.     

Molecular therapies for viral hepatitis

Current treatment modalities available for hepatitis B virus (HBV) or hepatitis C virus (HCV) infections are not efficient. The enormous disease burden caused by these two infections makes the development of novel therapies critical. For HCV, the development of an effective vaccine is urgent in view of the escalating number of infected individuals. Molecular therapies for HBV and HCV infection can be directed at reducing viral load by interfering with the life cycle of the viruses or at generating immune response against viral epitopes. The antiviral approaches consist of the delivery or expression of antisense RNAs, ribozymes or dominant negative proteins. Viral biology can be interrupted by attacking various potential targets within the two viruses. DNA-based vaccination strategies are being explored for both prevention and treatment of these diseases. Both non-viral and recombinant viral vectors are being developed for safe, effective and long-term gene transfer to the liver. Although no "ideal" vector is available at this time, the ingenuity of numerous investigators is leading to the improvement of the vector systems, promising successful application of gene therapy to the prevention and treatment of viral hepatitis in the foreseeable future.     

Dose rate constant and energy spectrum of interstitial brachytherapy sources

In the past two years, several new manufacturers have begun to market low-energy interstitial brachytherapy seeds containing 125I and 103Pd. Parallel to this development, the National Institute of Standards and Technology (NIST) has implemented a modification to the air-kerma strength (S(K)) standard for 125I seeds and has also established an S(K) standard for 103Pd seeds. These events have generated a considerable number of investigations on the determination of the dose rate constants (inverted V) of interstitial brachytherapy seeds. The aim of this work is to study the general properties underlying the determination of dose rate constant and to develop a simple method for a quick and accurate estimation of dose rate constant. As the dose rate constant of clinical seeds is defined at a fixed reference point, we postulated that dose rate constant may be calculated by treating the seed as an effective point source when the seed's source strength is specified in S(K) and its source characteristics are specified by the photon energy spectrum measured in air at the reference point. Using a semi-analytic approach, an analytic expression for dose rate constant was derived for point sources with known photon energy spectra. This approach enabled a systematic study of dose rate constant as a function of energy. Using the measured energy spectra, the calculated dose rate constant for 125I model 6711 and 6702 seeds and for 192Ir seed agreed with the AAPM recommended values within +/-1%. For the 103Pd model 200 seed, the agreement was 5% with a recently measured value (within the +/-7% experimental uncertainty) and was within 1% with the Monte Carlo simulations. The analytic expression for dose rate constant proposed here can be evaluated using a programmable calculator or a simple spreadsheet and it provides an efficient method for checking the measured dose rate constant for any interstitial brachytherapy seed once the energy spectrum of the seed is known.     

Dose distributions produced by shielded applicators using 241Am for intracavitary irradiation of tumors in the vagina.

Dosimetric characteristics of shielded vaginal applicators containing encapsulated 241Am sources are investigated in this work. Encapsulated 241Am sources emit primarily 60-keV photons which are more effectively shielded by thin layers of high atomic number materials than the 662-keV photons from 137Cs sources. With 241Am, it is possible to achieve almost unidirectional irradiation of localized vaginal tumors. The drastic decrease in irradiation volume on the contralateral side (uninvolved with tumor) is observed to decrease dose by up to 20%, even in the forward direction (unshielded side toward the tumor) of the applicator. A possible explanation for the observed effects of shields in both the forward and backward directions is the reduction of scattered photon fluence due to absorption of photons in the lead shield via photoelectric effect. Current theoretical models do not include this perturbation effect caused by shields on brachytherapy applicators.