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Immunoexpression of the selected compounds of the SMN complex in spinal cord neurons in patients with sporadic amyotrophic lateral sclerosis (sALS)

100%
Dziewulska D., Sulejczak D., Chrzanowska H., Ogonowska W., Rafalowska J.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr 1
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease leading to degeneration and loss of motoneurons in the spinal cord anterior horns. Although etiology of the disease is unknown there is a hypothesis assuming that survival motor neuron protein (SMN) may save motoneurons from degeneration not only in spinal muscular atrophy (SMA) but also in ALS. In animal models of ALS the neuroprotective role of SMN was observed but it is not known whether the phenomenon is present in humans. Therefore we decided to examine immunoexpression of SMN and functionally associated with it gemin 2, 3 and 4 in the anterior horn neurons of patients with sporadic form of ALS (sALS). Material and methods: The material was composed of 10 spinal cords of patients with sALS who died at the age of 52–87 years 1–8 years after the onset of the disease. On formalin-fixed and paraffin-embedded spinal cords immunohistochemistry was applied. The immunohistochemical reactions were performed with antibodies against SMN and gemin 2, 3 and 4 according to the avidin-biotin-peroxidase method. Results: In all the examined cases expression of SMN and gemin 3 in spinal cord neurons was found although intensity of the immune reactions was diverse. The immunolabel were the most intense in patients with acute course of sALS and gradually decreased with longevity of the disease. Not only motoneurons but also interneurons and sensory neurons revealed immunoexpression of SMN and gemin 3. The immune reaction to gemin 2 was negative. The immunoreactivity for gemin 4 was also negative or very weak. Conclusions: (1) In humans, expression of SMN and gemin 3 in neurons is present through the whole lifespan. (2) In sALS, expression of gemin 2 and 4 is abnormal: absent or diminished respectively. (3) Presence of all components of the SMN-gemin complex is probably necessary for its normal functioning. (4) Since the immunoreactivity for SMN, and gemin 2, 3 and 4 was similar in all the examined cases and 6 from the 10 cases were at the age of 65–87 years it seems that advanced age has no influence on expression of the investigated proteins. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640
2

IFNγ production profile in turkeys of different immunological status after TRT vaccination

100%
Smialek M., Tykalowski B., Dziewulska D., Kowalczyk J., Koncicki A.
Journal of Veterinary Research
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2020
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tom 64
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nr 2
3

Is SMN immunoexpression in hypertrophied Nisl granulations in amyotrophic lateral sclerosis a morphological equivalent of reinnervation ?

86%
Dziewulska D., Sulejczak D., Gogol A., Gogol P., Ogonowska W., Modrzewska-Lewczuk M., Rafalowska J.
Acta Neurobiologiae Experimentalis
|
2013
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tom 73
|
nr Suppl.1
Reinnervation observed in early stage of amyotrophic lateral sclerosis (ALS) is a compensatory mechanism for motoneuron loss. Since survival motor neuron (SMN) protein could be involved not only in neuroprotection but also in the transport of mRNAs in motoneuron axons, we examined its immunoexpression in anterior horn motoneurons of ALS patients with reinnervation in EMG. SMN immunolabel was observed in neuron cytoplasm and neurities but it was particularly intense in enlarged Nissl granules. This finding may mirror increased synthesis of the protein in rough endoplasmic reticulum being not only an attempt of motoneuron to selfprotection but also necessary for nerve sprouting. Study supported by the Ministry of Sciences and Higher Education grant NN 401 014 640.
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Differentiation of infectious bronchitis virus vaccine strains Ma5 and 4/91 by TaqMan real-time PCR

86%
Stenzel T., Dziewulska D., Smialek M., Tykalowski B., Kowalczyk J., Koncicki A.
Polish Journal of Veterinary Sciences
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2017
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tom 20
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nr 3
The aim of this study was to develop rapid molecular assays for differentiating vaccine strains Ma5 and 4/91 of the infectious bronchitis virus (IBV). Specific primers and probes for S1 and N genes were designed based on the nucleotide sequences of both vaccine strains. Cross-reactivity was not observed. Assay sensitivity was 2.373 x 10³ copies of the Ma5 strain, and 3.852 x 10³ copies of the 4/91 strain. Samples belonging to a known genotype demonstrated that the designed assays supported rapid and sensitive detection of Ma5 and 4/91 vaccine strains of IBV.
5

Phytoncides in the prevention and therapy of blackhead disease and their effect on the turkey immune system

86%
Tykalowski B., Smialek M., Kowalczyk J., Dziewulska D., Stenzel T., Koncicki A.
Journal of Veterinary Research
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2021
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tom 65
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nr 1
6

Immunoreactivities of some proteins forming SMN protein complex within spinal cord in rat model of fALS

86%
Rafalowska J., Sulejczak D., Gadamski R., Wojda R., Mordzewska-Lewczuk M., Dziewulska D.
Acta Neurobiologiae Experimentalis
|
2013
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tom 73
|
nr 1
Introduction: Amyotrophic lateral sclerosis (ALS) is a major neurodegenerative disease to afflict the adult human population. ALS causes a progressive motoneuron degeneration within anterior horns of the spinal cord. Recent data indicate the presence of mutations in the SMN (Survival Motor Neuron) gene that cause a deficits in the level of the functional SMN protein and may be an exacerbating factor in the disease development of rat model of fALS. SMN forms the multiprotein complex with selected gemins (i.a. gemin 2, 3 and 4). It is known, that the complex is important for motoneuron development in ontogenesis as well as in the proper functioning of mature motoneuron. However, the level of the SMN and individual gemin expression during the life both in humans and rats still become uncovered. The aim of our study was to determine the immunoreactivities of SMN and gemins 2, 3 and 4 in rat model of fALS during all life span. Material and method: Male rats mutated in SOD-1 were subjected to experiments. Animals at age of 60 days (group 1), 90 days (group 2), 120 days (group 3) were asymptomatic. The last group involving symptomatic rats was created from animals older than 120 days. Rats were perfused in deep anaesthesia. The spinal cords were removed and processed in routine histological staining techniques as well as in immunohistochemical methods (to detect SMN and selected gemins proteins). Labelling sections of spinal cords were analyzed with light and fluorescent microscope. Result: SMN and all investigated gemins were present in spinal cord motoneurons in rats from all experimental groups. However, the level of staining was weaker in the paretic rats. In the opposition to other examined proteins the immunoreaction of gemin 2 was weaker starting from 90 day of life. Conclusion: The SMN protein complex is present in motoneurons within the spinal cord during all animal lifespan in the rat model of familiar ALS. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640
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