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Biomedical subjects

C C Wang

Publications and source records attributed to C C Wang.

At least 19 recordsLinked to original sources
PubMed1992

Mouse ornithine decarboxylase is stable in Trypanosoma brucei.

The cDNA encoding mouse ornithine decarboxylase (ODC) was incorporated into a transforming vector pTSA-NEO2 carrying a procyclic acidic repetitive protein promoter and a neomycin phosphotransferase gene. The plasmid thus constructed, pMOD300, was introduced into the procyclic forms of Trypanosoma brucei via electroporation, and the transformants, selected under G418, expressed an ODC activity 100 times above the background level. Contrary to the commonly observed short half-life of mouse ODC in mammalian cells, however, the mouse ODC activity expressed in T. brucei remained stable for at least 6 h when protein synthesis was inhibited by cycloheximide. Pulse labelings and chase experiments with the irreversible ODC inhibitor [3,4-3H]difluoromethylornithine followed by gel electrophoresis, or with L-[35S] methionine followed by immunoprecipitation and gel electrophoresis indicated that the stable mouse ODC expressed in T. brucei has the same subunit molecular weight as the native enzyme. By an in vitro assay of protein stability in rabbit reticulocyte lysates (Loetscher, P., Pratt, G., and Rechsteiner, M. (1991) J. Biol. Chem. 266, 11213-11220), the native mouse ODC and the enzyme expressed in T. brucei had the same degree of instability. Thus, the mouse ODC expressed in T. brucei is probably identical to the native mouse ODC. Its remarkable stability in T. brucei must be due to the absence in trypanosomes of the proteolytic machinery present in mammalian cells responsible for rapid degradation of mouse ODC.

Animals↗
PubMed1992

Usefulness of predischarge electrophysiologic study in predicting late outcome after surgical ablation of the accessory pathway in the Wolff-Parkinson-White syndrome.

A predischarge electrophysiologic study was performed in 113 patients with the Wolff-Parkinson-White (WPW) syndrome who had undergone surgical ablation of the accessory pathway. The study was performed 5 to 20 (mean 10 +/- 3) days after surgery. There were 82 male and 31 female patients (aged 4 to 58 years, mean 36 +/- 13). Sixty-one patients (54%) had manifest, 52 (46%) had concealed and 12 (11%) had multiple accessory pathways. All but 1 patient had atrioventricular reentrant tachycardia incorporating single or multiple accessory pathways during the control electrophysiologic study. The accessory pathways were located in the left ventricular free wall in 60% of cases, right ventricular free wall in 22%, posteroseptum in 13%, and anteroseptum in 5%. The predischarge electrophysiologic study showed that the accessory pathway was capable of anterograde and retrograde conductions in 4 patients (all with manifest WPW syndrome). Four patients showed induction of supraventricular tachycardia, including 2 with atrioventricular reentrant tachycardia, and 2 with atrioventricular nodal reentrant tachycardia. Recurrence of supraventricular tachycardia was noted in 5 patients during a follow-up of 28 +/- 26 months. Of these 5 patients, 2 had inducible and 3 had no inducible supraventricular tachycardia during the predischarge electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Proton nuclear Overhauser effect study of the heme active site structure of chloroperoxidase.

Chloroperoxidase, a glycoprotein from the mold Caldariomyces fumago, has been investigated in its ferric low-spin cyanide-ligated form through use of nuclear Overhauser effect (NOE) spectroscopy to provide information on the heme pocket electronic/molecular structure. Spin-lattice relaxation times for the hyperfine-shifted heme resonances were found to be three times less than those in horseradish peroxidase. This must reflect a slower electronic relaxation rate for chloroperoxidase than for horseradish peroxidase as a consequence of axial ligation of cysteine in the former versus histidine in the latter enzyme. Isoenzymes A1 and A2 of chloroperoxidase show the largest chemical shift differences near the heme propionate on the basis of NOE measurements. This suggests that the primary structure differences for the two isoenzymes are communicated to the heme group through the ring propionate substituents. A downfield peak has been detected in chloroperoxidase with chemical shift, T1, and line width characteristics similar to those of the C epsilon-H proton of the distal histidine residue. The NOE pattern and T1's of the peaks in the 0.0 to -5.0 ppm upfield region are consistent with the presence of an arginine amino acid residue in the heme pocket near either the 1-CH3 or 3-CH3 group. Existence of catalytically important distal histidine and arginine amino acid residues in chloroperoxidase shows it to be structurally similar to peroxidases rather than to the often compared monooxygenase, cytochrome P-450. This result supports the earlier conclusions of Sono et al. [Sono, M., Dawson, J.H., Hall, K., & Hager, L.P. (1986) Biochemistry 25, 347-356].

Arginine↗
PubMed1992

Steady-state kinetics of the schistosomal hypoxanthine-guanine phosphoribosyltransferase.

Schistosomiasis is a trematode infection of some 200 million people. The hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) of the major etiologic agent, Schistosoma mansoni, has been proposed as a potential target for antischistosomal chemotherapy [Dovey, H. F., McKerrow, J. H., & Wang, C. C. (1984) Mol. Biochem. Parasitol, 11, 157-167]. The steady-state kinetic mechanism for the schistosomal HGPRTase has been determined by including both hypoxanthine and guanine in the forward and reverse reactions under identical conditions. Double-reciprocal plots of initial velocity versus the concentration of one substrate, at a series of fixed concentrations of the other, give groups of intersecting straight lines indicating a sequential mechanism for the schistosomal HGPRTase-catalyzed reactions. In product inhibition studies, the results show that magnesium pyrophosphate (MgPPi) is a noncompetitive inhibitor with respect to dimagnesium phosphoribose pyrophosphate (Mg2PRPP), hypoxanthine, and guanine. Also, magnesium inosine monophosphate (MgIMP) and magnesium guanosine monophosphate (MgGMP) are noncompetitive inhibitors with respect to hypoxanthine or guanine, respectively, but are competitive inhibitors to Mg2PRPP. Furthermore, Mg2PRPP is a competitive inhibitor with respect to MgIMP and MgGMP but is a non-competitive inhibitor to MgPPi. The minimum kinetic model which fits the experimental data is an ordered bi-bi mechanism, where the substrates bind to the enzyme in a defined order (first Mg2PRPP followed by the purine bases), while products are released in sequence (first MgPPi followed by MgIMP or MgGMP).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Expression, purification, and characterization of the functional dimeric cytoplasmic domain of human erythrocyte band 3 in Escherichia coli.

The cytoplasmic domain of the human erythrocyte membrane protein, band 3 (cdb3), contains binding sites for hemoglobin, several glycolytic enzymes, band 4.1, band 4.2, and ankyrin, and constitutes the major linkage between the membrane skeleton and the membrane. Although erythrocyte cdb3 has been partially purified from proteolyzed red blood cells, further separation of the water-soluble 43-kDa and 41-kDa proteolytic fragments has never been achieved. In order to obtain pure cdb3 for crystallization and site-directed mutagenesis studies, we constructed an expression plasmid that has a tandemly linked T7 promoter placed upstream of the N-terminal 379 amino acids of the erythrocyte band 3 gene. Comparison of several Escherichia coli strains led to the selection of the BL21 (DE3) strain containing the pLysS plasmid as the best host for efficient production of cdb3. About 10 mg of recombinant cdb3 can be easily purified from 4 L of E. coli culture in two simple steps. Comparison of cdb3 released from the red blood cell by proteolysis with recombinant cdb3 reveals that both have the same N-terminal sequence, secondary structure, and pH-dependent conformational change. The purified recombinant cdb3 is also a soluble stable dimer with the same Stokes radius as erythrocyte cdb3. The affinities of the two forms of cdb3 for ankyrin are essentially identical; however, recombinant cdb3 with its unblocked N-terminus exhibits a slightly lower affinity for aldolase.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1992

The translation initiation site of recombinant Trypanosoma brucei ornithine decarboxylase varies with different promoters.

Expression of the Trypanosoma brucei ornithine decarboxylase (ODC) gene in Escherichia coli behind the lambda phage PR promoter led to the production of a recombinant enzyme having the same subunit molecular weight as the native enzyme [4]. However, when the same gene is expressed behind the tac promoter or the phoA promoter, the ODCs produced by the transformed E. coli have subunit molecular weights approximately 2 kDa higher than that of the native enzyme. Amino terminal sequencing of the recombinant proteins indicates that the ODC synthesized under control of the lambda PR promoter actually starts at the second methionine (Met23) of the open reading frame, whereas those produced in the latter two cases begin at the first methionine (Met1). Analysis of the 5'-end of T. brucei ODC mRNA supports the conclusion that translation initiates at Met23. We postulate that, for the lambda PR promoter, translation initiates at Met23 instead of Met1 because of the formation of a stable secondary structure in the region of the Met1 and the presence of a good E. coli consensus translation initiation site upstream of Met23. We have constructed a new plasmid using the pho A promoter to express recombinant T. brucei ODC starting at Met23 in large quantities.

Amino Acid Sequence↗
PubMed1992

Transient inhibition of protein synthesis accompanies differentiation of Trypanosoma brucei from bloodstream to procyclic forms.

It has been widely believed that bloodstream forms of Trypanosoma brucei must be first transformed into intermediary and/or short-stumpy forms in the bloodstream of the mammalian host before differentiation to the procyclic culture form can occur. In our recent studies, the pleomorphic T. brucei strain TREU667 was found to differentiate directly from the long-slender bloodstream form to the procyclic form in Cunningham's medium at 26 degrees C [7]. In the present investigation, the same was found true for another pleomorphic strain of T. brucei, STIB366D. Four independent monomorphic strains of T. brucei were tested; two, #427 and EATRO164, were found capable of differentiating in vitro directly into procyclic forms, whereas the other two, TREU667/RP-56 and EATRO110, could not. There is thus no correlation between the capability of differentiating in vitro and the ability of being converted from long-slender to intermediary and short-stumpy bloodstream forms. Two additional markers for following differentiation, other than observing morphological changes, were tested. Assays for the emerging phosphoenolpyruvate carboxykinase (PEPCK) by immunoblottings worked well, with results agreeing closely with the morphological change. But immunoblottings of glycosomal phosphoglycerate kinase (gPGK) failed to demonstrate a significant decrease in the protein level upon completion of differentiation. Apparently, gPGK has a rather long half-life and is unsuitable as a marker of differentiation. When temperature was dropped from 37 degrees C to 26 degrees C at the starting point of in vitro differentiation, protein synthetic activity in the pleomorphic T. brucei TREU667 bloodstream form was decreased by 4-fold. When the activity was gradually brought back to and beyond the original level after a day's incubation, the profile of newly synthesized proteins was that of the procyclic form. A monomorphic variant of TREU667, RP-56, which is incapable of differentiating in vitro, has a much higher protein synthetic activity than its pleomorphic parent in the bloodstream form. This high activity and the bloodstream profile of proteins thus synthesized were unaffected by the decreased temperature in Cunningham's medium until cell death. We thus conclude that a general inhibition of protein synthesis in bloodstream forms caused by temperature drop may be among the early events triggering differentiation into the procyclic form.

Animals↗
PubMed1992

Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique.

OBJECTIVES: A comprehensive electrophysiologic study followed by selective radiofrequency ablation from three sites was performed in patients with atrioventricular (AV) node reentrant tachycardia to better delineate the nature of the tachycardia circuit. BACKGROUND: We postulated that the retrograde fast pathway is the anterior superficial group of transitional cells and the slow pathway is the compact node with its posterior input of transitional cells. Twenty-three consecutive patients were studied. In nine, the atria could be dissociated from the tachycardia by delivery of an atrial extrastimulus during tachycardia. METHODS: Radiofrequency ablation was performed with three approaches. The anterior approach was designed to interrupt the anterior superficial atrial input to the compact node, the posterior approach to interrupt the posterior atrial input to the compact node and the inferior approach to destroy the compact node itself. RESULTS: Selective ablation of the retrograde fast pathway was achieved in seven patients, six with the anterior and one with the inferior approach. Anterograde fast pathway conduction was not affected, whereas retrograde fast pathway conduction was either abolished or markedly depressed. None had induction of echoes or tachycardia after ablation. Selective ablation of the slow pathway was successful in 13 patients, 1 with anterior, 3 with posterior and 9 with inferior approaches. In these 13 patients, both anterograde and retrograde fast pathway conduction were not affected, the dual pathway physiology was abolished and the tachycardia was not inducible after ablation. Ablation of both the retrograde fast pathway and the slow pathway occurred with the inferior approach in three patients. CONCLUSIONS: We conclude that the retrograde fast pathway is likely to be the anterior superficial group of transitional cells, whereas the slow pathway is the compact node and its posterior input of transitional cells. A barrier seems to exist between the atrium and the tachycardia circuit. In a broad view of the AV node structure, the tachycardia circuit is confined to the node.

Atrial Function↗
PubMed1992

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.

Cardiac Pacing, Artificial↗
PubMed1992

In vivo import of firefly luciferase into the glycosomes of Trypanosoma brucei and mutational analysis of the C-terminal targeting signal.

The compartmentalization of glycolytic enzymes into specialized organelles, the glycosomes, allows the bloodstream form of Trypanosoma brucei to rely solely on glycolysis for its energy production. The biogenesis of glycosomes in these parasites has been studied intensively as a potential target for chemotherapy. We have adapted the recently developed methods for stable transformation of T. brucei to the in vivo analysis of glycosomal protein import. Firefly luciferase, a peroxisomal protein in the lantern of the insect, was expressed in stable transformants of the procyclic form of T. brucei, where it was found to accumulate inside the glycosomes. Mutational analysis of the peroxisomal targeting signal serine-lysine-leucine (SKL) located at the C-terminus of luciferase showed that replacement of the serine residue (Serine548) with a small neutral amino acid (A, C, G, H, N, P, T) still resulted in an import efficiency of 50-100% of the wild-type luciferase. Lysine549 could be substituted with an amino acid capable of hydrogen bonding (H, M, N, Q, R, S), whereas the C-terminal leucine550 could be replaced with a subset of hydrophobic amino acids (I, M, Y). Thus, a peroxisome-like C-terminal SKL-dependent targeting mechanism may function in T. brucei to import luciferase into the glycosomes. However, a few significant differences exist between the glycosomal targeting signals identified here and the tripeptide sequences that direct proteins to mammalian or yeast peroxisomes.

Animals↗
PubMed1992

Seroepidemiology and evaluation of passive surveillance during 1988-1989 measles outbreak in Taiwan.

A seroepidemiological study was carried out to explore the risk factors of a measles outbreak that occurred among school children at a rural village (Li-Tse) in Taiwan. Among the 1166 participants, the percentage susceptible before the outbreak was 10.5% (122/1158) which was estimated as the sum of measles IgG-negative (29/1158) and IgM-positive (93/1166) individuals. Among 340 vaccinated children, 16 (4.7%) were measles IgM-positive and 10 (2.9%) were measles IgG-negative; therefore the vaccine failure rate was estimated to be 7.6% (26/340) and vaccine efficacy was 79.7% (95% confidence interval [CI] : 65.0-88.5). The most important risk factors for acquiring measles infection were the presence of other measles cases in the family (Odds Ratio [OR] = 32.5, P = 0.002) and the presence of more than two cases in a class (OR = 29.1, P = 0.003). The physician reporting rate was 6.1% (4/66), and the sensitivity of passive measles surveillance was only 4.3% (4/93) by active serosurvey. A concomitant rubella epidemic also amplified the inaccuracy of a passive reporting system based only on clinical diagnosis. Five children developed measles IgM but did not experience any symptoms, indicating that asymptomatic measles infection can occur. Our experience has highlighted three important areas for future measles elimination: (1) the need for serological evaluation of vaccinees, particularly those who were born during the introduction of mass immunization; (2) improvement in measles vaccine efficacy; and (3) further investigations on the role of asymptomatic transmission and susceptibles who remain after mass immunization.

Adolescent↗
PubMed1992

Maintenance of CD4+ cells by thymopentin in asymptomatic HIV-infected subjects: results of a double-blind, placebo-controlled study.

OBJECTIVE: To assess the efficacy and safety of thymopentin in HIV-infected patients who had not yet developed AIDS. DESIGN: Patients were stratified into asymptomatic or symptomatic groups and randomized to receive either thymopentin (50 mg) or placebo, subcutaneously, double-blind for 24 or 52 weeks, three times a week. SETTING: Patients were enrolled at three sites (two hospital clinics and one private practice). PATIENTS: Of 91 HIV-seropositive patients (52 asymptomatic and 39 symptomatic) from whom HIV could be isolated from peripheral blood, 45 were enrolled for 24 weeks and 46 for 52 weeks of double-blind evaluation. MAIN OUTCOME MEASURES: Virological, immunological and clinical evaluations were performed before and during treatment. RESULTS: Thymopentin-treated asymptomatic patients had more CD4+ cells, as demonstrated by a greater area under the percentage CD4+ cells curve (P = 0.03) and a shorter median time to a 20% increase in percentage of CD4+ cells (P = 0.04) in the first 24 weeks, with similar trends in the 52-week study. By 24 weeks no asymptomatic thymopentin-treated and two placebo-treated patients (9.1%, Kaplan-Meier estimate) had progressed to constitutional symptoms (P = 0.12; two-tailed Wilcoxon-Gehan test), with only one further progression in a placebo-treated patient in the subset followed for 52 weeks. Symptomatic patients receiving thymopentin or placebo were similar in both CD4+ cell levels and disease progression (two progressions to AIDS in each group). No serious adverse effects attributable to thymopentin were observed. CONCLUSIONS: These results, if confirmed, indicate that thymopentin, by maintaining CD4+ cells, could slow or arrest immune decline and consequent disease progression at the asymptomatic stage of HIV infection.

Amino Acid Sequence↗
PubMed1992

Idiopathic hypercalciuria causing osteoporosis and hypocalcemia.

Idiopathic hypercalciuria, though a common cause of nephrolithiasis, has not been recognized to cause hypocalcemia and severe bone disease. We describe an adolescent with idiopathic hypercalciuria who presented initially with severe hypocalcemia and osteoporosis and this was later complicated by recurrent renal calculi formation after calcium and vitamin D supplement. After treatment with thiazide, hypercalciuria was controlled and serum biochemistry normalized. While idiopathic renal hypercalciuria may cause a negative calcium balance in adults, a variant of this syndrome with severe renal calcium leak occurring in a growing subject could lead to severe hypocalcemia and osteoporosis.

Adolescent↗
PubMed1992

Differential regulation of the genes encoding platelet-derived growth factor receptor and its ligand in rat lung during microvascular and alveolar wall remodeling in hyperoxia.

The growth factors that operate while the lung remodels in hyperoxia are not known. At the lung periphery, high oxygen levels cause cell hypertrophy and hyperplasia, and this results in a thickening of the alveolar-capillary membrane and the walls of its associated microvessels. The present study examines gene expression of platelet-derived growth factor (PDGF) receptor and its ligand in this region of the lung of rats breathing 87% oxygen and compares this with the levels of expression in normal lung. In similar peripheral lung tissue, the proliferative response of specific cell populations has been assessed by [3H]thymidine incorporation and autoradiography. Normal lung expresses PDGF alpha-receptor subunit transcripts of 6.5 and 4.7 kb and PDGF beta-receptor transcripts of 5.5 and 4.5 kb. PDGF A-chain transcripts of 2.9, 2.3, and 1.7 kb are also expressed, each being at 10-fold higher levels than the single 3.5-kb transcript detected for PDGF B-chain. Within hours of breathing high concentrations of oxygen, mRNA levels change rapidly for the PDGF receptor subunits. These levels return to normal after 1 day and then decline over the next 28 days of exposure. PDGF A-chain mRNA increases 12 to 18 h after exposure, but then returns to normal levels. It is the PDGF B-chain mRNA that responds most to hyperoxia by increasing 10-fold on day 3. This increase immediately precedes the proliferative response on day 4 of microvascular adventitial fibroblasts, precursor smooth muscle cells, and epithelial cells but not smooth muscle cells, which do not proliferate until day 28.

Animals↗
PubMed1992

Does Hakka ethnic group have higher incidence of thalassemia traits in Taiwanese population?

The purpose of this survey is to find out whether Hakka group has higher incidence of thalassemia traits in our population. A total of 1,115 healthy employees from a company were screened by complete blood count (CBC) with indices. Those subjects with mean corpuscular volume (MCV) less than 80 fl were further evaluated by hemoglobin electrophoresis and modified hemoglobin H (Hb H) inclusion staining to confirm the diagnosis of beta- and alpha-thalassemia traits, respectively. We evaluated and compared the crude occurrence rates of thalassemia traits in Hakka, non-Hakka, and Taiwanese. Subjects with one or both Hakka parents had higher crude incidence of alpha-thalassemia traits than other groups of subjects, but this phenomenon wasn't found in beta-thalassemia traits.

Adult↗
PubMed1992

[Chemical synthesis and cloning of Plasmodium falciparum 45 peptide antigen gene].

We have synthesized a 162 bp gene of human Plasmodium falciparum hybrid peptide antigen by the solid-phase phosphoramidite method with ABI 381A DNA synthesizer. The gene encodes three fragments of the relative molecules 83 kDa, 55 kDa and 35 kDa merozoite-specific proteins and two CS repeats or four peptides. The gene with the designed two cohesive ends was divided into 8 fragments to be synthesized. All synthetic fragments were annealed and ligated with T4 DNA ligase to form double DNA chain. This synthetic gene was recombined with P-Blue script as vector and transformed into E. coli JM109. The positive recombinants were screened out by dot hybridization and enzyme analysis. The DNA sequence analysis showed that the synthesized human Plasmodium falciparum hybrid peptide antigen gene was identical with the designed one. (Figs. 1-4).

Amino Acid Sequence↗
PubMed1991

Menadione-induced DNA damage in a human tumor cell line.

The nature and extent of menadione (MD)-induced DNA damage were explored using the human breast cancer cell line MCF-7. Concentration-dependent single-strand (ss) and double-strand (ds) DNA breaks were detected in MD-treated MCF-7 cells using the alkaline- and neutral-elution techniques, respectively. The repair of ss and ds DNA breaks was extensive but not complete after a 6-hr incubation in drug-free medium. Evidence was found for the production of DNA interstrand cross-links in MCF-7 cells treated with the bifunctional alkylating agent, mitomycin C, but not for cells treated with MD. Exposure of MCF-7 cells to etoposide (VP-16), mitoxantrone and camptothecin resulted in the detection of significant amounts of protein-linked DNA breaks, whereas none were found in MD-treated cells. These results support the proposition that MD-induced DNA damage is not likely to be mediated via topoisomerases, nor do significant amounts of protein-linked DNA form in MD-treated cells. Thus, MD serves as a good model for examination of the role of the quinone moiety in DNA damage in relation to redox cycling. Future studies directed at elucidation of the biochemical determinants mediating formation of reactive oxygen species effecting the MD-induced DNA damage are necessary and underway.

Breast Neoplasms↗