Despite the prevalence of the painful condition, women are fearful and frustrated with limited management options, according to Cedars-Sinai research published in the Journal of Urology.
Women who participated in the study were critical of healthcare providers for failing to understand their experiences while over-prescribing antibiotics as a treatment option.
“We were inspired to conduct the study due to the large number of women coming to us feeling hopeless and helpless when it came to the management of their UTIs,” said lead author Victoria Scott, MD, a urologist at the Female Pelvic Medicine and Reconstructive Surgery clinic at Cedars-Sinai.
To help give voice to those suffering with recurrent urinary tract infections, researchers led a focus group study of 29 women who experienced recurrent UTIs to learn about gaps in their care. UTIs are infections of any part of the urinary tract, including the kidneys, ureters, bladder or the urethra. The term is most commonly used to describe a bladder infection.
One of the biggest concerns expressed by study participants revolved around the frequent prescribing of antibiotics and fears of the potential adverse and long-term effects of the medication.
“Many of the participants were aware of the risks of bacteria developing resistance to antibiotics,” Scott said. “They also were aware of the ‘collateral damage’ of antibiotics and disruption they can have on the normal balance of good and bad bacteria throughout the body.”
The focus group discussions also reported concern with the medical system and limited research efforts to investigate new non-antibiotic management strategies.

Researchers from the University of Notre Dame and the University of Florida have developed a sensor that could diagnose a heart attack in less than 30 minutes, according to a study published in Lab on a Chip.
Currently, it takes health care professionals hours to diagnose a heart attack. Initial results from an echocardiogram can quickly show indications of heart disease, but to confirm a patient is having a heart attack, a blood sample and analysis is required. Those results can take up to eight hours.
“The current methods used to diagnose a heart attack are not only time intensive, but they also have to be applied within a certain window of time to get accurate results,” said Pinar Zorlutuna, the Sheehan Family Collegiate Professor of Engineering at Notre Dame and lead author of the paper. “Because our sensor targets a combination of miRNA, it can quickly diagnose more than just heart attacks without the timeline limitation.”
By targeting three distinct types of microRNA or miRNA, the newly developed sensor can distinguish between an acute heart attack and a reperfusion — the restoration of blood flow, or reperfusion injury, and requires less blood than traditional diagnostic methods to do so. The ability to differentiate between someone with inadequate blood supply to an organ and someone with a reperfusion injury is an unmet, clinical need that this sensor addresses.
“The technology developed for this sensor showcases the advantage of using miRNA compared to protein-based biomarkers, the traditional diagnostic target,” said Hsueh-Chia Chang, the Bayer Professor of Chemical and Biomolecular Engineering at Notre Dame and co-author of the paper. “Additionally, the portability and cost efficiency of this device demonstrates the potential for it to improve how heart attacks and related issues are diagnosed in clinical settings and in developing countries.”
A patent application has been filed for the sensor and the researchers are working with Notre Dame’s IDEA Center to potentially establish a startup company that would manufacture the device.
Bioengineers Chang and Zorlutuna are both affiliated with Notre Dame’s Institute for Precision Health. Additional co-authors from Notre Dame are Stuart Ryan Blood, Cameron DeShetler, Bradley Ellis, Xiang Ren, George Ronan and Satyajyoti Senapati. Co-authors from the University of Florida are David Anderson, Eileen Handberg, Keith March and Carl Pepine. The study was funded by the National Institutes of Health National Heart, Lung, and Blood Institute.
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Materials provided by University of Notre Dame. Original written by Brandi Wampler. Note: Content may be edited for style and length.

A team led by researchers at Weill Cornell Medicine, the New York Genome Center, Harvard Medical School, Massachusetts General Hospital and the Broad Institute of MIT and Harvard has profiled in unprecedented detail thousands of individual cells sampled from patients’ brain tumors. The findings, along with the methods developed to obtain those findings, represent a significant advance in cancer research, and ultimately may lead to better ways of detecting, monitoring and treating cancers.
As the researchers reported Sept. 30 in Nature Genetics, they used advanced techniques to record gene mutations, gene activity and gene-activity-programming marks on DNA called methylations, within individual tumor cells sampled from patients with gliomas, the most common type of brain cancer. In this way they mapped distinct tumor cell behaviors or “states” in gliomas, and identified key programming marks that appear to shift glioma cells from one state to another. These programming marks, in principle, could be targeted with future drugs.
Combining their single-cell methods with a molecular-clock technique, the researchers created “ancestral trees” for the sampled tumor cells, depicting their histories of state changes.
“It’s like having a time machine — we can take a sample from a patient’s tumor and infer many details of how that tumor has been developing,” said co-senior author Dr. Dan Landau, an associate professor of medicine in the Division of Hematology and Medical Oncology and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine, and a core member of the New York Genome Center.
“We’ve been able to make observations here that have fundamental implications for how we should think about treating gliomas,” said co-senior author Dr. Mario Suva, an associate professor of pathology at Harvard Medical School, a pathologist at Massachusetts General Hospital and a member of the Broad Institute of MIT and Harvard.
Tumors cells traditionally have been characterized in bulk, rather than individually, and in relatively simple ways, for example by their cell type of origin and by the receptors they bear on their surfaces. Drs. Landau and Suva, however, have helped pioneer the use of “single-cell multi-omics” methods to profile tumor cells individually and in much more detail.

COVID-19 may bring high risks of severe disease and death in many patients by disrupting key metabolic signals and thereby triggering hyperglycemia, according to a new study from researchers at Weill Cornell Medicine and NewYork-Presbyterian.
In the study, reported Sept. 15 in Cell Metabolism, the researchers found that hyperglycemia — having high blood sugar levels — is common in hospitalized COVID-19 patients and is strongly associated with worse outcomes. The researchers also found evidence suggesting that SARS-CoV-2, the coronavirus that causes COVID-19, can induce hyperglycemia by disrupting fat cells’ production of adiponectin, a hormone that helps regulate blood sugar levels.
“We normally don’t think that fat cells are very active, but in fact they synthesize many protective proteins for your body — and it appears that SARS-CoV-2 may disable that protection in many patients,” said Dr. James Lo, an associate professor of medicine in the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center.
Hyperglycemia, the core feature of diabetes, is associated with inflammation and weakened immunity against infections, and was recognized as a significant risk factor for severe COVID-19 early in the pandemic. However, doctors later began finding evidence that COVID-19 is associated with hyperglycemia in patients who have no history of diabetes.
To better understand this important but mysterious aspect of COVID-19, Dr. Lo and colleagues analyzed the records of 3,854 patients who were hospitalized with COVID-19 at NewYork-Presbyterian /Weill Cornell Medical Center, NewYork-Presbyterian Queens and NewYork-Presbyterian Lower Manhattan Hospital. in the first few months of the pandemic in the United States.
They found that a remarkably high proportion (49.7 percent) of these patients presented with hyperglycemia or developed it during their hospital stays.

Researchers at Michigan State University have made a surprising discovery about the human gut’s enteric nervous system that itself is filled with surprising facts. For starters, there’s the fact that this “second brain” exists at all.
“Most people don’t even know that they have this in their guts,” said Brian Gulbransen, an MSU Foundation Professor in the College of Natural Science’s Department of Physiology.
Beyond that, the enteric nervous system is remarkably independent: Intestines could carry out many of their regular duties even if they somehow became disconnected from the central nervous system. And the number of specialized nervous system cells, namely neurons and glia, that live in a person’s gut is roughly equivalent to the number found in a cat’s brain.
“It’s like this second brain in our gut,” Gulbransen said. “It’s an extensive network of neurons and glia that line our intestines.”
Neurons are the more familiar cell type, famously conducting the nervous system’s electrical signals. Glia, on the other hand, are not electrically active, which has made it more challenging for researchers to decipher what these cells do. One of the leading theories was that glial cells provide passive support for neurons.
Gulbransen and his team have now shown that glial cells play a much more active role in the enteric nervous system. In research published online on Oct. 1 in the Proceedings of the National Academy of Sciences, the Spartans revealed that glia act in a very precise way to influence the signals carried by neuronal circuits. This discovery could help pave the way for new treatments for intestinal illness that affects as much as 15% of the U.S. population.

SharecloseShare pageCopy linkAbout sharingImage source, MerckAn experimental drug for severe Covid cuts the risk of hospitalisation or death by about half, interim clinical trial results suggest. The tablet – molnupiravir – was given twice a day to patients recently diagnosed with the disease. US drug-maker Merck said its results were so positive that outside monitors had asked to stop the trial early.It said it would apply for emergency use authorisation for the drug in the US in the next two weeks.Volunteers take part in Covid-19 drug trialFirst oral treatmentIf authorised by regulators, molnupiravir would be the first oral antiviral medication for Covid-19. The pill, which was originally developed to treat influenza, is designed to introduce errors into the genetic code of the virus, preventing it from spreading in the body.An analysis of 775 patients in the study found:7.3% of those given molnupiravir were hospitalisedthat compares with 14.1% of patients who were given a placebo or dummy pillthere were no deaths in the molnupiravir group, but eight patients who were given a placebo in the trial later died of CovidThe data was published in a press release and has not yet been peer-reviewed. Unlike most Covid vaccines, which target the spike protein on the outside of the virus, the treatment works by targeting an enzyme the virus uses to make copies of itself. Merck, known by the name MSD in the UK, said that should make it equally effective against new variants of the virus as it evolves in the future. Daria Hazuda, Merck’s vice-president of infectious disease discovery, told the BBC: “An antiviral treatment for people who are not vaccinated, or who are less responsive to immunity from vaccines, is a very important tool in helping to end this pandemic.” Trial results suggest molnupiravir needs to be taken early after symptoms develop to have an effect. An earlier study in patients who had already been hospitalised with severe Covid was halted after disappointing results.Global approvalMerck is the first company to report trial results of a pill to treat Covid, but other companies are working on similar treatments. Its US rival Pfizer has recently started late-stage trials of two different antiviral tablets, while Swiss company Roche is working on a similar medication.Merck has said it expects to produce 10 million courses of molnupiravir by the end of 2021. The US government has already agreed to buy $1.2bn (£885m) worth of the drug if it receives approval from the regulatory body, the FDA. The company said it is in ongoing discussion with other countries, including the UK, and has also agreed licensing deals with a number of generic manufacturers to supply the treatment to low and middle-income countries.Prof Penny Ward, from King’s College London, who was not involved in the trial, said: “It is greatly hoped that the antiviral task force has, like the vaccines taskforce, pre-ordered courses of this medication.”[This is] so that the UK can, at last, properly manage this condition by treating vaccine breakthrough disease, and relieve pressure on the NHS during the forthcoming winter.”Prof Peter Horby, an expert in infectious diseases at University of Oxford, said: “A safe, affordable, and effective oral antiviral would be a huge advance in the fight against Covid. “Molnupiravir has looked promising in the lab, but the real test was whether it shows benefit in patients. Many drugs fail at this point, so these interim results are very encouraging.”LOOK-UP TOOL: How many cases in your area?SYMPTOMS: What are they and how to guard against them?YOUR QUESTIONS: We answer your queriesTREATMENTS: What progress are we making to help people?NEW VARIANTS: How worried should we be?

It’s Time to Get a Flu ShotChristine HauserReporting on the flu season ��Can the flu shot be given with other vaccines, such as one for Covid-19?Yes. The C.D.C. says the flu vaccine may be administered at the same time as a vaccine against Covid-19.Reactions to the vaccines are generally similar when they are given simultaneously as when they are administered alone.Common reactions to the flu vaccine can be a sore arm, and some people might get a little tired, experts say.

The COVID-19 pandemic has been an especially stressful time for cancer patients undergoing chemotherapy, which attacks not only the cancer, but also the immune cells needed to defend the body from infections. New research at the University of Arizona Health Sciences found that patients undergoing active chemotherapy had a lower immune response to two doses of the COVID-19 vaccine, but a third dose increased response.
“We wanted to make sure we understand the level of protection the COVID-19 vaccines are offering our cancer patients, especially as restrictions were being eased and more contagious variants were starting to spread,” said Rachna Shroff, MD, MS, chief of Gastrointestinal Medical Oncology at the UArizona Cancer Center and director of the Cancer Center Clinical Trials Office.
To answer this question, Dr. Shroff and a team of UArizona Health Sciences researchers looked at 53 Cancer Center patients on immunosuppressive active cancer therapy, such as chemotherapy. They compared the immune response following the first and second dose of the Pfizer-BioNTech COVID-19 vaccine with that of 50 healthy adults. Their results were published online in the journal Nature Medicine.
After two vaccine doses, most of the cancer patients showed some immune response to the vaccine, meaning they had antibodies for SARS-CoV-2, the virus that causes COVID-19.
“We were pleasantly surprised,” said Deepta Bhattacharya, PhD, professor of immunobiology in the College of Medicine — Tucson and a member of the Cancer Center and BIO5 Institute. “We looked at antibodies, B cells and T cells, which make up the body’s defense system, and found the vaccine is likely to be at least partially protective for most people on chemotherapy.”
However, the immune response was much lower than in healthy adults, and a few of the patients had no response to the COVID-19 vaccine. This translates to less protection against SARS-CoV-2, especially the delta variant that is now the dominant strain in the United States.
Twenty patients returned for a third shot, which boosted the immune response for most. The overall group immune response after the third shot reached levels similar to those of people who were not on chemotherapy after two doses.
The interdisciplinary research team was formed not long after the Pfizer-BioNTech vaccine was approved in late 2020. To get the clearest answer possible, they focused on patients with solid tumors, such as breast or gastrointestinal cancer, and excluded people on immunotherapy.
“The fact that we could answer this question in such a short time speaks to what can happen when you leverage the varied expertise we have within UArizona Health Sciences,” said Dr. Shroff, who also is a member of the BIO5 Institute. “Cancer Center clinicians went above and beyond to enroll their patients in the study because we all had a unified goal to protect our patients.”
Coauthors include: Pavani Chalasani, MD, MPH, associate professor of medicine in the Cancer Center; Bonnie LaFleur, biostatistics research professor in the BIO5 Institute; Michael D. Dake, MD, senior vice president of UArizona Health Sciences; Aaron J. Scott, MD, associate professor of medicine; Janko Nikolich-Žugich, MD, PhD, head of the Department of Immunobiology; Michael Worobey, DPhil, head of the Department of Ecology and Evolutionary Biology; Ryan Sprissler, PhD, manager of the University of Arizona Genetics Core; research assistant professor Mladen Jergovic, PhD; associate research scientist Jennifer L Uhrlaub; postdoctoral researcher Marta V. Schoenle, PhD; graduate students Grace Quirk and Tyler J. Ripperger; research assistant Shelby Dalgai; research specialist Alexander Wolf; clinical research coordinator Hytham Hammad; Cancer Center program manager Daniel Pennington; research nurse Amy Carrier, RN; and research technician Ran Wei.
This study was funded in part by the National Institutes of Health (R01AI099108, R01AI129945, R37AG020719, T32AG058503).

Promising news in the effort to develop drugs to treat obesity: University of Virginia scientists have identified 14 genes that can cause and three that can prevent weight gain. The findings pave the way for treatments to combat a health problem that affects more than 40% of American adults.
“We know of hundreds of gene variants that are more likely to show up in individuals suffering obesity and other diseases. But ‘more likely to show up’ does not mean causing the disease. This uncertainty is a major barrier to exploit the power of population genomics to identify targets to treat or cure obesity. To overcome this barrier, we developed an automated pipeline to simultaneously test hundreds of genes for a causal role in obesity. Our first round of experiments uncovered more than a dozen genes that cause and three genes that prevent obesity,” said Eyleen O’Rourke of UVA’s College of Arts & Sciences, the School of Medicine’s Department of Cell Biology and the Robert M. Berne Cardiovascular Research Center. “We anticipate that our approach and the new genes we uncovered will accelerate the development of treatments to reduce the burden of obesity.”
OBESITY AND OUR GENES
O’Rourke’s new research helps shed light on the complex intersections of obesity, diet and our DNA. Obesity has become an epidemic, driven in large part by high-calorie diets laden with sugar and high-fructose corn syrup. Increasingly sedentary lifestyles play a big part as well. But our genes play an important role too, regulating fat storage and affecting how well our bodies burn food as fuel. So if we can identify the genes that convert excessive food into fat, we could seek to inactivate them with drugs and uncouple excessive eating from obesity.
Genomicists have identified hundreds of genes associated with obesity — meaning the genes are more or less prevalent in people who are obese than in people with healthy weight. The challenge is determining which genes play causal roles by directly promoting or helping prevent weight gain. To sort wheat from chaff, O’Rourke and her team turned to humble worms known as C. elegans. These tiny worms like to live in rotting vegetation and enjoy feasting on microbes. However, they share more than 70% of our genes, and, like people, they become obese if they are fed excessive amounts of sugar.
The worms have produced great benefits for science. They’ve been used to decipher how common drugs, including the antidepressant Prozac and the glucose-stabilizing metformin, work. Even more impressively, in the last 20 years three Nobel prizes were awarded for the discovery of cellular processes first observed in worms but then found to be critical to diseases such as cancer and neurodegeneration. They’ve also been fundamental to the development of therapeutics based on RNA technology.
In new work just published in the scientific journal PLOS Genetics, O’Rourke and her collaborators used the worms to screen 293 genes associated with obesity in people, with the goal of defining which of the genes were actually causing or preventing obesity. They did this by developing a worm model of obesity, feeding some a regular diet and some a high-fructose diet.
This obesity model, coupled to automation and supervised machine learning-assisted testing, allowed them to identify 14 genes that cause obesity and three that help prevent it. Enticingly, they found that blocking the action of the three genes that prevented the worms from becoming obese also led to them living longer and having better neuro-locomotory function. Those are exactly the type of benefits drug developers would hope to obtain from anti-obesity medicines.
More work needs to be done, of course. But the researchers say the indicators are encouraging. For example, blocking the effect of one of the genes in lab mice prevented weight gain, improved insulin sensitivity and lowered blood sugar levels. These results (plus the fact that the genes under study were chosen because they were associated with obesity in humans) bode well that the results will hold true in people as well, the researchers say.
“Anti-obesity therapies are urgently needed to reduce the burden of obesity in patients and the healthcare system,” O’Rourke said. “Our combination of human genomics with causality tests in model animals promises yielding anti-obesity targets more likely to succeed in clinical trials because of their anticipated increased efficacy and reduced side effects.”
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Materials provided by University of Virginia Health System. Note: Content may be edited for style and length.

Where does your mind wander when you have idle time? A University of Arizona-led study published in Scientific Reports may offer some clues, and the findings reveal a surprising amount about our mental health.
78 participants were trained to voice their thoughts aloud for 10 minutes while sitting alone in a room without access to electronic devices. Researchers used audio equipment to record those thoughts, then transcribed the recordings and analyzed them for content. In total, more than 2,000 thoughts were analyzed.
“We wanted to mimic the small breaks we have throughout the day, such as when waiting in line at a café, taking a shower, lying in bed at night and so on. These are all times during which external demands are minimal and internal thoughts tend to creep in,” said first author Quentin Raffaelli, a graduate student in the UArizona Department of Psychology.
Most psychology research addressing human thought either tells people what to think about, asks participants to remember what they were thinking about minutes before, or uses self-report questionnaires to capture freeze-frame snapshots of thoughts at different moments in time, according to the authors.
“While insightful in its own right, this snapshot approach doesn’t tell us much about how thoughts unfold and transition over time — features of thinking that we think are important for our mental health. To capture these dynamic properties of thinking, we need a method that records thoughts in real time and for extended periods,” said co-author Jessica Andrews-Hanna, an assistant professor of psychology who oversaw the research in her lab.
Other co-authors include Caitlin Mills, an assistant professor at the University of New Hampshire, as well as UArizona associate professors of psychology Mary-Frances O’Connor, Matthias Mehl and Matthew Grilli, graduate student Eric Andrews, undergraduates Kate Chambers, Nadia-Anais de Stefano and Surya Fitzgerald, lab coordinator Ramsey Wilcox, as well as Kalina Christoff, a professor at the University of British Columbia.