| 41. |
- Abdelkader, Amal F., 1969, et al.
(författare)
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High salt stress induces swollen prothylakoids in dark-grown wheat and alters both prolamellar body transformation and reformation after irradiation
- 2007
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Ingår i: Journal of Experimental Botany. - : Oxford University Press (OUP). - 0022-0957 .- 1460-2431. ; 58:10, s. 2553-2564
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Tidskriftsartikel (refereegranskat)abstract
- High salinity causes ion imbalance and osmotic stress in plants. Leaf sections from 8-d-old dark-grown wheat (Triticum aestivum cv. Giza 168) were exposed to high salt stress (600 mM) and the native arrangements of plastid pigments together with the ultrastructure of the plastids were studied using low-temperature fluorescence spectroscopy and transmission electron microscopy. Although plastids from salt-treated leaves had highly swollen prothylakoids (PTs) the prolamellar bodies (PLBs) were regular. Accordingly, a slight intensity decrease of the short-wavelength protochlorophyllide (Pchlide) form was observed, but no change was found in the long-wavelength Pchlide form emitting at 656 nm. After irradiation, newly formed swollen thylakoids showed traversing stromal strands. The PLB dispersal was partly inhibited and remnants of the PLBs formed an electron-dense structure, which remained after prolonged (8 h) irradiation. The difference in fluorescence emission maximum of the main chlorophyll form in salt-stressed leaves (681 nm) and in control leaves (683 nm) indicated a restrained formation of the photosynthetic apparatus. Overall chlorophyll accumulation during prolonged irradiation was inhibited. Salt-stressed leaves returned to darkness after 3 h of irradiation had, compared with the control, a reduced amount of Pchlide and reduced reformation of regular net-like PLBs. Instead, the size of the electron-dense structures increased. This study reports, for the first time, the salt-induced swelling of PTs and reveals traversing stromal strands in newly formed thylakoids. Although the PLBs were intact and the Pchlide fluorescence emission spectra appeared normal after salt stress in darkness, plastid development to chloroplasts was highly restricted during irradiation.
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| 42. |
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| 43. |
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| 44. |
- Abdula, Rahimaisa, 1976
(författare)
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Climate Change Policy of Bio-Energy: A Computable General Equilibrium Analysis
- 2005
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Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
- This paper explores the intersectoral and land-use dynamics behind bio-energyâ??s development as a climate change policy. Bio-energy from agriculture and forestry can potentially mitigate the emissions of carbon dioxide (CO2) from energy use and land-use changes (LUC) by its substitution to fossil fuels and its diversion of land-use to biomass plantation. Two major issues concerning its interplay with the other sectors of the economy and other land-use options are mapped in the study, namely its competition with other energy sources and sectors of similar production structure such as the crops and livestock sector; and its competition for land with other land-use based CO2 mitigation option of afforestation. By employing a computable general equilibrium with a land-use change model, the study was able to depict the various interfaces of bio-energy with the rest of the economy and with the land market. Moreover, the model enabled the mapping of policy implications upon the economy, welfare, and pattern of land-use changes and its subsequent contribution to CO2 emissions. The main policy considered in this study is the carbon taxation with revenues geared towards the reduction of direct taxes and towards the finance of bio-energy subsidy. Results showed that the carbon taxation per se does not ensure the growth of the bio-energy sector, unless the tax base is extended to land-use changes and unless the proceeds are directed to subsidize the sector or to buttress the incomes and consumptions of rural households; the main users of bio-energy. Investment in bio-energy as a complementary mitigation policy to carbon taxation has resulted into the improvements in the domestic capacity for energy sourcing and the welfare of the rural households. It successfully lowered the cost of mitigation by shifting reliance away from fossil fuels and by inducing land-use conversion to bio-energy and forestry purposes, without instigating dramatic transformations in the land-use system and without producing catastrophic burden upon the agricultural sector. Moreover, despite the competition for scarce land resource of the different land-use based mitigation options, synergies between developing carbon offset through bio-energy and building carbon sink through afforestation can be achieved through the market mechanism. The same benefits are presented by integrating land-use changes emissions into the carbon tax coverage.
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| 45. |
- Abdulle, Sahra, 1970, et al.
(författare)
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Cerebrospinal fluid viral load and intrathecal immune activation in individuals infected with different HIV-1 genetic subtypes
- 2008
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 3:4
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: HIV-1 exhibits a high degree of genetic diversity and is presently divided into 3 distinct HIV-1 genetic groups designated major (M), non-M/non-O (N) and outlier (O). Group M, which currently comprises 9 subtypes (A-D, F-H, J and K), at least 34 circulating recombinant forms (CRFs) and several unique recombinant forms (URFs) is responsible for most of the HIV-1 epidemic. Most of the current knowledge of HIV-1 central nervous system (CNS) infection is based on subtype B. However, subtypes other than subtype B account for the majority of global HIV-1 infections. Therefore, we investigated whether subtypes have any influence on cerebrospinal fluid (CSF) markers of HIV-1 CNS infection. METHODOLOGY/PRINCIPAL FINDINGS: CSF HIV-1 RNA, CSF neopterin and CSF white blood cell (WBC) count were measured in patients infected with different HIV-1 subtypes. Using multivariate regression analysis, no differences in the CSF WBC count, neopterin and viral load were found between various HIV-1 subtypes. CONCLUSIONS: We did not find any subtype-dependent differences in the markers evaluated in this study.
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| 46. |
- Abdulle, Sahra, 1970, et al.
(författare)
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Continuing intrathecal immunoactivation despite two years of effective antiretroviral therapy against HIV-1 infection
- 2002
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Ingår i: Aids. ; 16:16, s. 2145-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To study the effect of antiretroviral combination treatment on intrathecal immunoactivation in HIV-1 infection. METHOD: Lumbar punctures were performed at baseline, and after 4 months, 1 and 2 years on 30 neurologically asymptomatic, treatment-naive HIV-1-infected patients started on antiretroviral treatment with three or more drugs. Levels of neopterin, beta2-microglobulin and HIV-1 RNA were measured in cerebrospinal fluid (CSF) and blood. RESULTS: All patients continued the study until the 4-month follow-up, although seven discontinued before the 1-year control, and an additional five discontinued before the control after 2 years. Neopterin, beta2-microglobulin and HIV-1 RNA decreased significantly both in CSF and blood, but although 100% of the patients decreased their CSF concentrations of beta2-microglobulin and HIV-1 RNA to normal levels, only 55% had normal CSF neopterin concentrations after 2 years treatment. CONCLUSIONS: In addition to CSF viral load, antiretroviral combination therapy substantially decreases the intrathecal immunoactivation as reflected by CSF neopterin and beta2-microglobulin in neuroasymptomatic HIV-1-infected patients. However, almost half of the patients still have slightly increased CSF neopterin concentrations after 2 years of effective treatment, which might reflect an ongoing low-grade viral replication in brain tissue.
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| 47. |
- Abdulle, Sahra, 1970, et al.
(författare)
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CSF neurofilament protein (NFL) - a marker of active HIV-related neurodegeneration.
- 2007
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Ingår i: Journal of neurology. - : Springer Science and Business Media LLC. - 0340-5354 .- 1432-1459. ; 254:8, s. 1026-32
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND METHODS : The light subunit of the neurofilament protein (NFL), a major structural component of myelinated axons, is a sensitive indicator of axonal injury in the central nervous system (CNS) in a variety of neurodegenerative disorders. Cerebrospinal fluid (CSF) NFL concentrations were measured by ELISA (normal < 250 ng/l) in archived samples from 210 HIV-infected patients not taking antiretroviral treatment: 55 with AIDS dementia complex (ADC), 44 with various CNS opportunistic infections/tumours (CNS OIs), 95 without neurological symptoms or signs, and 16 with primary HIV infection (PHI). The effect of highly active antiretroviral treatment (HAART) was studied by repeated CSF sampling in four of the ADC patients initiating treatment. RESULTS : CSF NFL concentrations were significantly higher in patients with ADC (median 2590 ng/l, IQR 780-7360) and CNS OIs (2315 ng/l, 985-7390 ng/l) than in neuroasymptomatic patients (<250 ng/l, <250-300) or PHI (<250 ng/l, <250-280), p < 0.001. Among patients with ADC, those with more severe disease (stage 2-4) had higher levels than those with milder disease (stage 0.5-1), p < 0.01. CSF NFL declined during HAART to the limit of detection in parallel with virological response and neurological improvement in ADC.CSF NFL concentrations were higher in neuroasymptomatic patients with lower CD4-cell strata than higher, p < 0.001. This increase was less marked than in the ADC patients and noted in 26/58 neuroasymptomatic patients with CD4 counts <200/mul compared to 1/37 with CD4-cells >/=200/mul. CONCLUSIONS : The findings of this study support the value of CSF NFL as a useful marker of ongoing CNS damage in HIV infection. Markedly elevated CSF NFL concentrations in patients without CNS OIs are associated with ADC, follow the grade of severity, and decrease after initiation of effective antiretroviral treatment. Nearly all previously suggested CSF markers of ADC relate to immune activation or HIV viral load that do not directly indicate brain injury. By contrast NFL is a sensitive marker of such injury, and should prove useful in evaluating the presence and activity of ongoing CNS injury in HIV infection.
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| 48. |
- Abdulle, Sahra, 1970, et al.
(författare)
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Effects of antiretroviral treatment on blood-brain barrier integrity and intrathecal immunoglobulin production in neuroasymptomatic HIV-1-infected patients.
- 2005
-
Ingår i: HIV medicine. - : Wiley. - 1464-2662 .- 1468-1293. ; 6:3, s. 164-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To study the effect of antiretroviral combination therapy on blood-brain barrier (BBB) integrity and intrathecal immunoglobulin G (IgG) production. METHODS: Lumbar punctures were performed on 38 neurologically asymptomatic, treatment-naive HIV-1-infected patients prior to and during treatment at intervals of approximately 4 months, 1 year and 2 years. Albumin ratio and IgG index were analysed as markers of BBB integrity and intrathecal IgG synthesis. RESULTS: HIV-1 RNA decreased to < 50 HIV-1 RNA copies/mL in the cerebrospinal fluid (CSF) of all patients and in the plasma of all but one patient. Only 5% of patients had elevated albumin ratio values at baseline, while 56% had an elevated IgG index. There was no significant reduction of the albumin ratio or the IgG index. After 2 years of treatment all patients had normal albumin ratio values, while 41% still had increased IgG index levels. CONCLUSIONS: Up to 2 years after the initiation of treatment, the favourable impact of antiretroviral combination treatment on CSF viral load was not accompanied by a similar reduction of intrathecal IgG production. BBB function, measured as the albumin ratio, was not significantly changed in this cohort of neurologically asymptomatic HIV-1-infected patients.
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| 49. |
- Abdulle, Sahra, 1970
(författare)
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HIV-1 infection of the central nervous system. Markers of pathogenesis and antiretroviral treatment effects
- 2006
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Human immunodeficiency virus type 1 (HIV-1) invades the central nervous system (CNS) early in the course of infection and either directly or through opportunistic infections causes a spectrum of neurological complications. The most severe manifestation of HIV-1 CNS infection is AIDS Dementia Complex (ADC), which occurs in approximately 20% of untreated patients with AIDS. ADC is considered the result of a complex interplay between immune activation effects and viral replication in the brain, which ultimately leads to neuronal injury and death. Reliable markers to diagnose HIV-1 associated CNS injury, track disease progression, and identify patients at risk of developing ADC are lacking. Such markers would also be beneficial in evaluating the efficacy of antiretroviral treatment (ART) in the CNS, as well as to provide insights into the pathogenesis of HIV-1 CNS infection.HIV-1 elicits intrathecal cell-mediated and humoral immune activation. We found that ART effectively decreased the cerebrospinal fluid (CSF) concentrations of neopterin and beta2-microglobulin, but had little effect on the elevated IgG index. However, almost half of the patients still had slightly elevated levels of neopterin after 2 years of follow-up. Phylogenetic analyses have identified 3 distinct HIV-1 genetic groups. Group M, which is responsible for most of the global HIV-1 epidemic is further subdivided into subtypes and circulating recombinant forms (CRFs). Most of the current knowledge of HIV-1 CNS infection is based on studies of subtype B, which is predominant in the western world. However, subtypes other than subtype B are responsible for most of the epidemic outside the western world, and HIV-1 infections due to subtypes other than B are rapidly increasing across Europe. Markers of HIV-1 CNS infection such as HIV-1 RNA, neopterin, and white blood cell (WBC) count in CSF were measured and compared in patients infected with different HIV-1 subtypes. We did not find any significant subtype-specific differences in the neuromarkers evaluated in this study. Thus, subtypes do not appear to influence neuropathogenesis.Although there is no evidence of productive infection of neurons the end-result of HIV-1 CNS infection is neuronal damage and loss. We investigated the potential of CSF neurofilament (NFL), a sensitive indicator of axonal injury, as a marker of HIV-1 associated neurodegeneration. CSF NFL concentrations were higher in patients with ADC than in neuroasymptomatic patients, or patients with primary HIV-1 infection. Patients with severe ADC had higher CSF NFL levels compared to those with milder disease. CSF NFL declined with ART to the limit of detection in parallel with virological response and neurological improvement in patients suffering from ADC.Neurocognitive impairment remains a major concern in HIV-1 infection despite the success of ART. Studies on the pathogenesis, epidemiology, and the effects of ART on HIV-1 CNS infection are important to improve patient management.
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| 50. |
- Abdurahman, Samir, 1965-, et al.
(författare)
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Activity of the small modified amino acid alpha-hydroxy glycineamide on in vitro and in vivo human immunodeficiency virus type 1 capsid assembly and infectivity
- 2008
-
Ingår i: Antimicrobial Agents and Chemotherapy. - 0066-4804 .- 1098-6596. ; 52:10, s. 3737-3744
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Tidskriftsartikel (refereegranskat)abstract
- Upon maturation of the human immunodeficiency virus type 1 (HIV-1) virion, proteolytic cleavage of the Gag precursor protein by the viral protease is followed by morphological changes of the capsid protein p24, which will ultimately transform the virus core from an immature spherical to a mature conical structure. Virion infectivity is critically dependent on the optimal semistability of the capsid cone structure. We have reported earlier that glycineamide (G-NH(2)), when added to the culture medium of infected cells, inhibits HIV-1 replication and that HIV-1 particles with aberrant core structures were formed. Here we show that it is not G-NH(2) itself but a metabolite thereof, alpha-hydroxy-glycineamide (alpha-HGA), that is responsible for the antiviral activity. We show that alpha-HGA inhibits the replication of clinical HIV-1 isolates with acquired resistance to reverse transcriptase and protease inhibitors but has no effect on the replication of any of 10 different RNA and DNA viruses. alpha-HGA affected the ability of the HIV-1 capsid protein to assemble into tubular or core structures in vitro and in vivo, probably by binding to the hinge region between the N- and C-terminal domains of the HIV-1 capsid protein as indicated by matrix-assisted laser desorption ionization-mass spectrometry results. As an antiviral compound, alpha-HGA has an unusually simple structure, a pronounced antiviral specificity, and a novel mechanism of antiviral action. As such, it might prove to be a lead compound for a new class of anti-HIV substances.
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