Tag Archives: disease

AM Briefing from Bowlersdesk.com for April 30, 2014

It is hot and windy in San Diego County. The National Weather Service issued a high wind warning for most of San Diego County and hot temperatures along with low humidity are hitting us too. However there is no “Red Flag” … that’s a high fire danger warning… Yet.

Pertussis or whooping cough is sweeping through San Diego. San Diego County Health and Human Services Agency says that this year alone there have been 298 pertussis cases reported. That’s about six times as many cases when compared to the same time period for last year. Last week alone 18 people reported having the disease.

Dr. Wilma Wooten says “Pertussis has shown no signs of slowing down … The vaccine’s effectiveness lessens over time so it’s very important that adults get their booster shots and that they make sure their children have the necessary doses of the vaccine at the recommended ages.”

Veteran San Diego Police officer Gilbert Anthony Lorenzo is being arraigned this morning at 8:00 in Department 2 of El Cajon’s courthouse. 31-year-old Lorenzo is accused of domestic violence. After his arrest by La Mesa police he was placed on unpaid leave.

In San Diego’s courthouse at 1:30 Todd Francis is being sentenced. Francis is the owner of a gun his daughter and a neighbor boy were playing with when it fired killing the boy. Francis pleaded guilty to child endangerment.

San Diego City Council has a busy day today.

First at 9:00 AM the Economic Development and Intergovernmental Relations Committee is meeting about a ballot proposal to increase the minimum wage in San Diego. Then at 2:00 the council’s Smart Growth and Land Use Committee is talking about the community plan for Ocean Beach.

This morning at 9:00 the County Board of Supervisors is meeting and on the agenda is a multimillion-dollar water quality monitoring contract.

The 50th anniversary of Dr. Martin Luther King Jr.’s speech at San Diego State University is being honored with the unveiling of a plaque at SDSU’s Open Air Theater.

And finally tonight at 7:00 San Diego city councilman Ed Harris is hosting a town hall meeting at Bay Park Elementary School.

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San Diego Plague Warning

[youtube:http://youtu.be/vJcAZpSOafk%5D

San Diego County is warning outdoors people to stay away from squirrels because they could have the plague.

Three captured squirrels tested positive for the disease and fleas on the little animals spread the infamous disease.

According to San Diego County’s Department of Environmental Health (DEH) Director Jack Miller

“The big thing is to avoid contact with squirrels and the fleas they carry … If you’re camping, set your tents up away from squirrel burrows. If you’re hiking, don’t feed squirrels and don’t let your kids play with them”.

The DEH say to:

• Avoid contact with ground squirrels, chipmunks, and other wild animals.
• Do not feed, touch or handle wild animals.
• Do not rest, camp or sleep near animal burrows in the ground.
• Protect pets by keeping them on a leash, use flea control, or best of all, leave pets at home.
• Contact your doctor immediately if you become ill within one week of visiting a known plague area.
• Symptoms include a sudden onset of fever, chills and tender swollen lymph nodes.
• Do not touch sick or dead animals.

They also warns people to keep their pets from touching or playing with the rodents. They say to keep you pets on leashes and to use flea control like Advantage.

Contact a doctor immediately if you think you are infected. Symptoms include tender and swollen lymph nodes, chills, and fever.

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AM Briefing from Bowlersdesk.com for April 18, 2013

[youtube:http://youtu.be/PdufJmvpXMM%5D

San Diego’s first Red Flag Warning of the season is in effect. A dangerous weather cocktail of gusty winds, low humidity, and high temperatures are why the National Weather Service in San Diego issued the warning. The warning is in effect until 5:00 PM Friday.

San Diego County’s Health and Human Services is investigating two confirmed and two possible cases of meningococcal disease. Commonly known as meningitis. A 22-year-old man hospitalized on April 9th died from the disses and a 47-year-old man is still in the hospital. The disease is spread through close contact like sharing a drinking glass or kissing. Symptoms include fever, headache, lethargy, stiff neck and a rash. Health Officials say if you’ve had close contact with an infected person to seek medical treatment.

This morning at 6am Goodwill Industries and Kaiser Permantente are hosting an e-waste recycling event. If you have any old electronics you can take them to 4405 Vandever Ave.

At 10:00 AM University of California at San Diego students are going to sort through a thousand pounds of trash to show how most garbage still has many things in it that can be recycled.

And at 1:00 PM in Bonita Cove the San Diego Triathlon is having its pre-race expo. No word yet on any enhanced security because of the Boston Marathon bombing. The woman’s race is on Friday and the men Saturday.

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Scripps Research Institute Scientists Help Unravel Central Alzheimer’s Disease Mystery

Scripps Research Institute reported a major break though in Alzheimer’s disease research.

They say that Alzheimer’s caused brain damage could be because of an enzyme with links to obesity and inulin production.

It is all very sciencey and interesting but over my head to explain.

The press release Scripp’s Institute sent out is the best thing for you to read to begin to understand what this is and means.

“LA JOLLA, CA – April 10, 2013 – Scientists at The Scripps Research Institute (TSRI) have shed light on one of the major toxic mechanisms of Alzheimer’s disease. The discoveries could lead to a much better understanding of the Alzheimer’s process and how to prevent it.

The findings, reported in the April 10, 2013 issue of the journal Neuron, show that brain damage in Alzheimer’s disease is linked to the overactivation of an enzyme called AMPK. When the scientists blocked this enzyme in mouse models of the disease, neurons were protected from loss of synapses—neuron-to-neuron connection points—typical of the early phase of Alzheimer’s disease.

“These findings open up many new avenues of investigation, including the possibility of developing therapies that target the upstream mechanisms leading to AMPK overactivation in the brain,” said TSRI Professor Franck Polleux, who led the new study.

Alzheimer’s disease, a fatal neurodegenerative disorder afflicting more than 25 million people worldwide, currently has no cure or even disease-delaying therapy.

In addition to having implications for Alzheimer’s drug discovery, Polleux noted the findings suggest the need for further safety studies on an existing drug, metformin. Metformin, a popular treatment for Type 2 Diabetes, causes AMPK activation.

Tantalizing Clues to Alzheimer’s

Researchers have known for years that people in the earliest stages of Alzheimer’s disease begin to lose synapses in certain memory-related brain areas. Small aggregates of the protein amyloid beta can cause this loss of synapses, but how they do so has been a mystery.

Until recently, Polleux’s laboratory has been focused not on Alzheimer’s research but on the normal development and growth of neurons. In 2011, he and his colleagues reported that AMPK overactivation by metformin, among other compounds, in animal models impaired the ability of neurons to grow output stalks, or axons.

Around the same time, separate research groups found clues that AMPK might also have a role in Alzheimer’s disease. One group reported that AMPK can be activated in neurons by amyloid beta, which in turn can cause a modification of the protein tau in a process known as phosphorylation. Tangles of tau with multiple phosphorylations (“hyperphosphorylated” tau) are known to accumulate in neurons in affected brain areas in Alzheimer’s. These results, published two years ago, reported abnormally high levels of activated AMPK in these tangle-ridden neurons.

Polleux decided to investigate further, to determine whether the reported interactions of AMPK with amyloid beta and tau can in fact cause the damage seen in the brains of Alzheimer’s patients. “Very little was known about the function of this AMPK pathway in neurons, and we happened to have all the tools needed to study it,” he said.

In Search of Answers

Georges Mairet-Coello, a postdoctoral research associate in the Polleux lab, performed most of the experiments for the new study. He began by confirming that amyloid beta, in the small-aggregate (“oligomer”) form that is toxic to synapses, does indeed strongly activate AMPK; amyloid beta oligomers stimulate certain neuronal receptors, which in turn causes an influx of calcium ions into the neurons. He found that this calcium influx triggers the activation of an enzyme called CAMKK2, which appears to be the main activator of AMPK in neurons.

The team then showed that this AMPK overactivation in neurons is the essential reason for amyloid beta’s synapse-harming effect. Normally, the addition of amyloid beta oligomers to a culture of neurons causes the swift disappearance of many of the neurons’ dendritic spines—the rootlike, synapse-bearing input stalks that receive signals from other neurons. With a variety of tests, the scientists showed that amyloid beta oligomers can’t cause this dendritic spine loss unless AMPK overactivation occurs—and indeed AMPK overactivation on its own can cause the spine loss.

For a key experiment the team used J20 mice, which are genetically engineered to overproduce mutant amyloid beta, and eventually develop an Alzheimer’s-like condition. “When J20 mice are only three months old, they already show a strong decrease in dendritic spine density, in a set of memory-related neurons that are also affected early in human Alzheimer’s,” Mairet-Coello said. “But when we blocked the activity of CAMKK2 or AMPK in these neurons, we completely prevented the spine loss.”

Next Mairet-Coello investigated the role of the tau protein. Ordinarily it serves as a structural element in neuronal axons, but in Alzheimer’s it somehow becomes hyperphosphorylated and drifts into other neuronal areas, including dendrites where its presence is associated with spine loss. Recent studies have shown that amyloid beta’s toxicity to dendritic spines depends largely on the presence of tau, but just how the two Alzheimer’s proteins interact has been unclear.

The team took a cue from a 2004 study of Drosophila fruit flies, in which an AMPK-like enzyme’s phosphorylation of specific sites on the tau protein led to a cascade of further phosphorylations and the degeneration of nerve cells. The scientists confirmed that one of these sites, S262, is indeed phosphorylated by AMPK. They then showed that this specific phosphorylation of tau accounts to a significant extent for amyloid beta’s synapse toxicity. “Blocking the phosphorylation at S262, by using a mutant form of tau that can’t be phosphorylated at that site, prevented amyloid beta’s toxic effect on spine density,” Mairet-Coello said.

The result suggests that amyloid beta contributes to Alzheimer’s via AMPK, mostly as an enabler of tau’s toxicity.

More Studies Ahead

Mairet-Coello, Polleux and their colleagues are now following up with further experiments to determine what other toxic processes, such as excessive autophagy, are promoted by AMPK overactivation and might also contribute to the long-term aspects of Alzheimer’s disease progression. They are also interested in the long-term effects of blocking AMPK overactivation in the J20 mouse model as well as in other mouse models of Alzheimer’s disease, which normally develop cognitive deficits at later stages. “We already have contacts within the pharmaceuticals industry who are potentially interested in targeting either CAMKK2 or AMPK,” says Polleux.

The other contributors to the study, “The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of amyloid beta oligomers through tau phosphorylation,” were Julien Courchet, Simon Pieraut, Virginie Courchet and Anton Maximov, all of TSRI.

The study was supported in part by the National Institutes of Health (RO1 AG031524) and by Novartis (ADI program).

About The Scripps Research Institute

The Scripps Research Institute (TSRI) is one of the world’s largest independent, not-for-profit organizations focusing on research in the biomedical sciences. TSRI is internationally recognized for its contributions to science and health, including its role in laying the foundation for new treatments for cancer, rheumatoid arthritis, hemophilia, and other diseases. An institution that evolved from the Scripps Metabolic Clinic founded by philanthropist Ellen Browning Scripps in 1924, the institute now employs about 3,000 people on its campuses in La Jolla, CA, and Jupiter, FL, where its renowned scientists—including three Nobel laureates—work toward their next discoveries. The institute’s graduate program, which awards PhD degrees in biology and chemistry, ranks among the top ten of its kind in the nation. For more information, see www.scripps.edu.”

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