| 1. |
- Atefi, Seyed Reza, et al.
(författare)
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Stroke Damage Detection Using Classification Trees on Electrical Bioimpedance Cerebral Spectroscopy Measurements
- 2013
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Ingår i: Sensors. - : MDPI AG. - 1424-8220. ; 13:8, s. 10074-10086
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Tidskriftsartikel (refereegranskat)abstract
- After cancer and cardio-vascular disease, stroke is the third greatest cause of death worldwide. Given the limitations of the current imaging technologies used for stroke diagnosis, the need for portable non-invasive and less expensive diagnostic tools is crucial. Previous studies have suggested that electrical bioimpedance (EBI) measurements from the head might contain useful clinical information related to changes produced in the cerebral tissue after the onset of stroke. In this study, we recorded 720 EBI Spectroscopy (EBIS) measurements from two different head regions of 18 hemispheres of nine subjects. Three of these subjects had suffered a unilateral haemorrhagic stroke. A number of features based on structural and intrinsic frequency-dependent properties of the cerebral tissue were extracted. These features were then fed into a classification tree. The results show that a full classification of damaged and undamaged cerebral tissue was achieved after three hierarchical classification steps. Lastly, the performance of the classification tree was assessed using Leave-One-Out Cross Validation (LOO-CV). Despite the fact that the results of this study are limited to a small database, and the observations obtained must be verified further with a larger cohort of patients, these findings confirm that EBI measurements contain useful information for assessing on the health of brain tissue after stroke and supports the hypothesis that classification features based on Cole parameters, spectral information and the geometry of EBIS measurements are useful to differentiate between healthy and stroke damaged brain tissue.
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| 2. |
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| 3. |
- Degerman, Johan, 1976, et al.
(författare)
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An automatic system for in vitro cell migration studies
- 2009
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Ingår i: Journal of Microscopy. - : Wiley. - 0022-2720 .- 1365-2818. ; 233:1, s. 178-191
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Tidskriftsartikel (refereegranskat)abstract
- This paper describes a system for in vitro cell migration analysis. Adult neural stem/progenitor cells are studied using time-lapse bright-field microscopy and thereafter stained immunohistochemically to find and distinguish undifferentiated glial progenitor cells and cells having differentiated into type-1 or type-2 astrocytes. The cells are automatically segmented and tracked through the time-lapse sequence. An extension to the Chan-Vese Level Set segmentation algorithm, including two new terms for specialized growing and pruning, made it possible to resolve clustered cells, and reduced the tracking error by 65%. We used a custom-built manual correction module to form a ground truth used as a reference for tracked cells that could be identified from the fluorescence staining. On average, the tracks were correct 95% of the time, using our new segmentation. The tracking, or association of segmented cells, was performed using a 2-state Hidden Markov Model describing the random behaviour of the cells. By re-estimating the motion model to conform with the segmented data we managed to reduce the number of tracking parameters to essentially only one. Upon characterization of the cell migration by the HMM state occupation function, it was found that glial progenitor cells were moving randomly 2/3 of the time, while the type-2 astrocytes showed a directed movement 2/3 of the time. This finding indicates possibilities for cell-type specific identification and cell sorting of live cells based on specific movement patterns in individual cell populations, which would have valuable applications in neurobiological research.
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| 4. |
- Degerman, Johan, et al.
(författare)
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Modeling stem cell migration by Hidden Markov
- 2004
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Ingår i: Proceedings of the Swedish Symposium on Image Analysis, SSBA 2004. ; , s. 122-125
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 5. |
- Hartelius, Lena, 1957, et al.
(författare)
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Short-term effects of repetitive transcranial magnetic stimulation on speech and voice in individuals with Parkinson's disease.
- 2010
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Ingår i: Folia phoniatrica et logopaedica : official organ of the International Association of Logopedics and Phoniatrics (IALP). - : S. Karger AG. - 1421-9972. ; 62:3, s. 104-9
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Tidskriftsartikel (refereegranskat)abstract
- The main characteristics of dysarthria in Parkinson's disease (PD) are monotony of pitch and loudness, reduced stress, variable speech rate, imprecise consonants, and breathy and harsh voice. Earlier treatment studies have shown that dysarthria is less responsive to both pharmacological and surgical treatments than other gross motor symptoms. Recent findings have suggested that repetitive transcranial magnetic stimulation (rTMS) may have a beneficial effect on vocal function in PD. In the present study, 10 individuals with mild PD and no or minimal dysarthria were treated with rTMS as well as placebo stimulation in a blinded experiment. Stimulation was delivered using a frequency of 10 Hz and a stimulation intensity of 90% of the motor threshold. The site of stimulation was the cortical area corresponding to the hand, on the hemisphere contralateral to the patient's most affected side. The participants were audio-recorded before and after both rTMS and sham stimulation. Acoustic analysis was performed on 3 sustained /a:/ for each of the 4 conditions, and analyzed both for the whole group as well as for men and women separately. Results showed that there were no significant differences between any of the conditions regarding duration of sustained fricative or sustained vowel phonation, diadochokinetic rates or intelligibility. Above all, the results of acoustic analyses showed an effect of placebo; there was a significant reduction in fundamental frequency (F(0)) variation, pitch period perturbation, amplitude period perturbation, noise-to-harmonics ratio and coefficient of variation in F(0) between the recordings performed before compared to after sham stimulation.
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| 6. |
- Leonova, Julia, et al.
(författare)
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Endothelin-1 decreases glutamate uptake in primary cultured rat astrocytes.
- 2001
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Ingår i: American journal of physiology. Cell physiology. - 0363-6143. ; 281:5
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Tidskriftsartikel (refereegranskat)abstract
- Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is also known to induce a wide spectrum of biological responses in nonvascular tissue. In this study, we found that ET-1 (100 nM) inhibited the glutamate uptake in cultured astrocytes expressing the glutamate/aspartate transporter (GLAST); astrocytes did not express the glutamate transporter-1 (GLT-1). The V(max) and the K(m) of the glutamate uptake were reduced by 57% and 47%, respectively. Application of the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 partly inhibited the ET-1-evoked decrease in the glutamate uptake, whereas the nonspecific ET receptor antagonist bosentan completely inhibited this decrease. Incubation of the cultures with pertussis toxin abolished the effect of ET-1 on the uptake. The ET-1-induced decrease in the glutamate uptake was independent of extracellular free Ca(2+) concentration, whereas the intracellular Ca(2+) antagonists thapsigargin and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester abolished the effect of ET-1 on the glutamate uptake. Incubation with the protein kinase C (PKC) antagonist staurosporine, but not with the fatty acid-binding protein bovine serum albumin, prevented the ET-1-induced decrease in the glutamate uptake. These results suggest that ET-1 impairs the high-affinity glutamate uptake in cultured astrocytes through a G protein-coupled mechanism, involving PKC and changes in intracellular Ca(2+).
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| 7. |
- Naylor, Andrew Stuart, 1977, et al.
(författare)
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Extended voluntary running inhibits exercise-induced adult hippocampal progenitor proliferation in the spontaneously hypertensive rat.
- 2005
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Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 93:5, s. 2406-14
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Tidskriftsartikel (refereegranskat)abstract
- Previous work has shown that voluntary running increases cell proliferation and neurogenesis in the dentate gyrus of the adult hippocampus. Here we report that long-term running for 24 days results in a down-regulation of hippocampal progenitor proliferation to one-half the level of nonrunning controls compared with a fivefold increase in progenitor proliferation seen after 9 days of voluntary running (short-term running). The negative effects seen on proliferation after 24 days of running were prevented by restricting daily running distances (by 30-50%) during 24 days. Long-term running for 24 days increases the response of the hypothalamic-pituitary-adrenal axis, with an increase in adrenal gland weight and increased plasma corticosterone levels, as well as decreased thymus weight, indicating a stress response as a possible mediator of decreased progenitor proliferation. Furthermore, the negative effects seen on the observed stress response after 24 days of running were prevented by restricting daily running distance. Short-term running did not alter these stress parameters compared with nonrunning controls. However, it increased phosphorylated cyclic AMP response element binding protein (pCREB) in the dentate gyrus, an increase that was not seen in nonrunning controls or after 24 days of running. Taken together, these data suggest that voluntary running does not always enhance proliferation and that the decrease in progenitor proliferation seen in long-term running is possibly mediated by mechanisms involving a stress response in the animal. However, a moderate level of long-term running was able to prevent the negative stress-related changes seen in unrestricted long-term running.
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| 8. |
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| 9. |
- Persson, Anders I., 1973, et al.
(författare)
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Comparison of immunoblotted delta opioid receptor proteins expressed in the adult rat brain and their regulation by growth hormone.
- 2005
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Ingår i: Neuroscience research. - : Elsevier BV. - 0168-0102. ; 52:1, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- It has previously been suggested that exogenous growth hormone (GH) affect quality of life and higher brain functions through the endogenous opioid system. Recently, we showed that GH down-regulate 72 and 48 kDa delta opioid receptor (DOR) proteins in the adult rat cerebral cortex and cerebellum. In the present study, we found that an antiserum raised against the N-terminus of the DOR also recognizes a 36 kDa protein, not recognized by a C-terminus-directed antiserum. We aimed to investigate the identity of the 72, 48 and 36 kDa proteins and to further study the effects of GH on their expression in different brain regions. The expression was studied in hypophysectomized (Hx) and untreated normal female rats. One subgroup of Hx rats received GH as a daily subcutaneous injection for 19 days. Our data show that treatment with GH in Hx rats normalized the expression of the 72 kDa protein in the cerebral cortex, whereas no significant effect were observed for the 48 or 36 kDa proteins. However, GH significantly reduced the ratio between the 72 and 36 kDa proteins in different brain regions of Hx rats. Our data suggest that GH reduces the levels of a 72 kDa DOR that likely represents a dimeric form of a 36 kDa DOR post-translationally truncated at the C-terminus, and that altered receptor dimerization may be involved in GH induced effects in the central nervous system.
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| 10. |
- Persson, Anders I., 1973, et al.
(författare)
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Differential regulation of hippocampal progenitor proliferation by opioid receptor antagonists in running and non-running spontaneously hypertensive rats.
- 2004
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Ingår i: The European journal of neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 19:7, s. 1847-55
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Tidskriftsartikel (refereegranskat)abstract
- Voluntary running in mice and forced treadmill running in rats have been shown to increase the amount of proliferating cells in the hippocampus. Little is known as yet about the mechanisms involved in these processes. It is well known that the endogenous opioid system is affected during running and other forms of physical exercise. In this study, we evaluated the involvement of the endogenous opioids in the regulation of hippocampal proliferation in non-running and voluntary running rats. Nine days of wheel running was compared with non-running in spontaneously hypertensive rats (SHR), a rat strain known to run voluntarily. On the last 2 days of the experimental period all rats received two daily injections of the opioid receptor antagonists naltrexone or naltrindole together with injections of bromodeoxyuridine to label dividing cells. Brain sections from the running rats showed approximately a five-fold increase in newly generated cells in the hippocampus, and this increase was partly reduced by naltrexone but not by naltrindole. By contrast, both naltrexone and naltrindole increased hippocampal proliferation in non-running rats. In non-running rats the administration of naltrexone decreased corticosterone levels and adrenal gland weights, whereas no significant effects on these parameters could be detected for naltrindole. However, adrenal gland weights were increased in naltrexone- but not in naltrindole-administered running rats. In addition, in voluntary running rats there was a three-fold increase in the hippocampal levels of Met-enkephalin-Arg-Phe compared with non-runners, indicating an increase in opioid activity in the hippocampus during running. These data suggest an involvement of endogenous opioids in the regulation of hippocampal proliferation in non-running rats, probably through hypothalamic-pituitary-adrenal axis modulation. During voluntary running in SHR naltrexone altered hippocampal proliferation via as yet unknown mechanisms.
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