Coil embolization of a fistula from the right inferior phrenic artery to the right pulmonary artery with involvement of further arteries: A rare case report.

A 51-year-old female patient was presenting dyspnea for more than a year with no previous lung infections or surgery. Initially, a diagnostic computed tomography was made, showing a rare arterio-arterial malformation between the right inferior phrenic and right pulmonary artery leading into a vascular bundle in the middle lung lobe. Due to the patients' dyspnea and massive extent of malformation, the indication for transcatheter arterial embolization was made. The first transcatheter arterial embolization procedure involved the inferior phrenic and a selective branch of the internal thoracic artery. Interventional angiography as well as computed tomography revealed further extend of the malformation showing a connection of right lateral thoracic, hepatic, and inferior epigastric artery to the fistula. After one month, a second transcatheter arterial embolization of these arteries as well as a second approach of the proximal internal thoracic artery was performed. In the follow-up the patient described a substantial improvement of her dyspnea and showed no signs of infections. A phrenic artery to pulmonary artery fistula is an extremely rare case occurring congenital or acquired. Patients may be asymptomatic or present, among others, dyspnea, hemoptysis, pulmonary infections and congestive heart failure. Symptomatic patients require treatment using transcatheter arterial embolization or surgical resection. The patient had dyspnea and a substantial extent of malformation with possibly complicated clinical course. The recommended less invasive treatment using transcatheter arterial embolization was successfully performed. In conclusion, our patient represented a rare congenital case of systemic and pulmonary artery communication, which we were able to treat sufficiently with coil embolization.

Flow cytometric characterization of the response of Fanconi's anemia cells to mitomycin C treatment.

DNA flow histogram analysis, using 33342 Hoechst as a stain, has been used to detect the effect of the potentially bifunctional alkylating agent, mitomycin C (MMC) on dermal fibroblasts from patients with Fanconi's anemia (FA), a hereditary human disease characterized by pancytopenia, hypersensitivity to DNA-crosslinking agents, congenital abnormalities and a predisposition for neoplasia. At 24 or 48 hr after a 2-hr exposure to 0.05 or 0.10 micrograms/ml MMC, (3)HdT incorporation was reduced to a greater extent in FA cells than in normal cells. Cells sorted from the last half of S phase showed a slightly greater inhibition of (3)HdT incorporation than did those sorted from the first half of S. Fanconi's anemia cells exhibited a marked accumulation in the G(2) + M peak of flow histograms following exposure to MMC. Twenty-four hr after treatment with .0.5 micrograms/ml MMC, the G(2) + M fraction of FA cells (eight lines) increased to more than 0.5 from a control value of approximately 0.02. Both normals (six lines) and heterozygotes (eight lines) showed, on the average, much less of a G(2) + M increment than did FA cells, even after exposure to 0.1 micrograms/ml MMC. Examination of cells sorted from the G(2) + M peak revealed that MMC-treated FA cells were blocked prior to mitosis. To determine whether the response of FA cells was specific for bifunctional alkylating agent, cells were also treated with ethylmethanesulfonate, a monofunctional agent. Twenty-four hours after exposure to 0.25 or 0.5 mg/ml ethylmethanesulfonate, FA and normal cells showed similar, small increases in the G(2) + M peak. The results suggest the utility of flow cytometry in the diagnostic evaluation of fibroblasts from patients suspected of having Fanconi's anemia.

Cytogenetic and flow cytometric studies of cells from patients with Fanconi's anemia.

Cells from patients wtih Fanconi's anemia are unusually sensitive to agents which are capable of crosslinking DNA. This increased sensitivity can be detected both by cytogenetic and flow cytometric methods. An elevated frequency of chromosome aberrations, which is further exaggerated by exposure of cells to DNA crosslinking agents, is a general feature of Fanconi's anemia. Information about the formation of sister chromatid exchanges in this disease is less consistent. Cytogenetic analysis of cells from patients with Fanconi's anemia can be compromised by a low mitotic index. This is reflected in an accumulation of cells In the G2 phase of the cycle, after exposure to the bifunctional alkylating agent, mitomycin C. New methods for differentiating individuals with Fanconi's anemia from unaffected individuals should be of empirical use and might also facilitate mechanistic studies of this disease.

Interactions between pairs of DNA-binding dyes: results and implications of chromosome analysis.

A number of DNA-binding dyes, with spectral properties making them suitable as components of energy donor-acceptor pairs, are described. If such pairs are used to stain metaphase chromosomes, and if the energy acceptor (e.g., actinomycin D or methyl green) has a binding specificity opposite to the binding or fluorescence specificity of the donor (e.g., 33258 Hoechst, quinacrine or chromomycin A3), contrast in donor fluorescence can be enhanced, leading to patterns selectively highlighting standard or reverse chromosome bands or particular polymorphic regions. Such results presumably reflect chromosomal regions enriched in 10-20 base pair clusters to which the donor binds and fluoresces but to which the acceptor cannot bind. For other pairs, involving counterstains such as netropsin or echinomycin, which are not suitable as energy acceptors, specific changes observed in polymorphic region fluorescence are most likely due to binding competition between dyes. Dye pairs producing contrast by either method can be used to differentiate between homologous chromosomes or to facilitate detection of specific chromosomal rearrangements. Preliminary data indicate that contrast enhancement generated in fixed metaphase chromosomes spread on microscopic slides can also be observed in suspensions of unfixed metaphase chromosomes, reinforcing the expectation that the methodology described will be of use in flow cytometry.

Induction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.

Sister chromatid exchanges, which may reflect chromosome repair in response to certain types of DNA damage, provide a means of investigating the increased chromosome fragility characteristic of Fanconi's anemia. By a recently developed technique using 33258 Hoechst and 5-bromodeoxyuridine, it was observed that the baseline frequency of sister chromatid exchanges in phytohemagglutinin-stimulated lymphocytes from four males with Fanconi's anemia differed little from that of normal lymphocytes. However, addition of the bifunctional alkylating agent mitomycin C (0.01 or 0.03 mug/ml) to the Fanconi's anemia cells during culture induces less than half of the increase in exchanges found in identically treated normal lymphocytes. This reduced increment in exchanges in accompanied by a partial suppression of mitosis and a marked increase in chromatid breaks and rearrangements. Many of these events occur at sites of incomplete chromatid interchange. The increase in sister chromatid exchanges induced in Fanconi's anemia lymphocytes by the monofunctional alkylating agent ethylmethane sulfonate (0.25 mg/ml) was slightly less than that in normal cells. Lymphocytes from two sets of parents of the patients with Fanconi's anemia exhibited a normal response to alkylating agents, while dermal fibroblasts from two different patients with Fanconi's anemia reacted to mitomycin C with an increase in chromatid breaks, but a nearly normal increment of sister chromatid exchanges. The results suggest that chromosomal breaks and rearrangements in Fanconi's anemia lymphocytes may result from a defect in a form of repair of DNA damage.

Recent developments in the detection of deoxyribonucleic acid synthesis by 33258 Hoechst fluorescence.

A number of applications of the detection of deoxyribonucleic acid synthesis by fluorescence microscopy are illustrated. These include (a) the analysis of sister chromatid exchanges and sister chromatid segregation at mitosis, (b) the location of chromosome regions containing deoxyribonucleic acid with an asymmetric distribution of thymine residues between polynucleotide chains and (c) the detection of late replicating regions in metaphase chromosomes. The suppression of 33258 Hoechst fluorescence by 5-bromodeoxyuridine incorporated biosynthetically into interphase nuclei is demonstrated both in fixed cytologic preparations and in unfixed cultured cells. Many of the cytologic observations described might form a basis for future biochemical studies.