Too-low diastolic blood pressure can be deadly for CKD patients

Main Category: Urology / Nephrology
Article Date: 20 Aug 2013 - 1:00 PDT Current ratings for:
Too-low diastolic blood pressure can be deadly for CKD patients

Having too-low diastolic blood pressure (DBP) may be deadly for patients with chronic kidney disease (CKD). Blood pressure (BP) recommendations are stricter for patients with CKD than for the general population and focus on lowering actual BP (the measurement of both systolic BP [SBP] and DBP) without consideration for achieving a DBP that is too low.

Researchers reviewed health records for 651,749 U.S. veterans with CKD to assess the association between BP and death. Both actual BP and measurements of SBP and DBP considered separately were assessed.

The researchers found that having a systolic blood pressure of 130 to 159 mm Hg and diastolic blood pressure of 70 to 89 mm Hg was associated with the lowest risk for death. Patients with a DBP less than 70 mm Hg, regardless of their SBP, had higher mortality rates.

An accompanying editorial highlights some of the limitations of the study. Among them, the authors suggest that it may not be BP combination but instead the characteristics of the persons with that combination that lead to greater mortality risk.

Blood Pressure and Mortality in U.S. Veterans With Chronic Kidney Disease: A Cohort Study, Csaba P. Kovesdy, MD; Anthony J. Bleyer, MD; Miklos Z. Molnar, MD, PhD; Jennie Z. Ma, PhD; John J. Sim, MD; William C. Cushman, MD; L. Darryl Quarles, MD; and Kamyar Kalantar-Zadeh, MD, PhD, Ann Intern Med. 2013;159(4):233-242. doi:10.7326/0003-4819-159-4-201308200-00004

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Susceptibility to deadly fungal infection increased by methamphetamine

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Neurology / Neuroscience;  Alcohol / Addiction / Illegal Drugs;  Respiratory / Asthma
Article Date: 31 Jul 2013 - 2:00 PDT Current ratings for:
Susceptibility to deadly fungal infection increased by methamphetamine

Methamphetamine use can make a person more susceptible to the lung infection cryptococcosis, according to a study published in mBio®, the online open-access journal of the American Society for Microbiology.

Researchers found that injected methamphetamine (METH) significantly enhanced colonization of the lungs by Cryptococcus neoformans and accelerated progression of the disease and the time to death in mouse models. C. neoformans is usually harmless to healthy individuals, but METH causes chinks in the blood-brain barrier that can permit the fungus to invade the central nervous system, where it causes a deadly brain infection.

"The highest uptake of the drug is in the lungs," says corresponding author Luis Martinez of Long Island University-Post, in Brookville, New York and of Albert Einstein College of Medicine in The Bronx. "This may render the individual susceptible to infection. We wanted to know how METH would alter C. neoformans infection."

Thirteen million people in the US have abused METH in their lifetimes, and regular METH users numbered approximately 353,000 in 2010, the most recent year for which data are available. A central nervous system stimulant that adversely impacts immunological responses, recent studies show that injected METH accumulates in various sites in the body, but the lungs seem to accumulate the highest concentrations, says Martinez, which could well impact how the lung responds to invading pathogens.

To study the impact this accumulation might have on pulmonary infection, Martinez and his colleagues injected mice with doses of METH over the course of three weeks, then exposed those mice to the C. neoformans fungus. In humans, C. neoformans initially infects the lungs but often crosses the blood-brain barrier to infect the central nervous system and cause meningitis. In their experiments, METH significantly accelerated the speed with which the infected mice died, so that nine days after infection, 100% of METH treated mice were dead, compared to 50% of the control mice.

Using fluorescent microscopy to examine lung tissue in METH-treated and control mice, the researchers found that METH enhanced the interaction of C. neoformans with epithelial cells in the lining of the lung. Seven days after exposure to the fungus, the lungs of METH-treated mice showed large numbers of fungi surrounded by vast amounts of gooey polysaccharide in a biofilm-like arrangement. METH-treated mice also displayed low numbers of inflammatory cells early during infection and breathed faster than controls, a sign of respiratory distress.

Martinez says this greater ability to cause disease in the lung may be due in part to simple electrical attraction. Their analysis shows that METH imparts a greater negative charge on the surface of the fungal cells, possibly lending them a greater attraction to the surface of the lung and an enhanced ability to form a biofilm that can protect its members from attack by the immune system. The fungus also releases more of its capsular polysaccharide in METH-treated mice, which can help the organism colonize and persist in the lung.

"When the organism senses the drug, it basically modifies the polysaccharide in the capsule. This might be an explanation for the pathogenicity of the organism in the presence of the drug, but it also tells you how the organism senses the environment and that it will modify the way that it causes disease," Martinez says.

But the fungus doesn't stop in the lungs. "The drug stimulates colonization and biofilm formation in the lungs of these animals," says Martinez. "And this will follow to dissemination to the central nervous system by the fungus."

C. neoformans in the lung moved on to the bloodstream and then into the central nervous system. The brains of METH-treated mice had higher numbers of C. neoformans cells, greater quantities of the fungus' polysaccharide, and larger lesions than control mice, indicating that METH has a detrimental effect on the blood-brain barrier, permitting the pathogen to cross more easily from the bloodstream to infect the central nervous system.

"METH-induced alterations to the molecules responsible to maintain the integrity of the blood-brain barrier provide an explanation for the susceptibility of METH abuser to brain infection by HIV and other pathogens," write the authors.

Martinez and his colleagues plan to follow up on the work by investigating how aspects of the immune system might be involved in changes the drug causes to the blood-brain barrier.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

Patel D, Desai GM, Frases S, Cordero RJB, DeLeon-Rodriguez CM, Eugenin EA, Nosanchuk JD, Martinez LR. 2013. Methamphetamine Enhances Cryptococcus neoformans Pulmonary Infection and Dissemination to the Brain, mBio 4(4):e00400-13. doi:10.1128/mBio.00400-13.

American Society for Microbiology

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New approach for studying deadly brain cancer

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience
Article Date: 25 Jul 2013 - 1:00 PDT Current ratings for:
New approach for studying deadly brain cancer

Human glioblastoma multiforme, one of the most common, aggressive and deadly forms of brain cancer, is notoriously difficult to study. Scientists have traditionally studied cancer cells in petri dishes, which have none of the properties of the brain tissues in which these cancers grow, or in expensive animal models.

Now a team of engineers has developed a three-dimensional hydrogel that more closely mimics conditions in the brain. In a paper in the journal Biomaterials, the researchers describe the new material and their approach, which allows them to selectively tune up or down the malignancy of the cancer cells they study.

The new hydrogel is more versatile than other 3-D gels used for growing glioma (brain cancer) cells in part because it allows researchers to change individual parameters - the gel's stiffness, for example, or the presence of molecular signals that can influence cancer growth - while minimally altering its other characteristics, such as porosity.

Being able to adjust these traits individually will help researchers tease out important features associated with the initial growth of a tumor as well as its response to clinical therapies, said University of Illinois chemical and biomolecular engineering professor Brendan Harley, who led the study with postdoctoral researcher Sara Pedron and undergraduate student Eftalda Becka. Harley is an affiliate of the Institute for Genomic Biology at Illinois.

The researchers found that they could increase or decrease the malignancy of glioma cells in their hydrogel simply by adding hyaluronic acid, a naturally occurring carbohydrate found in many tissues, especially the brain.

Hyaluronic acid (HA) is a key component of the extracellular matrix that provides structural and chemical support to cells throughout the body. HA contributes to cell proliferation and cell migration, and local changes in HA levels have been implicated in tumor growth.

"Hyaluronic acid is one of the major building blocks in the brain," Harley said. "The structure of a newly forming brain tumor has some of this HA within it, but there's also a lot of the HA in the brain surrounding the tumor."

Previous studies have used hydrogels made out of nothing but hyaluronic acid to study gliomas, Harley said. "The problem there is that HA is structurally not very strong." It also is difficult to adjust the amount of HA that the glioma cells are exposed to if their environment is 100 percent HA, he said.

In the new study, Pedron observed how glioma cells behaved in two different hydrogels - one based on methacrylated gelatin (GelMA) and the other using a more conventional polyethylene glycol (PEG) biomaterial. These two materials vary in one important trait: GelMA is a naturally derived material that contains adhesive sites that allow cells to latch onto it; synthetic PEG does not.

"The purpose of having these two systems was to isolate the effect of HA on glioma cells," Pedron said. If changing HA levels produced different effects in different gels, that would indicate that the gels were contributing to those effects, she said.

Instead, Harley and Pedron found that additions of HA to glioma cells had "very similar" effects in both materials. Adding too little or too much HA led to reduced malignancy, while incorporating just enough HA led to significantly enhanced malignancy. This held true for multiple types of glioblastoma multiforme cells. This suggests that "it's the HA itself that is likely the cause for this malignant change," Harley said.

"If you have a material that allows you to selectively tune up or down malignancy, that will allow you to ask lots of questions about treatment methods for more malignant or less malignant forms of glioma. It also will allow scientists to try to get a response that's closer to what you see in the body," he said.

"If you talk to pathologists, they'll say a biomaterial will never allow you to grow a full brain tumor, which is probably true," Harley said. "But it's realistic to think that a well-designed biomaterial will allow you to study aspects of glioma growth and treatment in a way that's much richer than simply looking in a petri dish and much more accessible than trying to study tumor development within the brain itself."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.

The U. of I. department of chemical and biomolecular engineering, the Institute for Genomic Biology and the Campus Research Board supported this research.

University of Illinois at Urbana-Champaign

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