Category Archives: Health

Diet, disease, Health, Public health

Can the Ketogenic Diet Be a Breakthrough in Halting Neuroendocrine Tumor Progression?

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Neuroendocrine tumors (NETs) have been on the rise in recent years, and among them, pancreatic neuroendocrine tumors (PanNETs) pose a significant health concern. However, a recent Cell Death and Disease study offers hope in the fight against these tumors. This groundbreaking research explores the effects of a ketogenic dietary intervention on the onset and progression of PanNETs, shedding light on a potential therapeutic approach.

Pancreatic Neuroendocrine Tumors: A Growing Concern
PanNETs, a subtype of NETs, are rare but have become increasingly prevalent. These tumors originate from pancreatic islet cells and can be functional or non-functional. While functional PanNETs produce hormones that lead to hormone syndromes, non-functional PanNETs, which comprise most cases, do not exhibit these characteristics.

The progression of PanNETs often involves the development of liver metastases, making them challenging to treat. Traditional treatments have shown limited success in shrinking these tumors, emphasizing the need for innovative interventions.

Understanding the Role of Insulin
The study draws attention to the role of insulin in PanNET development. Both human and mouse models have revealed a connection between elevated insulin levels and increased tumor growth. Conversely, reducing insulin levels has been associated with decreased tumor development.

Enter the Ketogenic Diet
The ketogenic diet, known for its low carbohydrate and high-fat composition, has gained recognition for its potential health benefits. In the context of cancer, previous research has suggested that a ketogenic diet can lower insulin levels without adverse effects.

In this study, researchers fed a ketogenic diet to mice with non-functional PanNETs using a Pancreatic β-cell-specific Men1 deficient mouse model. The results were promising.

Ketogenic Diet: A Game Changer
The findings demonstrated that a ketogenic diet could significantly suppress the onset and progression of non-functional PanNETs in the mouse model. What is more, this dietary intervention also had a positive impact on pituitary NET development in the mice.

The Implications for Human PanNET Patients
These results open up exciting possibilities for PanNET patients. High blood glucose levels have been associated with poorer outcomes in PanNET patients, especially those undergoing chemotherapy. Metformin, a blood sugar-reducing drug, has shown promise in improving chemotherapy effects for PanNET patients.

Therefore, reducing blood glucose levels through a ketogenic diet could enhance the prognosis for human PanNET patients. This treatment approach also holds promise for other cancers that rely on the insulin-regulated PI3K-Akt-mTOR pathway.

In conclusion, this study offers hope in the battle against PanNETs and potentially other NETs. The ketogenic diet’s ability to suppress tumor progression in a mouse model suggests a novel therapeutic intervention that could benefit patients in the future. Further research is needed, but this study paves the way for innovative approaches to combating neuroendocrine tumors.

Using the ketogenic diet as a therapeutic intervention for PanNETs may have potential side effects. However, it is essential to note that this research is still in its early stages, and further human studies are needed to understand the risks thoroughly. Some potential side effects of the ketogenic diet may include:

  1. Keto Flu: When transitioning to a ketogenic diet, some people experience “keto flu” symptoms, including fatigue, headaches, nausea, and dizziness.
  2. Nutritional Deficiencies: A restrictive diet may lead to nutritional deficiencies, especially if not carefully planned. Monitoring vitamin and mineral intake is crucial.
  3. Gastrointestinal Issues: Constipation and diarrhea can occur due to changes in dietary fiber and fat consumption.
  4. Liver and Kidney Function: There are concerns about how the diet may affect liver and kidney function, as they play a role in metabolizing ketone bodies.
  5. Increased Cholesterol Levels: Some individuals may experience increased cholesterol levels when on a high-fat diet, which could pose cardiovascular risks.
  6. Bone Health: The ketogenic diet may impact bone health due to its potential for calcium loss.

Regarding the use of Metformin, it is generally considered a safe and well-tolerated medication. However, like any medication, it can have side effects. Common side effects of Metformin may include gastrointestinal symptoms such as diarrhea, nausea, and abdominal discomfort. In some cases, it may also lead to vitamin B12 deficiency or, rarely, a serious condition called lactic acidosis. The risk of side effects should be weighed against the potential benefits of Metformin as part of PanNET treatment.

The following steps in research to determine the effectiveness of the ketogenic diet in human PanNET patients involve conducting clinical trials. These trials would involve carefully controlled studies on human participants to assess the diet’s impact on tumor growth, blood glucose levels, and overall health. Researchers would monitor for potential side effects and evaluate the diet’s efficacy in improving patient outcomes.

Additionally, research may explore the combination of a ketogenic diet with other treatment modalities, such as chemotherapy or targeted therapies, to determine if synergistic effects could enhance the treatment of PanNETs. Ultimately, conducting well-designed clinical trials will be essential to providing more concrete evidence of the diet’s effectiveness and safety in humans.

Cited Works:

Barrea, Luigi, Sara Cacciapuoti, Matteo Megna, Ludovica Verde, Claudio Marasca, Rosa Vono, Elisabetta Camajani, et al. “The effect of the ketogenic diet on Acne: Could it be a therapeutic tool?.” Critical Reviews in Food Science and Nutrition (2023): 1–20.

Cohen, Yotam, Rafael Valdés-Mas, and Eran Elinav. “The Role of Artificial Intelligence in Deciphering Diet–Disease Relationships: Case Studies.” Annual Review of Nutrition 43 (2023).

Rana, Avinash, and Monika Arora. “Ketogenic diet: Assessing YouTube video information using quality, reliability, and text analytics methods.” Nutrition and Health (2023): 02601060231193789.

Behavioral Science, Culture, disease, Education, Health, mental health, Public health

Is Your Night Owl Lifestyle Putting You at Risk for Type 2 Diabetes?

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Night owls, beware! If you feel groggy in the morning but perky in the evening, you might identify as a night owl, inclined to stay up late and sleep in. While this sleep pattern may seem harmless, a recent study has uncovered a concerning connection between being a night owl and an increased risk of developing type 2 diabetes and several unhealthy lifestyle habits.

Photo by cottonbro studio on Pexels.com

Lead author Sina Kianersi, a postdoctoral research fellow at Brigham and Women’s Hospital and Harvard Medical School in Boston, explains, “When we looked at the relationship between chronotype and diabetes, we found night owls had a 72% increased risk of developing diabetes over the eight years of our study.”

Even more alarming is that night owls exhibit various unhealthy behaviors that contribute to chronic diseases like type 2 diabetes. They were more likely to have a poor diet, be less physically active, consume higher quantities of alcohol, maintain an unhealthy BMI (body mass index), smoke, and either sleep less or more than the recommended seven to nine hours per night.

Even when the study accounted for these unhealthy habits, night owls still faced a 19% increased risk of developing type 2 diabetes compared to early birds. This suggests that genetic factors or other unaccounted variables also play a role.

Dr. Bhanu Prakash Kolla, a sleep medicine specialist at the Mayo Clinic, emphasizes the importance of awareness for evening-oriented individuals. He suggests moderating alcohol use, quitting smoking, increasing physical activity, getting adequate sleep, and managing other risks as best as possible.

Our internal body clocks, or circadian rhythms, control our sleep patterns, which are subject to genetic and environmental influences. Early birds have circadian rhythms that promote early mornings, while night owls have rhythms that delay peak activity until the afternoon or evening. When these rhythms are disrupted, it can lead to a domino effect of adverse health consequences, including an increased risk of diabetes and cardiovascular disease.

Studies have consistently shown that early birds perform better in school, are more active throughout the day, and have a lower risk of cardiovascular disease. In contrast, night owls tend to develop unhealthy habits that can lead to early mortality.

The study, which followed nearly 64,000 nurses over eight years, found that the association between being a night owl and developing type 2 diabetes was more significant for those who worked during the day than for night owls who had later work hours or worked overnight shifts. This suggests that personalized work scheduling could help mitigate some of the risks of being a night owl.

While genetics may play a role in one’s chronotype, maintaining a healthy lifestyle remains crucial. Night owls can reduce their risk of developing type 2 diabetes and other chronic illnesses by adopting a healthier way of living. So, consider this a wake-up call for all the night owls to prioritize their health and well-being.

Genetic, environmental, and lifestyle factors affect being a night owl or having a preference for staying up late and sleeping in. While the exact genetic factors contributing to night owl behavior are still being studied, here are some insights into the genetic aspects that may play a role:

  1. Clock Genes: Clock genes are one of the critical genetic factors in regulating our sleep-wake patterns. These genes control our circadian rhythms, the internal body clock determining when we feel alert and sleepy. The PERIOD genes (PER1, PER2, and PER3) and the CLOCK gene are examples of genes that influence circadian rhythms. Variations in these genes can lead to differences in the timing of sleep.
  2. Melatonin Receptors: Melatonin is a hormone that plays a crucial role in regulating sleep. The genes responsible for coding melatonin receptors, such as MTNR1A and MTNR1B, can impact how individuals respond to melatonin production, which varies throughout the day. Genetic variations in these receptors can affect an individual’s sleep-wake preferences.
  3. DEC2 Gene: Some studies have identified the DEC2 gene as a potential contributor to being a night owl. This gene is associated with short sleep patterns and is linked to people who can function well with fewer hours of sleep.
  4. PER3 Gene: The PER3 gene regulates the circadian rhythm’s sensitivity to light. Variations in this gene can affect how individuals respond to light cues and influence their sleep patterns.
  5. RORA Gene: The RORA gene regulates sleep duration and timing. Variations in this gene have been linked to differences in circadian rhythms and sleep preferences.
  6. Genetic Variability: It is essential to note that multiple genetic variations can contribute to being a night owl. These genetic factors can interact with each other and with environmental influences, making it a complex trait influenced by both nature and nurture.

While genetics plays a role, it is essential to recognize that environmental factors, such as work schedules, lifestyle choices, and exposure to light, can also significantly impact an individual’s sleep-wake patterns. Genetic predispositions do not determine behavior definitively but can make specific sleep patterns more likely.

Research in this field is ongoing, and our understanding of the genetic basis of night owl behavior continues to evolve as more studies are conducted.

Cite Works:

Okeefe, Christine. “From early birds to night owls: a review of chronobiology.” (2023).

Zhou, Ke, Marios Constantinides, Daniele Quercia, and Sanja Šćepanović. “How Circadian Rhythms Extracted From Social Media Relate to Physical Activity and Sleep.” In Proceedings of the International AAAI Conference on Web and Social Media, vol. 17, pp. 948-959. 2023.

Schilling, Ray. “Lung Cancer Screening Program.” Lung Cancer (2023).

Migliaccio, Gian Mario. The Science of Deep Sleep, Towards Success: Unleashing energies in Sports and Life thanks to quality sleep. Sport Science Lab srl, 2023.

disease, Health, Public health, Science

A New Hope for Pancreatic Cancer: Targeting the SE-Regulated RNA-Binding Protein Cascade

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Introduction

In a recent breakthrough study published in Nature Communications, researchers have uncovered a promising therapeutic target for one of the deadliest forms of cancer—pancreatic ductal adenocarcinoma (PDAC). This malignancy, responsible for over 90% of pancreatic cancer cases, has long presented a formidable challenge in the field of oncology. The study sheds light on a novel approach to combating this lethal disease.

The Enigma of Pancreatic Ductal Adenocarcinoma

Despite extensive research, the driving forces behind PDAC, including the role of the Myc master regulator and KRAS oncogene mutations, have remained elusive. Limited understanding of the super-enhancers (SEs) orchestrating sustained translation increases in this cancer type has made it more difficult to find effective treatments for PDAC.

The Study’s Quest

In this groundbreaking study, researchers embarked on a mission to map the genomic locations of SEs in 16 different human pancreatic cancer cell lines. The result was the identification of 876 SEs—a critical discovery in the battle against PDAC. To validate these findings, the researchers turned to clinical samples of PDAC and examined the expression of heterogeneous nuclear ribonucleoprotein (hnRNP) F protein, an RNA-binding protein linked to polyadenylation, alternative splicing, and messenger RNA (mRNA) stability regulation.

The Functional Role of SEs

To find out what role SEs play in increasing hnRNPF levels and tumor growth, researchers deleted certain parts of the genome in the SEs of the MIA PaCa-2 PDAC cell line. Subsequently, they injected these modified cells into the pancreases of immunodeficient mice to observe the in vivo effects on tumor growth.

A Closer Look at the Findings

The study’s findings highlighted the relevance of SE-regulated hnRNP F expression in PDAC. The researchers noted that H3 lysine 27 acetylation (H3K27ac), a common SE marker, was more prominent in pancreatic cancer cell lines than normal cells. This observation underscored the significance of SE-regulated hnRNP F expression in PDAC.

Members of the activator protein-1 (AP-1) family, like JUN, FOS, and ATF, were found in large amounts in SEs according to a study of transcription factor motif analysis. This suggests that they play a role in controlling hnRNP F.

Crucially, the deletion of SE elements led to an 80% reduction in hnRNP F transcript levels and a subsequent 35% reduction in protein levels. SE deletion also impacted chromatin accessibility at the hnRNP F SE.

Functional Consequences

The consequences of SE deletion were profound. Cells lacking the hnRNP F SE displayed reduced proliferation in two-dimensional (2D) cultures and formed smaller colonies in three-dimensional (3D) in vitro assays. We were surprised that adding hnRNP F back to these cells partially restored their ability to divide, showing that hnRNP F is the main SE-driven gene that causes PDAC cells to divide.

The Role of hnRNP F in mRNA Stability

The study also found that hnRNP F helps keep mRNAs stable. One of these is PRMT1, which controls tumor growth by creating new proteins through Ubap2l.

Unveiling a Targetable Pathway

That is interesting; the researchers discovered that the Myc oncogene controlled hnRNP F, PRMT1, and Ubap2l, creating a network that was essential for protein production. This discovery unveiled a targetable pathway to hinder PDAC growth.

Conclusion

Pancreatic ductal adenocarcinoma has long presented a formidable challenge in cancer research. But a new study has found a promising way to treat the disease: the SE-regulated RNA-binding protein cascade, which is made up of hnRNP F, PRMT1, and Ubap2l. By inhibiting PRMT1, this newfound understanding opens doors to novel treatments for PDAC and potentially other cancers. Importantly, these treatments may offer a safer alternative to existing SE-targeted therapies, mitigating severe toxicities. As the fight against pancreatic cancer continues, this discovery brings renewed hope to patients and researchers alike.

Cited Works:
Class, I. P. C., and AC12Q168FI USPC. “Patent application title: TRANSLATIONAL DYSFUNCTION BASED THERAPEUTICS Inventors: Gordon A. Jamieson, Jr.(Arlington, MA, and US) Katherine LB Borden (St. Laurent, and CA) Biljana Culjkovic (Montreal, CA) Alex Kentsis (New et al.) Assignees: Translational Therapeutics, Inc.” (2014).

Pelletier, Jerry, Marie-Ève Bordeleau, Lisa Lindqvist, Robert Francis, and Junichi Tanaka. “Chemotherapeutic agents for inhibition of protein translation.” U.S. Patent 8,008,346, issued on August 30, 2011.

disease, genetics, Health, Public health

Deciphering the DNA Code of Blood Sugar: Groundbreaking Insights from a GWAS Meta-Analysis

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Introduction

In a groundbreaking study published in Nature Genetics, researchers have embarked on a journey to decode the intricate genetic web that underlies blood glucose regulation. This genome-wide association study (GWAS) meta-analysis, conducted on an astonishingly vast scale, offers unparalleled insights into the pathophysiology of diabetes, its complications, and potential avenues for personalized treatment strategies.

The Complex World of Blood Glucose Regulation

Glucose, the primary fuel for our bodies, is under strict genetic control. Imbalances in glucose regulation play a pivotal role in developing type 2 diabetes (T2D). While previous studies have explored the genetic factors influencing glucose levels in response to various challenges, this study takes a broader perspective by examining random glucose (RG) levels. Although inherently more variable than standardized measures, RG provides a comprehensive snapshot of the complex processes governing glucose regulation across multiple organ systems.

The Study Unveiled

In this ambitious study, researchers conducted a GWAS meta-analysis involving 476,326 non-diabetic individuals of diverse ancestries. They meticulously adjusted their analyses for factors like sex, age, and the time elapsed since their last meal. The study excluded individuals with diabetes or hyperglycemia and employed sophisticated statistical models to select the most relevant covariates.

The results of this colossal undertaking were nothing short of remarkable. The researchers identified a whopping 150 distinct signals within 120 loci, with 53 signals being reported for the first time in the context of glycemic traits. Intriguingly, some signals identified in individuals of European ancestry exhibited nominal significance in people of other ancestries. Furthermore, two-thirds of these RG signals overlapped with loci related to T2D, highlighting the intricate interplay between blood glucose regulation and diabetes.

Unraveling the Genetic Complexity

Perhaps one of the most fascinating discoveries was the presence of sex dimorphism at 13 RG loci. The study also revealed common and low-frequency coding variants in genes such as THADA, RREB1, TET2, NMT1, and RFX1. These variants, with varying minor allele frequencies, exerted diverse effects on RG levels, further emphasizing the genetic complexity of glucose regulation.

The Role of GLP1R in Blood Glucose Regulation

The researchers prioritized GLP1R, a known target for T2D treatment, for functional analysis. They used RG data to develop a framework for predicting responses to GLP-1R agonists. The study showed that the functional impact of specific GLP1R variants could be linked to blood glucose homeostasis, validating the critical role of this gene in glucose regulation.

A Glimpse into Tissue and Cell Types

The researchers conducted comprehensive analyses to uncover the tissues and cell types involved in glucose metabolism. Their findings highlighted the importance of the colon, ileum, cartilage, adrenal glands, pancreas, and adrenal cortex. These insights could pave the way for a deeper understanding of how different body parts contribute to glucose regulation.

Intestinal Health and Genetic Associations

It was also interesting to see how RG variants are related to intestinal health, especially in two genera (Collinsella and Lachnospiraceae-FCS020) that are involved in making glucose from galactose and lactose. This multi-omics approach provided substantial evidence for the associations between RG variants and gut microbiota.

Blood Glucose’s Impact on Lung Function

Lastly, the study examined the genetic correlations between RG and other phenotypes. Positive genetic correlations were found with squamous cell lung cancer and lung cancer, while inverse correlations were observed with lung function-associated traits like FEV1 and FVC. Bidirectional Mendelian randomization demonstrated the causal effects of T2D and RG on lung function decline, uncovering a new diabetes complication.

Conclusion

In summary, this monumental GWAS meta-analysis has unveiled 44 additional loci associated with glycemic traits, validated the role of GLP1R in glucose regulation, and shed light on underexplored mediators of glycemic control, particularly the intestines. Furthermore, it confirmed the causal relationship between glycemic dysregulation and lung function decline, elevating lung dysfunction as a new complication of diabetes. This study deepens our understanding of blood glucose regulation and opens exciting avenues for future research and personalized diabetes management.

Cited Works
Reik, Anna. “Genetic and dietary predictors for the postprandial glucose response and possible implications of the postprandial metabolic phenotype on weight management.” PhD diss., Technische Universität München, 2023.

Fradin, Delphine, and Pierre Bougneres. “T2DM: Why Epigenetics?”” Journal of Nutrition and Metabolism 2011 (2011).

Foreman, Judy. A nation in pain: Healing our biggest health problem. Oxford University Press, USA, 2014.

disease, Health, Public health

Revealing the Hidden Battlefront: How Cryo-EM Unlocks the Secrets of Mucosal Host-Pathogen Warfare

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Introduction

In a recent study published on the bioRxiv* preprint server, researchers delved deep into the intricate world of mucosal host-pathogen interactions. Using cutting-edge cryogenic-electron microscopy (cryo-EM), they have unveiled the detailed structures of secretory immunoglobulin A (sIgA) complexes with Streptococcus pyogenes M4 and human CD89. This groundbreaking research offers a fascinating glimpse into the molecular battleground where our immune system confronts microbial invaders, shedding light on the mechanisms that govern these crucial interactions.

*Disclaimer: It is important to note that BioRxiv publishes preliminary scientific reports that are not peer-reviewed and should not be considered conclusive or used to guide clinical practice.

Understanding the Basics

Before diving into the study’s findings, let us lay some essential groundwork. Immunoglobulin A, or IgA, exists in monomeric (mIgA) and secretory (sIgA). While mIgA circulates in the bloodstream, sIgA is found in mucosal secretions, such as saliva and tears. Both forms of IgA possess fragment antigen-binding (Fab) and Fc regions, but sIgA is the frontline defender against pathogens at mucosal surfaces.

The research was mostly about how sIgA interacts with two essential parts of the host-pathogen relationship: CD89, a human receptor, and Streptococcus pyogenes M4 (GAS M4), a virulence factor. GAS M4 and other M proteins play a pivotal role in modulating the host immune response, binding to IgA, and influencing the course of infection.

The Stakes Are High

Understanding these interactions is more than just an academic exercise. Streptococcus pyogenes, responsible for conditions like tonsillitis and more severe invasive infections, poses a significant global health threat. It is estimated that over 1.78 million new GAS-related invasive infections occur annually, leading to more than 160,000 deaths worldwide. Therefore, gaining insights into how these bacteria interact with the host’s immune system is paramount.

The Study Unveiled

The researchers in this study employed cryo-EM to examine the structures of sIgA-M4 and sIgA-CD89 complexes at remarkably high resolutions. This technology allowed them to scrutinize the atomic details of these complexes, shedding light on their intricate architectures.

One key finding was that CD89 and M4 shared five common amino acid residues in their interactions with sIgA but displayed distinct binding stoichiometry. This suggests that while these binding sites were conserved on both sIgA forms, they exhibited different accessibility to host receptors and microbial proteins.

A Twist in the Tale

One of the most intriguing discoveries was that the sIgA-M4 complex exhibited a steric 1:1 M4:sIgA stoichiometry, leading to an asymmetric sIgA structure. This meant that M4 bound to sIgA in a way that was different from its binding to other regions, opening up exciting possibilities for future research.

Additionally, the study found variations in the binding of CD89 to sIgA in different contexts. The orientation and spacing of bound CD89 molecules differed between sIgA and mIgA. This means that each sIgA may have its own CD89 binding sites, which could change how CD89 clusters and, in turn, how IgA effector functions.

Implications and Future Directions

The study’s findings imply that sIgA may have significantly shaped the evolution of Streptococcus pyogenes. Understanding these interactions could be pivotal for developing strategies to combat GAS and other pathogenic bacteria effectively.

Moreover, the concept that host sIgA effector functions are crucial in the antimicrobial response extends beyond GAS. Other pathogenic bacterial species like S. aureus and S. pneumoniae have been found to bind to sIgA, potentially modulating their virulence and host responses.

In conclusion, this cryo-EM study represents a significant step in understanding mucosal host-pathogen interactions. It provides valuable insights into Streptococcus pyogenes and opens up exciting avenues for future research, offering hope for improved strategies to combat infectious diseases and enhance our understanding of the intricate dance between our immune system and microbial invaders.

Cited Works
Responses – viagrawithoutdoc. https://viagrawithoutdoc.com/tag/responses

Genomic sequencing supports a long-term infection as source of SARS-CoV-2 Omicron – JUSTBALANCINGHEALTH. https://justbalancinghealth.com/health-news/genomic-sequencing-supports-a-long-term-infection-as-source-of-sars-cov-2-omicron/

Georgia State Researchers Survey Antibodies to SARS-CoV-2 in Blood Samples of Local Residents – Georgia State University News – Institute for Biomedical Sciences, Press Releases, Research, University Research – Health & Wellness. https://news.gsu.edu/2020/05/01/georgia-state-researchers-survey-antibodies-to-sars-cov-2-in-blood-samples-of-local-residents/

Hao, Ya, et al. “A Prospective on Multiple Biological Activities of Lactoferrin Contributing to Piglet Welfare.” Biochemistry and Cell Biology, 2021, https://doi.org/10.1139/bcb-2020-0078.

Andargie, Temesgen E., and Ermias D. Ejara. “Pro- and Anti-inflammatory Cytokines in Visceral Leishmaniasis.” Journal of Cell Science & Therapy, 2016, https://doi.org/10.4172/2157-7013.1000206.

Behavioral Science, Culture, Health, meditation, mental health, Philosophy and Religion, positive thinking, Public health

Unlocking the Power of Meditation: Techniques, Benefits, and Scientific Insights

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Culture, Health, Public health

Revolutionizing Kidney Health: Artificial Kidney Implant Sparks Hope for a Brighter Future

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Culture, disease, genetics, Health, mental health, Public health

Cracking the Code of Autism’s Neural Mysteries: The Game-Changing Twin Study You Need to Know About

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Culture, disease, Health, mental health, Public health

Unlocking the Mystery of Aphantasia: The Astonishing World of the Mind’s Eye Gone Dark

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Culture, environmental, Health, Public health

Nature or Nurture? Unraveling the Complexity of People-Pleasing Behavior

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