Health24.com | ‘Help! My baby’s cough sounds like a dog’s bark’

Croup is a viral illness which triggers the swelling of your baby’s voice box and windpipe.

The high-pitched or barking cough develops when air is forced against a constricted airway during a breath in or a cough.

The smaller your child is, the more distinctive and noticeable the sound.

Some children with severe croup get a harsh, tight sound while breathing in. This is called stridor.

When does it happen?

The virus associated with the development of croup can be passed on by breathing in respiratory droplets from a cough, or from playing with toys that have the virus on them.

Croup normally affects infants and children between the ages of 6 months and 3 years.

As children grow, so do their airways. Therefore, children above the age of 6 rarely get diagnosed with croup.

What are the symptoms?

You may notice the typical symptoms of a cold, like a runny nose and fever. Usually, the barky cough begins at night, and gets worse when your child gets upset and cries.

Croup typically lasts 3-5 days.

How is croup diagnosed?

The doctor will usually listen for a cough and stridor.

They may also ask if your child has had any recent illnesses that caused a fever and congestion and whether the child has a history of croup or upper airway problems.

He may also perform an X-ray if the croup is severe and doesn’t get better after treatment.

An X-ray in this case will help show the top of the airway narrowing to a point, which doctors call a “steeple sign”, which is a tapering or narrowing of the airway below the vocal cords.

Home treatment for croup 

If your child wakes up in the middle of the night with croup, try to keep him calm as this will help him breathe better.

Crying can make croup worse.

For a fever, medicine like paracetamol, also known as acetaminophen or, only for kids older than 6 months, ibuprofen; can help make your child more comfortable.

Ask your doctor for guidance in giving your child the medicine. 

Help your child breathe in moist air. This can make him feel better.

  • Use a cool-mist humidifier or run a hot shower to create a steam-filled bathroom where you can sit with your child for 10 minutes. Breathing in the mist will sometimes stop the severe coughing.
  • In cooler weather, take your child outside to help ease symptoms so they can breathe fresh air. 
  • Make sure your child is well hydrated. If needed, give small amounts of liquid more often using a spoon or medicine dropper. Children with croup should also get lots of rest.

When to call the doctor

If you are concerned that your child’s croup is not improving, contact your child’s doctor, especially if  these symptoms persist:

  • A sound that gets louder with each breath
  • If your child speaks or makes verbal sounds for lack of breath
  • Seems to be struggling to catch his breath
  • Has bluish lips or fingernails
  • Has stridor when resting
  • Drools or has extreme difficulty swallowing saliva

References: WebMD, KidMed, HealthyChildren, KidsHealth, Remedy

Image credit: iStock

Share Button

Health24.com | 5 common gym injuries and how to prevent them

Ankle sprain

You may think that an ankle sprain is only possible when running outdoors, but jogging on a treadmill could also lead to an injury.

It’s easy to hurt your ankle on the treadmill because you might lose focus while jogging and could accidentally step half on and half off the moving machine.

Don’t jump off the treadmill too quickly either! You could roll your ankle into an unnatural position. 

To prevent treadmill ankle injuries, attach a clip from your clothes to the machine, which will stop it if you fall.

If you plan on running outdoors, stick to even or paved grounds. 

Shin splints

Commonly known as a shin splint, pain and muscle inflammation along the inner edge of your shinbone usually develops if you exercise often.

The risk is increased if you work out on uneven ground, on hills or have recently increased the intensity of your workout. 

Prevent shin splints by wearing shoes designed for working out, slowly increasing your workout intensity by no more than 10% a week and warming up before running or jogging.

Lower-back strains

A sudden, sharp ache or shock in your lower back? It could be a sign that you’ve overworked your back while exercising.

Deadlifts or squats could lead to lower back injuries so it’s important to do them with the correct form.

Twisting motions and side bends could also lead to lower back injuries. 

If you’re a beginner doing squats or deadlifts, first learn how to maintain a neutral back. To find your neutral spine, lay on your back with your knees bent and your feet flat on the floor.

Your spine should touch the floor under your neck and lower back, allowing the natural curves of your back to absorb the shock.

If you’re a beginner, get your form correct first by asking a qualified trainer for advice before adding weights.

Biceps tendinitis

Overuse can happen after repetitive motions during exercises like weightlifting, swimming, tennis and even golf.

This causes biceps tendinitis. It’s the inflammation of the tendon that’s attached to your upper bicep muscle to the bones of your shoulder.

If you feel pain in the front of your shoulder or have upper arm weakness, you may have this injury.

Try cross-training to prevent repetitive overhead movements, keep your posture correct while exercising and rest enough between workouts.

Pectoral injury

A pectoral injury can easily happen if you lose control of a dumbbell or barbell during a heavy bench press.

Too much weight can lead to a tear in your pectoral muscle (large muscle in your upper chest).

See your doctor immediately if you feel a tearing sensation along with blue or black upper arm bruising, as you might need surgery.

Prevent this kind of injury by controlling the amount of weight you’re lifting. You could also ask someone to spot for you (support you during an exercise like weightlifting) so you don’t lose control of the weights while you lift. 

References: Livestrong, WebMD

Image credit: iStock

NEXT ON HEALTH24X

Share Button

Athletes have poor teeth despite brushing

Are sugary sports drinks and gels the problem?

Share Button

Light-matter interaction without interference

An efficient light-matter interface might constitute the foundation of quantum communication. However, certain structures that are formed during the growth process interfere with the signal.

Certain semiconductor structures, so-called quantum dots, might constitute the foundation of quantum communication. They are an efficient interface between matter and light, with photons (light particles) emitted by the quantum dots transporting information across large distances. However, structures form by default during the manufacture of quantum dots that interfere with communication. Researchers at the University of Basel, Ruhr-Universität Bochum, and Forschungszentrum Jülich have now successfully eliminated these interferences. They’ve published their report in the journal Communications Physics from 9 August 2019.

Light particles capable of transporting information across large distances

Quantum dots can be realised in semiconductors if researchers lock an electron and an electron hole — i.e. a positive charge at a position where an electron should exist — in a constricted space. Together, electron and electron hole form an excited state. When they recombine, the excited state disappears and a photon is generated. “That photon might be usable as information carrier in quantum communication across large distances,” says Dr. Arne Ludwig from the Chair for Applied Solid State Physics in Bochum.

The quantum dots manufactured in Bochum are generated in the semiconductor material indium arsenide. The researchers grow the material on a gallium arsenide substrate. In the process, a smooth indium arsenide layer forms at a thickness of a mere one and a half atomic layers — the so-called wetting layer. Subsequently, the researchers generate small islands with a diameter of 30 nanometres and a height of a few nanometres. These are the quantum dots.

Interfering photons from wetting layer

The wetting layer that has to be deposited in the first step causes problems, because it, too, contains excited electron hole states that decay and may release photons. In the wetting layer, these states decay even more easily than in the quantum dots. The photons emitted in the process can’t be used in quantum communication, however; rather, they generate a static noise in the system.

“The wetting layer covers the entire surface while the quantum dots only cover a thousandth of the semiconductor chip, which is why the interfering light is approximately a thousand times stronger than the light emitted by the quantum dots,” explains Andreas Wieck, Head of the Chair for Applied Solid State Physics in Bochum. “The wetting layer radiates photons at a slightly higher frequency and at a much higher intensity than the quantum dots. It’s as if the quantum dots emitted the chamber pitch A, whereas the wetting layer emitted an B that was a thousand times louder.”

Additional layer eliminates interferences

“We have been able to ignore those interferences by exciting only the required energy states,” says Matthias Löbl from the University of Basel. “However, if quantum dots are to be used as information units for quantum applications, it might be ideal to charge them with more electrons. But in that case, the energy levels in the wetting layer would be likewise excited,” adds Arne Ludwig.

The research team has now eliminated this interference by adding an aluminium arsenide layer grown above the quantum dots in the wetting layer. The energy states in the wetting layer are thus removed, which, in turn, makes it less likely for electrons and electron holes to recombine and emit photons.

Collaboration between three research institutes

The samples for the current project were generated by Dr. Sven Scholz at the RUB Chair of Applied Solid State Physics, whose work was awarded with the dissertation prize by the Wilhelm and Else Heraeus Foundation in June 2019. The measurements of the size of interferences with and without the aluminium arsenide layer were conducted by the team at the University of Basel, under the auspices of Matthias Löbl, Dr. Immo Söllner and Professor Richard Warburton. The group at Forschungszentrum Jülich captured high-resolution microscope images of the samples.

Story Source:

Materials provided by Ruhr-University Bochum. Original written by Julia Weiler; translated by Donata Zuber. Note: Content may be edited for style and length.

Share Button

Stay healthy by making friends

Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission.

Advertising & Sponsorship

Mayo Clinic Marketplace

Check out these best-sellers and special offers on books and newsletters from Mayo Clinic.

Share Button

Heart attack patients with mild cognitive impairment get fewer treatments

A new study finds people who have mild cognitive impairment (MCI), which lies on the continuum of cognitive decline between normal cognition and dementia, are less likely to receive proven heart attack treatment in the hospital.

Researchers found no evidence that those with MCI would derive less benefit from evidence-based treatment that’s offered to their cognitively normal peers who have heart attacks, says lead author Deborah Levine, M.D., MPH.

“Patients should get the treatments they would want if they were properly informed,” says Levine, an associate professor of internal medicine and neurology at Michigan Medicine, the academic medical center of the University of Michigan.

Some people with thinking, memory and language problems have MCI. Unlike dementia, which severely interferes with daily functioning and worsens over time, MCI does not severely interfere with daily functioning and might not worsen over time. Although people with MCI have an increased risk of developing dementia, it’s not an inevitable next step, Levine says.

“While some may progress to dementia, many will persist in having MCI, and a few will actually improve and revert to normal cognition,” says Levine, also a member of the University of Michigan Institute for Healthcare Policy and Innovation. “Many older adults with MCI live years with good quality of life, and so face common health risks of aging like heart attack and stroke.

“Clinicians, patients and families might be overestimating the risk of dementia after a mild cognitive impairment diagnosis even without realizing it. These older adults with MCI should still receive evidence-based treatments when indicated.”

The research, published in the Journal of General Internal Medicine, found pre-existing MCI was associated with significantly lower use of guideline-concordant care after a heart attack, whether catheter-based or open surgery. The study measured 609 adults ages 65 and older who were hospitalized for a heart attack between 2000 and 2011.

Levine notes both cardiac catheterization (35% less likely in patients with pre-existing MCI) and coronary revascularization (45% less likely in patients with pre-existing MCI) have been shown to be highly effective at reducing deaths and improving physical functioning after heart attack in multiple large clinical trials.

‘A timely issue’

Physicians must weigh the competing risks of all health problems that increase with age, Levine says, including heart disease and cognitive decline. Many families are dealing with both concerns at once in their older loved ones.

“This is a timely issue because as the population ages, the number of seniors 85 years old and older has become the fastest-growing segment of the U.S. population,” Levine says. “Seniors 85 and older are most likely to have MCI, and their incidence of heart attack has surged.”

However, cardiovascular disease, including heart attack and stroke, is still the leading cause of death and serious morbidity in older adults, whether they have MCI or normal cognitive functioning.

Up to 1 in 5 adults ages 65 and older has MCI, although many may be undiagnosed, Levine says. Since the Affordable Care Act mandated coverage of cognitive impairment assessments for Medicare beneficiaries, MCI diagnoses are expected to increase, she adds.

The need to question decision-making

Although much recent medical literature addresses overtreatment, Levine says this research shows undertreatment with high-value therapies can also be a problem.

Her team’s ongoing research finds physicians might not be recommending invasive treatments as often after an older patient with some memory and thinking problems has a heart attack. She encourages clinicians to reflect on the influence of MCI in their decision-making.

“It’s important for providers to consider whether they are recommending against treating a patient just because they have MCI,” Levine says. “Physicians can think about offering treatments to all patients when clinically indicated.”

Invasive treatments may not be indicated in those with advanced dementia or a limited life expectancy, she says, but MCI does not fall in that category.

This potential disconnect in provider recommendations provides an opportunity for patients and families to empower themselves by having conversations about the care they’d want if they become ill, she says. People with MCI can still participate in these types of discussions, and families don’t need to wait until an event happens to start the conversation.

“In these discussions, patients and families often think about catastrophic illnesses where life support measures may be used, but heart attacks and stroke are much more common, and they’re treatable,” Levine says.

“Because dementia is so feared among older adults and their families, it’s understandable and appropriate that it may weigh heavily on the decisions for all types of care, including heart attack care,” adds co-author Kenneth Langa, M.D., Ph.D., a professor of internal medicine at Michigan Medicine and a member of the Institute for Healthcare Policy and Innovation. “Our study emphasizes the importance of differentiating between MCI and dementia and of educating patients, families and clinicians on the relative risks of further cognitive decline versus common cardiovascular conditions for people with MCI.”

An ongoing effort

Levine and colleagues used data from the Health and Retirement Study, a nationally representative longitudinal study of older Americans that’s based at U-M.

Heart attack, or acute myocardial infarction, was an appealing lens to research whether patients with MCI receive guideline-based treatment, Levine says. Heart attacks are acute, emergent medical problems that are common in seniors and have robust evidence of effective treatment, she adds.

Levine’s team is also studying the effect of pre-existing MCI on treatment for acute ischemic stroke, and the reasons physician recommendations and patient preferences for effective treatment after stroke or heart attack might be different if the patient already has MCI.

“Studies like this are an important first step in raising awareness on MCI so that providers, like cardiologists, can make sure they offer the best therapies available during heart attacks,” says senior author Brahmajee Nallamothu, M.D., MPH, an interventional cardiologist and professor of internal medicine at Michigan Medicine.

Share Button

Evolution designed by parasites

While analyzing interactions between parasites and hosts, a substantial amount of research has been devoted to studying the methods parasitic organisms use to control host behavior. In “Invisible Designers: Brain Evolution Through the Lens of Parasite Manipulation,” published in the September 2019 issue of The Quarterly Review of Biology, Marco Del Giudice explores an overlooked aspect of this relationship by systematically discussing the ways in which parasitic behavior manipulation may encourage the evolution of mechanisms in the host’s nervous and endocrine systems. Examining this evolutionary history, Del Giudice investigates the hypothetical methods hosts may have adopted to counteract attempts at behavioral hijacking.

Parasites, such as viruses, insects, helminths, and bacteria, seek to manipulate host behavior for numerous reasons. Parasitic organisms may induce behavioral changes in order to increase their chances of transmission from one host to another. In a similar vein, parasites may disrupt a host’s normal neural functioning to prompt the organism to travel to an environment that is more hospitable for the parasite or more conducive for reproduction. Host bodies are sometimes co-opted and utilized as safe environments for the development of the parasite’s offspring.

The means by which parasites attempt to alter host behavior also vary. Parasites may use an immunological approach by disrupting responses in an organism’s immune system. A more direct option may be to employ neuropharmacological manipulation by secreting substances that interfere with the host’s neurotransmitters. Parasites may also take the genomic/proteomic route by changing gene expression.

Expanding beyond the motivations and tactics of parasites, Del Giudice posits that attacks from these biochemical mechanisms place significant pressure on the nervous system to adapt and develop countermeasures. Drawing upon previous literature and real-world examples, the article proposes four categories of potential host countermeasures. Analyzing this taxonomy, Del Giudice argues that when encountering manipulation, hosts may prevent parasites from bypassing the brain’s protective barrier, force parasites to work harder and release greater amounts of neuroactive substances, make signals more complex, or strengthen the brain’s ability to endure disturbances.

Elaborating further on these countermeasures, the author considers the potential evolutionary constraints and the associated “robustness-fragility tradeoffs.” Although countermeasures may increase complexity and deter parasites, new adaptations may simultaneously weaken another section of the system and provide alternative targets for parasites.

Taking into account the proposed effectiveness of the mechanisms discussed, the article suggests studying host-parasite interactions could aid in furthering neuroscience and psychopharmacology research. By studying adaptations to parasitic attacks, neuroscientists could gain additional perspective into how continuous evolutionary battles produce inefficiency or how once-critical mechanisms over time serve unrelated functions. In psychopharmacology, the biochemical methods parasites use mimic those of pharmacological drugs. Researchers could analyze the ways brain structures reject pharmacological interventions by parasites and, in turn, use that information to make psychoactive drugs more effective for patients.

“The unrelenting pressure exerted by parasites must have shaped the evolution of nervous and endocrine systems at all levels, with important consequences even for animals that are not (or no longer) manipulation targets. If this is true, many aspects of neurobiology are destined to remain mysterious or poorly understood until parasites — the brain’s invisible designers — are finally included in the picture,” Del Giudice writes.

Story Source:

Materials provided by University of Chicago Press Journals. Note: Content may be edited for style and length.

Share Button

A novel technology for genome-editing a broad range of mutations in live organisms

The ability to edit genes in living organisms offers the opportunity to treat a plethora of inherited diseases. However, many types of gene-editing tools are unable to target critical areas of DNA, and creating such a technology has been difficult as living tissue contains diverse types of cells.

Now, Salk Institute researchers have developed a new tool — dubbed SATI — to edit the mouse genome, enabling the team to target a broad range of mutations and cell types. The new genome-editing technology, described in Cell Research on August 23, 2019, could be expanded for use in a broad range of gene mutation conditions such as Huntington’s disease and the rare premature aging syndrome, progeria.

“This study has shown that SATI is a powerful tool for genome editing,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases.”

Techniques that modify DNA — notably the CRISPR-Cas9 system — have generally been most effective in dividing cells, such as those in the skin or the gut, using the cells’ normal DNA repair mechanisms. The Izpisua Belmonte lab previously showed that their CRISPR/Cas9-based gene-editing technology, called HITI (for homology-independent targeted integration), could target both dividing and non-dividing cells. Protein-coding regions function like recipes for making proteins, while areas called non-coding regions act as chefs deciding how much food to make. These non-coding regions make up the vast majority of DNA (~98%) and regulate many cellular functions including turning genes off and on, so could be a valuable target for future gene therapies.

“We sought to create a versatile tool to target these non-coding regions of the DNA, which would not affect the function of the gene, and enable the targeting of a broad range of mutations and cell types,” says Mako Yamamoto, co-first author on the paper and a postdoctoral fellow in the Izpisua Belmonte lab. “As a proof-of-concept, we focused on a mouse model of premature aging caused by a mutation that is difficult to repair using existing genome-editing tools.”

The new gene knock-in method, which the scientists call SATI (short for intercellular linearized Single homology Arm donor mediated intron-Targeting Integration) is an advancement of the previous HITI method to enable it to target additional areas of the genome. SATI works by inserting a normal copy of the problematic gene into the non-coding region of the DNA before the mutation site. This new gene then becomes integrated into the genome alongside the old gene via one of several DNA repair pathways, relieving the organism of the detrimental effects of the original, mutated gene, without risking damage associated with fully replacing it.

The scientists tested the SATI technology in living mice with progeria, which is caused by a mutation in the LMNA gene. Both humans and mice with progeria show signs of premature aging, cardiac dysfunction and dramatically shortened life span due to the accumulation of a protein called progerin. By using SATI, a normal copy of LMNA gene was inserted in the progeria mice. The researchers were able to observe diminished features of aging in several tissues including the skin and spleen, along with an extension of life span (45% increase compared to untreated progeria mice). A similar extension of life span, when translated to humans, would be more than a decade. Thus, the SATI system represents the first in vivo gene correction technology that can target non-coding regions of DNA in multiple tissue types.

Next, the team aims to improve the efficiency of SATI by increasing the number of cells that incorporate the new DNA.

“Specifically, we will investigate the details of the cellular systems involved in DNA repair to refine the SATI technology even further for better DNA correction,” says Reyna Hernandez-Benitez, co-first author on the paper and a postdoctoral fellow in the Izpisua Belmonte lab.

Other authors included Keiichiro Suzuki, Rupa Devi Soligalla, Emi Aizawa, Fumiyuki Hatanaka, Masakazu Kurita, Pradeep Reddy, Alejandro Ocampo, Tomoaki Hishida, Masahiro Sakurai, Amy N. Nemeth, Concepcion Rodriguez Esteban of Salk; Zhe Li, Christopher Wei and Kun Zhang of the University of California San Diego; Estrella Nuñez Delicado of Universidad Catolica San Antonio de Murcia; Jun Wu of University of Texas Southwestern Medical Center; Josep M. Campistol of the Hospital Clinic of Barcelona in Spain; Pierre Magistretti of the King Abdullah University of Science and Technology in Saudi Arabia; Pedro Guillen of the Clinica CEMTRO in Spain; Jianhui Gong, Yilin Yuan and Ying Gu of the BGI-Shenzhen in China; Guang-Hui Liu of the Chinese Academy of Sciences; and Carlos López-Otín from the Universidad de Oviedo in Spain.

The work was funded by the 2016 Salk Women & Science Special Award, the JSPS KAKENHI (15K21762 and 18H04036), the Takeda Science Foundation, The Uehara Memorial Foundation, the National Institutes of Natural Sciences (BS291007), The Sumitomo Foundation (170220), The Naito Foundation, The Kurata Grants (1350), the Mochida Memorial Foundation, The Inamori Foundation, the Guangdong Provincial Key Laboratory of Genome Read and Write (No. 2017B030301011), Guangdong Provincial Academician Workstation of BGI Synthetic Genomics (No. 2017B090904014), the Shenzhen Peacock Plan (No. KQTD20150330171505310), The Leona M. and Harry B. Helmsley Charitable Trust (2012-PG-MED002), the G. Harold and Leila Y. Mathers Charitable Foundation, the National Institutes of Health (R01HL123755 and 5 DP1 DK113616), The Progeria Research Foundation, The Glenn Foundation, KAUST, The Moxie Foundation, the Fundación Dr. Pedro Guillen, the Asociación de Futbolistas Españoles, and Universidad Católica San Antonio de Murcia (UCAM).

Share Button

Migrating mule deer don’t need directions, study finds

How do big-game animals know where to migrate across hundreds of miles of vast Wyoming landscapes year after year?

Among scientists, there are two camps of thought. First is that animals use local cues within their vicinity to determine where to migrate. Animals might move up to areas with greener forage — often termed green-wave surfing — or move down from mountains with deeper snow. The second idea is that animals develop memory of the landscape where they live and then use that information to guide their movements.

Recent research from the University of Wyoming has found that memory explains much of deer behavior during migration: Mule deer navigate in spring and fall mostly by using their knowledge of past migration routes and seasonal ranges.

The study found that the location of past years’ migratory route and summer range had 2-28 times more influence on a deer’s choice of a migration path than environmental factors such as tracking spring green-up, autumn snow depth or topography.

“These animals appear to have a cognitive map of their migration routes and seasonal ranges, which helps them navigate tens to hundreds of miles between seasonal ranges,” says the lead author of the paper, Jerod Merkle, assistant professor and Knobloch Professor in Migration Ecology and Conservation in the Department of Zoology and Physiology at UW.

The findings recently were published in Ecology Letters, a leading journal within the field of ecology. Co-authors of the paper included Hall Sawyer, with Western EcoSystems Technology Inc.; Kevin Monteith and Samantha Dwinnell, with UW’s Haub School of Environment and Natural Resources; Matthew Kauffman, with the U.S. Geological Survey Wyoming Cooperative Fish and Wildlife Research Unit at UW; and Gary Fralick, with the Wyoming Game and Fish Department.

Scientists had long presumed that migratory behavior was dictated by availability of food resources and other external factors. Where you find resources, you will find species that exploit them, the theory went.

The UW team found it is not that simple. Without the intrinsic factor of landscape memory to guide deer between seasonal ranges, the long-distance corridors of western Wyoming’s Green River Basin, for example — exceeding 300 miles round-trip in some cases — would not exist in their present form.

“It appears that green-wave surfing helps them determine when to move within a kind of ‘map’ in their brain,” Merkle says. “The timing of spring green-up determines when an animal should migrate, but spatial memory determines where to migrate.”

The finding has important conservation implications. Because landscape memory so strongly underlies mule deer migratory behavior, the loss of a migratory population also will destroy the herd’s collective mental map of how to move within a landscape, making it very difficult to restore lost migration routes. Patches of potential habitat likely will go unused.

“This is yet another study that makes clear that animals must learn and remember how to make these incredible journeys,” say Kauffman, who leads the Wyoming Cooperative Fish and Wildlife Research Unit, where the research was conducted. “This is critical for conservation, because it tells us that, to conserve a migration corridor, we need to conserve the specific animals who have the knowledge necessary to make the journey.”

The study bolsters the findings of a 2018 paper in the journal Science by a UW-led team that found translocated bighorn sheep and moose with no knowledge of the landscape can take anywhere from several decades to a century to learn how to migrate to vacant habitats.

Similarly, strategies such as off-site restoration or mitigation may be unsuccessful if restored habitats are not “discovered” and integrated into the memory of individuals.

The study further makes a case that biologists will not be able to successfully predict migration corridors — or optimally manage populations — based on environmental information or range quality alone. Managers will find it difficult to evaluate potential conservation actions without directly gathering movement data, crucial information that reveals the migration knowledge that animals carry around in their heads.

Moreover, the research shows that migrants can obtain greater forage benefits during spring migration using memory of a vast landscape, compared to migrants that rely simply on foraging cues in their local area.

This suggests that the migratory routes we see today are optimized across generations for green-wave surfing in large landscapes. These learned migration corridors are not readily discoverable by animals if they cannot access the memories established by past generations.

Share Button

Health24.com | How your workout may affect your vagina

Whether it’s chafing, itching or even bruising, working out can take its toll on your lady parts. While there is no doubt that working out is beneficial for your health, it’s important not to forget to take care of your vaginal area during and after exercise.

Here’s what can go wrong, and what you can do about it:

1. Chafing, itching and burning during and after a run

Ever ran a marathon, only to strip off your clothes afterwards and feel the painful burn from chafing as soon as you hit the shower? Sweaty clothes, frequent rubbing and impact for hours, and delicate skin are a combination that can lead to horrible chafing, itching, burning and rashes. This tends to happen especially around the groin area. Exposing your bits to damp, sweaty running tights and underwear for too long may also increase your risk for yeast infections.

Here’s what you should do: Switch to well-fitting, moisture-wicking running tights and underwear. Avoid underwear with prominent seams, as these can cause chafing during a run. Apply a lubricant such as Vaseline, a body glide product or even nappy ointment (Fissan Paste works well) on all the vulnerable areas before you go for a run.

Afterwards, take off the sweaty tights and shower as soon as possible while avoiding too hot water. Dry properly and carefully and apply ointment again to soothe sensitive skin.

2. Yeast infections after swimming

Swimming is a great form of exercise, but the exposure to chlorine and wet material may not always be kind to your nether regions. If you make a habit of lounging around or chatting to your friends while in your wet costume straight out of the pool, stop it immediately.

Water from the pool is not the direct cause of a yeast infection, but the prolonged exposure to wet fabric may increase your risk of yeast overgrowth, which can lead to itching, burning and a discharge.

Here’s what you should do: Always take along a dry set of clothes when you go swimming. If you plan to lounge around the pool, a dry swimming costume might be a good idea. Rinse your body and change into dry clothes straight after swimming if you are prone to yeast infections.

3. Burning and bruising after spinning

Being in the saddle for a prolonged period may lead to pressure sores, which can present in the form of cracked, red skin or even blisters. As with running, chafing can also be a problem when cycling. 

Here’s what you should do:  Invest in a padded pair of cycling shorts, as these can help alleviate pressure sores. If you prefer hitting the road on your own bike instead of sweating away in a spin class, you have the option of investing in a gel-padded seat cover for extra cushioning.

As with long runs, protecting your delicate skin with a lubricant beforehand can also make a difference and help prevent chafing.

General gym-hygiene:

Workout clothes, as comfy as they are, become breeding grounds for bacteria as soon as they become sweaty. Follow good hygiene after your workout routine to minimise your risk for infections. These tips may help:

  • Don’t sit around in the same workout pants and underwear. Even if you can’t shower immediately after your workout, dry underwear can make a big difference.
  • Avoid any perfumed shower gels or soaps when washing, as these can disturb the delicate pH balance of the skin and lead to itching, burning and infections.
  • Wash with lukewarm water.
  • Try to wash your workout clothes as soon as possible to avoid festering in the laundry basket for too long. You can invest in a detergent made specifically for workout gear to help maintain and protect the moisture-wicking properties of your workout clothes.
  • Wear well-fitting workout pants and underwear to minimise chafing.
  • When you need to wax or groom your pubic hair, read these tips to help avoid post-waxing rashes.

Image credit: iStock 

Share Button