Anonymous asked:

How successful is surgery for someone w/ advanced Parkinson's Disease? How likely are you to develop a brain tumor if someone in your family had one? (if you live a healthy lifestyle,taking only heredity into consideration)

Parkinson’s disease is a neurodegenerative disorder. Dopamine-generating cells situated in the midbrain decay, which produces the symptoms (related to movements at first, it can lead to behavioral issues).

I don’t know a lot about Parkinson’s disease. I have read that people with very advanced Parkinson’s disease are not good candidates for surgery, probably because of the nature of the disease and also because with age come different problems which render surgery difficult (heart problems, etc). There are a few surgical options to either stimulate a part of the brain or on the contrary destroy a small part of the brain which is causing symptoms. Though it is a fact that there is no cure for Parkinson’s disease yet, and the surgery is used to alleviate symptoms to relieve patients of some medication and side effects.

As for your other questions, it depends ! Depends on the tumor (see here for hereditary brain tumors), depends on the gene involved. Cancer is very complicated so of course I won’t go into great detail here, but basically it can be caused by a great number of things. Genetic risk factors can be involved, and they’re generally called “risk factors” because most of them won’t directly cause a cancer. Only a small subset of genes involved in very critical cellular processes will cause cancer if mutated. Otherwise, a risk factor will increase the chance of developing a cancer. On the other hand, living a healthy lifestyle will decrease that chance, although random mutations do happen whether we watch out for them or not. 

h1ppo asked:

We seek your boundless intellect for counsel on the realm of spiders. I've heard they technically don't have brains but instead have a primitive system of ganglia. Nor do they they feel pain? Does this make spiders, in a sense, automatons?

No one really knows if spiders feel pain, though in recent years it has come to light that animals like crabs and shrimps that also rely on a ganglia control, might feel pain. Pain doesn’t require a full brain, just a viable circuit of nerves and the right receptors and chemicals. For one thing, spiders are sensible to drugs. So why not pain ?

Intelligence is another debate, surely it would seem like ganglia are more primitive, though we know that a great deal of an octopus’ neurons are inside its arms and I wouldn’t call this creature dumb. In all cases an automaton won’t really be able to react to its environment, which is an amazing feature shared by spiders, octopuses and humans alike.

The neuromuscular junction connects the nervous system to the muscular system via synapses between efferent nerve fibers and muscle fibers, also known as muscle cells.
Picture : The frog developing neuromuscular junctions are labeled with a marker of synaptic vesicles (green) and a marker of acetylcholine receptors (red).

The neuromuscular junction connects the nervous system to the muscular system via synapses between efferent nerve fibers and muscle fibers, also known as muscle cells.

Picture : The frog developing neuromuscular junctions are labeled with a marker of synaptic vesicles (green) and a marker of acetylcholine receptors (red).

Movement difficulties in people with Parkinson’s disease arise because of the disturbed electrical activity of nerve cells in the brain.  Excessive rhythmic activities called ‘beta oscillations’ are one key disturbance. Research carried out at the Unit has given new insights into why and how these beta oscillations might emerge throughout the Parkinsonian brain.  By matching the electrical activity of individual nerve cells to their connections, members of the Magill group have discovered that two different types of cell in a brain area called the external globus pallidus (GPe) could perform a division of labour to control many other areas important for movement.  In their published paper, the team also reveal a novel type of GPe cell that provides massive and specific connections to the striatum, a brain area that is of central importance in Parkinson’s.  Because these remarkable GPe cells are positioned to cast wide nets of influence over their targets, they were termed “arkypallidal neurons” (from ancient Greek αρκυς [arkys] for ‘hunter’s net’).  Dr. Magill commented, “Exposing the striking diversity of GPe cells is a game changer for the field.  The challenge ahead now is to explain the building blocks and necessity of this diversity”.
Figure : Parasagittal section of the striatum and external globus pallidus (to the left and right, respectively), showing immunofluorescence for parvalbumin (green), preproenkephalin (red), and the pan-neuronal marker HuCD (blue). Prototypic neurons of the globus pallidus express parvalbumin (green/turquoise), whereas arkypallidal neurons instead express preproenkephalin (evident as pink signal). The single arkypallidal neuron in the foreground (soma/dendrites in red, axon in white) exclusively innervates striatum, another hallmark of this novel cell type. 

Movement difficulties in people with Parkinson’s disease arise because of the disturbed electrical activity of nerve cells in the brain.  Excessive rhythmic activities called ‘beta oscillations’ are one key disturbance. Research carried out at the Unit has given new insights into why and how these beta oscillations might emerge throughout the Parkinsonian brain.  By matching the electrical activity of individual nerve cells to their connections, members of the Magill group have discovered that two different types of cell in a brain area called the external globus pallidus (GPe) could perform a division of labour to control many other areas important for movement.  In their published paper, the team also reveal a novel type of GPe cell that provides massive and specific connections to the striatum, a brain area that is of central importance in Parkinson’s.  Because these remarkable GPe cells are positioned to cast wide nets of influence over their targets, they were termed “arkypallidal neurons” (from ancient Greek αρκυς [arkys] for ‘hunter’s net’).  Dr. Magill commented, “Exposing the striking diversity of GPe cells is a game changer for the field.  The challenge ahead now is to explain the building blocks and necessity of this diversity”.

Figure : Parasagittal section of the striatum and external globus pallidus (to the left and right, respectively), showing immunofluorescence for parvalbumin (green), preproenkephalin (red), and the pan-neuronal marker HuCD (blue). Prototypic neurons of the globus pallidus express parvalbumin (green/turquoise), whereas arkypallidal neurons instead express preproenkephalin (evident as pink signal). The single arkypallidal neuron in the foreground (soma/dendrites in red, axon in white) exclusively innervates striatum, another hallmark of this novel cell type. 

"Visualizing the dynamic behaviors of immune cells in living tissue has dramatically increased our understanding of how cells interact with their surroundings, contributing important insights into mechanisms of leukocyte trafficking, tumor cell invasion, and T cell education by dendritic cells, among others. Despite substantial advances with various intravital imaging techniques including two-photon microscopy and the generation of multitudes of reporter mice, there is a growing need to assess cell interactions in the context of specific extracellular matrix composition and microvascular functions, and as well, simpler and more widely accessible methods are needed to image cell behaviors in the context of living tissue physiology. Here we present an antibody-based method for intravital imaging of cell interactions with the blood, lymphatic, and the extracellular matrix compartments of the living dermis while simultaneously assessing capillary permeability and lymphatic drainage function."
Figure 4. Live immunostaining detects only extracellular basement membrane-bound CCL21, while staining on fixed tissue reveals intracellular as well as extracellular CCL21.
(a–b) In the live ear dermis CCL21 accumulated in patches (arrowheads) and along continuous lymphatic segments (arrows), and co-localized with (a) perlecan and (b) collagen IV, both basement membrane components of the collecting lymphatic vessels. (c) Occasionally observed CCL21-positive (green) initial lymphatic vessels (iLy) stained more weakly for collagen IV (red). (d) Extracellular CCL21 deposits (green) were seen around lymphatic vessels in the exposed ear skin did not correlate with injured blood vessel, as determined by i.v. injection of TRITC-dextran (cyan) that leaked from areas of injured vessels (arrowheads). The tissue was pre-stained for perlecan and CCL21 before dextran injection. Scale bars in a, b and d (left), 400 µm; c and d (right), 100 µm.
Kilarski et al. (2013) Intravital Immunofluorescence for Visualizing the Microcirculatory and Immune Microenvironments in the Mouse Ear Dermis.

"Visualizing the dynamic behaviors of immune cells in living tissue has dramatically increased our understanding of how cells interact with their surroundings, contributing important insights into mechanisms of leukocyte trafficking, tumor cell invasion, and T cell education by dendritic cells, among others. Despite substantial advances with various intravital imaging techniques including two-photon microscopy and the generation of multitudes of reporter mice, there is a growing need to assess cell interactions in the context of specific extracellular matrix composition and microvascular functions, and as well, simpler and more widely accessible methods are needed to image cell behaviors in the context of living tissue physiology. Here we present an antibody-based method for intravital imaging of cell interactions with the blood, lymphatic, and the extracellular matrix compartments of the living dermis while simultaneously assessing capillary permeability and lymphatic drainage function."

Figure 4. Live immunostaining detects only extracellular basement membrane-bound CCL21, while staining on fixed tissue reveals intracellular as well as extracellular CCL21.

(a–b) In the live ear dermis CCL21 accumulated in patches (arrowheads) and along continuous lymphatic segments (arrows), and co-localized with (a) perlecan and (b) collagen IV, both basement membrane components of the collecting lymphatic vessels. (c) Occasionally observed CCL21-positive (green) initial lymphatic vessels (iLy) stained more weakly for collagen IV (red). (d) Extracellular CCL21 deposits (green) were seen around lymphatic vessels in the exposed ear skin did not correlate with injured blood vessel, as determined by i.v. injection of TRITC-dextran (cyan) that leaked from areas of injured vessels (arrowheads). The tissue was pre-stained for perlecan and CCL21 before dextran injection. Scale bars in a, b and d (left), 400 µm; c and d (right), 100 µm.

Kilarski et al. (2013) Intravital Immunofluorescence for Visualizing the Microcirculatory and Immune Microenvironments in the Mouse Ear Dermis.

Figure 1. Immunohistofluorescence for ornithine decarboxylase (ODC) (Cy3, red) and nuclei (DAPI, blue). A–E: urothelium from five different normal control subjects. F–J: urothelium from five different subjects with overactive bladder syndrome (OAB). Staining conditions were identical for all 10 patients. There is higher expression of ODC in OAB urothelium compared with control. Scale bar: 100 μm.
Li et al. Augmented bladder urothelial polyamine signaling and block of BK channel in the pathophysiology of overactive bladder syndrome. American Journal of Physiology

Figure 1. Immunohistofluorescence for ornithine decarboxylase (ODC) (Cy3, red) and nuclei (DAPI, blue). A–E: urothelium from five different normal control subjects. F–J: urothelium from five different subjects with overactive bladder syndrome (OAB). Staining conditions were identical for all 10 patients. There is higher expression of ODC in OAB urothelium compared with control. Scale bar: 100 μm.

Li et al. Augmented bladder urothelial polyamine signaling and block of BK channel in the pathophysiology of overactive bladder syndrome. American Journal of Physiology