The researchers gave 10 mutant
mice bone marrow from healthy mice.
The team then added IGF2BP3 to
mouse bone marrow.
• Piero Anversa at New York Medical College in Valhalla, New York, and Donald Orlic at the National Human Genome Research Institute in Bethesda, Maryland, used
mouse bone marrow to repair damaged mouse hearts.
To gauge the effect off the loss of imprinting control on the maintenance of the quiescent hematopoietic stem cell pool, Venkatraman analyzed the numbers of quiescent, active and differentiated hematopoietic stem cells in
mouse bone marrow.
Employing the advanced technology of the Institute's Cytometry, Imaging and Histology centers, the researchers examined the relationship between megakaryocytes and hematopoietic stem cells in
mouse bone marrow.
Reiser's team used a «humanized» mouse model that utilizes patients» peripheral blood stem cells to communicate signals to
mouse bone marrow immature myeloid cells.
Regulation of STAT signaling in
mouse bone marrow derived dendritic cells by respiratory syncytial virus.
An example of this type of circuitry analysis includes measuring and interpreting all of these parameters over a time course, following stimulation of
mouse bone marrow - derived dendritic cells with bacterial lipopolysaccharides (LPS) endotoxin.
In separate experiments reported in Nature — one with mice, the other transplanting human stem cells into
mouse bone marrow — researchers demonstrated techniques with the potential to produce all types of blood cells.
Differential expression of surface markers in
mouse bone marrow mesenchymal stromal cell subpopulations with distinct lineage commitment.
When BubR1H / H; INK - ATTAC
mouse bone marrow cells were pushed into senescence in vitro by the PPAR - γ - activating drug rosiglitazone, a subpopulation of the cells exhibited high levels of INK - ATTAC expression and GFP, coupled with SAβ - gal staining; subsequent to treatment with the INK - ATTAC activating drug, these cells rapidly entered into apoptosis, and within 48 h were either destroyed or in the cell death process.
To achieve efficient and synchronous reprogramming, the authors expressed reprogramming factors (OSKM) in
mouse bone marrow - derived pre-B cells exposed to the C / EBPα transcription factor, leading to nearly 100 % reprogramming within 4 to 8 days.
Not exact matches
In
mice undergoing a
bone marrow transplant, ATG16L1 - deficient
mice were three times more likely to die or show signs of transplant rejection than
mice with the protective action of ATG16L1 in place.
Bone marrow transplant cured compulsive behaviour in
mice whose OCD symptom seems to be the result of a mutation in a gene never before linked to behaviour.
In a study published in Nature Communications, the investigators report that hyperglycemic
mice (or
mice with type 2 diabetes) have a 24-fold higher accumulation of succinate, an intermediate metabolite, in the metabolic pathways of their
bone marrow stromal cells.
A drug used to stop immune cells from gobbling up transplanted organs and
bone marrow has been caught boosting the immune response to a virus in
mice and monkeys.
Jerrold Olefsky and colleagues at the University of California, San Diego, killed the
bone marrow cells in
mice that make immune cells called macrophages.
In the study, «Succinate and its G - protein - coupled receptor stimulate osteoclastogenesis,» the researchers took samples of
bone marrow from hyperglycemic male
mice and healthy
mice.
When placed beneath the skin in
mice, the implant grew into a
bone - like structure and produced a working
marrow.
He and his boss, stem cell researcher Donald Phinney, wondered whether those
mice were also protected from the fattening of the
bone marrow that accompanies a high - fat diet.
In a
mouse model in which they simulated the development of CML by adding Bcr - Abl to the
bone marrow, a shortage of Gab2 led to a clear weakening or even a lack of symptoms.
Researchers have designed a nanoparticle - based therapy that is effective in treating
mice with multiple myeloma, a cancer of immune cells in the
bone marrow.
Researchers at Washington University School of Medicine in St. Louis have developed a nanotherapy that is effective in treating
mice with multiple myeloma, a cancer of
bone marrow immune cells.
«When we transplanted our labeled blood stem cells from the
bone marrow into other
mice, only a few stem cells were active in the recipients, and many stem cells were lost,» Rodewald explains.
Nayernia says that researchers have produced the same early - stage sperm cells in
mice from
bone marrow cells taken from female
mice.
He proved it in 2003 by first X-raying
mice to kill off all the stem cells in their
bone marrow, then repopulating the
bone with stem cells tagged with a fluorescent marker.
Now a report in this month's issue of Nature Medicine may provide an explanation: A key
bone marrow protein causes immune cells in
mouse transplant recipients to self - destruct.
Then scientists reported that members of a class of RNA molecules called microRNAs direct the development of blood and
bone marrow cells in
mice.
The researchers used «humanized
mice,» which have had their immune systems replaced with human immune system cells, thymus tissue and
bone marrow.
Studying
mouse monocytes in more detail, the researchers found that the increase in TNF levels that occurs with age causes premature release of immature monocytes from the
bone marrow into the blood stream.
Furthermore, examination of aged
mice showed dramatically reduced levels of Cbf - beta in
bone marrow cells, as compared to younger
mice.
Bone marrow mesenchymal stem cells and bone cells from the skulls of Cbf - beta - deficient mice showed increased expression of adipocyte ge
Bone marrow mesenchymal stem cells and
bone cells from the skulls of Cbf - beta - deficient mice showed increased expression of adipocyte ge
bone cells from the skulls of Cbf - beta - deficient
mice showed increased expression of adipocyte genes.
Deletion of the CXCR4 gene led to sustained T - ALL remission within a month in similar
mice, as well as movement of the cancerous blood cells away from the
bone marrow.
Subsequent transplant of millions of human T - ALL cells into normal
mice that were then treated with an anti-CXCR4 drug induced remission within two weeks, with diseased spleen and
bone marrow tissue nearly returning to normal.
In experiments in
mice and human cells, researchers found that blocking CXCR4 — a so - called homing receptor protein molecule that helps T cells mature and attracts blood cells to the
bone marrow — halted disease progression in
bone marrow and spleen tissue within two weeks.
As part of the new study, researchers deleted CXCL12 production specifically from
bone marrow vasculature in leukemic
mice.
To test this idea, the researchers utilized two
mouse models of human breast cancer metastasis and found dormant disseminated tumor cells residing upon the membrane microvasculature of lung,
bone marrow and brain tissue.
The researchers used
mice in which the telomerase gene was eliminated; specifically in
bone marrow cells.
Prior research with cultured tissue had shown that a mix of chemicals could change
bone marrow stem cells from
mice to those resembling brain cells, but when a team led by neurologist Lorraine Iacovitti of Thomas Jefferson University in Philadelphia tried the same brew on human cells, the number altered was modest.
BMT was effective in
mice, but in humans resulted in death before the new
bone marrow grew and expanded (called engraftment) in treated patients.
• A Yale research team led by Diane Krause turned a single stem cell from the
bone marrow of an adult
mouse into lung, liver, intestinal, and skin cells for other
mice.
Flow cytometry analysis using
mouse blood showed that MSCs were released from
bone marrow to the blood in cinnamtannin B -1-administered
mice.
Case Western Reserve research associate Amar Desai, PhD, worked between the Markowitz and Gerson laboratories to determine the effect of SW033291 on
mice that had received lethal doses of radiation and then received a partial
bone marrow transplant.
In a study published in the June 12 edition of Science, they detail how a new drug repaired damage to the colon, liver and
bone marrow in animal models — even going so far as to save the lives of
mice who otherwise would have died in a
bone marrow transplantation model.
Both the number and activity of osteoblasts — cells that produce and reshape
bone tissue — were increased within the
bone marrow of
mice with lung tumors compared with cancer - free animals; and reducing the number of osteoblasts in
mice not only limited neutrophil infiltration of tumors but also interrupted tumor progression.
Gerson and Markowitz partnered to show the SW033291 drug is effective for regenerating
bone marrow in
mice.
Desai, Case Western Reserve, performed experiments that showed that SW033291 works in
bone marrow transplantation in
mice.
This rejuvenated the stem cells in the
bone marrow of the older
mice that replenish their blood, and led to a wave of studies comparing the blood of old and young
mice to try and identify the youth - giving substance.
She and her colleagues then collected stem cells from the
bone marrow of drowsy and of well - rested
mice and injected them into 12
mice that had received what would normally be a lethal dose of radiation.
Then they injected the cell into a
mouse whose
bone marrow had been destroyed by radiation.