Podcasts about differentially

Link to original articleWelcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Please stop publishing ideas/insights/research about AI, published by Tamsin Leake on May 2, 2024 on LessWrong. Basically all ideas/insights/research about AI is potentially exfohazardous. At least, it's pretty hard to know when some ideas/insights/research will actually make things better; especially in a world where building an aligned superintelligence (let's call this work "alignment") is quite harder than building any superintelligence (let's call this work "capabilities"), and there's a lot more people trying to do the latter than the former, and they have a lot more material resources. Ideas about AI, let alone insights about AI, let alone research results about AI, should be kept to private communication between trusted alignment researchers. On lesswrong, we should focus on teaching people the rationality skills which could help them figure out insights that help them build any superintelligence, but are more likely to first give them insights that help them realize that that is a bad idea. For example, OpenAI has demonstrated that they're just gonna cheerfully head towards doom. If you give OpenAI, say, interpretability insights, they'll just use them to work towards doom faster; what you need is to either give OpenAI enough rationality to slow down (even just a bit), or at least not give them anything. To be clear, I don't think people working at OpenAI know that they're working towards doom; a much more likely hypothesis is that they've memed themselves into not thinking very hard about the consequences of their work, and to erroneously feel vaguely optimistic about those due to cognitive biases such as wishful thinking. It's very rare that any research purely helps alignment, because any alignment design is a fragile target that is just a few changes away from unaligned. There is no alignment plan which fails harmlessly if you fuck up implementing it, and people tend to fuck things up unless they try really hard not to (and often even if they do), and people don't tend to try really hard not to. This applies doubly so to work that aims to make AI understandable or helpful, rather than aligned - a helpful AI will help anyone, and the world has more people trying to build any superintelligence (let's call those "capabilities researchers") than people trying to build aligned superintelligence (let's call those "alignment researchers"). Worse yet: if focusing on alignment is correlated with higher rationality and thus with better ability for one to figure out what they need to solve their problems, then alignment researchers are more likely to already have the ideas/insights/research they need than capabilities researchers, and thus publishing ideas/insights/research about AI is more likely to differentially help capabilities researchers. Note that this is another relative statement; I'm not saying "alignment researchers have everything they need", I'm saying "in general you should expect them to need less outside ideas/insights/research on AI than capabilities researchers". Alignment is a differential problem. We don't need alignment researchers to succeed as fast as possible; what we really need is for alignment researchers to succeed before capabilities researchers. Don't ask yourself "does this help alignment?", ask yourself "does this help alignment more than capabilities?". "But superintelligence is so far away!" - even if this was true (it isn't) then it wouldn't particularly matter. There is nothing that makes differentially helping capabilities "fine if superintelligence is sufficiently far away". Differentially helping capabilities is just generally bad. "But I'm only bringing up something that's already out there!" - something "already being out there" isn't really a binary thing. Bringing attention to a concept that's "already out there" is an ex...

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Please stop publishing ideas/insights/research about AI, published by Tamsin Leake on May 2, 2024 on LessWrong. Basically all ideas/insights/research about AI is potentially exfohazardous. At least, it's pretty hard to know when some ideas/insights/research will actually make things better; especially in a world where building an aligned superintelligence (let's call this work "alignment") is quite harder than building any superintelligence (let's call this work "capabilities"), and there's a lot more people trying to do the latter than the former, and they have a lot more material resources. Ideas about AI, let alone insights about AI, let alone research results about AI, should be kept to private communication between trusted alignment researchers. On lesswrong, we should focus on teaching people the rationality skills which could help them figure out insights that help them build any superintelligence, but are more likely to first give them insights that help them realize that that is a bad idea. For example, OpenAI has demonstrated that they're just gonna cheerfully head towards doom. If you give OpenAI, say, interpretability insights, they'll just use them to work towards doom faster; what you need is to either give OpenAI enough rationality to slow down (even just a bit), or at least not give them anything. To be clear, I don't think people working at OpenAI know that they're working towards doom; a much more likely hypothesis is that they've memed themselves into not thinking very hard about the consequences of their work, and to erroneously feel vaguely optimistic about those due to cognitive biases such as wishful thinking. It's very rare that any research purely helps alignment, because any alignment design is a fragile target that is just a few changes away from unaligned. There is no alignment plan which fails harmlessly if you fuck up implementing it, and people tend to fuck things up unless they try really hard not to (and often even if they do), and people don't tend to try really hard not to. This applies doubly so to work that aims to make AI understandable or helpful, rather than aligned - a helpful AI will help anyone, and the world has more people trying to build any superintelligence (let's call those "capabilities researchers") than people trying to build aligned superintelligence (let's call those "alignment researchers"). Worse yet: if focusing on alignment is correlated with higher rationality and thus with better ability for one to figure out what they need to solve their problems, then alignment researchers are more likely to already have the ideas/insights/research they need than capabilities researchers, and thus publishing ideas/insights/research about AI is more likely to differentially help capabilities researchers. Note that this is another relative statement; I'm not saying "alignment researchers have everything they need", I'm saying "in general you should expect them to need less outside ideas/insights/research on AI than capabilities researchers". Alignment is a differential problem. We don't need alignment researchers to succeed as fast as possible; what we really need is for alignment researchers to succeed before capabilities researchers. Don't ask yourself "does this help alignment?", ask yourself "does this help alignment more than capabilities?". "But superintelligence is so far away!" - even if this was true (it isn't) then it wouldn't particularly matter. There is nothing that makes differentially helping capabilities "fine if superintelligence is sufficiently far away". Differentially helping capabilities is just generally bad. "But I'm only bringing up something that's already out there!" - something "already being out there" isn't really a binary thing. Bringing attention to a concept that's "already out there" is an ex...

On this episode, we discuss the Antikythera Mechanism, a device found in a Roman shipwreck off the Greek Island of Antijythera.  Retrieved with several other treasures, due to it's advanced state of petrification and other issues, it wasn't even looked at much after it was initially brought up.  But over time, people have discovered this uncanny device that simulates the movement of the heavens created in the time of Before Common Era using a differential gear which otherwise doesn't show up for another 1300 years.  We discuss the devices discovery and the theories about it in this man learning stuff is fun episode of the Family Plot Podcast!Become a supporter of this podcast: https://www.spreaker.com/podcast/family-plot--4670465/support.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Slim overview of work one could do to make AI go better (and a grab-bag of other career considerations), published by Chi on March 22, 2024 on The Effective Altruism Forum. Many kinds of work one could do to make AI go better and a grab-bag of other career considerations I recently found myself confused about what I'd like to work on. So, I made an overview with the possible options for what to work on to make AI go well. I thought I'd share it in case it's helpful for other people. Since I made this overview for my own career deliberations, it is tailored for myself and not necessarily complete. That said, I tried to be roughly comprehensive, so feel free to point out options I'm missing. I redacted some things but didn't edit the doc in other ways to make it more comprehensible to others. In case you're interested, I explain a lot of the areas in the "Humans in control" and the "Misalignment" worlds here and to some extent here. What areas could one work on? What endpoints or intermediary points could one aim for? Note that I redacted a bunch of names in "Who's working on this" just because I didn't want to bother asking them and I wasn't sure they had publicly talked about it yet, not because of anything else. "?" behind a name or org means I don't know if they actually work on the thing (but you could probably find out with a quick google!) World it helps The area (Note that this doesn't say anything about the type of work at the moment. For example, I probably should never do MechInterp myself because of personal fit. But I could still think it's good to do something that overall supports MechInterp.) Biggest uncertainty Who's working on this Hu- mans in con- trol ASI governance | human-control Who is in control of AI, what's the governance structure etc. Digital sentience [...] Is this tractable and is success path-dependent? Will MacAskill, [redacted]?, indirectly: cybersec. folk?, some AI governance work? Acausal interactions | human-control Metacognition Decision theory Values of future civilisation SPIs [redacted] SPIs for causal interactions | human-control CLR Mis- align- ment Prevent sign flip and other near misses Is this a real concern? Nobody? Acausal interactions | misalignment Decision theory Value porosity Is this tractable? [redacted]? [redacted]? Reducing conflict-conducive preferences for causal interactions & SPIs | misalignment CLR Main- stream AI safety best thing to work on Reduction of malevolence in positions of influence through improving awareness (also goes into the "Humans in control" category) [redacted]? Nobody? Differentially support responsible AI labs For some of these: Would success be net good or net bad? If good: How good? How high is the penalty for being less neglected? Influence AI timelines [redacted], [redacted], [redacted]?, maybe misc. policy people? AI control (and ideas like paying AIs) Redwood Research Model capabilities evaluations METR, Apollo?, maybe AI labs policy teams, maybe misc. Other policy people? Alignment (more comprehensive overview): MechInterp ELK (L)AT Debate COT oversight Infrabayesianism Natural abstractions Understanding intelligence [...] Overview post on LessWrong Human epistemics during early AI ~Forecasting crowd, nobody? Growing the AI safety and EA community or improving its branding or upskilling people in the community (e.g. fellowships) Constellation, Local groups, CEA, OpenPhilanthropy, … Improving the AI safety and EA community and culture socially CEA Threat modelling, scenario forecasting etc. [redacted], … Make it harder to steal models Cybersecurity folk Regulate Open Source capabilities Policy folk? Nobody? What types of work are there? Which world Type of work Broad category of work Can be in any of the three areas above Offering 1-1 support (mental, operational, and debugging) Proj...

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Memo on some neglected topics, published by Lukas Finnveden on November 11, 2023 on The Effective Altruism Forum. I originally wrote this for the Meta Coordination Forum. The organizers were interested in a memo on topics other than alignment that might be increasingly important as AI capabilities rapidly grow - in order to inform the degree to which community-building resources should go towards AI safety community building vs. broader capacity building. This is a lightly edited version of my memo on that. All views are my own. Some example neglected topics (without much elaboration) Here are a few example topics that could matter a lot if we're in the most important century, which aren't always captured in a normal "AI alignment" narrative: The potential moral value of AI. [1] The potential importance of making AI behave cooperatively towards humans, other AIs, or other civilizations (whether it ends up intent-aligned or not). Questions about how human governance institutions will keep up if AI leads to explosive growth. Ways in which AI could cause human deliberation to get derailed, e.g. powerful persuasion abilities. Positive visions about how we could end up on a good path towards becoming a society that makes wise and kind decisions about what to do with the resources accessible to us. (Including how AI could help with this.) (More elaboration on these below.) Here are a few examples of somewhat-more-concrete things that it might (or might not) be good for some people to do on these (and related) topics: Develop proposals for how labs could treat digital minds better, and advocate for them to be implemented. (C.f. this nearcasted proposal.) Advocate for people to try to avoid building AIs with large-scale preferences about the world (at least until we better understand what we're doing). In order to avoid a scenario where, if some generation of AIs turn out to be sentient and worthy of rights, we're forced to choose between "freely hand over political power to alien preferences" and "deny rights to AIs on no reasonable basis". Differentially accelerate AI being used to improve our ability to find the truth, compared to being used for propaganda and manipulation. E.g.: Start an organization that uses LLMs to produce epistemically rigorous investigations of many topics. If you're the first to do a great job of this, and if you're truth-seeking and even-handed, then you might become a trusted source on controversial topics. And your investigations would just get better as AI got better. E.g.: Evaluate and write-up facts about current LLM's forecasting ability, to incentivize labs to make LLMs state correct and calibrated beliefs about the world. E.g.: Improve AI ability to help with thorny philosophical problems. Implications for community building? …with a focus on "the extent to which community-building resources should go towards AI safety vs. broader capacity building". Ethics, philosophy, and prioritization matter more for research on these topics than it does for alignment research. For some issues in AI alignment, there's a lot of convergence on what's important regardless of your ethical perspective, which means that ethics & philosophy aren't that important for getting people to contribute. By contrast, when thinking about "everything but alignment", I think we should expect somewhat more divergence, which could raise the importance of those subjects. For example: How much to care about digital minds? How much to focus on "deliberation could get off track forever" (which is of great longtermist importance) vs. short-term events (e.g. the speed at which AI gets deployed to solve all of the world's current problems.) But to be clear, I wouldn't want to go hard on any one ethical framework here (e.g. just utilitarianism). Some diversity and pluralism seems ...

BUFFALO, NY- September 25, 2023 – A new research paper was published in Oncotarget's Volume 14 on September 22, 2023, entitled, “Transcriptomic analysis identifies four novel receptors potentially linking endometrial cancer with polycystic ovary syndrome and generates a transcriptomic atlas.” Polycystic Ovary Syndrome (PCOS) is associated with a 3 to 4-fold increased risk of endometrial cancer (EC), but molecular mechanisms are unclear. Upregulation of the IGF1 gene in PCOS endometrium may increase EC risk, but this is uncertain. In this new study, researchers Fatma Alqutami, Mahmood Hachim, Charlie Hodgman, and William Atiomo from the Mohammed Bin Rashid University of Medicine and Health Sciences and the University of Nottingham aimed to investigate links between EC and PCOS, by analyzing publicly available transcriptomic data. “The original aim of this study was to investigate the links between EC and PCOS, by analysing publicly available transcriptomic data and investigate IGF-1 and IGFBP gene expression in the endometrium of women with PCOS and EC compared with normal endometrium.” The NCBI Gene Expression Omnibus was used to identify relevant studies. Differentially expressed genes (DEGs) were identified and analyzed using Metascape to identify pathways of interest. PCOS DEGs that encode proteins secreted into blood were identified using the Human Protein Atlas blood protein database. EC DEGs that are cellular receptors were identified using EcoTyper. These were intersected to identify which EC receptors interact with PCOS secreted proteins. Seven receptors were identified in EC but only PTPRF, ITGA2, ITGA3, and ITGB4 genes were expressed on epithelial cells. Pathway enrichment of these genes showed that the major and common pathway involved was that of the PI3K-AKT signaling pathway which was consistent with a link between PCOS and EC. However, IGF1 was down regulated in PCOS and EC. “Our conclusions at this stage do not support a link between IGF-1 and IGFBP genes in PCOS and EC. However, we have identified four novel receptors which may underpin the risk of EC in PCOS, and we believe our findings provide sufficient evidence to form the basis for a transcriptomic atlas to underpin future research into the links between PCOS and EC and the molecular mechanisms underpinning both diseases.” DOI - https://doi.org/10.18632/oncotarget.28513 Correspondence to - William Atiomo - william.atiomo@mbru.ac.ae Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28513 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, polycystic ovary syndrome, endometrial cancer, transcriptomics, IGF1, in-silico About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.25.550567v1?rss=1 Authors: Chen, J. A., Tsai, Y.-H., Linden, A. K., Kessler, J. A., Peng, C.-Y. Abstract: WW domain-containing transcription regulator 1 (TAZ) and Yes-associated protein (YAP) are transcriptional co-activators traditionally studied together as a part of the Hippo pathway and best known for their roles in stem cell proliferation and differentiation. Despite their similarities, TAZ and YAP can exert divergent cellular effects by differentially interacting with other signaling pathways that regulate stem cell maintenance or differentiation. In the developing central nervous system, In this study, we show that TAZ regulates astrocytic differentiation and maturation of postnatal neural stem and progenitor cells (NPCs), and that TAZ mediates some but not all of the effects of bone morphogenetic protein (BMP) signaling on astrocytic development. By contrast, TAZ and YAP both mediate effects on NPC fate of {beta}1-integrin and integrin-linked kinase (ILK) signaling, and these effects are dependent on extracellular matrix (ECM) cues. These findings demonstrate that TAZ and YAP perform divergent functions in the regulation of astrocyte differentiation, where YAP regulates cell cycle states of astrocytic progenitors and TAZ regulates differentiation and maturation from astrocytic progenitors into astrocytes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.24.550111v1?rss=1 Authors: Sharples, S. A., Broadhead, M. J., Gray, J. A., Miles, G. B. Abstract: The size principle is a key mechanism governing the orderly recruitment of motor units and is believed to be dependent on passive properties of the constituent motoneurons. However, motoneurons are endowed with voltage-sensitive ion channels that create non-linearities in their input-output functions. Here we describe a role for the M-type potassium current, conducted by KCNQ channels, in the control of motoneuron recruitment in mice. Motoneurons were studied with whole-cell patch clamp electrophysiology in transverse spinal slices and identified based on delayed (fast) and immediate (slow) onsets of repetitive firing. M-currents were larger in delayed compared to immediate firing motoneurons, which was not reflected by variations in the expression of Kv7.2 or Kv7.3 subunits. Instead, a more depolarized spike threshold in delayed-firing motoneurons afforded a greater proportion of the total M-current to become activated within the subthreshold voltage range, which translated to a greater influence on their recruitment with little influence on their firing rates. Pharmacological activation of M-currents also influenced motoneuron recruitment at the population level, producing a rightward shift in the recruitment curve of monosynaptic reflexes within isolated mouse spinal cords. These results demonstrate a prominent role for M-type potassium currents in regulating the function of motor units, which occurs primarily through the differential control of motoneuron subtype recruitment. More generally, these findings highlight the importance of active properties mediated by voltage-sensitive ion channels in the differential control of motoneuron recruitment, which is a key mechanism for the gradation of muscle force. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.21.550014v1?rss=1 Authors: Boi, L., Johansson, Y., Tonini, R., Moratalla, R., Fisone, G., Silberberg, G. Abstract: Parkinson's disease (PD) is characterized by motor impairments caused by degeneration of dopamine neurons in the substantia nigra pars compacta. In addition to these symptoms, PD patients often suffer from non-motor co-morbidities including sleep and psychiatric disturbances, which are thought to depend on concomitant alterations of serotonergic and noradrenergic transmission. A primary locus of serotonergic neurons is the dorsal raphe nucleus (DRN), providing brain-wide serotonergic input. Here, we identified electrophysiological and morphological parameters to classify serotonergic and dopaminergic neurons in the murine DRN under control conditions and following striatal injection of the catecholamine toxin, 6-hydroxydopamine (6-OHDA). Electrical and morphological properties of both neuronal populations were altered by 6-OHDA. In serotonergic neurons, most changes were reversed when 6-OHDA was injected in combination with desipramine, a noradrenaline reuptake inhibitor, protecting the noradrenergic terminals. Our results show that the depletion of both noradrenaline and dopamine in the 6-OHDA mouse model causes changes in the DRN neural circuitry. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.15.549177v1?rss=1 Authors: M, S., Paul, P., Ramakrishna, S., Ghose, V., Dey, G., Muddashetty, R., Jain, S., Purushottam, M., Viswanath, B., Sud, R. Abstract: ApoE4 isoform contributes to increased risk for Alzheimers Disease (AD) over the life course of individuals. Much remains unknown about the biological pathways that connect APOE4 genotype with the development of pathology that eventually leads to AD, nor do we know how early in life these cellular alterations begin. To answer these questions, we derived neural precursor cells (NPCs) from induced pluripotent stem cells (IPSCs) that were CRISPR-edited at the APOE locus. We intended to characterize the protein expression landscape in the NPCs subsequent to targeted deletion of E4 from a parent IPSC line of APOE3/4 genotype. Differentially expressed proteins (DEPs) following mass spectrometric analysis were determined from the protein abundance fold change values obtained for each protein. Proteins which showed greater than 1.5-fold difference with FDR adjusted P-value less than 0.05 were considered differentially expressed. DEPs were mapped to the STRING database (v11.5) for retrieval of interacting proteins and functional enrichment. CRISPR-editing of E4 from the parent line revealed 98 differential expressed proteins. Of these, 54 were upregulated, and 44 were downregulated. Further analysis of the DEPs via STRING database showed that these changes primarily affect pathways linked to RNA processing, plasma membrane repair, and cytoskeleton organization. Indeed, we find the effects of E4 extend beyond proteins considered central to AD pathology. Knowing more about the protein interactions regulated by ApoE, in an isoform-specific manner, can reveal new mechanistic insights into development of AD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Go online to PeerView.com/GYW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease and has a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. The FDA has recently approved a noninvasive, first-in-class cardiac myosin inhibitor specifically indicated for the treatment of HCM—meaning timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment. In this activity, based on a recent live symposium, expert panelists present practical skills and guidance to accurately diagnose HCM and apply recent treatment advances to patients with various clinical presentations of HCM. They begin by sharing the rationale for maintaining a high index of suspicion for HCM and review diagnostic strategies. The Clinical Consults portion of this activity features case examples to demonstrate current practices in diagnosis and offer practical guidance for treating patients—focusing on personalized care with new and emerging therapeutic options. Concluding with an engaging Q&A, this activity is for anyone involved in the care of patients with HCM interested in loosening the grip of this increasingly treatable disease. Upon completion of this activity, participants should be better able to: Suspect the presence of HCM based on clinical symptoms, pathologic features, and/or family history; Differentially diagnose patients suspected of having HCM consistent with current guidance to promote early diagnosis and timely treatment; and Individualize treatment for patients with HCM based on the efficacy, safety, and potential ability of the therapeutic strategy to address the underlying disease pathophysiology.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: RLHF does not appear to differentially cause mode-collapse, published by Arthur Conmy on March 20, 2023 on LessWrong. Epistemic status: confident but not certain. This post is part of the work done at Conjecture. TL;DR: the results in Mysteries of mode collapse do not reproduce in text-davinci-003, a model trained with RLHF. In fact, there are cases where RLHF models exhibit higher entropy outputs than base models. We observe that the mode collapse phenomenon occurs more for the public OpenAI GPT-3 model trained with supervised finetuning (text-davinci-002) than RLHF, and present early experiments and theory to support this. Background Mysteries of mode collapse details how "mode collapse" (which we operationalize as a large increase in model output confidence and decreases in entropy of output distribution) arises more in text-davinci-002 than the base model davinci, and speculates about how this connects to RLHF training. At the time, OpenAI was very unclear on the training process for this model, and later (as @janus points out in the edited introduction to the post) it was revealed that this model was finetuned on highly-rated samples rather than trained with RLHF. However, the connection between RLHF and mode collapse has stuck, and several posts written since assume a connection. Results In this section, we compare the base model (davinci code-davinci-002, thanks commenters!) with the supervised fine-tuned model (text-davinci-002) and the RLHF model (text-davinci-003). We recommend trying some prompts for yourself in the OpenAI playground. The first result is that the mode collapse to “ 97” for the completion of the first prompt from @janus' does not occur in the RLHF model: In fact, when we try another prompt we get that the base model has the lowest entropy: (ETA: this result is somewhat weaker than hoped, since text-davinci-002 seems to not output " 0" - " 100" here. davinci does exhibit collapses on other prompts, but commenters pointed out this is not the base model) The finding that mode collapse occurs in finetuned models is not robust. Comparing two of the prompts from the original post and two more, there is no noticeable pattern where the base model has higher entropy than the other models: (the uncertainty bars represent the maximum possible entropy if the model had uniform probability on all tokens other than “ 0”, . , “ 100” - the OpenAI API doesn't provide probabilities for all tokens) Reproducing the qualitative examples What about the other examples from the mode-collapse post? We found that the Blake Lemoine result was reproduced by davinci. On the Blake Lemoine greentext prompt with temperature 0.3, davinci gave completions where anon leaves after at most 5 lines. Most other results quickly led into repetitions of 3-4 sentences, something that occurred more frequently with the base language model. Overall, extrapolation from just the responses of one language model risks overstating conclusions, in this case about how unlikely the completion "leaving" was. Interpretation It appears as if the finetuning used for text-davinci-002 does cause mode collapses on the first two prompts. Arguably this is not surprising; RLHF training has a KL penalty to the base model's outputs, which constrains the entropy of the RLHF model's outputs to be close to that of the base model. Directly finetuning on new samples does not have this property since KL penalties to the base model are generally not so ubiquitous in standard finetuning (though lack of training details limits the conclusions that can be made here). Inferences about the phenomenon of mode collapse must be compatible with the evidence from both text-davinci-002 and text-davinci-003. For example, the author speculates that FeedME's reliance on samples from RLHF models may be responsible for text-davi...

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/FSW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Explore new horizons in complement-targeted treatments with two leading experts who share fresh insights into the underlying pathophysiology of complement-associated kidney diseases and provide evidence-based guidance on their diagnosis and treatment. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of complement-associated kidney diseases, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets; Differentially diagnose patients with complement-associated kidney diseases in a timely manner using evidence-based tools and strategies; and Describe current and emerging treatments for complement-associated kidney diseases, including data from recent clinical trials.

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/ACR860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert discusses how to utilize the American Gastroenterological Association's Clinical Care Pathway for the risk stratification and management of patients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Upon completion of this activity, participants should be better able to: List the disease pathways and mechanisms that define NASH as a metabolic disease; Identify the pathophysiology and role of GLP-1 as a therapeutic target in NASH; Differentially diagnose NASH in a timely manner; Integrate current and emerging agents into early management plans for patients with NASH based on the AGA NASH Clinical Care Pathway

Go online to PeerView.com/KHN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert on hypertrophic cardiomyopathy (HCM) discusses guideline-recommended diagnostic approaches and therapeutic strategies to improve symptoms and preserve quality of life. Upon completion of this activity, participants should be better able to: Recognize the clinical characteristics and pathologic features suggestive of HCM; Differentially diagnose patients suspected of having HCM consistent with current guidance and evidence to promote early diagnosis and timely treatment; Assess the efficacy, safety, and ability of available therapeutic strategies to address the underlying pathophysiology and desired treatment goals; and Individualize treatment regimens for HCM consistent with patient preferences and goals of care.

Go online to PeerView.com/KHN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert on hypertrophic cardiomyopathy (HCM) discusses guideline-recommended diagnostic approaches and therapeutic strategies to improve symptoms and preserve quality of life. Upon completion of this activity, participants should be better able to: Recognize the clinical characteristics and pathologic features suggestive of HCM; Differentially diagnose patients suspected of having HCM consistent with current guidance and evidence to promote early diagnosis and timely treatment; Assess the efficacy, safety, and ability of available therapeutic strategies to address the underlying pathophysiology and desired treatment goals; and Individualize treatment regimens for HCM consistent with patient preferences and goals of care.

Go online to PeerView.com/KHN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert on hypertrophic cardiomyopathy (HCM) discusses guideline-recommended diagnostic approaches and therapeutic strategies to improve symptoms and preserve quality of life. Upon completion of this activity, participants should be better able to: Recognize the clinical characteristics and pathologic features suggestive of HCM; Differentially diagnose patients suspected of having HCM consistent with current guidance and evidence to promote early diagnosis and timely treatment; Assess the efficacy, safety, and ability of available therapeutic strategies to address the underlying pathophysiology and desired treatment goals; and Individualize treatment regimens for HCM consistent with patient preferences and goals of care.

Go online to PeerView.com/KHN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert on hypertrophic cardiomyopathy (HCM) discusses guideline-recommended diagnostic approaches and therapeutic strategies to improve symptoms and preserve quality of life. Upon completion of this activity, participants should be better able to: Recognize the clinical characteristics and pathologic features suggestive of HCM; Differentially diagnose patients suspected of having HCM consistent with current guidance and evidence to promote early diagnosis and timely treatment; Assess the efficacy, safety, and ability of available therapeutic strategies to address the underlying pathophysiology and desired treatment goals; and Individualize treatment regimens for HCM consistent with patient preferences and goals of care.

Go online to PeerView.com/KHN860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert on hypertrophic cardiomyopathy (HCM) discusses guideline-recommended diagnostic approaches and therapeutic strategies to improve symptoms and preserve quality of life. Upon completion of this activity, participants should be better able to: Recognize the clinical characteristics and pathologic features suggestive of HCM; Differentially diagnose patients suspected of having HCM consistent with current guidance and evidence to promote early diagnosis and timely treatment; Assess the efficacy, safety, and ability of available therapeutic strategies to address the underlying pathophysiology and desired treatment goals; and Individualize treatment regimens for HCM consistent with patient preferences and goals of care.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/WKU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is estimated to affect as many as 15 to 20 million people worldwide. However, it remains frequently undetected, because its symptoms are often nonspecific or mistaken for more common conditions. In this discussion-based activity, leading experts on HCM get to the heart of the matter, diagnosis and treatment, as they review guideline recommendations on imaging for diagnosis and examine current and novel treatment options, including small-molecule myosin inhibitors, as a means to improve patient outcomes and quality of life. Upon completion of this activity, participants should be better able to: Differentially diagnose patients suspected of having HCM consistent with current guidance using appropriate cardiac imaging techniques; Apply the latest recommendations and current guidance for diagnosing, evaluating, and managing patients with HCM in a collaborative care model; and Incorporate emerging therapies for managing patients with HCM based on their efficacy, safety, and ability to address the unmet needs of patients and the pathophysiology of HCM.

Go online to PeerView.com/JCU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in complement 3 glomerulopathy (C3G) discusses evidence-based approaches to differentially diagnose patients with C3G and reviews the evidence for current and emerging treatment strategies. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of C3G, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets, Differentially diagnose patients with C3G using evidence-based tools and strategies, Identify the mechanisms of action for agents targeted at specific complement inhibitors (eg, Factors B, C5a, C3, etc), Incorporate the latest findings for approved and emerging pharmacotherapies to optimize the management of patients with C3G.

Go online to PeerView.com/JCU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in complement 3 glomerulopathy (C3G) discusses evidence-based approaches to differentially diagnose patients with C3G and reviews the evidence for current and emerging treatment strategies. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of C3G, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets, Differentially diagnose patients with C3G using evidence-based tools and strategies, Identify the mechanisms of action for agents targeted at specific complement inhibitors (eg, Factors B, C5a, C3, etc), Incorporate the latest findings for approved and emerging pharmacotherapies to optimize the management of patients with C3G.

Go online to PeerView.com/JCU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in complement 3 glomerulopathy (C3G) discusses evidence-based approaches to differentially diagnose patients with C3G and reviews the evidence for current and emerging treatment strategies. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of C3G, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets, Differentially diagnose patients with C3G using evidence-based tools and strategies, Identify the mechanisms of action for agents targeted at specific complement inhibitors (eg, Factors B, C5a, C3, etc), Incorporate the latest findings for approved and emerging pharmacotherapies to optimize the management of patients with C3G.

Go online to PeerView.com/JCU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in complement 3 glomerulopathy (C3G) discusses evidence-based approaches to differentially diagnose patients with C3G and reviews the evidence for current and emerging treatment strategies. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of C3G, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets, Differentially diagnose patients with C3G using evidence-based tools and strategies, Identify the mechanisms of action for agents targeted at specific complement inhibitors (eg, Factors B, C5a, C3, etc), Incorporate the latest findings for approved and emerging pharmacotherapies to optimize the management of patients with C3G.

Go online to PeerView.com/JCU860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in complement 3 glomerulopathy (C3G) discusses evidence-based approaches to differentially diagnose patients with C3G and reviews the evidence for current and emerging treatment strategies. Upon completion of this activity, participants should be better able to: Explain the pathophysiology of C3G, highlighting the rationale for using complement proteins and proteinuria as therapeutic targets, Differentially diagnose patients with C3G using evidence-based tools and strategies, Identify the mechanisms of action for agents targeted at specific complement inhibitors (eg, Factors B, C5a, C3, etc), Incorporate the latest findings for approved and emerging pharmacotherapies to optimize the management of patients with C3G.

References Dr. Guerra's lipid lecture notes Cancer Res. 2018 Apr 1; 78(7): 1713–1725. Progress in Lipid Research Volume 74, April 2019, Pages 145-159 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support