New University at Buffalo research demonstrates how defects in an important neurological pathway in early development may be responsible for the onset of schizophrenia later in life.
The UB findings, published in Schizophrenia Research (paper at http://bit.ly/Wq1i41), test the hypothesis in a new mouse model of schizophrenia that demonstrates how gestational brain changes cause behavioral problems later in life – just like the human disease.
Partial funding for the research came from New York Stem Cell Science (NYSTEM).
The genomic pathway, called the Integrative Nuclear FGFR 1 Signaling (INFS), is a central intersection point for multiple pathways of as many as 160
While looking for mechanisms that might be relevant to restoring regenerative potential in older skeletal muscle, HSCI Executive Committee member, Amy Wagers, PhD, and her team, thought about mechanisms that had been studied for a long time evolutionarily as regulating lifespan and longevity. One example of such a mechanism is reduced calorie intake in the absence of malnutrition, also know as calorie restriction, which has been show to extend lifespan in many organisms.
In order to address the question of whether calorie restriction could also affect skeletal muscle regeneration, Wagers and her colleagues placed mice for 12 weeks
(…) At the age of 29, Bhoir underwent a surgery to correct deformity in his legs. Although the limb length improved, there was no change in muscle strength. He then decided to consult Dr Pradeep Mahajan to be treated by stem cell therapy.
“A personalized treatment protocol was prepared comprising of 1 session of autologous cellular therapy combined with physiotherapy, yoga and diet modifications.
Hundreds of mutations exist in leukemia cells at the time of diagnosis, but nearly all occur randomly as a part of normal aging and are not related to cancer, new research shows.
Scientists at Washington University School of Medicine in St. Louis have found that even in healthy people, stem cells in the blood routinely accumulate new mutations over the course of a person’s lifetime. And their research shows that in many cases only two or three additional genetic changes are required to transform a normal blood cell already dotted with mutations into acute myeloid leukemia (AML).
Hematopoietic stem cells (HSCs) give rise to all other blood cell types, but their development and how their fate is determined has long remained a mystery. In a paper published online this week in Nature, researchers at the University of California, San Diego School of Medicine elaborate upon a crucial signaling pathway and the role of key proteins, which may help clear the way to generate HSCs from human pluripotent precursors, similar to advances with other kinds of tissue stem cells.
Principal investigator David Traver, PhD, professor in the Department of Cellular and Molecular Medicine, and colleagues focused on the