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Sökning: WFRF:(Ankerst Jaro)

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1.
  • Andersson, Anders, et al. (författare)
  • Hyperhomocysteinemia and changed plasma thiol redox status in chronic obstructive pulmonary disease
  • 2001
  • Ingår i: Clinical Chemistry and Laboratory Medicine. - 1434-6621. ; 39:3, s. 229-233
  • Tidskriftsartikel (refereegranskat)abstract
    • Reduced and total homocysteine, cysteine, glutathione and cysteinylglycine in plasma were investigated in 19 patients with chronic obstructive pulmonary disease and in 29 healthy subjects. The purpose was to examine the influence of pro-oxidant activity caused by the lung disease on the metabolism of homocysteine and other plasma thiols. We observed a decreased concentration of reduced glutathione and a decreased ratio of reduced/total glutathione in the patients compared to the healthy individuals, which supports the hypothesis of an association between free radicals and pathogenesis in some lung diseases. We also observed an increased total plasma homocysteine. The influence of a possible extracellular pro-oxidant activity on the concentration of total plasma homocysteine is discussed.
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2.
  • Andersson, S., et al. (författare)
  • Tumour Localization by Means of Laser-Induced Fluorescence in Hematoporphyrin Derivative (HPD) — Bearing Tissue
  • 1985
  • Ingår i: Laser Spectroscopy VII : Proceedings of the Seventh International Conference, Hawaii, June 24-28, 1985 - Proceedings of the Seventh International Conference, Hawaii, June 24-28, 1985. - Berlin, Heidelberg : Springer Berlin Heidelberg. - 9783662152539 - 9783540396642 ; , s. 401-406
  • Konferensbidrag (refereegranskat)abstract
    • Following systemic injection, hematoporphyrin derivative (HPD) is known to be selectively retained in malignant tissue. This property can be used in a two-fold way: a) for localizing tumours by observing the characteristic dual-peaked laser-induced fluorescence from HPD, and b) for photodynamic therapy (HPD-PDT) using a localized HPD-assisted singlet oxygen release induced by irradiation of 630 nm laser light. This rapidly developing field has recently been reviewed by DOUGHERTY.
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3.
  • Ankerst, Jaro, et al. (författare)
  • Adenovirous type 9-induced tumorigenesis in the rat mammary gland related to sex hormonal state
  • 1989
  • Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 81:4, s. 294-298
  • Tidskriftsartikel (refereegranskat)abstract
    • Adenovirus type 9 was inoculated sc into newborn Wistar/Furth rats, divided into four groups: (1) six male rats, not treated further; (2) 11 male rats, castrated at 4 weeks of age; (3) 12 male rats, castrated at 4 weeks of age and subsequently treated repeatedly with estrogen; and (4) 12 female rats, not treated further. All of the rats in group 3 developed mammary hyperplasia and tumors (fibroadenomas and lipomas), in some cases with malignant histologic structure. Rats in group 4 developed similar mammary tumors, but with later appearance and significantly slower growth. A fifth group of rats, not virus inoculated but castrated and estrogen treated as in group 3, did not develop any demonstrable mammary lesions. The results show that the effects of the virus on the mammary gland are dependent upon an estrogenic background, which by itself cannot cause tumor development in males. It is suggested that viral DNA is incorporated into the cellular DNA in such a way that it influences the synthesis and/or activity of steroid receptors, triggering tumor development.
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7.
  • Ankerst, Jaro, et al. (författare)
  • Complete remission in a patient with acute myelogenous leukemia treated with leukocyte α-interferon and cimetidine
  • 1984
  • Ingår i: Cancer Immunology Immunotherapy. - 0340-7004. ; 17:1, s. 69-71
  • Tidskriftsartikel (refereegranskat)abstract
    • A 76-year-old woman with acute myelogenous leukemia with approximately 65% myeloblasts on bone marrow examination was treated daily with a combination of 4 megaU of leukocyte interferon IM and 1,000 mg cimetidine PO. During therapy there was a gradual decrease of bone marrow myeloblasts down to 9% and a normalization of peripheral white blood cells. The treatment was discontinued after 6 weeks because of increasing fatigue and anorexia. The general condition improved greatly during the following weeks and the patient entered complete remission, which has continued for 6 months so far. In the course of therapy there was a gradual appearance of antibodies showing a selective binding capacity to autochthonous leukemic cells with no tendency to increased binding to remission cells. The aim of this report is to stimulate a further evaluation of this form of therapy in additional AML patients whenever this might be justified as an alternative to conventional chemotherapy.
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8.
  • Ankerst, Jaro, et al. (författare)
  • Cross‐reacting tstas in adeno 7 and 12 tumors demonstrated by 51CR‐Cytotoxicity and isograft rejection tests
  • 1969
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 4:3, s. 279-287
  • Tidskriftsartikel (refereegranskat)abstract
    • Antisera of mice hyperimmunized against syngeneic X‐irradiated adeno 12 tumor cells were tested for complement‐dependent cytotoxicity against an adeno 7 and an adeno 12 hamster tumor by a 51Cr‐cytotoxic test, developed to work on non‐lymphoid target cells. Significant isotope release above the level of release obtained after exposure to control sera was recorded with both tumors. There was no similar release from BHK‐C13 control hamster cells. The cytotoxic effect on hamster adeno 7 tumor cells was confirmed by the colony inhibition technique. Furthermore, it was demonstrated by transplantation tests in mice that the hamster adeno 7 tumor cells were immunogenic, causing an isograft immunity to adeno 12 tumors similar to that induced by adeno 12 hamster and mouse tumor cells.
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9.
  • Ankerst, Jaro (författare)
  • Demonstration And Identification Of Cytotoxic Antibodies And Antibodies Blocking The Cell-Mediated Antitumor Immunity Against Adenovirus Type 12 Induced Tumors
  • 1971
  • Ingår i: Cancer Research. - 0008-5472. ; 31:7, s. 997-1003
  • Tidskriftsartikel (refereegranskat)abstract
    • Hyperimmune mouse antisera against syngeneic adenovirus type 12 induced tumors and their 7 S and 19 S fractions of immunoglobulins obtained after combined diethylaminoethyl cellulose and Sephadex G-200 separation were tested against a rat adenovirus type 12 induced tumor by 51 Cr release technique. The same sera and their fractions were investigated with the colony inhibition technique for ability to abrogate the inhibitory effect of mouse lymph node cells specifically immunized against syngeneic adenovirus type 12 induced tumors on rat adenovirus 12 target tumor cells. It was found that (a) hyperimmune antisera from mice which had received many immunization doses were cytotoxic to rat adenovirus 12 induced tumor cells at 37° in the presence of complement; (b) the same hyperimmune antisera abrogated specifically the inhibitory effect of specifically immune mouse lymph node cells on rat adenovirus 12 tumor cells; (c) the cytotoxic activity of the hyperimmune antisera at 37° in the presence of complement was found in 19 S fractions of γ-globulins; and (d) the serum factors causing abrogation of immune lymph node cells in vitro were found in 7 S fractions of immunoglobulins.
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10.
  • Ankerst, Jaro, et al. (författare)
  • Demonstration of two group‐specific TSTAs in adenovirus‐induced tumors
  • 1970
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 6:1, s. 84-92
  • Tidskriftsartikel (refereegranskat)abstract
    • Infection of mice and rats with any one of five tested human adenovirus types belonging to groups A and B (types 3, 7, 12, 18 and 31) induced an immunity to the TSTAs of type 12 tumors as detected by the colony inhibition (CI) test. No immunity was found against an adenovirus type 1 tumor. Two adenovirus types belonging to group C (types 1 and 5) were similarly tested and found to induce a clear‐cut immunity to the adenovirus type 1 tumor but not to tumors induced by adenovirus of groups A and B. The only tested virus type of group D (type 4) did not induce any clear‐cut immunity to either adenovirus 12 tumors or the adenovirus 1 tumor. Immunization of rats with rat adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 mouse tumor cells but not to a mouse polyoma tumor. Adenovirus 1 rat tumor cells induced no such immunity. Immunization of rats with syngenic adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 rat and mouse tumors and an adenovirus 7 hamster tumor, but not to an adenovirus 1 rat tumor or BHK‐C13 control hamster cells. The result of a tumor prevention experiment is consistent with the existence of a common TSTA induced by types 7 and 12 and a different TSTA induced by type 5 virus. It is concluded that the highly oncogenic group A and the weakly oncogenic group B adeno virus types all induce a common TSTA. Another TSTA is induced by the group C viruses, while no evidence has been obtained for the existence of any TSTA induced by a group D virus type.
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