| 1. |
- Bhuiyan, Hasanuzzaman, et al.
(författare)
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Lateral elements inside synaptonemal complex-like polycomplexes in ndt80 mutants of yeast bind DNA
- 2003
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Ingår i: Genetics. - : Genetics. - 0016-6731. ; 163:2, s. 539-544
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Tidskriftsartikel (refereegranskat)abstract
- The synaptonemal complex (SC) keeps the synapsed homologous chromosomes together during pachytene in meiotic prophase I. Structures that resemble stacks of SCs, polycomplexes, are sometimes found before or after pachytene. We have investigated ndt80 mutants of yeast, which arrest in pachytene. SCs appear normal in spread chromosome preparations, but are only occasionally found in intact nuclei examined in the electron microscope. Instead, large polycomplexes occur in almost every ndt80 mutant nucleus. Immunoelectron microscopy using DNA antibodies show strong preferential labeling to the lateral element parts of the polycomplexes. In situ hybridization using chromosome-specific probes confirms that the chromosomes in ndt80 mutants are paired and attached to the SCs. Our results suggest that polycomplexes can be involved in binding of chromosomes and possibly also in synapsis.
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| 2. |
- Chang, Tingru, et al.
(författare)
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A novel methodology to study antimicrobial properties of high-touch surfaces used for indoor hygiene applications-A study on Cu metal
- 2021
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Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 16:2
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Tidskriftsartikel (refereegranskat)abstract
- Metal-based high-touch surfaces used for indoor applications such as doorknobs, light switches, handles and desks need to remain their antimicrobial properties even when tarnished or degraded. A novel laboratory methodology of relevance for indoor atmospheric conditions and fingerprint contact has therefore been elaborated for combined studies of both tarnishing/corrosion and antimicrobial properties of such high-touch surfaces. Cu metal was used as a benchmark material. The protocol includes pre-tarnishing/corrosion of the high touch surface for different time periods in a climatic chamber at repeated dry/wet conditions and artificial sweat deposition followed by the introduction of bacteria onto the surfaces via artificial sweat droplets. This methodology provides a more realistic and reproducible approach compared with other reported procedures to determine the antimicrobial efficiency of high-touch surfaces. It provides further a possibility to link the antimicrobial characteristics to physical and chemical properties such as surface composition, chemical reactivity, tarnishing/corrosion, surface roughness and surface wettability. The results elucidate that bacteria interactions as well as differences in extent of tarnishing can alter the physical properties (e.g. surface wettability, surface roughness) as well as the extent of metal release. The results clearly elucidate the importance to consider changes in chemical and physical properties of indoor hygiene surfaces when assessing their antimicrobial properties.
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| 3. |
- Chang, Tingru, et al.
(författare)
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The interplay between atmospheric corrosion and antimicrobial efficiency of Cu and Cu5Zn5Al1Sn during simulated high-touch conditions
- 2021
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Ingår i: Corrosion Science. - : Elsevier BV. - 0010-938X .- 1879-0496. ; 185
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Tidskriftsartikel (refereegranskat)abstract
- The interplay between atmospheric corrosion and antimicrobial efficiency of bare Cu and Cu5Zn5Al1Sn was studied upon exposures simulating high-touch surface conditions. The survival of the bacteria Bacillus subtilis during surface contact with Cu and Cu5Zn5Al1Sn was examined under different degrees of surface oxidation, tarnishing, wettability and copper ion release. Depending on surface conditions complete bacteria inhibition was obtained within 4 min on Cu and within 6-10 min on Cu5Zn5Al1Sn. The antibacterial efficiency increases slightly with copper release rate and is governed by complex interactions between the corroded metal surface, bacteria and extracellular polymeric substances produced by the bacteria.
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| 4. |
- Dahlfors, Gunilla
(författare)
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Action and interaction of growth factors and regulatory molecules in vascular cells : With special reference to the IGF-I-system
- 2000
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Vascular function is greatly influenced by growth factors and regulatory molecules that can interact with each other in a complex pattern in the vascular wall. In this thesis we studied how different substances of special interest in the pathogenesis of vascular disease interact and regulate each other's expressions in endothelial cells and vascular smooth muscle cells (VSMCs).In VSMCs, angiotensin II was shown to delay PDGF-BB induced cell growth. This transient inhibitory effect of angiotensin II was mediated by the AT1-receptor, did not involve autocrine action of transforming growth factor-ß1 (TGF-ß1) and acted at a site downstream of PDGF-ß receptor phosphorylation.The interaction of the insulin-like growth factor-system (IGF-system) with various growth factors, glucose and nitric oxide (NO) was studied in vascular cells. Vascular endothelial growth factor (VEGF) and transforming growth factor-ß1 (TGF-ß1) regulated the expression of insulin-like growth factor-binding proteins (IGFBPs) in large vessel endothelial cells in a way that might cause an increased bioavailability of IGF-I locally in the subendothelial space. Angiotensin II, IGF-I and insulin did not affect IGFBP expression in these cells. The expression of IGFBPs was studied for the first time in human micro vessel endothelial cells. No effect of high glucose treatment on IGFBP expression was seen in either large vessel endothelial cells or microvessel endothelial cells. A possible interaction between NO and the IGF-system was studied in VSMCs. IGF-I did not have any significant effect on NO production in VSMCs and neither exogenous nor endogenous NO had any effect on IGFBP expression.In conclusion, we found that angiotensin II interacts with PDGF-BB in the regulation of VSMC growth. The IGF-system is regulated by VEGF and TGF-ß1 in endothelial cells while no effect of angiotensin II, IGF-I, insulin or high glucose was seen. We found no evidence for interaction of NO and the IGF-system in VSMCs.
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| 5. |
- Dahlfors, Gunilla, et al.
(författare)
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Effect of nitric oxide on vascular smooth muscle cell proliferation and insulin-like growth factor binding protein expression
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- A possible interaction between nitric oxide (NO) and the insulin-like growth factor (IGF)-system was studied in cultured rat aortic smooth muscle cells. The NO-donor SNAP markedly inhibited basal and sernm-induced DNA synthesis while addition of L-NAME, an inhibitor of endogenous NO production, had no effect. L-NAME did also not significantly affect IGF-I, angiotensin II or TGF-ß1- induced effects on DNA synthesis. IGF-I was shown to stimulate the expression of IGFBP-4 mRNA, as measured by an RNase-protection assay, and angiotensin II inhibited expression of IGFBP-2 mRNA. Addition of L-NAME did not significantly change the effect of IGF-I or angiotensin II on IGFBP mRNA expression, neither did L-NAME or SNAP affect basal expression of IGFBP-2, -4 or -6 mRNA. In conclusion, we found no evidence for interaction of NO with the IGF-system in smooth muscle cells. Nitric oxide did not regulate the expression of IGFBPs and IGF-I-induced smooth muscle cell proliferation was not affected by inhibition of endogenous NO production.
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| 6. |
- Dahlfors, Gunilla, et al.
(författare)
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Expression of insulin-like growth factor binding proteins and transforming growth factor-ß1 in human microvascular endothelial and bovine aortic endothelial cells, no effects of high glucose
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Vascular complications are the major cause of morbidity and mortality in patients with diabetes mellitus. Insnlin-like growth factor-I (IGF-I) and transforming growth factor-ß1 (TGF-ß1) are two growth factors that regnlate vascular smooth muscle cell function in vivo and might be involved in the development of diabetic vascnlar complications. In this study we measnred the expression of IGF-binding proteins (IGFBPs) and TGF-ß1 in human dermal microvessel endothelial cells (HDMEC). We also studied the effect of high glucose levels on the expression of IGFBPs and TGF-ß1 in cnltured HDMEC and bovine aortic endothelial cells (BAEC). Gene expression was measured by an RNase-protection assay and proteins secreted into conditioned medium by ELISA or Western blot. The HDMEC expressed mRNAs for IGF-I and IGFBP-2 through -6 of which IGFBP-4 was the most excessively expressed and IGFBP-2 and -4 were detected in conditioned medium. Culture of HDMEC in high glucose (25 mM) for two passages did not change mRNA expressions for IGFBP-2, -3 or -4 significantly. Neither did low glucose+ mannitol (5.6 mM+ 20 mM) have any effect. In BAEC, high glucose (25 mM) for 48 h or 96 h did not affect IGFBP-3, -4 or -5 mRNA or protein and exposnre of BAEC to high glucose for two passages did also not affect IGFBP mRNA. TGF-ß1 mRNA was expressed by both BAEC and HDMEC. High glucose for two passages did not alter TGF-ß1 gene expression in either BAEC or HDMEC. In conclusion, we show that HDMEC express IGFBPs and TGF-ß1 andthat high glucose does not affect the expression in either HDMEC or BAEC.
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| 7. |
- Dahlfors, Gunilla
(författare)
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Growth factors and their interaction in the regulation of vascular cells : with special reference to diabetes
- 1999
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Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Proliferation of vascular smooth muscle cells plays an important role in the development of atherosclerosis and in restenosis following balloon angioplasty. This study focuses on growth factors associated with diabetic vascular disease and their interaction in the regulation of vascular smooth muscle cell growth.The effect of streptozotocin-induced diabetes on proliferation of cells in aortic media two days after balloon angioplasty was studied. All proliferating cells in the aortic media were smooth muscle cells. In diabetic rats, the amount of proliferating cells was lower than in control rats. This was not accompanied by a change of transforming growth factor-ß1 (TGF-ß1) gene expression. Total TGF-ß1 levels in serum of diabetic rats was slightly lower and might possibly contribute to the inhibited proliferation of smooth muscle cells.The effect of angiotensin II on platelet-derived growth factor-BB(PDGF-BB)-induced growth was studied in cultured rat vascular smoothmuscle cells. Angiotensin II, acting through the AT1 receptor, transientlyinhibited the growth effect of PDGF-BB for approximately 6 hours. Thiswas not due to an autocrine effect of TGF-ß1, a growth factor consideredto mediate growth inhibitory actions of angiotensin II. Inhibition wasneither due to inhibition of PDGF-ß receptor phosphorylation.Large vessel endothelial cells from bovine aorta were shown to express and secrete insulin-like growth factor binding proteins (IGFBPs). Vascular endothelial growth factor (VEGF) and TGF-ß1, both associated with diabetic vascular complications, modulated the expression of IGFBPs in a way that might suggest increased bioavailability of insulin-like growth factor-I (IGF-I) locally in the vessel wall. VEGF, which is highly specific for endothelial cells, and TGF-ß1, might in this way indirectly regulate smooth muscle cell growth.In conclusion, we have shown that experimental diabetes has an inhibitory effect on smooth muscle cell proliferation in vivo, that interaction of growth factors, as shown for angiotensin II and PDGF-BB, might be of great importance for regulation of smooth muscle cell growth and that VEGF and TGF-ß1 regulate the IGF-system in large vessel endothelial cells with possible implications for regulation of smooth muscle cell function.
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| 8. |
- Dahlfors, Gunilla, et al.
(författare)
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Inhibitory effect of diabetes on proliferation of vascular smooth muscle after balloon injury in rat aorta
- 2000
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Ingår i: Experimental Diabetes Research. - 1687-5214 .- 1687-5303. ; 1:2, s. 101-109
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Tidskriftsartikel (refereegranskat)abstract
- The effect of streptozotocin-induced diabetes on cell proliferation in rat aortic intima-media, as well as on local gene expression of transforming growth factor-β1 (TGF-β1) was studied. TGF-β1 mRNA was measured by solution hybridization and TGF-β1 protein by ELISA. Proliferation was measured by bromodeoxyuridine incorporation into DNA two days after balloon injury. All BrdU-labelled cells observed were smooth muscle cells. After a diabetes duration of 2 and 4 weeks, labelled cells were significantly fewer compared with controls. Circulating levels of total TGF-β1 were lowered in rats with 2 weeks diabetes. Although the balloon injury procedure by itself stimulated the gene expression of TGF-β1, no significant difference in TGF-β1 mRNA content between diabetic and control rats after injury was found. In conclusion: vascular smooth muscle proliferation in vivo is inhibited by the diabetic state in this model of insulin deficient diabetes and this inhibition is not related to an impaired local expression of TGF-β1.
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| 9. |
- Dahlfors, Gunilla, et al.
(författare)
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PDGF-BB-induced DNA synthesis is delayed by angiotensin II in vascular smooth muscle cells
- 1998
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Ingår i: American Journal of Physiology. Heart and Circulatory Physiology. - 0363-6135 .- 1522-1539. ; 274:5, s. H1742-H1748
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Tidskriftsartikel (refereegranskat)abstract
- The interaction of ANG II with platelet-derived growth factor (PDGF)-BB-induced DNA synthesis was studied in cultured rat aortic smooth muscle cells. PDGF-BB-induced DNA synthesis was delayed (∼6–8 h) by ANG II as shown by a time-course experiment. Losartan, an AT1-receptor antagonist, blocked the transient inhibitory effect of ANG II, whereas the AT2-receptor antagonist PD-123319 had no effect. Autocrine- or paracrine-acting transforming growth factor-β1 (TGF-β1), believed to be a mediator of ANG II-induced inhibitory effects, was not responsible for the delay of PDGF-BB-induced DNA synthesis, because a potent TGF-β1 neutralizing antibody could not reverse this effect of ANG II, nor was the delay of the PDGF-BB effect caused by inhibition of PDGF-β-receptor phosphorylation as shown by Western blot analysis of immunoprecipitated PDGF-β receptor. In conclusion, our results show that ANG II can exert a transient inhibitory effect on PDGF-BB-induced proliferation via the AT1 receptor.
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| 10. |
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