• currentsinbiology:

HeLa Cell
Mr. Tomasz Szul
University of Alabama at Birmingham
Birmingham, AL, USA
Technique: Confocal

    currentsinbiology:

    HeLa Cell

    Mr. Tomasz Szul

    University of Alabama at Birmingham

    Birmingham, AL, USA

    Technique: Confocal

    9 months ago
  • currentsinbiology:

Psychosis association with Parkinson’s disease
Psychosis is a common non-motor symptom of Parkinson’s disease whose pathogenesis remains poorly understood. Parkinson’s disease in conjunction with psychosis has been shown to induce injury to extracorticospinal tracts as well as within some cortical areas. Jingmei Zhong and colleagues from First People’s Hospital of Yunnan Province, China conducted a diffusion tensor imaging study in parkinson’s disease patients with psychosis who did not receive antipsychotic treatment and those without psychosis, to determine whether the degree of white-matter fiber injury in brain regions associated with psychiatric symptoms is different from that which occurs in the extrapyramidal motor system. Results revealed that damage to the white-matter fibers in the brain regions associated with psychiatric symptoms were greater than that which occurs in the extrapyramidal motor system, which might explain why psychosis often occurs in Parkinson’s disease patients. Using fractional anisotropy ratios of several brain regions, diffusion tensor imaging can be used to observe the relative degree of injury in brain regions associated with mental diseases, information that is valuable in the clinic and in scientific research. 
Zhong JM, Wu SY, Zhao Y, Chen H, Zhao NW, Zheng KW, Zhao Z, Chen WL, Wang B, Wu KH. Why psychosis is frequently associated with Parkinson’s disease? Neural Regen Res. 2013;8(27):2548-2556.
Caption: This shows the establishment of locations and voxels (diffusion weighted imaging) of the hippocampus (top ovals voxel) and substantia nigra (bottom rectangles voxel) in a female 76-year-old patient with psychosis associated with Parkinson’s disease.
Credit: Neural Regeneration Research

    currentsinbiology:

    Psychosis association with Parkinson’s disease

    Psychosis is a common non-motor symptom of Parkinson’s disease whose pathogenesis remains poorly understood. Parkinson’s disease in conjunction with psychosis has been shown to induce injury to extracorticospinal tracts as well as within some cortical areas. Jingmei Zhong and colleagues from First People’s Hospital of Yunnan Province, China conducted a diffusion tensor imaging study in parkinson’s disease patients with psychosis who did not receive antipsychotic treatment and those without psychosis, to determine whether the degree of white-matter fiber injury in brain regions associated with psychiatric symptoms is different from that which occurs in the extrapyramidal motor system. Results revealed that damage to the white-matter fibers in the brain regions associated with psychiatric symptoms were greater than that which occurs in the extrapyramidal motor system, which might explain why psychosis often occurs in Parkinson’s disease patients. Using fractional anisotropy ratios of several brain regions, diffusion tensor imaging can be used to observe the relative degree of injury in brain regions associated with mental diseases, information that is valuable in the clinic and in scientific research. 

    Zhong JM, Wu SY, Zhao Y, Chen H, Zhao NW, Zheng KW, Zhao Z, Chen WL, Wang B, Wu KH. Why psychosis is frequently associated with Parkinson’s disease? Neural Regen Res. 2013;8(27):2548-2556.

    Caption: This shows the establishment of locations and voxels (diffusion weighted imaging) of the hippocampus (top ovals voxel) and substantia nigra (bottom rectangles voxel) in a female 76-year-old patient with psychosis associated with Parkinson’s disease.

    Credit: Neural Regeneration Research

    9 months ago
  • do you ever feel like your math grade is literally ruining your life

    image

    THIS IS ORGANIC CHEMISTRY FOR ME.

    (Source: annakushiina, via lolsofunny)

    10 months ago
  • currentsinbiology:

Magelona mirabili - a marine worm
Dr. Monika C. M. Mueller
Osnabrück, GermanyTechnique: Confocal

    currentsinbiology:

    Magelona mirabili - a marine worm

    Dr. Monika C. M. Mueller

    Osnabrück, GermanyTechnique: Confocal

    11 months ago
  • ucsdsenior:

    Every time I study enantiomers,this is the song that is playing in my mind. 

    Mirror mirror images of each other, baby! 


    1 year ago
  • Evolution of Choosing a Mate| T-Shirt Experiment


    1 year ago
  • currrentbiology:


First bees, now birds (PAN)
Prairie bird populations are falling in many Midwestern states, from ring-necked pheasants to horned larks to sparrows. Scientists now say insecticides are a primary culprit.

    currrentbiology:

    First bees, now birds (PAN)

    Prairie bird populations are falling in many Midwestern states, from ring-necked pheasants to horned larks to sparrows. Scientists now say insecticides are a primary culprit.

    (Source: currentsinbiology)

    1 year ago
  • millrick10:

Sir, you are a genius.

    millrick10:

    Sir, you are a genius.

    (via developingbiologist)

    1 year ago
  • ucsdhealthsciences:

Chronic myeloid leukemia blood cells.
Enzyme Accelerates Malignant Stem Cell Cloning in Chronic Myeloid LeukemiaAn international team, headed by researchers at the University of California, San Diego School of Medicine, has identified a key enzyme in the reprogramming process that promotes malignant stem cell cloning and the growth of chronic myeloid leukemia (CML), a cancer of the blood and marrow that experts say is increasing in prevalence.The findings are published in the Dec. 24 online early edition of the Proceedings of the National Academy of Sciences (PNAS).Despite the emergence of new therapies, such as tyrosine kinase inhibitors, CML and other leukemias remain problematic because some cancer stem cells avoid destruction and eventually regenerate themselves, a stem cell process known as self-renewal that can result in a return and spread (metastasis) of the disease.In the PNAS paper, principal investigator Catriona H. M. Jamieson, MD, PhD, associate professor of medicine at UC San Diego, with colleagues in the United States, Canada and Italy, report that inflammation – long associated with the development of cancer – boosts activity of  an enzyme called adenosine deaminase or ADAR1. Expressed during embryogenesis to help blood cell development, ADAR1 subsequently turns off and is triggered by viral infections where it protects normal hematopoietic stem cells from attack. In leukemia stem cells, however, overexpression of ADAR1 enhances the missplicing of RNA, which leads to greater self-renewal and therapeutic resistance of malignant stem cells. The findings build upon previous studies by Jamieson and others that elucidate the effects of RNA missplicing and instability. “People normally think about DNA instability in cancer, but in this case, it’s how the RNA is edited by enzymes that really matters in terms of cancer stem cell generation and resistance to conventional therapy.” The described RNA editing process, which occurs in the context of human and other primate specific sequences, also underscores the importance of addressing inflammation as “an essential driver of cancer relapse and therapeutic resistance,” Jamieson said. It also presents a new target for future therapies.“ADAR1 is an enzyme that we may be able to specifically target with a small molecule inhibitor, an approach we have already used effectively with other inhibitors,” said Jamieson. “If we can block the capacity of leukemia stem cells to use ADAR1, if we can knock down that pathway, maybe we can put stem cells back on the right track and stop malignant cloning.”CML is a cancer initiated by a mutant gene called BCR-ABL in blood forming stem cells that leads to an expansion of white blood cells and their precursors. It is typically slow-growing and often not diagnosed until its later stages when there can be a sudden, dramatic increase in malignant cells, known as blast crisis. Median age of diagnosis is 66 years; incidence of the disease increases with age.  Despite tremendous advances in BCR-ABL tyrosine kinase inhibitor therapies, the majority of patients relapse if therapy is discontinued, in part as a result of dormant cancer stem cell resistance.  This work suggests a novel mechanism for overcoming cancer stem cell resistance to therapy that may prevent relapse and progression.The estimated prevalence of CML in the United States is 70,000 persons with the disease, projected to steadily increase to approximately 181,000 by 2050. CML is initiated by the mutant BCR-ABL gene, but scientists have not yet identified the cause of the mutation.

    ucsdhealthsciences:

    Chronic myeloid leukemia blood cells.

    Enzyme Accelerates Malignant Stem Cell Cloning in Chronic Myeloid Leukemia

    An international team, headed by researchers at the University of California, San Diego School of Medicine, has identified a key enzyme in the reprogramming process that promotes malignant stem cell cloning and the growth of chronic myeloid leukemia (CML), a cancer of the blood and marrow that experts say is increasing in prevalence.

    The findings are published in the Dec. 24 online early edition of the Proceedings of the National Academy of Sciences (PNAS).

    Despite the emergence of new therapies, such as tyrosine kinase inhibitors, CML and other leukemias remain problematic because some cancer stem cells avoid destruction and eventually regenerate themselves, a stem cell process known as self-renewal that can result in a return and spread (metastasis) of the disease.

    In the PNAS paper, principal investigator Catriona H. M. Jamieson, MD, PhD, associate professor of medicine at UC San Diego, with colleagues in the United States, Canada and Italy, report that inflammation – long associated with the development of cancer – boosts activity of  an enzyme called adenosine deaminase or ADAR1.

    Expressed during embryogenesis to help blood cell development, ADAR1 subsequently turns off and is triggered by viral infections where it protects normal hematopoietic stem cells from attack. In leukemia stem cells, however, overexpression of ADAR1 enhances the missplicing of RNA, which leads to greater self-renewal and therapeutic resistance of malignant stem cells.

    The findings build upon previous studies by Jamieson and others that elucidate the effects of RNA missplicing and instability. “People normally think about DNA instability in cancer, but in this case, it’s how the RNA is edited by enzymes that really matters in terms of cancer stem cell generation and resistance to conventional therapy.”

    The described RNA editing process, which occurs in the context of human and other primate specific sequences, also underscores the importance of addressing inflammation as “an essential driver of cancer relapse and therapeutic resistance,” Jamieson said. It also presents a new target for future therapies.

    “ADAR1 is an enzyme that we may be able to specifically target with a small molecule inhibitor, an approach we have already used effectively with other inhibitors,” said Jamieson. “If we can block the capacity of leukemia stem cells to use ADAR1, if we can knock down that pathway, maybe we can put stem cells back on the right track and stop malignant cloning.”

    CML is a cancer initiated by a mutant gene called BCR-ABL in blood forming stem cells that leads to an expansion of white blood cells and their precursors. It is typically slow-growing and often not diagnosed until its later stages when there can be a sudden, dramatic increase in malignant cells, known as blast crisis. Median age of diagnosis is 66 years; incidence of the disease increases with age.  Despite tremendous advances in BCR-ABL tyrosine kinase inhibitor therapies, the majority of patients relapse if therapy is discontinued, in part as a result of dormant cancer stem cell resistance.  This work suggests a novel mechanism for overcoming cancer stem cell resistance to therapy that may prevent relapse and progression.

    The estimated prevalence of CML in the United States is 70,000 persons with the disease, projected to steadily increase to approximately 181,000 by 2050. CML is initiated by the mutant BCR-ABL gene, but scientists have not yet identified the cause of the mutation.

    1 year ago