RCMP say a 50-year-old man died and a 60-year-old man is in hospital following a crash involving a CP Rail train Friday morning.

France defender Samuel Umtiti has picked up a calf injury in just the second session since Barcelona returned to training from the cornonavirus quarantine.

The peroxisome is a subcellular organelle that functions in essential metabolic pathways, including biosynthesis of plasmalogens, fatty acid β-oxidation of very-long-chain fatty acids, and degradation of hydrogen peroxide. Peroxisome biogenesis disorders (PBDs) manifest as severe dysfunction in multiple organs, including the central nervous system (CNS), but the pathogenic mechanisms in PBDs are largely unknown. Because CNS integrity is coordinately established and maintained by neural cell interactions, we here investigated whether cell-cell communication is impaired and responsible for the neurological defects associated with PBDs. Results from a noncontact co-culture system consisting of primary hippocampal neurons with glial cells revealed that a peroxisome-deficient astrocytic cell line secretes increased levels of brain-derived neurotrophic factor (BDNF), resulting in axonal branching of the neurons. Of note, the BDNF expression in astrocytes was not affected by defects in plasmalogen biosynthesis and peroxisomal fatty acid β-oxidation in the astrocytes. Instead, we found that cytosolic reductive states caused by a mislocalized catalase in the peroxisome-deficient cells induce the elevation in BDNF secretion. Our results suggest that peroxisome deficiency dysregulates neuronal axogenesis by causing a cytosolic reductive state in astrocytes. We conclude that astrocytic peroxisomes regulate BDNF expression and thereby support neuronal integrity and function.

Assembled α-synuclein in nerve cells and glial cells is the defining pathological feature of neurodegenerative diseases called synucleinopathies. Seeds of α-synuclein can induce the assembly of monomeric protein. Here, we used sucrose gradient centrifugation and transiently transfected HEK 293T cells to identify the species of α-synuclein from the brains of homozygous, symptomatic mice transgenic for human mutant A53T α-synuclein (line M83) that seed aggregation. The most potent fractions contained Sarkosyl-insoluble assemblies enriched in filaments. We also analyzed six cases of idiopathic Parkinson's disease (PD), one case of familial PD, and six cases of multiple system atrophy (MSA) for their ability to induce α-synuclein aggregation. The MSA samples were more potent than those of idiopathic PD in seeding aggregation. We found that following sucrose gradient centrifugation, the most seed-competent fractions from PD and MSA brains are those that contain Sarkosyl-insoluble α-synuclein. The fractions differed between PD and MSA, consistent with the presence of distinct conformers of assembled α-synuclein in these different samples. We conclude that α-synuclein filaments are the main driving force for amplification and propagation of pathology in synucleinopathies.

Manganese (Mn) is an essential micronutrient required for the normal development of many organs, including the brain. Although its roles as a cofactor in several enzymes and in maintaining optimal physiology are well-known, the overall biological functions of Mn are rather poorly understood. Alterations in body Mn status are associated with altered neuronal physiology and cognition in humans, and either overexposure or (more rarely) insufficiency can cause neurological dysfunction. The resultant balancing act can be viewed as a hormetic U-shaped relationship for biological Mn status and optimal brain health, with changes in the brain leading to physiological effects throughout the body and vice versa. This review discusses Mn homeostasis, biomarkers, molecular mechanisms of cellular transport, and neuropathological changes associated with disruptions of Mn homeostasis, especially in its excess, and identifies gaps in our understanding of the molecular and biochemical mechanisms underlying Mn homeostasis and neurotoxicity.

12 March 2015 , Volume 91, Number 2

Invitation Only Research Event

Invitation Only Research Event

6 February 2014 , Volume 70, Number 1

Beautiful Kyiv has been brutalized

John M. Dietschy
Aug 1, 2004; 45:1375-1397
Thematic Reviews

Assembled α-synuclein in nerve cells and glial cells is the defining pathological feature of neurodegenerative diseases called synucleinopathies. Seeds of α-synuclein can induce the assembly of monomeric protein. Here, we used sucrose gradient centrifugation and transiently transfected HEK 293T cells to identify the species of α-synuclein from the brains of homozygous, symptomatic mice transgenic for human mutant A53T α-synuclein (line M83) that seed aggregation. The most potent fractions contained Sarkosyl-insoluble assemblies enriched in filaments. We also analyzed six cases of idiopathic Parkinson's disease (PD), one case of familial PD, and six cases of multiple system atrophy (MSA) for their ability to induce α-synuclein aggregation. The MSA samples were more potent than those of idiopathic PD in seeding aggregation. We found that following sucrose gradient centrifugation, the most seed-competent fractions from PD and MSA brains are those that contain Sarkosyl-insoluble α-synuclein. The fractions differed between PD and MSA, consistent with the presence of distinct conformers of assembled α-synuclein in these different samples. We conclude that α-synuclein filaments are the main driving force for amplification and propagation of pathology in synucleinopathies.

Manganese (Mn) is an essential micronutrient required for the normal development of many organs, including the brain. Although its roles as a cofactor in several enzymes and in maintaining optimal physiology are well-known, the overall biological functions of Mn are rather poorly understood. Alterations in body Mn status are associated with altered neuronal physiology and cognition in humans, and either overexposure or (more rarely) insufficiency can cause neurological dysfunction. The resultant balancing act can be viewed as a hormetic U-shaped relationship for biological Mn status and optimal brain health, with changes in the brain leading to physiological effects throughout the body and vice versa. This review discusses Mn homeostasis, biomarkers, molecular mechanisms of cellular transport, and neuropathological changes associated with disruptions of Mn homeostasis, especially in its excess, and identifies gaps in our understanding of the molecular and biochemical mechanisms underlying Mn homeostasis and neurotoxicity.

28 April 2020

Invitation Only Research Event

Invitation Only Research Event

Expert

Van Wedeen talks about the geometry of the brain's communication pathways.

Researcher: John A. Adam, Old Dominion University. John A. Adam explains the math and physics behind rainbows.

Tropical rainforests are the world's richest land habitats for biodiversity, harbouring stunning numbers of plant and animal species. The Amazon and the Congo basins, together with Asian rainforests, represent only 6 per cent of earth's land surface, and yet more than 50 per cent of global biodiversity can be found under their shade.

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The coach and rail journey app has launched a new AI voice app for automated disruption alerts

The peroxisome is a subcellular organelle that functions in essential metabolic pathways, including biosynthesis of plasmalogens, fatty acid β-oxidation of very-long-chain fatty acids, and degradation of hydrogen peroxide. Peroxisome biogenesis disorders (PBDs) manifest as severe dysfunction in multiple organs, including the central nervous system (CNS), but the pathogenic mechanisms in PBDs are largely unknown. Because CNS integrity is coordinately established and maintained by neural cell interactions, we here investigated whether cell-cell communication is impaired and responsible for the neurological defects associated with PBDs. Results from a noncontact co-culture system consisting of primary hippocampal neurons with glial cells revealed that a peroxisome-deficient astrocytic cell line secretes increased levels of brain-derived neurotrophic factor (BDNF), resulting in axonal branching of the neurons. Of note, the BDNF expression in astrocytes was not affected by defects in plasmalogen biosynthesis and peroxisomal fatty acid β-oxidation in the astrocytes. Instead, we found that cytosolic reductive states caused by a mislocalized catalase in the peroxisome-deficient cells induce the elevation in BDNF secretion. Our results suggest that peroxisome deficiency dysregulates neuronal axogenesis by causing a cytosolic reductive state in astrocytes. We conclude that astrocytic peroxisomes regulate BDNF expression and thereby support neuronal integrity and function.

β-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide. Previously, we demonstrated that lysosomal GBA1 and nonlysosomal GBA2 possess not only GlcCer hydrolase activity, but also transglucosylation activity to transfer the glucose residue from GlcCer to cholesterol to form β-cholesterylglucoside (β-GlcChol) in vitro. β-GlcChol is a member of sterylglycosides present in diverse species. How GBA1 and GBA2 mediate β-GlcChol metabolism in the brain is unknown. Here, we purified and characterized sterylglycosides from rodent and fish brains. Although glucose is thought to be the sole carbohydrate component of sterylglycosides in vertebrates, structural analysis of rat brain sterylglycosides revealed the presence of galactosylated cholesterol (β-GalChol), in addition to β-GlcChol. Analyses of brain tissues from GBA2-deficient mice and GBA1- and/or GBA2-deficient Japanese rice fish (Oryzias latipes) revealed that GBA1 and GBA2 are responsible for β-GlcChol degradation and formation, respectively, and that both GBA1 and GBA2 are responsible for β-GalChol formation. Liquid chromatography–tandem MS revealed that β-GlcChol and β-GalChol are present throughout development from embryo to adult in the mouse brain. We found that β-GalChol expression depends on galactosylceramide (GalCer), and developmental onset of β-GalChol biosynthesis appeared to be during myelination. We also found that β-GlcChol and β-GalChol are secreted from neurons and glial cells in association with exosomes. In vitro enzyme assays confirmed that GBA1 and GBA2 have transgalactosylation activity to transfer the galactose residue from GalCer to cholesterol to form β-GalChol. This is the first report of the existence of β-GalChol in vertebrates and how β-GlcChol and β-GalChol are formed in the brain.

(Institute for Operations Research and the Management Sciences) Job performance has long been understood to be the primary equalizing factor affecting promotions for men and women in the workplace, but research shows, women don't gain as much from the same performance improvements as men do. New research in the INFORMS journal Information Systems Research shows training plays an important part in promotions for women in the field of information technology.

The recent economic downturn has dealt a severe blow to many employees. However, for Shiu Yin-ming and Poon Man-kit, the crisis has brought them skill-upgrading opportunities.

Miss Shiu has over 30 years’ experience in the retail industry. Her last job was a salesperson at a lighting store. Struck by the competition with online stores and a series of protests, the shop closed in October last year and left her unemployed.

“I have got no choice. Many people in Hong Kong have mortgage burdens. It is the most worrying part. And it is frightening to see my account balance drop,” she said.

Miss Shiu spent several months trying to get a job but failed.

“Of course I was frustrated. Perhaps the employers think that young people are more hard-working. It is difficult for middle-aged people like me to get a job. It hurt my confidence and I hesitated to keep going."

Seeing the demand in the healthcare industry, Miss Shiu decided to swap careers. She joined the Love Upgrading Special Scheme and enrolled in the Foundation Certificate in Care-related Support Worker Training.

The course covered basic pathology and healthcare skills. It also arranged recruitment from the Hospital Authority in class. Miss Shiu said the special course helped her to find a job and she will soon work at a nursing home.

“It is like an admission ticket. During an interview at a nursing home, the interviewer asked how I would change a nappy for an elderly person. I answered what I had learnt from the course. Moreover, as I have not participated in an interview after so many years of work, the interview skills that I have learnt from the course have geared me up,” she said.

Better prospects

Young newcomers to the job market are also affected by the economic downturn.

Mr Poon has been engaged in casual work in the catering industry. The 19-year-old said there used to be plenty of casual job opportunities on career websites, but that is no longer the case. He has been underemployed in recent months and feels his family just see him as someone who is not in education, employment, or training.

“The full-time waiters have not got much work to do, and each of them is assigned to be responsible for a few positions. So, the restaurant does not need extra casual manpower. My relatives look down on me like I am a neet,” he said.

Mr Poon has enrolled in the Foundation Certificate in Barista Training to gain experience in different positions in the industry.

"Many coffee shops and hotels need people to make latte art. I think the course will help me get a job more easily. I plan to further enroll in other courses relating to pastry-making," he added.

Skills upgrade

The Love Upgrading Special Scheme, launched in last October, provides free training to employees affected by the recent economic downturn to upgrade their skills. The courses are conducted in full-time or part-time mode and offer special allowances.

According to the Employees Retraining Board, as of the end of March, more than 12,200 people have applied for the scheme. About one-third of them are aged between 50 to 59.

The applicants mainly come from the catering, retail, social and personal services industries.

The most popular course is the Foundation Certificate in Care-related Support Worker Training, followed by courses related to baker and pastry cook, barista and security training.

Employees Retraining Board Executive Director Byron Ng said the 66 courses under the scheme were specially selected.

“We want to help those employees in the hard-hit industries like tourism, catering, retail, hotel, construction, etc. Also, we want to provide courses in industries which demand heavy labour during this period, such as healthcare and innovative technology.”

The scheme does not impose any restrictions on the trainees’ industry and educational attainment.

“We hope to encourage all unemployed or underemployed employees, including those who are highly educated, and take these chances to upgrade their own skills so they can re-enter the market smoothly,” Mr Ng said.

He added that those who have completed a full-time vocational skills course will get a follow-up service that includes three months of employment.

The second phase of the scheme will be launched in July, and the monthly maximum allowance is expected to increase from $4,000 to $5,800.

(University of Virginia Health System) Focused ultrasound, the researchers hope, could revolutionize treatment for conditions from Alzheimer's to epilepsy to brain tumors -- and even help repair the devastating damage caused by stroke.

Every summer, rainstorms occur in Hong Kong occasionally, leading to loss of property or even casualties.

(Columbia University's Mailman School of Public Health) Researchers found that 92 percent of employers who responded to a survey on climate change and public health reported need for public health professionals with training in climate change will very likely increase in the next 5 to 10 years. While graduates of public health programs who focus on climate change are in demand in the current job market, these positions appear to be just a small proportion of the total number of jobs available in public health.

(University of Massachusetts Amherst) As physicians and families know too well, though Alzheimer's disease has been intensely studied for decades, too much is still not known about molecular processes in the brain that cause it. Now researchers at the University of Massachusetts Amherst say new insights from analytic theory and molecular simulation techniques offer a better understanding of amyloid fibril growth and brain pathology.