Dr. Howard Smith Reports

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Imagine this! A tiny device injectable through a needle and powered wirelessly offers a new approach for managing chronic pain and movement disorders. All this without the batteries, connecting wires, or surgically implanted hardware used in current pain control systems.

This technology was developed by NYU bioengineers and Cleveland Clinic  gastroenterologists sited in Abu Dhabi. It delivers electrical signals near a targeted nerve, controllable wirelessly from outside the body.

The device, named SEED, is the size of a small seed and designed to be delivered through a standard needle. Once positioned in a blood vessel near a target nerve using ultrasound and CT imaging, it receives power from outside the body and delivers programmable electrical pulses.

The researchers tested the technology in laboratory experiments and in living animals, including a rat model. They show that the device can activate nerves and produce controlled responses. 

These are early engineering achievements, but they are not evidence that SEED can relieve chronic pain in human patients. That remains for future randomized and controlled clinical trials.

The references for this report are available on my website.

#ChronicPain #MedicalTechnology #NerveStimulation #NYUResearch #HealthInnovation

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Persistent loneliness costs you up to nearly 6 years of healthy life. This from new research by Tulane University epidemiologists working with colleagues at the Harvard School of Public Health and published in the journal Nature.

The researchers analyzed health information from nearly 277,500 adults between the ages of 40 and 69. They examined how social isolation and loneliness were associated with the number of years people could expect to live without major physical illnesses, depression, or anxiety.

Among people experiencing both social isolation and loneliness, men had an estimated 5.8 fewer years free from depression and anxiety. For women, the estimated loss was approximately 3.7 years. Physical health was affected, too. Women experiencing both conditions had about 2.4 fewer years free from major physical diseases, while men had about 1.7 fewer years.

The investigators emphasize the difference between social isolation  and loneliness. Social isolation means having relatively few social connections or interactions. Loneliness is the distressing feeling that your relationships are insufficient or that you lack the connection you need. 

The study also uncovered an important difference in the role of health habits. Regular exercise, adequate sleep, a healthier diet, and non-smoking were associated with smaller losses of disease-free years among people experiencing social isolation. However, those lifestyle habits did not significantly offset the additional risks associated with loneliness itself.

That suggests that being physically healthy and feeling socially connected may be two different challenges. Exercise and good nutrition matter, but they may not replace meaningful relationships and emotional support.

So, what can you do?

Make time for people who matter to you. Reach out to a friend you have not spoken with recently. Consider a community group, volunteer activity, class, or regular social gathering. If loneliness persists or affects your daily life, speaking with a mental health professional may help.

And if someone you know seems withdrawn, a simple phone call or invitation can be a meaningful first step.

There is an important limitation to remember: this was an observational study. The findings show associations between loneliness, social isolation, and disease-free life expectancy; they do not prove that loneliness directly causes a specific number of lost healthy years. Further studies and clinical trials are needed to understand cause and effect.

The references for this report are available on my website.

#Loneliness #SocialIsolation #MentalHealth #HealthyAging #HealthResearch

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Yale orthopedic researchers now report in the journal Bioactive Materials that the epilepsy drug lacosamide, LCM for short and branded as Vimpat, injected periodically into a joint, reduces the pain of osteoarthritis and shifts cartilage cell activity toward repair rather than destruction. 

The Yale team finds that LCM inhibits a protein called Nav1.7 that helps nerve cells transmit pain signals and signals the cartilage cells, chondrocytes, to break down cartilage. The researchers tested LCM by delivering it into arthritic knee joints in a temperature-sensitive gel.

In mouse experiments, the researchers find that a single injection of the drug-containing hydrogel every four weeks effectively protects cartilage and leads to its repair. Their study did not measure pain reduction. 

It remains to planned controlled clinical trials to demonstrate that LCM Nav1.7 inhibition effectively and safely triggers cartilage repair as well as pain relief for those with osteoarthritis.

The references for this report are available on my website.

#Osteoarthritis #Lacosamide #CartilageRepair #YaleMedicine #MedicalResearch

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Stanford biologists have developed a molecule that converts a protein responsible for stimulating lymphoma growth into a trigger for cancer-cell death. Their mouse studies are now published in the journal Cell.

Their research focuses on diffuse large B-cell lymphoma, the most common type of non-Hodgkin lymphoma. Many of these cancers flourish under the influence of a protein called BCL6 that causes malignant cells to continue multiplying. Under normal circumstances, BCL6 helps immune cells multiply temporarily when the body needs to fight an infection by suppressing genes that would otherwise stop cell growth and initiate programmed cell death.

The Stanford team designed a molecule called TCIP23 to redirect the activity of BCL6. This designer molecule adds chemical tags that switch on genes to initiate the cancer cell’s own self-destruct process. 

The researchers tested TCIP23 in mice carrying tumors made from human lymphoma cells. After twice-daily treatment, the tumors disappeared within 11 days, while tumors in untreated control animals remained. The treated mice showed no obvious signs of toxicity during the experiment.

These findings are encouraging, but these results in mice cannot establish whether TCIP23 drug will be safe or effective in people. In addition to affecting tumor cells, it can also impact a patient’s own protective immunity. With careful modifications, TCIP23 may also be helpful for treating autoimmune disease. It remains for controlled clinical trials to demonstrate the usefulness of this approach for treating human cancer and immunity out of control.

The references for this report are available on my website.

#CancerResearch #Lymphoma #StanfordMedicine #CancerTreatment #MedicalScience

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Experiments in mice supported these findings. Animals receiving an antibiotic while consuming sucrose developed substantially larger populations of toxic intestinal bacteria than controls.

The researchers suggest that dietary sugar gives harmful bacteria additional fuel to grow while antibiotics weaken the competition. The precise mechanism still needs to be determined.

The researchers suggest that temporarily cutting back on sweets and other sources of added sugar during and possibly after antibiotic treatment would help limit microbiome disruption. But this remains a promising hypothesis, not a proven treatment. Clinical trials are needed to determine whether reducing sugar actually preserves beneficial bacteria or prevents infections.

The study limitation: the human participants were hospitalized patients with blood cancers, a group particularly vulnerable to infections and microbiome disturbances. The results cannot automatically be applied to everyone taking antibiotics.

For now, a sensible takeaway is to consume a balanced diet and avoid excessive added sugar while on antibiotics. If you have cancer, are undergoing a transplant, or have special nutritional needs, ask your clinical team before making substantial dietary changes.

The references for this report are available on my website.

#Antibiotics #GutMicrobiome #SugarIntake #NutritionScience #HealthResearch

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All of our knee cartilages deteriorate with age and injury due to an increase in the destructive enzyme 15-hydroxy prostaglandin dehydrogenase or 15-PGDH. Now, Stanford University biologists and orthopedic surgeons demonstrate that blocking this enzyme stops this process and even restores already damaged cartilage.

Their studies, published in the journal Science, involve mice with deteriorated cartilage due to aging and/or injuries. The data shows that blocking this enzyme restores the diseased cartilage. The treatment also helps protect against osteoarthritis after knee injuries resembling anterior cruciate ligament damage or ACL injuries suffered by humans.

he scientists find that in the absence of 15-PGDH, the existing cartilage cells called chondrocytes begin producing healthier cartilage. Rather than relying on stem cells to build new tissue, the treatment appears to encourage mature cells to adopt a more youthful pattern of behavior. The regenerated tissue is healthy hyaline cartilage, the type of smooth cartilage that effectively cushions the ends of bones and allows joints to move with minimal friction.

The researchers also tested cartilage removed from patients undergoing knee replacement surgery. After exposure to the experimental 15-PGDH inhibitor in the laboratory, the human tissue showed changes consistent with cartilage regeneration.

Osteoarthritis affects millions of Americans. Current therapy relieves pain and improves mobility, but does not restore lost articular cartilage. When joint damage becomes severe, knee or hip replacement becomes necessary. This treatment that could safely regenerate cartilage is a major advance.

Clinical research with carefully controlled human trials will be needed to establish whether 15-PGDH inhibitor therapy can safely and effectively restore cartilage, relieve pain, and improve function.

The references for this report are available on my website.

#CartilageRegeneration #Osteoarthritis #StanfordMedicine #JointHealth #MedicalResearch

CartilageRegeneration, Osteoarthritis, StanfordMedicine, JointHealth, MedicalResearch

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The diet appears to protect against cancer in one part of the gastrointestinal tract yet promote it in another? MIT biologists in collaboration with Harvard gastroenterologists document this phenomenon in their preclinical study published in the journal Nature.

Keto diets are high in fat and very low in carbohydrates. They encourage the body to burn fat for energy instead of relying primarily on carbohydrates. The researchers tested this diet in mice genetically predisposed to developing intestinal cancer. They were surprised to find that the ketogenic diet triggers more cancers in their small intestines yet suppresses tumor formation in the colon.

Seeking to understand the mechanisms for this, the researchers traced the increased small-intestinal tumor growth to the way intestinal stem cells process dietary fat. The fat we ingest is oxidized to so-called PPAR proteins that cause stem cells to multiply more rapidly. This action is both good and bad: the new stem cells help repair the intestinal lining, but the excessive cell division increases opportunities for cancer to develop.

With regard to the situation in the large intestine, the colon, previous studies have shown that the ketones generated by the diet protect against the development of colon cancers.

But a caveat: this was research in genetically susceptible mice and not proof that the ketogenic diet causes small-intestinal cancer in humans. Further research is needed to determine whether these findings translate to people and whether particular dietary fats influence the outcome.

The investigators advise those on the keto diet not to discontinue it without consulting their medical teams. But those at higher risk for gastrointestinal cancer, those with inflammatory bowel diseases including Crohn’s and or celiac disease or with a family thhistory of small bowel cancer, should only start a ketogenic diet on the advise of their medical professionals.

The references for this report are available on my website.

#KetoDiet #CancerResearch #MITResearch #NutritionScience #HealthNews

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#foodrecall #foodallergy #consumeralert #childsafety #fda

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#ProductRecall #ConsumerAlert #HomeSafety #cpsc #childsafety

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Neurosurgical cell biologists at the University of Michigan have bioengineered nanoparticles that sensitize deadly gliomas to radiation therapy.

Their study, published in Nature Communications, focused on those gliomas that carry a mutated form of the IDH1 gene. Malignant tumors bearing this gene easily activate a cellular recycling process called autophagy (au toff fa gee) thar helps tumor cells remove damaged material but also helps them repair the DNA damage caused by radiation.

To block these tumor-protective effects, researchers created nanoparticles capable of crossing the blood-brain barrier and penetrating into brain tumors to deliver mRNA molecules that trigger a shut-down of the autophagy pathway.

Using mouse models, they show that combining nanoparticle injections with radiation produces a phenomenal result: 60% of the animals are cured of their tumors and survive long-term without recurrence. The treatment produces no significant toxic side effects.

An added benefit: mice whose tumors are eliminated by the nanoparticle-radiation combo therapy develop active immunity against the tumor and able to destroy a newly implanted tumor without additional therapy.

*Bioengineered nanoparticles may offer a way to overcome radiation resistance in a select group of gliomas while also triggering lifesaving anti-tumor immunity. These animal model results are impressive, but it remains for human clinical trials to confirm whether this approach is safe and effective in patients.

The references for this report are available on my website.

#Glioma #BrainCancer #CancerResearch #Nanotechnology #RadiationTherapy