Increased number of cerebellar granule cells and astrocytes in the internal granule layer in sheep following prenatal intra-amniotic injection of lipopolysaccharide.

Chorioamnionitis is an important problem in perinatology today, leading to brain injury and neurological handicaps. However, there are almost no data available regarding chorioamnionitis and a specific damage of the cerebellum. Therefore, this study aimed at determining if chorioamnionitis causes cerebellar morphological alterations.

Age-related changes of neuron numbers in the frontal cortex of a transgenic mouse model of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by amyloid plaque accumulation, intracellular tangles and neuronal loss in selective brain regions. The frontal cortex, important for executive functioning, is one of the regions that are affected. Here, we investigated the neurodegenerative effects of mutant human amyloid precursor protein (APP) and presenilin 1 (PS1) on frontal cortex neurons in APP/PS1KI mice, a transgenic mouse model of AD, expressing two mutations in the human APP, as well as two human PS1 mutations knocked-in into the mouse PS1 gene in a homozygous (ho) manner.

Advanced microscopy techniques for quantitative analysis in neuromorphology and neuropathology research: current status and requirements for the future.

Visualizing neuromorphology and in particular neuropathology has been the focus of many researchers in the quest to solve the numerous questions that are still remaining related to several neurological and neuropsychiatric diseases. Over the last years, intense research into microscopy techniques has resulted in the development of various new types of microscopes, software imaging systems, and analysis programs. This review briefly discusses some key techniques, such as confocal stereology and automated neuron tracing and reconstruction, and their applications in neuroscience research.

Antibody effector mechanisms in myasthenia gravis-pathogenesis at the neuromuscular junction.

Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies that are either directed to the muscle nicotinic acetylcholine receptor (AChR) or to the muscle-specific tyrosine kinase (MuSK). These autoantibodies define two distinct subforms of the disease-AChR-MG and MuSK-MG. Both AChR and MuSK are expressed on the postsynaptic membrane of the neuromuscular junction (NMJ), which is a highly specialized region of the muscle dedicated to receive and process signals from the motor nerve.

Subchronic infusion of the product of inflammation prostaglandin J2 models sporadic Parkinson's disease in mice.

Background: Chronic neuroinflammation is implicated in Parkinson's disease (PD). Inflammation involves the activation of microglia and astrocytes that release high levels of prostaglandins. There is a profound gap in our understanding of how cyclooxygenases and their prostaglandin products redirect cellular events to promote PD neurodegeneration.

Extracorporeal shockwave application to the distal femur of rabbits diminishes the number of neurons immunoreactive for substance P in dorsal root ganglia L5.

Application of extracorporeal shockwaves to the musculoskeletal system can induce long-term analgesia in the treatment of chronic painful diseases such as calcifying tendonitis of the shoulder, tennis elbow and chronic plantar fasciitis. However, the molecular and cellular mechanisms underlying this phenomenon are largely unknown. Recently it was shown that application of extracorporeal shockwaves to the distal femur of rabbits can lead to reduced concentration of substance P in the shockwaves' focal zone.

Cyclic GMP in the pig vitreous and retina after experimental retinal detachment.

Purpose: Earlier studies have revealed a decreased level of cGMP in vitreous fluid obtained from patients with a retinal detachment. To further investigate this phenomenon, we developed an experimental retinal detachment model in pigs.

Methods: Experimental unilateral retinal detachments were induced in pig eyes by subretinal injection of 0.

Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection.

Neuroinflammation, initiated by cerebral infection, is increasingly postulated as an aetiological factor in neurodegenerative diseases such as Alzheimer's disease (AD). We investigated whether Chlamydia pneumoniae (Cpn) infection results in extracellular aggregation of amyloid beta (Abeta) in BALB/c mice. At 1 week post intranasal infection (p.