Hopkins Project Shows House Calls and Good Neighbors Can Benefit Patients and Hospitals

Four-year "J-CHiP" study helps hospitals operate more efficiently while helping patients in their homes...When people with chronic health problems couldn't get around town to their doctors' appointments, a four-year Johns Hopkins program brought the appointments to them

Newswise, January 3, 2017 — Johns Hopkins cardiologist and senior director for accountable care Scott Berkowitz, M.D., has published an extensive report of a four-year, $19 million Centers for Medicare and Medicaid Services grant in the journal Healthcare.

The grant, which wrapped up in late summer, was aimed at providing more efficient, less expensive care for people living with multiple chronic conditions in the Baltimore neighborhoods closest to The Johns Hopkins Hospital and Johns Hopkins Bayview Medical Center. Over the course of the grant, the Johns Hopkins Community Health Partnership (J-CHiP) provided East Baltimore residents care in community clinics, acute care hospitals, emergency departments, skilled nursing facilities and even people's homes.

J-CHiP had two components: one community-based and one acute-care based. The acute-care based program targeted the 40,000 adult patients admitted annually to The Johns Hopkins Hospital and the Johns Hopkins Bayview Medical Center. 

Those patients were screened for risks of hospital readmission. The community-based component scored 2,000 Medicare and 1,000 Medicaid patients on their risk of hospitalization.

The community-based program centered on community health workers — specially trained neighborhood residents — who helped identify “super users” of health care in the area and intervene. People who used the emergency department frequently, as well as those identified as high risk for hospital admission, were the program’s main targets.

Reducing hospital readmissions is a goal of government, payers and hospitals alike. Many government and private insurance payers are now refusing to pay for second hospital stays for the same condition. Thus, many hospitals are devising strategies to get patients more engaged in their own care, keeping them healthier and out of the hospital.

"The complex health and social needs of an urban community pose many challenges in the delivery of high-quality care," says Berkowitz, who led the study. "We've learned a lot over four years, and we look forward to learning even more, as the data rolls out in the months to come."

In the J-CHiP model, community health workers, paid by the grant, helped super users break down their barriers to paying regular visits to primary care providers. In addition to a community health worker, each super user was assigned a custom team of physicians, nurses, pharmacists and social workers. 

And finally, J-CHiP worked with skilled nursing facilities on standardizing transitions and keeping patients engaged and motivated.

Among Medicaid patients in the J-CHiP program, 38 percent listed transportation as the main barrier they faced to staying engaged with their own health care. In response, JCHiP provided bus tokens, cab vouchers or shuttle support to 550 patients.

Patients also faced barriers like unstable housing situations and an inability to pay for medicines or care. J-CHiP provided social workers, pharmacy assistance programs and pre-programmed mobile phones to patients who faced critical financial barriers.

Berkowitz says that J-CHiP aligned with Johns Hopkins Medicine goals for transforming care and improving population health. "We focused heavily on East Baltimore's health needs, as well as on innovation of care delivery across the settings where care takes place," he says.

In the report, Berkowitz cites Baltimore City Health Department statistics on life expectancy in the city. "The nearly 200,000 residents of East Baltimore, where life expectancy can be as many as 20 years shorter than nearby more affluent Baltimore neighborhoods, face many challenges to health and well-being," he says.

Berkowitz's article includes examples of J-CHiP team members helping patients overcome barriers to care. In one example, a patient with diabetes who made regular visits to her primary care doctor could no longer see well enough to read her insulin prescription. 

Embarrassed, the patient hid this fact from her doctor, who couldn't determine why her diabetes was so poorly managed. A community health worker visited the patient and saw the trouble she had measuring her insulin. 

After switching to a pre-measured pen system for insulin delivery, the patient also got an eye exam. After three months of her new regimen, both her blood sugar and her eyesight improved significantly.

The J-CHiP program was supported by grant number 1C1CMS331053-01-00 from the U.S. Department of Health and Human Services, Centers for Medicare and Medicaid Services. The content of this press release is solely the responsibility of the authors and does not necessarily represent the official views of the U.S. Department of Health and Human Services or any of its agencies.

To read the full report, click here.

Cedars-Sinai Neurologist Warns of Increased Risk of Strokes During and after the Holidays

Stroke Expert Explains How to Recognize Symptoms and Prevent Life-Threatening Complications by Acting Quickly

Newswise, January 3, 2017 — Along with increased cheer and festivities during the holidays comes an increased risk of stroke, one of the leading causes of death and disability in the U.S.

Patrick D. Lyden, MD, chair of the Cedars-Sinai Department of Neurology, said he sees a significant increase in stroke incidents during December and January, particularly on Christmas Day and New Year’s Day.

Lyden attributes the surge to holiday stress, sleep deprivation, dehydration, smoking, overindulging, and seasonal colds and influenza. He also says that changes in barometric pressure and lower temperatures can play a role.

“Holiday strokes can be an unexpected and even fatal problem because they often arrive with little warning,” said Lyden, director of the Cedars-Sinai Stroke Center. “The good news, however, is that with advanced tools and technology available to us, we may prevent life-threatening complications and even reverse the effects of a stroke if we administer treatment within six hours.”

Lyden says the number of stroke cases treated at Cedars-Sinai rises to about 100 from about 80 per month during the winter season. Stroke is the fifth-leading cause of death in the U.S. and a leading cause of disability, according to the American Stroke Association.

To recognize symptoms, leading stroke experts recommend memorizing an easy-to-remember acronym: FAST!

Face (drooping of the face)
Arm (arm weakness)
Speech (slurred speech)
Time (time counts -- call 911 immediately)

To reduce the risk of strokes, Lyden recommends that individuals reduce stress, eat and drink in moderation, be vigilant about taking prescribed medications, exercise, get rest and stop smoking.

“Studies show that 80 percent of strokes can be prevented,” said Lyden. “But if it occurs, the key is calling 911 fast. Every minute a stroke is untreated, the average patient loses about 1.9 million brain cells.”

Cedars-Sinai has been designated a Comprehensive Stroke Center by The Joint Commission, an independent, not-for-profit organization that accredits and certifies nearly 21,000 health care organizations and programs in the United States.

This advanced certification for comprehensive stroke centers recognizes the significant resources in staff and training that these centers must have to treat complex stroke cases. Cedars-Sinai was proud to be among the first five hospitals in the nation, and the first in Southern California, to receive this designation.

Ovarian Cancer Survival Rates Improve in Sanford Study

Sanford Research lab exploring role of protein in disease progression

Newswise, January 3, 2017– A Sanford Research lab is studying a protein’s role in improving survival in ovarian cancer patients. Findings published in Oncogenesis indicate a higher level of a specific protein correlates with an increased survival rate and decrease in the spreading of cancer cells.

Kristi Egland, Ph.D., an associate scientist in the Cancer Biology Research Center at Sanford Research, led the study, which retroactively looked at tumor samples from ovarian cancer patients. 

Her team noticed that patients with higher levels of the Sushi Domain Containing 2 protein, or SUSD2, experienced less metastasizing of cancer cells and thus survived an average of 18 months longer.

“We want to better understand how SUSD2 played a role in inhibiting the spread of cancer from the ovaries to other parts of the body,” said Egland. “Ovarian cancer is usually diagnosed in late stages and after it has spread, which makes it difficult to cure. The mechanisms that underlie SUSD2’s ability to reduce metastasizing of cancer cells could help us identify drugs that mimic its function and provide a target for therapy options that prolong survival.”

SUSD2 is a protein common in cancers that is responsible for telling cells where to attach to other cells. In ovarian cancer, cancer cells often attach to the lining of the abdominal cavity and spread to other organs in or adjacent to that area. Higher levels of SUSD2, according to Egland, seemed to stop the attachment of cancer cells to other organs.

The American Cancer Society reports that ovarian cancer accounts for more deaths than any other cancer of the female reproductive system and ranks fifth in cancer deaths among women. A woman's risk of getting ovarian cancer during her lifetime is about 1 in 75, and her lifetime chance of dying from ovarian cancer is about 1 in 100.

Egland’s lab at Sanford Research specializes in studying proteins for use as diagnostic markers and immunotherapy targets. In addition to exploring ovarian cancer, her lab also does work with breast cancer.

Oncogenesis is a peer-reviewed online journal focusing on the molecular basis of cancer and promoting diverse and integrated areas of molecular biology, cell biology, oncology and genetics.

About Sanford Research

Sanford Research is a non-profit research organization and is part of Sanford Health, an integrated health system headquartered in the Dakotas. Sanford Health is one of the largest health systems in the nation with a presence in nine states and four countries. 

More than $600 million in gifts from Denny Sanford has provided for an expansion of research initiatives in type 1 diabetes, breast cancer and genomics in internal medicine.

With a team of more than 200 researchers, Sanford Research comprises several research centers, including Children’s Health Research, Edith Sanford Breast Center, Cancer Biology, Center for Health Outcomes and Population and Sanford Sports Science Institute.

Regular Aspirin Use May Reduce Risk for Pancreatic Cancer

Newswise, January 3, 2017 — Regular use of aspirin by people living in Shanghai, China, was associated with decreased risk for developing pancreatic cancer, according to data published in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

Data from the new study and meta-analysis of data from 18 other studies suggest that over the past two decades, as the general population’s use of aspirin has increased, the effect of aspirin in decreasing pancreatic cancer risk has become more pronounced.

“Pancreatic cancer is one of the deadliest types of cancer—fewer than 8 percent of patients survive five or more years after diagnosis—so it is crucial that we find ways to prevent it,” said Harvey A. Risch, MD, PhD, professor of epidemiology in the Department of Chronic Disease Epidemiology at the Yale School of Public Health, Yale School of Medicine, and Yale Cancer Center in New Haven, Connecticut.

“We found that regular use of aspirin by a large group of people in Shanghai cut risk of pancreatic cancer almost in half."

“These new data are consistent with what has been seen in other populations around the world,” continued Risch. “Pancreatic cancer is relatively rare—just 1.5 percent of U.S. adults will be diagnosed with it at some point during life—and regular aspirin use can cause appreciable complications for some.

“Therefore, a person should consult his or her doctor about aspirin use. Nevertheless, the balance of evidence shows that people who use aspirin to reduce risk for cardiovascular disease or colorectal cancer can feel positive that their use likely also lowers their risk for pancreatic cancer.”

Risch and colleagues recruited patients newly diagnosed with pancreatic cancer at 37 Shanghai hospitals from December 2006 to January 2011. They also randomly selected controls from the Shanghai Residents Registry.

The 761 patients with pancreatic cancer and 794 controls were interviewed in person to determine when they started using aspirin, the number of years they used aspirin, and when they stopped using aspirin, among other things. Almost all aspirin users used aspirin daily.

Among the patients with pancreatic cancer, 11 percent reported regular use of aspirin. Eighteen percent of the controls reported regular use of aspirin.

After adjusting for a number of factors, including body mass index, smoking history, and history of diabetes, the researchers found that ever having used aspirin regularly was associated with a 46 percent decreased risk for pancreatic cancer. Risk decreased by 8 percent for each year of aspirin use.

In reviewing the literature, Risch and colleagues found 18 other studies that had investigated aspirin use and pancreatic cancer risk.

Meta-analysis of the data from these studies showed that if the studies were considered by the year at which the midpoint of when the aspirin exposures were ascertained in the study, the odds ratios for regular use of aspirin and pancreatic cancer risk significantly decreased by 2.3 percent per year through the present.

According to Risch, the main limitation of the Shanghai study is that it is a case-control study that relied on participants accurately reporting past aspirin use.

The study was supported by grants from the U.S. National Cancer Institute, the Science and Technology Commission of Shanghai Municipality, and the Shanghai Cancer Institute. Risch declares no conflicts of interest.

Brain Generates Replacement Cells After Stroke

Newswise, January 3, 2017— UCLA researchers have shown that the brain can be repaired — and brain function can be recovered — after a stroke in animals.

The discovery could have important implications for treating a mind-robbing condition known as a white matter stroke, a major cause of dementia.

White matter stroke is a type of ischemic stroke, in which a blood vessel carrying oxygen to the brain is blocked. Unlike large artery blockages or transient ischemic attacks, individual white matter strokes, which occur in tiny blood vessels deep within the brain, typically go unnoticed but accumulate over time.

They accelerate Alzheimer’s disease due to damage done to areas of the brain involved in memory, planning, walking and problem-solving.

“Despite how common and devastating white matter stroke is there has been little understanding of how the brain responds and if it can recover,” said Dr. Thomas Carmichael, senior author of the study and a professor of neurology at the David Geffen School of Medicine at UCLA.

“By studying the mechanisms and limitations of brain repair in this type of stroke, we will be able to identify new therapies to prevent disease progression and enhance recovery.”

In a five-year study, Carmichael’s team looked at white matter strokes in animals and found that the brain initiated repair by sending replacement cells to the site, but then the process stalled.

The team had a short list of molecular suspects from previous research that they thought might be responsible. Researchers identified a molecular receptor as the likely culprit in stalling the repair; when they blocked the receptor, the animals began to recover from the stroke.

“White matter stroke is an important clinical target for the development of new therapies,” Carmichael said.

Annually in the United States, about 795,000 suffer a stroke, resulting in nearly 130,000 deaths. Multiply the number of strokes by six, and you’ll have an estimate of the number of strokes that are “silent,” in that they do not produce symptoms that lead to hospitalization. Most of these silent strokes are white matter strokes.

The paper was published in the electronic edition of the Proceedings of the National Academy of Sciences.

The study was funded by National Institute of Neurological Disorders and Stroke, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, and the American Stroke Association/Bugher Foundation.

Study Details Molecular Roots of Alzheimer’s

Credit: Daniel L. Kober

A new study at Washington University School of Medicine in St. Louis details the structure of TREM2, a protein involved in Alzheimer's disease and other neurodegenerative disorders

Cellular 'housekeeping' molecule’s structure linked to neurodegeneration

Newswise, January 3, 2017 — Scientists at Washington University School of Medicine in St. Louis have detailed the structure of a molecule that has been implicated in Alzheimer’s disease.

Knowing the shape of the molecule — and how that shape may be disrupted by certain genetic mutations — can help in understanding how Alzheimer’s and other neurodegenerative diseases develop and how to prevent and treat them.

The idea that the molecule TREM2 is involved in cognitive decline — the hallmark of neurodegenerative diseases, including Alzheimer’s — has gained considerable support in recent years.

Past studies have demonstrated that certain mutations that alter the structure of TREM2 are associated with an increased risk of developing late-onset Alzheimer’s, frontal temporal dementia, Parkinson’s disease and sporadic amyotrophic lateral sclerosis (ALS).

Other TREM2 mutations are linked to Nasu-Hakola disease, a rare inherited condition that causes progressive dementia and death in most patients by age 50.

“We don’t know exactly what dysfunctional TREM2 does to contribute to neurodegeneration, but we know inflammation is the common thread in all these conditions,” said senior author Thomas J. Brett, PhD, an assistant professor of medicine.

“Our study looked at these mutations in TREM2 and asked what they do to the structure of the protein itself, and how that might impact its function. If we can understand that, we can begin to look for ways to correct it.”

The analysis of TREM2 structure, completed by first author, Daniel L. Kober, a doctoral student in Brett’s lab, revealed that the mutations associated with Alzheimer’s alter the surface of the protein, while those linked to Nasu-Hakola influence the “guts” of the protein. The difference in location could explain the severity of Nasu-Hakula, in which signs of dementia begin in young adulthood.

The internal mutations totally disrupt the structure of TREM2, resulting in fewer TREM2 molecules. The surface mutations, in contrast, leave TREM2 intact but likely make it harder for the molecule to connect to proteins or send signals as normal TREM2 molecules would.

TREM2 lies on the surface of immune cells called microglia, which are thought to be important “housekeeping” cells. Via a process called phagocytosis, such cells are responsible for engulfing and cleaning up cellular waste, including the amyloid beta that is known to accumulate in Alzheimer’s disease.

 If the microglia lack TREM2, or the TREM2 that is present doesn’t function properly, the cellular housekeepers can’t perform their cleanup tasks.

“Exactly what TREM2 does is still an open question,” Brett said. “We know mice without TREM2 have defects in microglia, which are important in maintaining healthy brain biology. Now that we have these structures, we can study how TREM2 works, or doesn’t work, in these neurodegenerative diseases.”

TREM2 also has been implicated in other inflammatory conditions, including chronic obstructive pulmonary disease and stroke, making the structure of TREM2 important for understanding chronic and degenerative diseases throughout the body, he added.

###

This work was supported by the National Institutes of Health (NIH), grant numbers R01-HL119813, R01-AG044546, R01-AG051485, R01-HL120153, R01-HL121791, K01-AG046374, T32-GM007067, K08-HL121168, and P50-AG005681-30.1; the Burroughs-Wellcome Fund; the Alzheimer’s Association, grant number AARG-16-441560; and the American Heart Association, grant number PRE22110004. Results were derived from work performed at Argonne National Laboratory (ANL) Structural Biology Center. ANL is operated by U. Chicago Argonne, LLC, for the U.S. DOE, Office of Biological and Environmental Research, supported by grant number DE-AC02-06CH11357.

Kober DL, Alexander-Brett JM, Karch CM, Cruchaga C, Colonna M, Holtzman MJ, Brett TJ. Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms. eLife. Dec. 20, 2016.

Washington University School of Medicine‘s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

UVA Discovers Powerful Defenders of the Brain -- with Big Implications for Disease and Injury

Rare immune cells found in unexpected place; may be missing link between brain and gut

• UVA researchers discover an influential type of immune cell in the membranes around the brain;
• These cells kick off powerful immune responses to disease or injury;
• Their presence around the brain comes as a surprise;
• The cells may play a vital role connecting the brain with our gut microbiota, which is essential for good health;
• The cells have a major effect on recovery from spinal cord injury, UVA shows;
• By targeting the cells, doctors may be able to develop new treatments for many neurological conditions, including migraines.

Newswise, January 3, 2017--A rare and powerful type of immune cell has been discovered in the meninges around the brain, suggesting the cells may play a critical but previously unappreciated role in battling Alzheimer's, multiple sclerosis, meningitis and other neurological diseases, in addition to supporting our healthy mental functioning. By harnessing the cells' power, doctors may be able to develop new treatments for neurological diseas

es, traumatic brain injury and spinal cord injuries – even migraines.

Further, School of Medicine researchers suspect the cells may be the missing link connecting the brain and the microbiota in our guts, a relationship already shown important in the development of Parkinson’s disease.

Unexpected presence

The cells, known as “type 2 innate lymphocytes,” previously have been found in the gut, lung and skin – the body’s barriers to disease. Their discovery in the meninges, the membranes surrounding the brain, comes as a surprise. 

They were found as UVA researcher Jonathan Kipnis, PhD, explored the implications of his lab’s game-changing discovery last year that the brain and the immune system are directly connected via vessels long thought not to exist.

“This all comes down to immune system and brain interaction,” said Kipnis, 

chairman of UVA’s Department of Neuroscience. 

“The two were believed to be completely not communicating, but now we’re slowly, slowly filling in this puzzle. Not only are these [immune] cells present in the areas near the brain, they are integral to its function. When the brain is injured, when the spinal cord is injured, without them, the recovery is much, much worse.”

Curiously, the immune cells were found along the vessels discovered by Kipnis’ team. “They’re right on the lymphatics, which is really weird,” noted researcher Sachin Gadani. “You have the lymphatics and they’re stacked right on top. 

They’re not inside of them – they’re around them.”

Important immune role

The immune cells play several important roles within the body, including guarding against pathogens and triggering allergic reactions. In exploring their role in protecting the brain, the Kipnis team has determined they are vital in the body’s response to spinal cord injuries. But it’s their role in the gut that makes Kipnis suspect they may be serving as a vital communicator between the brain’s immune response and our microbiomes. That could be of great importance, because our intestinal flora is critical for maintaining our health and wellbeing.

“These cells are potentially the mediator between the gut and the brain. They are the main responder to microbiota changes in the gut. They may go from the gut to the brain, or they may just produce something that will impact those cells. But you see them in the gut and now you see them also in the brain,” Kipnis said. 

“We know the brain responds to things happening in the gut. Is it logical that these will be the cells that connect the two? Potentially. We don’t know that, but it very well could be.”

While much more research needs to be done to understand the role of these cells in the meninges, Gadani noted that it’s almost certain that the cells are important in a variety of neurological conditions. 

“It would be inconceivable they’re not playing a role in migraines and certain conditions like that,” he said. “The long-term goal of this would be developing drugs for targeting these cells. I think it could be highly efficacious in migraine, multiple sclerosis and possibly other conditions.”

Findings published

The findings have been published online by the Journal of Experimental Medicine. The article is by Gadani, of UVA’s Medical Scientist Training Program; Igor Smirnov; Ashtyn T. Smith; Christopher C. Overall; and Kipnis, who, in addition to being department chairman, is the director of UVA’s Center for Brain Immunology and Glia (BIG).

The work was supported by the National Institutes of Health, grant NS081026.