A better understanding of Skp2 gene and its relation to cellular senescence can lead to the development of new agents that can suppress tumor growth in certain types of cancer, researchers at the University of Texas, MD Anderson Cancer Center and Memorial Sloan-Kettering Cancer Center report in the journal Nature. Journal Skp2 is involved in promoting cell cycle regulation, cell proliferation, cell growth and tumor formation, and is overexpressed in a variety of human cancers, according to lead author Hui-Kuan Lin, Ph.D., professor MD Anderson Cancer assistant molecular and cell biology.
Lin and colleagues found that inactivation oncogenes are overexpressed Skp2 after strangling cancer growth by inducing senescence – the irreversible loss of the ability of a cell to divide and grow. Harnessing the power of cellular senescence to push rapidly dividing cells in a dormant state could provide an alternative means of prevention or control of the common malignant tumors such as prostate cancer.
The sense of taste and smell can be lost or impaired after head trauma, according to a new study by scientists at the University of Montreal, Lucie Bruneau Rehabilitation Centre and the Centre for Interdisciplinary Research in Rehabilitation of Greater Montreal. Published in the journal Brain Injury, the survey found that mild to severe traumatic brain injury could cause loss of smell.
“The study clearly shows that olfactory deficits may occur in mild traumatic brain injury, and moderate and severe head trauma patients,” said study co-author and neuropsychologist Maurice Ptito, a professor in the School of University of Montreal optometry. “We also found that patients with frontal lesions were more likely to olfactory dysfunction.
The research team recruited 49 people with traumatic brain injury (73 percent of men with a mean age of 43) who completed a questionnaire and underwent two tests to measure the loss of smell the smell. The result: 55 percent of subjects had an impaired sense of smell, while 41 percent of the participants were aware of their olfactory deficit.
Researchers have discovered a genetic mutation associated with this typical motor neuron disease or amyotrophic lateral sclerosis, which has a pathological effect similar to certain genetic mutations have shown in previous studies. Ultimately, researchers hope that understanding what causes motor neuron disease (MND) will lead to new ways of treatment.
MDN is a progressive neurodegenerative disease that attacks the upper and lower motor neurons. The degeneration of motor neurons causes weakness and atrophy of muscles, causing increasing loss of mobility in the limbs, difficulty speaking, swallowing and breathing.
The new research, published today in the journal Proceedings of the National Academy of Sciences and conducted by researchers from Imperial College London, provides strong additional evidence that genetics is a disease caused by the protein reconstituted in motor neurons, cells that help control muscle movement.