Assessment of Human Sperm Cells Morphological Parameters

The quality of spermatozoa has a direct influence on the fertilization and developmental competence of embryos. The aim of this work was to review the methods of spermatozoa morphology assessment, features of the normal spermatozoa and the reasons of their several abnormalities. Three methods can be used for the evaluation of spermatozoa morphology in the in vitro fertilization (IVF) laboratory: (1) light microscopy of stained spermatozoa, (2) motile sperm organelle morphology examination (MSOME) and (3) polarized light microscopy. The analysis of spermatozoa morphology includes the assessment of head, neck, midpiece and tail. Morphologically abnormal spermatozoa are categorized into subgroups according to the defects of the head, neck, midpiece and/or tail. Before IVF and intracytoplasmic sperm injection (ICSI), the quality of spermatozoa must be estimated exactly, because this has the high influence on embryo development. Therefore the analysis of the morphological parameters of spermatozoa using the light microscopy, MSOME, in combination with precise head birefringence detection using the polarized microscopy, could give the best fertilization rate and embryo quality after IVF and ICSI

Glial Cells in Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is an adult motor neuron disease characterized by premature death of upper and lower motor neurons. Two percent of ALS cases are caused by the dominant mutations in the gene for superoxide dismutase 1 (SOD1) through a gain of toxic property of mutant protein. Genetic and chimeric mice studies using SOD1 models indicate that non-neuronal cells play important roles in neurodegeneration through non-cell autonomous mechanism. We review the contribution of each glial cell type in ALS pathology from studies of the rodent models and ALS patients. Astrogliosis and microgliosis are not only considerable hallmarks of the disease, but the intensity of microglial activation is correlated with severity of motor neuron damage in human ALS. The impaired astrocytic functions such as clearance of extracellular glutamate and release of neurotrophic factors are implicated in disease. Further, the damage within astrocytes and microglia is involved in accelerated disease progression. Finally, other glial cells such as NG2 cells, oligodendrocytes and Schwann cells are under the investigation to determine their contribution in ALS. Accumulating knowledge of active role of glial cells in the disease should be carefully applied to understanding of the sporadic ALS and development of therapy targeted for glial cells

Age-related morphological peculiarities of human testes

Background: This study aimed to compare the isolated testes size, volume, weight and density changes with age and to establish the suitability of three formulas of testicular volume calculation for 18–50 and 51–70-year-old men groups. Materials and methods: Two hundred and six testes of 103 men (59 of 18–50-year-old and 44 of 51–70-year-old men) were weighed and their size was measured by the sliding calliper. The accurate volume was determined by water displacement and compared with volume calculated using three formulas, and the density of testicular tissues was calculated. Results: The mean length and height of both testes and length and height of right and left testes decreased significantly with age. The mean width of both testes and width of right and left testes decreased with age insignificantly. The mean of water displacement volume and weight and volume and weight of right and left testes decreased with age significantly. The mean density of testicular tissues and the density of the right and left testes increased significantly with age. In the same age group, the size, water displacement volume and weight of right testes was insignificantly higher than that of the left ones, and the density of testicular tissues was similar in the right and left testes. Conclusions: The prolate spheroid formula was most suitable for calculation of testicular volume for 18–50-year-old men and prolate ellipsoid formula was most suitable for calculation of testicular volume in 51–70-year-old men

Neuregulin 1 confers neuroprotection in SOD1-linked amyotrophic lateral sclerosis mice via restoration of C-boutons of spinal motor neurons

Supplementary figures (Figure S1, S2, S3, and S4). (PDF 2135 kb

Ablation of Proliferating Cells in the CNS Exacerbates Motor Neuron Disease Caused by Mutant Superoxide Dismutase

Proliferation of glia and immune cells is a common pathological feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Here, to investigate the role of proliferating cells in motor neuron disease, SOD1G93A transgenic mice were treated intracerebroventicularly (ICV) with the anti-mitotic drug cytosine arabinoside (Ara-C). ICV delivery of Ara-C accelerated disease progression in SOD1G93A mouse model of ALS. Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1G93A transgenic mice. Exacerbation of disease was also associated with significant alterations in the expression inflammatory molecules IL-1β, IL-6, TGF-β and the growth factor IGF-1

Locomotor recovery following contusive spinal cord injury does not require oligodendrocyte remyelination

The contribution of oligodendrocytes to remyelination in functional recovery after spinal cord injury is not fully understood. Here, the authors show that oligodendrocyte progenitor cell differentiation is not required for functional recovery after spinal cord injury in mice

Human Neural Stem Cells Differentiate and Promote Locomotor Recovery in an Early Chronic Spinal coRd Injury NOD-scid Mouse Model

Traumatic spinal cord injury (SCI) results in partial or complete paralysis and is characterized by a loss of neurons and oligodendrocytes, axonal injury, and demyelination/dysmyelination of spared axons. Approximately 1,250,000 individuals have chronic SCI in the U.S.; therefore treatment in the chronic stages is highly clinically relevant. Human neural stem cells (hCNS-SCns) were prospectively isolated based on fluorescence-activated cell sorting for a CD133(+) and CD24(-/lo) population from fetal brain, grown as neurospheres, and lineage restricted to generate neurons, oligodendrocytes and astrocytes. hCNS-SCns have recently been transplanted sub-acutely following spinal cord injury and found to promote improved locomotor recovery. We tested the ability of hCNS-SCns transplanted 30 days post SCI to survive, differentiate, migrate, and promote improved locomotor recovery.hCNS-SCns were transplanted into immunodeficient NOD-scid mice 30 days post spinal cord contusion injury. hCNS-SCns transplanted mice demonstrated significantly improved locomotor recovery compared to vehicle controls using open field locomotor testing and CatWalk gait analysis. Transplanted hCNS-SCns exhibited long-term engraftment, migration, limited proliferation, and differentiation predominantly to oligodendrocytes and neurons. Astrocytic differentiation was rare and mice did not exhibit mechanical allodynia. Furthermore, differentiated hCNS-SCns integrated with the host as demonstrated by co-localization of human cytoplasm with discrete staining for the paranodal marker contactin-associated protein.The results suggest that hCNS-SCns are capable of surviving, differentiating, and promoting improved locomotor recovery when transplanted into an early chronic injury microenvironment. These data suggest that hCNS-SCns transplantation has efficacy in an early chronic SCI setting and thus expands the "window of opportunity" for intervention

Recruitment of endogenous CNS stem cells for regeneration in demyelinating disease.

Demyelinating diseases, such as multiple sclerosis (MS), are responsible for a significant portion of the neurological disability burden worldwide, especially in young adults. Demyelination can be followed by a spontaneous regenerative process called remyelination, in which new myelin sheaths are restored to denuded axons. However, in chronic demyelinating disease such as MS, this process becomes progressively less efficient. This chapter reviews the biology of remyelination and the rationale and strategies by which it can be enhanced therapeutically in acquired demyelinating disease

What is the potential of oligodendrocyte progenitor cells to successfully treat human spinal cord injury?

<p>Abstract</p> <p>Background</p> <p>Spinal cord injury is a serious and debilitating condition, affecting millions of people worldwide. Long seen as a permanent injury, recent advances in stem cell research have brought closer the possibility of repairing the spinal cord. One such approach involves injecting oligodendrocyte progenitor cells, derived from human embryonic stem cells, into the injured spinal cord in the hope that they will initiate repair. A phase I clinical trial of this therapy was started in mid 2010 and is currently underway.</p> <p>Discussion</p> <p>The theory underlying this approach is that these myelinating progenitors will phenotypically replace myelin lost during injury whilst helping to promote a repair environment in the lesion. However, the importance of demyelination in the pathogenesis of human spinal cord injury is a contentious issue and a body of literature suggests that it is only a minor factor in the overall injury process.</p> <p>Summary</p> <p>This review examines the validity of the theory underpinning the on-going clinical trial as well as analysing published data from animal models and finally discussing issues surrounding safety and purity in order to assess the potential of this approach to successfully treat acute human spinal cord injury.</p