| 1. |
- Bergqvist, A, et al.
(författare)
-
Loss of DNA-binding and new transcriptional trans-activation function in polyomavirus large T-antigen with mutation of zinc finger motif.
- 1990
-
Ingår i: Nucleic Acids Research. - 0305-1048 .- 1362-4962. ; 18:9, s. 2715-20
-
Tidskriftsartikel (refereegranskat)abstract
- A putative zinc finger in polyomavirus large T-antigen was investigated. We were unable to demonstrate unequivocally a requirement for zinc in specific DNA-binding using the chelating agent 1, 10-phenanthroline. An involvement of the putative zinc finger in specific DNA-binding was nevertheless suggested by the properties of a mutant protein with a cys----ser replacement in the finger motif. Probably as a result of the defective DNA-binding, the mutant protein had lost its activity in initiation of viral DNA-replication and in negative regulation of viral early transcription. However, the trans-activation of the viral late promoter was normal. The analysis also revealed a previously unrecognized activity of large T-antigen. The mutant protein trans-activated the viral early promoter. In the wild-type protein this activity is probably concealed by the separate, negative regulatory function.
|
|
| 2. |
- Bondeson, K, et al.
(författare)
-
Lactose repressor-operator DNA interactions : kinetic analysis by a surface plasmon resonance biosensor.
- 1993
-
Ingår i: Analytical Biochemistry. - 0003-2697 .- 1096-0309. ; 214:1, s. 245-51
-
Tidskriftsartikel (refereegranskat)abstract
- Lactose repressor binding to operator DNA and subsequent dissociation of the complex was monitored continuously by a biosensor, measuring surface plasmon resonance. In this analysis a synthetic, double-stranded oligonucleotide containing the operator site was immobilized on the sensor surface and repressor protein was passed over the surface. The formation of the repressor-operator complex was specific and could be inhibited by isopropyl-beta-D-thiogalactopyranoside inducer. From the association curve, the apparent kass was determined to be 1.8 x 10(6) M-1 s-1. Dissociation of the complex was, for the first time for the lac repressor, determined as an uncatalyzed reaction and the kdiss was determined to be 3.4 x 10(-4) s-1. As a reference, the repressor-operator interaction was analyzed by electrophoretic mobility shift assay under similar reaction conditions. With this method the equilibrium binding constant was calculated to be 2.4 (+/- 0.2) x 10(8) M-1. The corresponding value calculated from biosensor data was 5.1 x 10(9) M-1.
|
|
| 3. |
- Brantberg, K, et al.
(författare)
-
Asymmetric optokinetic afterresponse in patients with small acoustic neurinomas
- 1990
-
Ingår i: Journal of Vestibular Research: Equilibrium and Orientation. - 0957-4271. ; 1:3, s. 299-307
-
Tidskriftsartikel (refereegranskat)abstract
- Directional asymmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 20 patients with small acoustic neurinomas (< or = 20 mm), and results were compared to those for 24 normal controls. The optokinetic afterresponse was induced by 60 s of horizontal whole-field optokinetic stimulation in both directions. Among patients, the optokinetic afterresponse was asymmetric, OKAN I and OKAN II beating toward the lesioned ear being significantly weaker than the OKAN I and OKAN II beating toward the healthy ear. Hence, in these patients with gradual deterioration of vestibular function, the vestibular side-difference was reflected both in OKAN I and OKAN II. Although asymmetry in OKAN I was frequently observed among controls, it was significantly more pronounced among the patients. Moreover, patients could be distinguished by the occurrence of OKAN II, as it did not occur at all among controls exposed to the same stimulation.
|
|
| 4. |
- Brantberg, K, et al.
(författare)
-
Asymmetric optokinetic afterresponse in patients with vestibular neuritis
- 1990
-
Ingår i: Journal of Vestibular Research: Equilibrium and Orientation. - 0957-4271. ; 1:3, s. 89-279
-
Tidskriftsartikel (refereegranskat)abstract
- The symmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals. The patients were examined at onset of symptoms and at follow-up 3 and 12 months later. At onset, OKAN was found mainly to reflect the spontaneous nystagmus. Although the spontaneous nystagmus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups. OKAN beating toward the lesioned ear was weaker than the OKAN beating toward the healthy ear. Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II. Between the 3- and 12-month check-ups, asymmetry in OKAN declined, even among those patients who showed no improvement in caloric response during that time. The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus. Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side-difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.
|
|
| 5. |
- Brantberg, K, et al.
(författare)
-
Galvanically induced asymmetric optokinetic after-nystagmus
- 1990
-
Ingår i: Acta Oto-Laryngologica. - 0001-6489. ; 110:3-4, s. 95-189
-
Tidskriftsartikel (refereegranskat)abstract
- The effect of an asymmetric vestibular input on the symmetry of horizontal optokinetic after-nystagmus (OKAN) was studied in twenty healthy subjects. Optokinetic nystagmus (OKN) was elicited by a whole-field optokinetic drug, rotating at 90 degrees/s, and eye-movements were recorded by a DC electro-oculographic technique (EOG). The ratio of OKAN following right and left-beating OKN respectively was computed. An asymmetric vestibular input was generated by a continuous bi-polar, bi-aural galvanic stimulus (1 mA) to the vestibular nerves during the optokinetic stimulation and the recording of the OKAN. During galvanic stimulation the relation between left and right-beating OKAN was asymmetric, compared with the OKAN found after optokinetic stimulation only. The galvanic stimulus caused a preponderance for OKAN with the fast phase beating toward the cathode. Thus, the small vestibular asymmetry induced by the galvanic stimulus, which was not strong enough to produce nystagmus by itself, caused an asymmetric OKAN. These findings suggest that examination of OKAN may be of value to detect small vestibular asymmetries in peripheral vestibular disorders in man.
|
|
| 6. |
- Brantberg, K, et al.
(författare)
-
The dynamics of the vestibulo-ocular reflex in patients with vestibular neuritis
- 1990
-
Ingår i: American Journal of Otolaryngology - Head and Neck Medicine and Surgery. - 0196-0709. ; 11:5, s. 51-345
-
Tidskriftsartikel (refereegranskat)abstract
- The dynamics of the vestibulo-ocular reflex (VOR) were studied in 14 patients at the onset of vestibular neuritis, and at follow-up 1 year later. A velocity step stimulus of 150 degrees/s was used to investigate the VOR time constant and gain, and the results were related to the caloric response. In the acute, vertiginous phase of the disease, the VOR time constant was reduced but was almost normalized 1 year later, both among patients who regained normal caloric side-difference and among those who did not. However, the increase in VOR time constant was greater among those who regained normal caloric excitability, and regression analysis showed a correlation between the prolongation of the VOR time constant and the recovery of caloric excitability. These findings suggest that VOR dynamics are modulated during the acute phase of vestibular neuritis, and that there is recovery with vestibular compensation. Furthermore, the recovery of the VOR time constant is not solely dependent on the recovery of normal caloric excitability. This implies that central storage of velocity information may be involved in the VOR, even in cases of asymmetric vestibular input after vestibular compensation.
|
|
| 7. |
|
|
| 8. |
- Eng, H, et al.
(författare)
-
Beta 2-adrenergic receptor antibodies in myasthenia gravis.
- 1992
-
Ingår i: Journal of autoimmunity. - 0896-8411. ; 5:2, s. 213-27
-
Tidskriftsartikel (refereegranskat)abstract
- Although autoantibodies against the nicotinic acetylcholine receptor are the characteristic feature of the autoimmune disease myasthenia gravis (MG), no strong correlation is found between the autoantibody titer and the degree of clinical severity. Numerous studies have attempted to detect the presence of other autoantibody populations that might have a role in the pathology of the disease. We report, for the first time, that 18% of the MG patients we screened have antibodies in their serum to a peptide corresponding to the second extracellular loop of the human beta 2-adrenergic receptor (residues 172-197). Affinity purified antibodies to the beta 2-adrenergic receptor peptide 172-197 reacted with the human beta 2-adrenergic receptor protein obtained from transfected E. coli cell membrane extracts, but did not cross-react with the human AChR. Sufficient material was obtained from nine MG patients and it was found that the gamma globulin fraction from these patients immunoprecipitated the receptor, and that affinity purified IgG to peptide 172-197 competed for receptor binding with the beta-antagonist iodo-cyanopindolol. Using truncated peptides or amino acid modification procedures, no immunodominant B-cell epitope could be detected within region 172-197. Thus, a subpopulation of MG patients possesses anti-beta 2-adrenergic receptor antibodies which are a distinct set of autoantibodies with possible pharmacological activity.
|
|
| 9. |
- Guillet, J G, et al.
(författare)
-
Induction of a pharmacologically active clonotypic B cell response directed to an immunogenic region of the human beta 2-adrenergic receptor.
- 1992
-
Ingår i: Clinical and experimental immunology. - 0009-9104. ; 89:3, s. 461-7
-
Tidskriftsartikel (refereegranskat)abstract
- It has been reported that autoantibodies against the beta 2-adrenergic receptors are involved in the pathology of allergic disorders and of Chagas' disease. Therefore, the immune response against a peptide (H26Q) corresponding to the putative second extracellular loop of the human beta 2-adrenergic receptor, which could be a target for autoantibody attack, was analysed in view of its possible immunogenicity. The free peptide induced a T cell-mediated humoral response in the context of three different murine MHC haplotypes. The T cell epitope was found to be localized in the N-terminal region of the peptide. Highly specific T helper cells were capable of stimulating B cells with the potential to generate a large antibody repertoire reactive with the loop peptide. MoAbs were screened to analyse this B cell response for antibodies potentially interfering with receptor function and a MoAb was found that impaired ligand binding to the receptor.
|
|
| 10. |
- Magnusson, Måns, et al.
(författare)
-
Sensory stimulation promotes normalization of postural control after stroke
- 1994
-
Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 25:6, s. 1176-1180
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: In a randomized study of hemiparetic stroke patients with a median age of 75 years, functional recovery was significantly better in those who received additional sensory stimulation (n = 38), including electrostimulation, than in control patients (n = 40) given the same physiotherapy and occupational therapy; group differences for balance, mobility, and activities of daily living were significant. The present study was designed to investigate postural control in patients who survived more than 2 years after stroke onset. METHODS: The 48 survivors (mean, 2.7 years; range, 2.0 to 3.8 years), 22 from the treatment group and 26 from the control group, were compared with 23 age-matched healthy subjects. Subjects were perturbed by vibrators applied to calf muscles or with galvanic vestibular stimulation. We evaluated postural control in terms of sway variances or sway velocities and the dynamics of postural control as a feedback system using system identification with a model previously validated for human postural control. RESULTS: Significantly more patients of the treatment group than of the control group maintained stance during perturbations (P < .01). Among patients capable of maintaining stance during perturbation, the control patients were characterized by significant divergence from normal values in two of the three characteristic parameters of dynamic postural control (ie, swiftness and stiffness; P < .05) compared with the treatment subgroup or age-matched subjects. CONCLUSIONS: The course of sensory stimulation enhanced recovery of postural function, an enhancement still significant 2 years after the lesion and treatment. The differences and near normalization of characteristic parameters of dynamic postural control among treated patients suggest that improved recovery after sensory stimulation may be achieved by patients regaining normal or near normal dynamics of human postural control.
|
|
