He knows joy in all that he does: on the occasion of Jan Klein's 65th birthday.
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Biomedical subjects
Publications and source records attributed to I Vucak.
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The ventilatory function of the lung was studied in 100 patients (85 men and 15 women) suffering from ankylosing spondylitis. The mean age of the patients was 48 years (range: 29-72) and the mean duration of the disease was 18 years (range: 4-37). In 74% of the cases there was evidence of impaired ventilatory function of the lung. Most of the affected patients exhibited restrictive ventilation disorders (57 or 77%), the incidence of restrictive-obstructive (12 or 16.2%) and obstructive ventilation disorders (5 or 6.8%) being considerably lower. While there were no significant differences in the incidence of restrictive ventilation disorders with respect to the age of the patients (t = 0.84; P greater than 0.05) and the duration of the disease (t = 0.84; P greater than 0.05), a highly significant correlation was found between the functional stage of the disease and the severity of restrictive ventilation impairment (r = 0.46; P less than 0.001).
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Granulomatosis caused by four subcutaneous talc powder-suspension injections induced strong immunosuppression in rats. The disturbance included reduction of mononuclear white blood cell count in the peripheral blood, atrophy of the thymic cortex, spleen enlargement with predominance of red over the white pulp, increase in the number of lymph node germinal centres and a significant delay of the first-set and second-set allograft rejection. Neither phagocytic function of reticuloendothelial system nor erythrocyte count and humoral immune response were found to be altered. Indomethacin suppression of prostaglandin production did not normalize the allograft rejection dynamics. In contrast, splenectomy completely abolished the immunosuppressive effects of granulomatosis. In splenectomized, talc-treated animals WBC counts were not altered and the rejection of allografts was not delayed. Suppression of immune response to alloantigens was transferred to normal and splenectomized recipients by both serum and spleen cells of talc-injected animals. Also, in a cell mixture-transfer experiment, spleen cells from talc-granulomatosis-bearing donors suppressed the immune response induced by lymph node cells from immune donors in T cell-deficient rats. The inability of serum from splenectomized talc-injected rats to transfer the suppression suggested the crucial role of the spleen in the mechanisms leading to suppression in rats bearing talc-granulomatosis.
A total of 88 wild mice from the Dalmatian coast of Yugoslavia (35 animals), and Peloponnesus (30 animals) and Thebes (23 animals) on mainland Greece were karyotyped. In all but five animals Robertsonian translations were found. Mice from the Dalmatian region were homozygous for translocations Rb(5.15), Rb(6.12), Rb(8.17), Rb(9.13), and Rb(10.14); they were homo- or heterozygous for the translocation Rb(1.11). Some of them lacked the Rb(1.11) translocation altogether so that the diploid numbers in the Yugoslavian mice were 2n = 28, 29, 30, or 40. The mice from the vicinity of Olympia in northwestern Peloponnesus were homozygous for eight Robertsonian translocations: Rb(1.3), Rb(2.5), Rb(4.6), Rb(8.12), Rb(9.16), Rb(10.14), Rb(11.17), and Rb(13.15). Their diploid chromosome number was therefore 2n = 24. Mice from the vicinity of Patras in northwest Peloponnesus carried all except the first three of these eight translocations; their chromosome number was 2n = 30. Finally, the mice from Thebes were homozygous for translocations Rb(2.15), Rb(4.14), Rb(5.12), and Rb(10.13). They were homo- or heterozygous for Rb(6.9), Rb(8.17), and Rb(1.11); some mice lacked the Tb(1.11) translocation altogether. The translocations Rb(6.9)40Tu and Rb(10.13)42Tu represent new arm combinations not found previously in any wild mouse population. The remaining translocations have previously been found in different Mediterranean countries, in Scotland and in southern Germany. The findings suggest that each translocation arose only once and that different translocations have come together in different populations to generate a unique karyotype characterizing this population.
Twelve responder-stimulator combinations of mouse B10.W strains identical at K, D, and class II loci were tested for the generation of cytolytic T lymphocytes (CTL). No primary CTL could be obtained in any of the combinations but in nine combinations CTL were generated after priming in vivo. Six of these CTL are described. They define five antigenic determinants expressed exclusively in a small group of B10.W lines. The determinants appear to be part of the same system that resembles the Qa system originally defined in classic inbred strains. This resemblance rests on the observation that in vivo priming is necessary for the generation of the CTL, and that the CTL are not restricted in their reactivity by known H-2 loci. At least some of the determinants, however, appear to be controlled by a locus (or loci) associated with the K-rather than the D-end of the H-2 complex. Furthermore, some of the CTL directed against these Qa-like determinants cross-react with a molecule controlled by the K locus.
The B10.STA12 mouse congenic line inherited from the wild mouse parent not only the H-2w13 haplotype but also an allele at a minor H locus, which we designate H-41. This allele (H-41a) differentiates the B10.STA12 line from B10.STA10 and B10.LIB55, which carry identical H-2w13 haplotypes but a different H-41 allele (the H-41b, also present in the background strain C57BL/10Sn). The B10.STA12 and B10.STA10 lines reject each other's skin grafts and generate cytolytic T lymphocytes (CTL) after in vivo immunization and in vitro restimulation with cells of the partner strain. The B10.STA12 anti-B10.STA10 CTL react with B10.STA10, B10.LIB55, and B10.STA39 target cells and with cells of F1 hybrids between the responder strain B10.STA12 and strains C57BL/6, C57BL/10, C57L, BALB/c, A, AKR, WB, DBA/1, and DBA/2 but fail to react with (C3H x B10.STA12) F1 and (CBA x B10.STA12) F1 cells. The B10.STA10 anti-B10.STA12 CTL react with B10.STA12, B10.P, and C3H.NB cells but fail to react to (B6 x B10.STA10) F1 target cells. The CTL reactivity in both combinations is Dp restricted. The B10.STA10 anti-B10.STA12 CTL exhibit, in addition, a cross-reactivity with B10.SAA48 cells that may be directed at one of the alloantigens controlled by the H-2 haplotype of this strain.
B10.W females were immunized against syngeneic male cells (via the footpad and also i.p. in some strains) and their spleen cells were then restimulated in vitro and tested in the cell-mediated lympholysis assay for H-Y-specific killing of target cells. Only seven of the 33 tested lines were anti-H-Y responders. The effector cells obtained from each of the responder lines were then tested against male and female cells of other B10.W lines, as well as a number of classic B10 congenic lines, and the MHC molecules providing the context for H-Y recognition were identified. They were: Kk, Kw3, Kw7, Kw17, Kw27, Dk, and Dp. None of the strains generated effector cells capable of recognizing the H-Y antigen simultaneously in the context of the K and D molecules. The WOA1 females generated effector cells by using the Kw7 molecule for context of recognition, whereas the WR7 females produced cells recognizing the H-Y antigen exclusively in the context of the Dk molecule despite the fact that both lines share the Kw7 gene. Some of the effector cells cross-reacted with both male and female cells of other strains and this cross-reactivity could be attributed to the recognition of allogeneic MHC molecules controlled by K or D region genes. Interestingly, STA39 females generated Dp- but not Kw3-restricted anti-H-Y responses, whereas SAA48 females generated Kw3- but not Dw3-restricted responses; the Kw3-restricted cells cross-reacted with the Dp molecule. This cross-reaction might explain why the STA39 females do not mount a Kw3-restricted anti-H-Y response. Because the Kw3 + H-Y combination resembles Dp, the anti-Kw3 + H-Y T cells are functionally eliminated when tolerance of Dp molecules is attained in the STA39 mice.
Cell-mediated lymphocytotoxicity was generated in four strain combinations differing only by the cell-surface expression of the class II E molecule controlled by the H-2 complex. The four combinations were: B10.D2(R107) anti-B10.A(3R), B10.A(4R) anti-B10.A(2R), B10.GD anti-B10.D2(R101), and B10.S(7R) anti-B10.S(9R). In all four of these combinations, the stimulator expresses E molecules on the cell surface, while the responder does not. The cytolytic T lymphocytes generated in the B10.D2(R107) anti-B10.A(3R) and B10.A(4R) anti-B10.A(2R) combinations reacted not only with the stimulator but also with strains that do not express cell-surface E molecules, in particular, strains carrying the H-2f and H-2q haplotypes. The cross-reactivity with E-negative strains could be blocked by monoclonal antibodies specific for the Af or Aq molecules but not by antibodies recognizing determinants on E or class I (K) molecules. The anti-H-2f cross-reactivity could be inhibited by H-2q cold targets and, reciprocally, the anti-H-2q reactivity could be blocked by H-2f cold targets. These findings are interpreted as indicating that the cytolytic T lymphocytes stimulated by E molecules can recognize and lyse cells lacking E molecules but expressing A molecules. The observed E-A cross-reactivity supports the notion of structural and functional relatedness between the A and E molecules and suggests a common evolutionary origin of the A- and E-encoding loci.
The B10.STA62 strain carries the H-2w27 haplotype derived from a wild mouse captured in the vicinity of Ann Arbor, Michigan. Products of two class II loci composing this haplotype, A alpha and A beta, are serologically, biochemically (by tryptic peptide mapping), and functionally indistinguishable from products controlled by the Ab alpha and Ab beta genes of the B10.A(5R) strain. In contrast, the polypeptide chain controlled by the third class II locus, E beta, is different from that controlled by the Eb beta gene. This Ew27 beta chain lacks an antigenic determinant present on the Eb molecule and carries determinants lacking on the Eb molecule, the Eb beta and Ew27 beta peptide maps differ in at least six peptides, and cytotoxic T cells specific for the Eb beta chains do not react with B10.STA62 target cells. This great difference between the Eb beta and Ew27 beta chains suggests that the corresponding genes have not been derived from one another by a direct mutational conversion; instead, H-2w27 appears to be a recombinant haplotype derived by crossing-over between the A alpha A beta duplex and the E beta locus. This is the first recombinant discovered separating these class II loci.
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Professor B. Spisić is rightly referred to as founder of the Croatian orthopaedics and rehabilitation. Based on the principles formulated by Prof. B. Spisić the next generations of Croatian orthopaedists gave their contribution to the remarkable building of the orthopaedics. The First World War gave a strong impetus to the development of orthopaedics, as well as medical and social rehabilitation in Croatia. Dr. V. Cepulić was among the first who, as early as 1915, joined Dr. B. Spisić. Their close and fruitful collaboration was disrupted by Dr. V. Cepulić's long absence because of illness. Later on, Dr. V. Cepulić became a famous Croatian physiologist. Owing to his contribution in fighting tuberculosis in Croatia, as well as his merits for the Croatian Medical Association, he is among the most prominent Croatian doctors. On this occasion, the memory of his place in the history of Croatian orthopaedics, that is less known, is refreshed.
Prof. dr. Hugo Gjanković is among the most prominent Croatian doctors of this century. He has studied medicine in Austria and has been promoted in Wienna in 1920. First he worked unpaid in Ginecology Clinics in Wienna and then in 1922. he was accepted as assistant doctor at newly established Surgery Clinic of the Medical Faculty University of Zagreb. He worked hard to become respectable surgeon and university teacher. He was an effervescent member of the Croatian Medical Association--lecturing, publishing numerous papers and participating at many congresses in the country and abroad. His compulsory transfer, for political reasons, to the Department of Surgery of the State Hospital in Sarajevo during the Second World Was ment four years-long break in his academic career. Returned to afterwar Zagreb and to the Clinic as assistant professor he continued to improve the operation techniques, to establish the surgeons associations and to lecture for his colleagues, for the medical students and to the general public. He has published several textooks of surgery. Insulted by the measures taken by the Medical Faculty Authorities towards himself, he felt forced to leave Zagreb in 1953. In his 60th he has accepted the position of the Head of the Department of Surgery in the General Hospital in Dubrovnik. Next seven years he has invested in the through reconstruction of that hospital, particularly the Department of Surgery. He has proved helpful to his younger colleagues in their education and academic advancement. There is a lot to be learned from, not only his numerous papers and books, but from his biography, too.
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