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Biomedical subjects

D Zelenika

Publications and source records attributed to D Zelenika.

13 recordsLinked to original sources
PubMed2006

[Hospital outcome in acute coronary syndrome in the period 1987-2001 in West-Herzegovina canton--retrospective study].

Objective of the study is to show prevalence of hospital mortality of acute coronary syndrome in pre-war (1987-1991), war (1992-1996) and after war period (1997-2001) among inhabitants of West-Herzegovina canton living in the following municipalities: Siroki Brijeg, Posusje, Grude and Ljubuski (88,992 inhabitants). Collected were data on patients who were admitted in the hospital due to acute coronar syndrome (category I 20, 21, 22- X revision, ICD) in the above period in Mostar. Data were analyzed in regard to sex, age and disease output. Hospital morality in 15 year period for both sex were 15.0 %, men 12.1 %, and women 20.2 %. Statistically it was not found significant differences in the period 1987-2001 in regards to total hospital mortality of men and women and separate hospital mortality of men. Differences were found in women where considerable larger number was in pre-war and post-war period in comparison with war period. The largest hospital mortality was in total and for women in the pre-war period and for men was during the war period. The smallest hospital mortality was in total and for women during the war and for men in pre-war period. We find that lower hospital mortality in women was caused by lower hospital admission because of war time and problems with transport and that larger number of women deceased before admission to the hospital.

Angina, Unstable↗
PubMed2001

The role of CD4+ T-cell subsets in determining transplantation rejection or tolerance.

Peripheral tolerance to allogeneic organ grafts can be induced in rodents by treating with non-depleting CD4 and CD8 monoclonal antibodies. This tolerance is maintained by CD4+ T cells with a potent capacity to induce tolerance in further cohorts of T cells (i.e. infectious tolerance). We have cloned CD4+ T-cell subsets against the male transplantation antigen in vitro and find, in contrast to Th1 or Th2 clones that elicit rejection, that there is a distinct population of CD4+ T cells that suppress rejection by adoptive transfer (here called Treg). In order to identify molecular markers associated with tolerance and gain insights into the mechanisms of action of Treg cells, we carried out serial analysis of gene expression. We identified genes overexpressed in Treg compared to Th1 and Th2 cultures and found that some of these correlated in vivo with CD4-induced transplantation tolerance rather than rejection. The genes overexpressed in Treg cultures and within tolerated skin grafts were primarily expressed by mast cells (e.g. tryptophan hydroxylase and FcepsilonR1alpha), suggesting that regulatory cell activity and this form of tolerance may be associated with a localised but non-destructive form of Th2-like activation and a recruitment of mast cells.

Animals↗
PubMed1999

CD4 T cells can reject major histocompatibility complex class I-incompatible skin grafts.

We have re-investigated the roles of CD4 and CD8 T cell subsets in skin graft rejection across a single class I MHC disparity. Recipient mice were transplanted with skin from donors transgenic for the class I MHC molecule Kb. As expected, CD8 T cells were sufficient for rapid injection; but surprisingly, CD4 T cells were also competent to do the same. Rejection was dependent on one or the other subset, since elimination of both resulted in indefinite graft survival. The possibility that alloantibody was the downstream effector of CD4 mediated rejection was excluded because CD8-depleted mice rendered B cell deficient still rejected rapidly, but T cell-depleted recipients with pre-existing high titers of alloantibody were unable to do so. In addition, if CD4 cells act to reject by recruiting and/or activating macrophages then this was not dependent on CR3, IFN-gamma or TNF-alpha. Transplantation of skin grafts where the MHC class I disparity was at the level of passenger leukocytes only, demonstrated that transient bystander damage could occur, but that this was insufficient to result in full rejection. We surmise that for CD4 T cells to reject an MHC class I-incompatible graft it is necessary that an appropriate allogeneic peptide is processed and presented in the context of recipient MHC class II. CD4 T cells from B6 mice may fail to reject skin from MHC class I mutants because of the lack of such MHC class II-restricted presentation.

Animals↗
PubMed1998

Rejection of H-Y disparate skin grafts by monospecific CD4+ Th1 and Th2 cells: no requirement for CD8+ T cells or B cells.

We wished to determine whether CD4+ T cells could reject a skin graft that was discordant for a single minor transplantation Ag in the absence of CD8+ T cells or Ab. Transgenic A1(M) mice were constructed that express the rearranged V beta 8.2 and V alpha 10 TCR genes from a T cell clone that is specific for the male Ag (H-Y) in the context of H2-Ek. In addition, the RAG-1(-/-) background was bred onto these mice to eliminate any endogenous TCR rearrangements. As expected, clonal deletion was found to be complete in the thymus of male A1(M) x RAG-1(-/-) mice, while only CD4+ T cells were positively selected and found in the periphery of females. Female A1(M) x RAG-1(-/-) mice were able to rapidly reject (in <14 days) male (but not female) skin grafts in a CD4-dependent fashion. After multiple grafts, it was confirmed that no CD8+ T cells or surface Ig+ B cells were present. An immunofluorescent analysis of spleen cells after grafting showed that the majority of T cells expressed activation markers (CD44, CD25, and intracytoplasmic IL-2) and a significant proportion were making IFN-gamma and IL-4. Surprisingly, the transfer of either Th1 or Th2 CD4+ T cell lines from these mice into T cell-depleted recipients was sufficient to cause a specific rejection of male skin.

Animals↗
PubMed1995

A novel glial fibrillary acidic protein mRNA lacking exon 1.

Glial fibrillary acidic protein (GFAP) is the major intermediate filament protein in the mature astrocytes. We have assayed for the presence of GFAP mRNA gene in mouse tissues outside the nervous system. Nuclease S1 protection experiments show that RNAs lacking exon 1 are transcribed in bone marrow. From a mouse bone marrow cDNA library we isolated GFAP cDNAs which start in the 3' part of intron 1 and contain all the downstream GFAP exons. The new GFAP mRNAs, which we call GFAP gamma mRNAs, are already present in the brain at embryonic day 15 and in adult forebrain and cerebellum. Their presence in astrocytic cell lines suggests that astrocytes may be the site of in vivo expression of these mRNAs. In addition we have detected GFAP gamma mRNAs in mouse spleen. Furthermore in human an analogous GFAP mRNA containing the 3' part of intron 1 and lacking the exon 1 is also present in adult brain. These results suggest a new regulation of the GFAP gene expression.

Animals↗
PubMed1994

Identification of new human myelin basic protein transcripts in the immune and central nervous systems.

Five new myelin basic protein (MBP) transcripts were identified which each have preferential sites of expression in adult human brain and immune system. They contain a novel 5' coding region which presents extensive sequence similarity to the mouse 0' region. One of these ribonucleic acid (RNA) species, HMBPR1, is found essentially, if not only, in haemopoietic and immune cells. Two alternatively spliced transcripts called MBP2a and c are only expressed in the central nervous system (CNS). In addition, the two other transcripts are expressed in both immune and nervous systems. Thus, the MBP locus can generate multiple forms of RNA, whose start sites and splicing depend on the tissue in which they are expressed. The presence of an MBP transcript specifically expressed in the adult human immune system suggests previously unsuspected functions related to the pathogenesis of multiple sclerosis.

Amino Acid Sequence↗
PubMed1993

A new family of transcripts of the myelin basic protein gene: expression in brain and in immune system.

A cDNA clone (MBP2) corresponding to a novel mouse myelin basic protein (MBP) mRNA has been isolated from an adult mouse bone marrow cDNA library. It contains the MBP exons 1a-7 except exon 5. Using PCR experiments we have determined that this MBP2 mRNA belongs to a new MBP mRNA family initiated upstream from exon 1b. Their 5' end extends into exon 1a and/or the region 0' previously described. These mRNAs are generated by alternative splicing of the primary transcript involving excision of exon 1a, 1b, 2, 5, or 6. Thus, these new mRNAs are produced from a promoter(s) located upstream from the major promoter 1b. They are expressed in brain (at least from embryonic day 15), in bone marrow, and in other hemolymphopoietic tissues, particularly in macrophage cells. As their expression is not restricted to myelinating cells, the function of these novel MBP mRNAs and putative proteins might not be related to myelination.

Animals↗
PubMed1992

A novel transcript overlapping the myelin basic protein gene.

Myelin basic protein (MBP) is a major constituent of myelin synthesized by oligodendrocytes and Schwann cells. We have investigated the expression of mouse MBP RNAs outside the nervous system. Nuclease protection experiments indicate that RNAs containing exon 1 and not the six downstream exons of the MBP gene are transcribed in various hemopoietic tissues. We have isolated a hemopoietic MBP-related (HMBPR) cDNA clone from a mouse bone marrow cDNA library screened with an MBP cDNA probe. This clone contains exons 1a and 1b and a part of intron 1 of the MBP gene. An additional 5' region, encoded by at least three unidentified exons, lies upstream of exon 1a. The HMBPR clone corresponds to a 5-kb RNA expressed in bone marrow, spleen, thymus, and macrophagic cells. This transcript is expressed at a similar level in brain, although at a lower level than the classical 2-kb mRNA. These data indicate that a new transcript, overlapping the MBP transcription unit and controlled by a distinct promoter, is expressed in hemopoietic tissues. This RNA might encode a 21-kDa protein sharing a common domain with MBP.

Amino Acid Sequence↗
PubMed1991

Isolation of a novel cDNA corresponding to a transcript expressed in the choroid plexus and leptomeninges.

The CNS is composed of neurons and glial cells (i.e., astrocytes, oligodendrocytes, and microglia). The brain communicates with the blood circulation through choroid plexus and meninges as well as through the blood-brain barrier. To identify transcripts specifically expressed in a distinct brain cell type, we have previously constructed a subtracted cDNA library from the poly(A)+ RNAs of a velate protoplasmic-like astrocytic cell line, designated D19. This library was screened in order to isolate transcripts over-expressed in this astroglial cell line versus another astroglial cell line. Of the six recombinants which have been isolated, three sequences have not been described. Their sizes ranged from 100 to 200 bp and they hybridized to mRNAs expressed in vivo inside and outside the CNS. We have constructed a size-selected D19 cDNA library in order to obtain the full length cDNAs corresponding to the three undescribed sequences. We report here the isolation of a 1.6 kb cDNA corresponding to one of these recombinants, named p14. Its sequence has not yet been described and its deduced amino acid sequence codes for a 43 kDa protein with a putative signal peptide. In situ hybridization shows that this transcript is expressed at a high level in choroid plexus and leptomeninges and also in perivascular cells in the adult mouse brain. It is also expressed in cell subsets of kidney and gonads as well as in perivascular cells in skeletal and cardiac muscles. These localizations suggest that the encoded protein might be involved in transport processes and hormonally controlled.

Animals↗
PubMed1990

[Membrane abnormalities and cellular hyperreactivity in different models of hypertension].

In various models of hypertension of genetic origin, a hypersensitivity of phospholipase C has been demonstrated to participate in the hyperreactivity of platelets toward a variety of vasoactive agents. Since this abnormality could not be observed in the absence of cell stimulation, it could not account for the increase in free Ca2+ which has been reported in resting platelets in primary hypertension. Likewise, in hypertensive subjects, platelets behave hyperactive when stimulated by ADP, although the stimulus has been demonstrated to be a poor activator of phospholipase C. In order to gain insight into the membrane alteration that could account for the cellular hyperactivity which characterizes hypertensive subjects, we investigated, in resting platelets, the kinetics of radioactive labeling of major membrane phospholipids. Isolated platelets were prepared from SHR (4w and 17w of age), SHR-SP, Dahl salt-resistant and salt-sensitive rats fed either a low or a high salt diet, DOCA-salt hypertensive rats and from the appropriate normotensive controls. Irrespective of the radioactive precursor used (32P-orthophosphate, 3H-glycerol, 3H-choline), the labeling of phosphatidylcholine (PC) was markedly (up to 20 fold) enhanced in SHR (whichever their age) and SHR-SP compared with WKY. This increase, specific of PC, could not be accounted for by differences either in the actual amount of PC or in the uptake of various labels, suggesting an increased PC turnover. Such an increase was also observed in platelets of Dahl hypertensive rats but not in those of DOCA-salt hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Clinical and morphologic characteristics of adult IgA nephropathy].

Within the period 1987-1992 IgA nephropathy was diagnosed at the Nephrology Clinic of the Military Medical Academy in 61 patients aged from 17 to 41 years (mean +/- SD = 24.31 +/- 6.39). The aim of the study was to evaluate their importance as markers of progressive forms of IgA nephropathy by analysis of mutual relationship of clinical-laboratory and histopathological characteristics. Clinical form of the disease with recurrent macroscopic hematurias existed in 30 (49.2%) patients, and oligosymptomatic form in 31 (50.8%) patients. Acute renal failure of reversible oliguric character had 5 (8.2%) patients. Patients with recurrent macroscopic hematurias had more progressive course of IgA nephropathy which could be indirectly seen from the parameters of the global renal function. The most frequent histological form of IgA nephropathy was diffuse mesangioproliferative glomerulonephritis registered in 30 (49.2%) patients.

Adolescent↗