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New UCLA research finds that small group professional coaching can reduce physician burnout rates by up to 30%, suggesting that it is more effective than the traditional, and more expensive, one-on-one coaching method.

Nearly half of physicians in the US suffer from burnout, which is marked by emotional exhaustion, depersonalization and decreased personal accomplishment. These can lead to medical errors and other harmful consequences to the healthcare system and patient outcomes, said lead author Dr. Joshua Khalili, director of physician wellness in the UCLA Department of Medicine and assistant clinical professor of medicine at the David Geffen School of Medicine at UCLA.

Most current evidence related to professional coaching is related to individual coaching and its impact on reducing burnout. But individual coaching can be quite costly, which is a barrier to broad implementation.”

Dr. Joshua Khalili, director of physician wellness, UCLA Department of Medicine and assistant clinical professor of medicine, David Geffen School of Medicine at UCLA

The study will be published in the peer-reviewed Journal of General Internal Medicine.

Physician burnout is estimated to cost the US healthcare system about $4.6 billion annually, mostly due to costs associated with physician turnover and fewer clinical hours. 

The researchers conducted a randomized, wait-list controlled trial with 79 UCLA attending internal medicine physicians for just over a year starting in March 2023. The intervention consisted of six one-hour coaching sessions, with one-third of the group receiving one-on-one coaching via Zoom while another third were coached in small groups consisting of three physicians and one coach. The final third acted as control group, receiving no coaching during the first few months of the trial, and subsequently received six, one-on-one coaching sessions.

The primary outcome the researchers measured was overall burnout. They also examined areas of work life such as workload, control rewards, community, fairness, and values; work engagement such as vigor, dedication, and absorption; self-efficacy, and social support. They measured each of these outcomes before and after the intervention and again six months afterward.

They found that small group intervention participants experienced a nearly 30% reduction in burnout rate. Participants in the one-on-one coaching experienced a 13.5% burnout rate reduction. By contrast, the control group experienced an 11% increase in burnout rates. Burnout remained stable among the small group participants and continued to fall in the one-on-one group six months after the initial intervention.

Coaching for the one-on-one sessions cost $1000 per participant, compared with $400 for the small group coaching sessions.

“This new, small-group model of professional coaching can make a significant impact in physician burnout and costs much less than the one-on-one model,” Khalili said.

Study limitations include potential selection bias among participants who would most likely benefit from the intervention. The baseline overall burnout rate was higher in the small group coaching arm (70.4%) compared to the one-on-one group (40.0%); however, relative reductions in burnout were similar: 42% in the small group intervention compared to 34% the one-on-one group. In addition, the study was conducted at a large academic center whose physicians may not be comparable to those in other healthcare institutions.

The researchers are now providing coaching to physicians in the UCLA Department of Medicine and hope that this research encourages other health care institutions and organizations to implement professional coaching, Khalili said.

“By improving physicians’ well-being, engagement, and sense of support, interventions like coaching can enhance the quality of care patients receive, making this a public health priority, not just a workplace issue,” he said.

The study was co-authored by Dr. Karen Miotto, Dr. Tisha Wang, Dr. John Mafi, Elizabeth Kyababchyan, Jesse Sanford, Dr. David Elashoff, Jenny Brook, Yetunde Adebambo, Paige‑Ashley Smith, Emma Nguyen, and Dr. Sun Yoo.

The UCLA Department of Medicine funded the study.

Recently, the team led by Chief Physician Quan Zhang and Associate Professor Feng Liu at Tianjin Medical University General Hospital systematically evaluated the genetic associations between type 2 diabetes mellitus and subcortical brain structures using large-scale genome-wide association summary statistics and advanced statistical genetic methods. The related findings were published in Research under the title “Genome-wide pleiotropy analysis reveals shared genetic associations between type 2 diabetes mellitus and subcortical brain volumes”.

1. Research background

Type 2 diabetes mellitus (T2DM) is a highly prevalent metabolic disorder worldwide. Beyond glucose dysregulation, it exerts significant effects on the central nervous system. Epidemiological and neuroimaging evidence indicates that individuals with T2DM are at substantially increased risk of cognitive decline and dementia, which is closely linked to degenerative changes in brain structure—particularly within subcortical regions such as the hippocampus, amygdala, caudate, and thalamus. These regions play critical roles in memory, emotional regulation, and motor control, and have been shown to exhibit marked volume reduction and structural abnormalities in individuals with T2DM.

Current neuroimaging studies have systematically characterized the structural brain abnormalities associated with T2DM. However, the underlying genetic mechanisms driving these changes remain unclear. T2DM is a prototypical polygenic disorder, with large-scale genome-wide association studies (GWAS) having identified hundreds of associated genetic loci. Likewise, the volume and morphology of subcortical brain structures are known to be strongly influenced by genetic factors. Emerging evidence suggests potential genetic overlap between T2DM and brain structure. For instance, the T2DM risk gene TCF7L2 has been linked to amygdala volume, and the Hp 1-1 gene has been associated with hippocampal volume. Moreover, polygenic risk scores for glycated hemoglobin (HbA1c) have shown associations with gray matter volume, and the genetic risk of several hippocampal morphological traits has been related to T2DM. While these findings provide preliminary insights, a comprehensive investigation into the shared genetic architecture between T2DM and brain structural abnormalities is still lacking. Further research is needed to elucidate the underlying molecular pathways and biological mechanisms.

2. Research progress

The authors systematically evaluated the polygenic overlap and shared genetic architecture between T2DM and the volumes of subcortical brain structures, including the bilateral thalamus, caudate, putamen, pallidum, hippocampus, amygdala, and accumbens. MiXeR analysis revealed that T2DM has high polygenicity and low discoverability, and shares varying degrees of genome-wide genetic overlap with subcortical brain regions, with Dice coefficients ranging from 22.4% to 49.6% .

Using the conditional false discovery rate approach, the study identified 229 loci associated with T2DM (including 5 novel loci) and 220 loci associated with subcortical brain structures (including 16 novel loci). Furthermore, conjunctional false discovery rate analysis revealed 129 shared loci jointly associated with T2DM and subcortical volumes. Among them, rs429358 on chromosome 19 (located in the APOE gene) showed the strongest association with both bilateral accumbens volume and T2DM, and exhibited a high functional pathogenicity score.

In the functional annotation, most of the shared SNPs were located in intronic or intergenic regions. A total of 769 protein-coding genes were mapped from the candidate SNPs, showing high expression in pancreatic, hepatic, and cardiac tissues, and were involved in various biological processes including energy metabolism, neurogenesis, and nervous system development. Developmental trajectory analysis revealed that genes shared between T2DM and multiple subcortical brain regions were highly expressed during the fetal period and gradually declined after birth, suggesting their potential role in early brain development.

Further transcriptome-wide association analysis (TWAS) validated the dual association of several key genes (e.g., TUFM, JAZF1) with both T2DM and the volumes of specific brain regions.

3. Future perspectives

This study systematically revealed the genetic overlap between T2DM and subcortical brain structures, clarifying their shared genetic loci, shared genes and the potential biological pathways involved. This interdisciplinary work not only deepens our understanding of how T2DM affects brain health, but also promotes a shift in metabolic disease research from a traditional focus on peripheral metabolism to the central nervous system. The findings provide critical genetic evidence for risk prediction, biomarker identification, and early intervention strategies targeting T2DM-related brain structural alterations, offering new directions for clinical translation and precision prevention in the brain-metabolism interface.

Autoimmune diseases, such as multiple sclerosis (MS), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA), affect millions of people worldwide. These conditions arise when the body’s immune system fails to distinguish between “self” and “foreign” cells, and mistakenly attacks its own healthy cells, resulting in persistent inflammation and tissue damage. Central to these autoimmune responses are CD4⁺ T cells, a class of immune cells that can either promote or suppress the condition.

Regulatory T cells (T_reg) are a special subtype of CD4⁺ T cells that act as the immune system’s peacekeepers. T_reg cells, marked by protein Foxp3, help in suppressing harmful immune responses. However, when the function of T_reg cells is compromised, as seen in cases of MS and IBD, the immune response is dominated by the Th1 and Th17 cells (other CD4⁺T cell subtypes), which promote inflammation, further worsening the disease symptoms. Therefore, boosting the development and activity of T_reg cells is emerging as a promising therapeutic approach, but the mechanisms underlying its effective regulation remain unclear.

In pursuit of a deeper understanding of these mechanisms, a team of Chinese scientists led by Dr. Xiaojun Wu and Dr. Fei Huang from the Shanghai Key Laboratory of Compound Chinese Medicines, SHUTCM, China, and Dr. Weidong Pan from the Department of Neurology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China, explored the role of Early Growth Response Gene 1 (Egr-1) in promoting the activity of T_reg cells. The study was conducted in a well-established animal model of MS, called experimental autoimmune encephalomyelitis (EAE), to confirm the mechanisms. The findings of this study were published in Volume 8 of Research on April 15, 2025.

Elaborating more, Dr. Wu, the lead author of this study, says “We started by screening the genes that appeared different between mice with mild and severe EAE.” Further, he adds, “Among the top identified genes in CD4⁺ T cells, Egr-1 stood out as significantly downregulated in severe disease.”

After identifying Egr-1 as a regulatory gene, the team assessed its role by using genetically engineered mice lacking Egr-1 in CD4⁺ T cells. These mice were induced with EAE and tracked for disease progression. The researchers also analyzed the immune cell compositions in the spleen, lymph nodes, and central nervous system of these mice.

“The mice lacking Egr-1 showed worse disease, fewer T_reg cells, and more inflammatory TH17 and TH1 cells” explains Dr. Huang.

The researchers also conducted additional in vitro experiments. By analyzing isolated human CD4⁺ T cells from MS patients and healthy donors, they confirmed that both Egr-1 and Foxp3 levels were reduced in patient samples. Further, to determine whether Egr-1 directly regulates Foxp3, the researchers used chromatin immunoprecipitation, which revealed that Egr-1 binds to the Foxp3 promoter. Additionally, using luciferase reporter assays, they also confirmed that Egr-1 binding increases Foxp3 gene activity. They then traced the pathway to TGF-β (Transforming Growth Factor Beta) signaling via the Raf/Mek/Erk cascade, which activates Egr-1.

“We identified a unique mechanism of Egr-1,” explains Dr. Pan, “First, TGF-β activates the Raf/Mek/Erk cascade, which activates Egr-1. Egr-1 then directly binds to the Foxp3 promoter to enhance its expression, bypassing the classical Smad3-dependent pathway.”

What’s more, the researchers also investigated the effect of a natural compound, Calycosin, which acts as an Egr-1 agonist. Treatment with calycosin restored T_reg cell functions and improve clinical outcomes in mice with EAE, but only in those with functional Egr-1.

Overall, the study underscores the essential role of Egr-1 in T_reg cell development and function, identifying it as a central molecular switch in immune regulation. By elucidating its mechanism and validating the effect of a natural Egr-1 agonist, the study suggests that targeting Egr-1 may offer a promising treatment strategy, potentially transforming therapeutic approaches to autoimmune diseases.

Recently, a research team from Chongqing Medical University, led by Prof. Wei Huang, Dr. Wei Bao, and Dr. Yiting Lei, has successfully developed a novel engineered extracellular matrix (eECM) to address the challenge of cartilage repair. Their findings were published in Research under the title “Cytokine-Activated MSC-Derived ECM Facilitates Cartilage Repair by Maintaining Chondrocyte Homeostasis and Promoting Chondrogenic Differentiation of Recruited Stem Cells.”

Research background

Cartilage injuries are a common clinical issue, often caused by trauma, severe infections, or degenerative joint diseases. The lack of direct blood supply to cartilage and limited access to nutrients from the surrounding synovial fluid make it difficult for these injuries to heal on their own, often leading to osteoarthritis, which is characterized by joint deformity and functional impairment. Current strategies for cartilage repair, such as microfracture surgery, arthroscopic debridement, and cell-based therapies, face challenges including limited cell availability, risks of immune rejection, donor site morbidity, and logistical issues related to cell transport.

Research progress

The research team optimized the extracellular matrix (ECM) derived from mesenchymal stromal cells (MSCs) by preconditioning them with inflammatory cytokines, such as IL-6, TNF-α, and IFN-γ, to create a bioactive eECM. Immunofluorescence and scanning electron microscopy revealed that the decellularization process successfully removed cellular components while preserving key ECM components, including glycosaminoglycans (GAGs).

Further proteomic analysis showed significant changes in the expression levels of key ECM components, such as collagen, laminin, and matrix metalloproteinases, in the cytokine-preconditioned eECM. The eECM was also enriched with bioactive molecules like TGFBI, TGFB3, and SDF2, which play crucial roles in maintaining chondrocyte homeostasis and recruiting endogenous stem cells.

In vitro experiments demonstrated that the eECM significantly influenced the expression of cartilage matrix components. Specifically, IFN-γ-ECM restored type II collagen levels and reduced ADAMTS5 expression, promoting matrix synthesis and inhibiting degradation, thereby effectively maintaining cartilage homeostasis. Additionally, the eECM significantly enhanced chondrocyte recruitment and proliferation, with IFN-γ-ECM showing the strongest recruitment ability. It also reduced pro-inflammatory cytokine levels and enhanced chondrocyte proliferation, indicating significant anti-inflammatory effects and the potential to reverse cellular senescence.

In vivo experiments using an animal model showed that implanting IFN-γ-ECM into cartilage defects treated with microfracture surgery led to significantly better cartilage regeneration compared to controls treated with microfracture alone or with standard ECM. Histological analysis at 6 and 12 weeks post-surgery revealed that the IFN-γ-ECM group had superior hyaline cartilage regeneration, with repaired tissue showing rich type II collagen expression and minimal distinction from surrounding normal tissue.

Future prospects

This study not only provides a new strategy for cartilage repair but also offers new insights into the development of bioactive materials with specific functions. By selecting appropriate cytokines for MSC preconditioning, it is possible to customize eECMs with specific functions for cartilage repair and other tissue regeneration therapies. Future research will further explore the long-term safety and efficacy of eECM in vivo, as well as its potential applications in other tissue regeneration fields.

Announcing a new article publication for BIO Integration journal. Imbalances in the intestinal microbiome are closely associated with the occurrence and development of cancer, and can affect tumorigenesis by influencing the inflammatory response, regulating the immune system, producing specific metabolites, and participating in tumor signaling pathways.

This study investigated the relationships among intestinal microbial dynamics, metabolite profiles, and neoadjuvant chemotherapy (NAC) outcomes in patients with breast cancer. Patients were stratified by Miller-Payne (MP) grade into good (MP 4-5) or poor (MP 1-3) responders. Fecal samples from patients (pre- and post-NAC) were analyzed via 16S rRNA sequencing and untargeted metabolic analysis.

After neoadjuvant chemotherapy, the species diversity and abundance of the intestinal microbiome significantly decreased, and these trends were not correlated with neoadjuvant chemotherapy efficacy. Fusobacterium abundance remained significantly higher in poor responders than good responders post-NAC, thus suggesting its association with chemoresistance.

The Firmicutes/Bacteroidetes ratio was lower in patients with breast cancer than healthy controls, and was correlated with the therapeutic response: this ratio rose post-NAC but remained suboptimal in poor responders. Untargeted metabolomics identified upregulated amino acids (Thr-Thr and histidine) in poor responders and elevated lipids (C17-sphinganine) in good responders. ROC (receiver operating characteristic curve) analysis validated these metabolites (AUC >0.7) as predictive biomarkers. KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis highlighted enrichment in mTOR signaling, endocrine resistance, and estrogen signaling pathways.

These findings underscore the intestinal microbiome’s potential as a predictor of NAC efficacy and a therapeutic target. Modulating Fusobacterium or metabolite pathways may enhance chemotherapy response.

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