A sentiment analysis on online psychiatrist reviews to identify clinical attributes of psychiatrists that shape the therapeutic alliance.

Background: While online reviews from physician rating websites are increasingly utilized by healthcare providers to better understand patient needs, it remains difficult to objectively identify areas for improvement in providing psychiatric care. Objectives: To quantitatively characterize the sentiment of online written reviews of psychiatrists to determine clinical attributes that can be strengthened to improve psychiatrists' therapeutic alliance with their patients. Materials and methods: Sentiment scores of 6,400 written reviews of 400 US-based psychiatrists on a US-based online physician rating website were obtained through a natural-language-processing-based sentiment analysis. Relationships among sentiment scores, average star ratings, and demographics were examined. Linguistic analyses determined words and bigrams that were highly associated with reviews with the most positive and negative sentiment. Findings: Sentiment scores were significantly correlated with average star ratings of the psychiatrists (R = 0.737, p < 0.001). Psychiatrists who were younger (< 56 years old) and/or practiced in the Northeast had significantly higher average star ratings than those older and/or practicing in the Southwest. Frequency analysis showed that positive reviews most frequently contained "time" (N = 1,138) and "caring" (N = 784) while negative reviews most frequently contained "medication" (N = 495) and "time" (N = 379). Logistic regression analysis revealed that reviews were more likely to be considered positive when they included "great listener" (OR = 16.89) and "comfortable" (OR = 10.72) and more likely to be negative when they included "meds" (OR = 0.55) and "side effect" (OR = 0.59). Conclusion: Psychiatrists who are younger and located in the Northeast receive more positive reviews; there may be potential for demographic bias among patient reviewers. Patients positively rate psychiatrists who make them feel heard and comfortable but negatively rate encounters centered around medications and their side effects. Our study lends quantitative evidence to support the importance of thorough and empathetic communication of psychiatrists in building a strong therapeutic alliance.

An Update: National Institutes of Health Research Funding for Palliative Medicine 2016-2020.

Background: The evidence base to support palliative care clinical practice is inadequate and opportunities to improve the evidence base remain despite the field's rapid growth. Objective: The aim of this study was to examine current National Institutes of Health (NIH) funding of palliative medicine research and trends over time. Design: We sought to identify NIH funding of palliative medicine (2016-2020) in two stages: (1) we searched the NIH grant database, RePORTER, for grants with the keywords, "palliative care," "end-of-life care," "hospice," and "end of life," and (2) identified palliative care researchers likely to have secured NIH funding using three strategies. Methods: We abstracted (1) the first and last authors' names from original investigations published in major palliative medicine journals from 2016 to 2018; (2) names from a PubMed-generated list of original articles published in major medicine, nursing, and subspecialty journals using the above keywords; and (3) palliative medicine journal editorial board members and members of key palliative medicine initiatives. We cross-matched the pooled names against NIH grants funded from 2016 to 2021. Results: A crosswalk analysis of the author search and NIH RePORTER search identified 1658 grants. Of those, 541 were categorized as relevant to palliative medicine, which represented 419 unique principal investigators (mean of 1.34 grants per investigator). Compared with 2011-2015, the number of NIH-funded grants increased by 25%, NIH dollars increased by 35%, and the distribution of grant types remained stable. Conclusions: Despite the challenging NIH funding climate, the number of NIH grants and funding to palliative care have increased. Given the increased funding allocation toward Alzheimer's dementia and related dementia research at the congressional level, this increase in funding reflects this funding allocation and does not represent overall growth. Dedicated federal funding for palliative care research remains critical to grow the evidence base for persons living with serious illnesses and their families.

Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.

DNA inter-strand crosslinks (ICLs) are dangerous lesions that can be caused by a variety of endogenous and exogenous bifunctional compounds. Because covalently linking both strands of the double helix locally disrupts DNA replication and transcription, failure to remove even a single ICL can be fatal to the cell. Thus, multiple ICL repair pathways have evolved, with the best studied being the canonical Fanconi anemia (FA) pathway. However, recent research demonstrates that different types of ICLs (e.g., backbone distorting vs. non-distorting) can be discriminated by the cell, which then mounts a specific repair response using the FA pathway or one of a variety of FA-independent ICL repair pathways. This review focuses on the latter, covering current work on the transcription-coupled, base excision, acetaldehyde-induced, and SNM1A/RecQ4 ICL repair pathways and highlighting unanswered questions in the field. Answering these questions will provide mechanistic insight into the various pathways of ICL repair and enable ICL-inducing agents to be more effectively used as chemotherapeutics.

The yeast Hrq1 helicase stimulates Pso2 translesion nuclease activity and thereby promotes DNA interstrand crosslink repair.

DNA interstrand crosslink (ICL) repair requires a complex network of DNA damage response pathways. Removal of the ICL lesions is vital, as they are physical barriers to essential DNA processes that require the separation of duplex DNA, such as replication and transcription. The Fanconi anemia (FA) pathway is the principal mechanism for ICL repair in metazoans and is coupled to DNA replication. In Saccharomyces cerevisiae, a vestigial FA pathway is present, but ICLs are predominantly repaired by a pathway involving the Pso2 nuclease, which is hypothesized to use its exonuclease activity to digest through the lesion to provide access for translesion polymerases. However, Pso2 lacks translesion nuclease activity in vitro, and mechanistic details of this pathway are lacking, especially relative to FA. We recently identified the Hrq1 helicase, a homolog of the disease-linked enzyme RecQ-like helicase 4 (RECQL4), as a component of Pso2-mediated ICL repair. Here, using genetic, biochemical, and biophysical approaches, including single-molecule FRET (smFRET)- and gel-based nuclease assays, we show that Hrq1 stimulates the Pso2 nuclease through a mechanism that requires Hrq1 catalytic activity. Importantly, Hrq1 also stimulated Pso2 translesion nuclease activity through a site-specific ICL in vitro We noted that stimulation of Pso2 nuclease activity is specific to eukaryotic RecQ4 subfamily helicases, and genetic and biochemical data suggest that Hrq1 likely interacts with Pso2 through their N-terminal domains. These results advance our understanding of FA-independent ICL repair and establish a role for the RecQ4 helicases in the repair of these detrimental DNA lesions.