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biologicalmarginalia:

Extant cetaceans exhibit hyperphalangy, a condition where the finger have an increased number of bones. The first digit, however,has a reduced number of bones (so hypophalangy) and is actually absent in several baleen whales; only Pilot Whales have hyperphalangy on this digit. The fifth digit generally has the ancestral number of bones for baleen whales but toothed whales typically have reduction; Kogia is an exception with hyperphalangy. In toothed whales, the second and third digits have the most number of bones whereas in baleen whales it is the third and fourth digits.

First Image: (A) Orca, (B) Sperm Whale, (C) North Atlantic Right Whale, (D) Humpback Whale, (E) Ichthyosaur (Stenopterygius sp.)

Second Image: (A) Orca, (B) North Atlantic Right Whale, (C) Sei Whale

Cooper, L. et al. (2007) Evolution of Hyperphalangy and Digit Reduction in the Cetacean Manus. The Anatomical Record 290 654–672

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irinaivanov:

Hieronymus Bosch, detail The Garden of Earthly Delights, 1490-1510

irinaivanov:

Hieronymus Bosch, detail The Garden of Earthly Delights, 1490-1510

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theartistsmanifesto:

Peach Blossoms—Villiers–le–Bel by Childe Hassam (1887)

theartistsmanifesto:

Peach Blossoms—Villiers–le–Bel by Childe Hassam (1887)

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mineralia:

Bedside minerals: Quartz, Dioptase, Amazonite, Creedite, & Amethyst.

mineralia:

Bedside minerals: Quartz, Dioptase, Amazonite, Creedite, & Amethyst.

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bpod-mrc:

20 April 2014
Nuclear Deterioration
In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.
Written by Daniel Cossins
—
Image courtesy of Juan Carlos Izpisua Belmonte and colleaguesThe Salk Institute for Biological Studies, USA Copyright held by original authors Research published in Nature, November 2012
—
You can also follow BPoD on Twitter and Facebook

bpod-mrc:

20 April 2014

Nuclear Deterioration

In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.

Written by Daniel Cossins

Image courtesy of Juan Carlos Izpisua Belmonte and colleagues
The Salk Institute for Biological Studies, USA
Copyright held by original authors
Research published in Nature, November 2012

You can also follow BPoD on Twitter and Facebook

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スケートと都市

lvrkstr:

スケートと都市

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biologicalmarginalia:

Extant cetaceans exhibit hyperphalangy, a condition where the finger have an increased number of bones. The first digit, however,has a reduced number of bones (so hypophalangy) and is actually absent in several baleen whales; only Pilot Whales have hyperphalangy on this digit. The fifth digit generally has the ancestral number of bones for baleen whales but toothed whales typically have reduction; Kogia is an exception with hyperphalangy. In toothed whales, the second and third digits have the most number of bones whereas in baleen whales it is the third and fourth digits.

First Image: (A) Orca, (B) Sperm Whale, (C) North Atlantic Right Whale, (D) Humpback Whale, (E) Ichthyosaur (Stenopterygius sp.)

Second Image: (A) Orca, (B) North Atlantic Right Whale, (C) Sei Whale

Cooper, L. et al. (2007) Evolution of Hyperphalangy and Digit Reduction in the Cetacean Manus. The Anatomical Record 290 654–672

(via scientificillustration)

irinaivanov:

Hieronymus Bosch, detail The Garden of Earthly Delights, 1490-1510

irinaivanov:

Hieronymus Bosch, detail The Garden of Earthly Delights, 1490-1510

(via deteled)

theartistsmanifesto:

Peach Blossoms—Villiers–le–Bel by Childe Hassam (1887)

theartistsmanifesto:

Peach Blossoms—Villiers–le–Bel by Childe Hassam (1887)

(via deteled)

mineralia:

Bedside minerals: Quartz, Dioptase, Amazonite, Creedite, & Amethyst.

mineralia:

Bedside minerals: Quartz, Dioptase, Amazonite, Creedite, & Amethyst.

(via sexlovemarijuana)

4egis:

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4egis:

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bpod-mrc:

20 April 2014
Nuclear Deterioration
In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.
Written by Daniel Cossins
—
Image courtesy of Juan Carlos Izpisua Belmonte and colleaguesThe Salk Institute for Biological Studies, USA Copyright held by original authors Research published in Nature, November 2012
—
You can also follow BPoD on Twitter and Facebook

bpod-mrc:

20 April 2014

Nuclear Deterioration

In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.

Written by Daniel Cossins

Image courtesy of Juan Carlos Izpisua Belmonte and colleagues
The Salk Institute for Biological Studies, USA
Copyright held by original authors
Research published in Nature, November 2012

You can also follow BPoD on Twitter and Facebook

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