phd em stanford

Linda N. Geng, MD, PhD

• Clinical Associate Professor, Medicine - Primary Care and Population Health
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Clinical Focus

• Diagnostic Medicine
• Undiagnosed Diseases and Medical Mysteries
• Rare Disorders
• Post-Acute COVID-19 Syndrome (long COVID)
• Internal Medicine

Academic Appointments

Administrative appointments.

• Co-Director, Stanford Post-Acute COVID-19 Syndrome Clinic (2021 - Present)
• Director, Stanford Consultative Medicine Clinic (2019 - Present)
• Chief Resident, Stanford Internal Medicine Residency Program (2018 - 2019)

Honors & Awards

• Julian Wolfsohn Award (for clinical excellence, leadership, teaching, kindness), Stanford Internal Medicine Residency (2016)
• Harold M. Weintraub Graduate Student Award (National), Fred Hutchinson Cancer Research Center (2012)
• Alpha Omega Alpha (Medical Honor Society), Stanford University chapter (2019)
• Phi Beta Kappa (Honor Society), Rice University chapter (2006)

Professional Education

• Board Certification: American Board of Internal Medicine, Internal Medicine (2019)
• Visiting scholar, NIH, Undiagnosed Diseases Program (2019)
• Chief Resident, Stanford University Internal Medicine Residency (2019)
• Residency: Stanford University Internal Medicine Residency (2018) CA
• Medical Education: University of Washington School of Medicine (2015) WA
• Ph.D., University of Washington, Molecular and Cellular Biology (2011)
• Academic University - Academic staff Department: Med/Primary Care and Population Health Position: Clinical Associate Professor
• (650) 498-9000 (office)

Additional Clinical Info

• Stanford Health Care

Additional Info

• Stanford Post-Acute COVID-19 Syndrome (PACS) Clinic

Current Research and Scholarly Interests

My scholarly interests are focused on defining, studying, and improving patients' diagnostic journeys. What prolongs the journey to the correct diagnosis and how can we shorten it? With this question in mind, we are exploring crowdsourcing, informatics/AI, health data visualization, and advanced laboratory testing as ways to help tackle the toughest cases in medicine-- complex, rare, and mystery conditions. With the COVID pandemic, the puzzling and complex illness of post-acute COVID-19 syndrome (PACS) or long COVID came to light. Together with a multidisciplinary group of physicians and researchers, we launched a program here at Stanford to advance the care and understanding of PACS. Our goal is to better understand the natural history, clinical symptomatology, immunological response, risk factors, and subgroup stratification for PACS. We are also actively assessing management strategies that may be effective for heterogeneous PACS symptoms.

Clinical Trials

The purpose of this study is to compare whether being treated with Paxlovid (nirmatrelvir plus ritonavir) for 15 days works better than being treated with placebo (plus ritonavir) to reduce severe symptoms of Long Covid (the placebo does not have any active drug). Participants will have 5 planned visits to the study clinic over 15 weeks and will take the drug (or placebo) for the first 15 days. This study uses the term post-acute sequelae of SARS-CoV-2 (PASC), which is another name for "Long Covid."

Stanford is currently not accepting patients for this trial. For more information, please contact Study Team, 650-308-6788.

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2023-24 Courses

• Undergraduate Research MED 199 (Aut, Win, Spr)

2021-22 Courses

• Diagnostic Medicine on Television: Truths vs. Theatrics MED 291 (Win)

2020-21 Courses

All publications.

There is an urgent need to identify treatments for postacute sequelae of SARS-CoV-2 infection (PASC).To assess the efficacy of a 15-day course of nirmatrelvir-ritonavir in reducing the severity of select PASC symptoms.This was a 15-week blinded, placebo-controlled, randomized clinical trial conducted from November 2022 to September 2023 at Stanford University (California). The participants were adults with moderate to severe PASC symptoms of 3 months or longer duration.Participants were randomized 2:1 to treatment with oral nirmatrelvir-ritonavir (NMV/r, 300 mg and 100 mg) or with placebo-ritonavir (PBO/r) twice daily for 15 days.Primary outcome was a pooled severity of 6 PASC symptoms (fatigue, brain fog, shortness of breath, body aches, gastrointestinal symptoms, and cardiovascular symptoms) based on a Likert scale score at 10 weeks. Secondary outcomes included symptom severity at different time points, symptom burden and relief, patient global measures, Patient-Reported Outcomes Measurement Information System (PROMIS) measures, orthostatic vital signs, and sit-to-stand test change from baseline.Of the 155 participants (median [IQR] age, 43 [34-54] years; 92 [59%] females), 102 were randomized to the NMV/r group and 53 to the PBO/r group. Nearly all participants (n = 153) had received the primary series for COVID-19 vaccination. Mean (SD) time between index SARS-CoV-2 infection and randomization was 17.5 (9.1) months. There was no statistically significant difference in the model-derived severity outcome pooled across the 6 core symptoms at 10 weeks between the NMV/r and PBO/r groups. No statistically significant between-group differences were found at 10 weeks in the Patient Global Impression of Severity or Patient Global Impression of Change scores, summative symptom scores, and change from baseline to 10 weeks in PROMIS fatigue, dyspnea, cognitive function, and physical function measures. Adverse event rates were similar in NMV/r and PBO/r groups and mostly of low grade.The results of this randomized clinical trial showed that a 15-day course of NMV/r in a population of patients with PASC was generally safe but did not demonstrate a significant benefit for improving select PASC symptoms in a mostly vaccinated cohort with protracted symptom duration. Further studies are needed to determine the role of antivirals in the treatment of PASC.ClinicalTrials.gov Identifier: NCT05576662.

View details for DOI 10.1001/jamainternmed.2024.2007

View details for PubMedID 38848477

View details for DOI 10.1007/s10389-024-02284-1

View details for Web of Science ID 001238134000001

The glycosylation of IgG plays a critical role during human severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, activating immune cells and inducing cytokine production. However, the role of IgM N-glycosylation has not been studied during human acute viral infection. The analysis of IgM N-glycosylation from healthy controls and hospitalized coronavirus disease 2019 (COVID-19) patients reveals increased high-mannose and sialylation that correlates with COVID-19 severity. These trends are confirmed within SARS-CoV-2-specific immunoglobulin N-glycan profiles. Moreover, the degree of total IgM mannosylation and sialylation correlate significantly with markers of disease severity. We link the changes of IgM N-glycosylation with the expression of Golgi glycosyltransferases. Lastly, we observe antigen-specific IgM antibody-dependent complement deposition is elevated in severe COVID-19 patients and modulated by exoglycosidase digestion. Taken together, this work links the IgM N-glycosylation with COVID-19 severity and highlights the need to understand IgM glycosylation and downstream immune function during human disease.

View details for DOI 10.1038/s41467-023-44211-0

View details for PubMedID 38195739

Post-acute sequelae of SARS-CoV-2 (PASC) is a significant public health concern. We describe Patient Reported Outcomes (PROs) on 590 participants prospectively assessed from hospital admission for COVID-19 through one year after discharge. Modeling identified 4 PRO clusters based on reported deficits (minimal, physical, mental/cognitive, and multidomain), supporting heterogenous clinical presentations in PASC, with sub-phenotypes associated with female sex and distinctive comorbidities. During the acute phase of disease, a higher respiratory SARS-CoV-2 viral burden and lower Receptor Binding Domain and Spike antibody titers were associated with both the physical predominant and the multidomain deficit clusters. A lower frequency of circulating B lymphocytes by mass cytometry (CyTOF) was observed in the multidomain deficit cluster. Circulating fibroblast growth factor 21 (FGF21) was significantly elevated in the mental/cognitive predominant and the multidomain clusters. Future efforts to link PASC to acute anti-viral host responses may help to better target treatment and prevention of PASC.

View details for DOI 10.1038/s41467-023-44090-5

View details for PubMedID 38172101

View details for PubMedCentralID PMC10764789

Post-acute sequelae of SARS-CoV-2 (PASC), or long COVID, is characterized by persistent symptoms after acute SARS-CoV-2 infection that can vary from patient to patient. Here, we present a case series of four patients with a history of SARS-CoV-2 infection referred to the Post-Acute COVID-19 Syndrome (PACS) Clinic at Stanford University for evaluation of persistent symptoms, who also experienced new-onset alcohol sensitivity. Alcohol reactions and sensitivity are not well characterized in the literature as it relates to post-viral illness. While there have been some anecdotal reports of new alcohol sensitivity in PASC patients in the media, there is a paucity of published data in the medical literature about this topic. During their medical consultation, the patients self-reported new changes in their symptoms or behaviors following the use of alcohol. A new onset of alcohol sensitivities should be assessed along with other post-COVID-19 symptoms and may provide novel avenues to explore the pathobiology of illness and potential interventions.

View details for DOI 10.7759/cureus.51286

View details for PubMedID 38288178

View details for PubMedCentralID PMC10823305

The global prevalence of Post-Acute Sequelae of SARS-CoV-2 Infection (PASC) stands at approximately 43 % among individuals who have previously had acute COVID-19. In contrast, in the United States, the National Center for Health Statistics (NCHS) estimates that around 11 % of individuals who have been infected with SARS-CoV-2 go on to experience long COVID. The underlying causes of PASC remains under investigation, and there are no currently established FDA-approved therapies. One of the leading hypotheses for the cause of PASC is the persistent activation of innate immune cells with increase systemic inflammation. Naltrexone is a medication with anti-inflammatory and immunomodulatory properties that has been used in other conditions that overlap with PASC. We performed a retrospective review of a clinical cohort of 59 patients at a single academic center who received low-dose naltrexone (LDN) off-label as a potential therapeutic intervention for PASC. The use of LDN was associated with a fewer number of symptoms, improved clinical symptoms (fatigue, post-exertional malaise, unrefreshing sleep, and abnormal sleep pattern), and a better functional status. This observation warrants testing in rigorous, randomized, placebo-controlled clinical trials.

View details for DOI 10.1016/j.intimp.2023.110966

View details for PubMedID 37804660

Millions of people are suffering from Long COVID or post-acute sequelae of COVID-19 (PASC). Several biological factors have emerged as potential drivers of PASC pathology. Some individuals with PASC may not fully clear the coronavirus SARS-CoV-2 after acute infection. Instead, replicating virus and/or viral RNA-potentially capable of being translated to produce viral proteins-persist in tissue as a 'reservoir'. This reservoir could modulate host immune responses or release viral proteins into the circulation. Here we review studies that have identified SARS-CoV-2 RNA/protein or immune responses indicative of a SARS-CoV-2 reservoir in PASC samples. Mechanisms by which a SARS-CoV-2 reservoir may contribute to PASC pathology, including coagulation, microbiome and neuroimmune abnormalities, are delineated. We identify research priorities to guide the further study of a SARS-CoV-2 reservoir in PASC, with the goal that clinical trials of antivirals or other therapeutics with potential to clear a SARS-CoV-2 reservoir are accelerated.

View details for DOI 10.1038/s41590-023-01601-2

View details for PubMedID 37667052

View details for PubMedCentralID 8755397

The global prevalence of PASC is estimated to be present in 0·43 and based on the WHO estimation of 470 million worldwide COVID-19 infections, corresponds to around 200 million people experiencing long COVID symptoms. Despite this, its clinical features are not well-defined.We collected retrospective data from 140 patients with PASC in a post-COVID-19 clinic on demographics, risk factors, illness severity (graded as one-mild to five-severe), functional status, and 29 symptoms and principal component symptoms cluster analysis. The Institute of Medicine (IOM) 2015 criteria were used to determine the Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) phenotype.The median age was 47 years, 59.0% were female; 49.3% White, 17.2% Hispanic, 14.9% Asian, and 6.7% Black. Only 12.7% required hospitalization. Seventy-two (53.5%) patients had no known comorbid conditions. Forty-five (33.9%) were significantly debilitated. The median duration of symptoms was 285.5 days, and the number of symptoms was 12. The most common symptoms were fatigue (86.5%), post-exertional malaise (82.8%), brain fog (81.2%), unrefreshing sleep (76.7%), and lethargy (74.6%). Forty-three percent fit the criteria for ME/CFS, majority were female, and obesity (BMI > 30 Kg/m2) (P = 0.00377895) and worse functional status (P = 0.0110474) were significantly associated with ME/CFS.Most PASC patients evaluated at our clinic had no comorbid condition and were not hospitalized for acute COVID-19. One-third of patients experienced a severe decline in their functional status. About 43% had the ME/CFS subtype.

View details for DOI 10.3389/fneur.2023.1090747

View details for PubMedID 36908615

View details for PubMedCentralID PMC9998690

Importance: SARS-CoV-2 infection is associated with persistent, relapsing, or new symptoms or other health effects occurring after acute infection, termed postacute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID. Characterizing PASC requires analysis of prospectively and uniformly collected data from diverse uninfected and infected individuals.Objective: To develop a definition of PASC using self-reported symptoms and describe PASC frequencies across cohorts, vaccination status, and number of infections.Design, Setting, and Participants: Prospective observational cohort study of adults with and without SARS-CoV-2 infection at 85 enrolling sites (hospitals, health centers, community organizations) located in 33 states plus Washington, DC, and Puerto Rico. Participants who were enrolled in the RECOVER adult cohort before April 10, 2023, completed a symptom survey 6 months or more after acute symptom onset or test date. Selection included population-based, volunteer, and convenience sampling.Exposure: SARS-CoV-2 infection.Main Outcomes and Measures: PASC and 44 participant-reported symptoms (with severity thresholds).Results: A total of 9764 participants (89% SARS-CoV-2 infected; 71% female; 16% Hispanic/Latino; 15% non-Hispanic Black; median age, 47 years [IQR, 35-60]) met selection criteria. Adjusted odds ratios were 1.5 or greater (infected vs uninfected participants) for 37 symptoms. Symptoms contributing to PASC score included postexertional malaise, fatigue, brain fog, dizziness, gastrointestinal symptoms, palpitations, changes in sexual desire or capacity, loss of or change in smell or taste, thirst, chronic cough, chest pain, and abnormal movements. Among 2231 participants first infected on or after December 1, 2021, and enrolled within 30 days of infection, 224 (10% [95% CI, 8.8%-11%]) were PASC positive at 6 months.Conclusions and Relevance: A definition of PASC was developed based on symptoms in a prospective cohort study. As a first step to providing a framework for other investigations, iterative refinement that further incorporates other clinical features is needed to support actionable definitions of PASC.

View details for DOI 10.1001/jama.2023.8823

View details for PubMedID 37278994

View details for DOI 10.14218/ERHM.2022.00045

BACKGROUNDProlonged symptoms after SARS-CoV-2 infection are well documented. However, which factors influence development of long-term symptoms, how symptoms vary across ethnic groups, and whether long-term symptoms correlate with biomarkers are points that remain elusive.METHODSAdult SARS-CoV-2 reverse transcription PCR-positive (RT-PCR-positive) patients were recruited at Stanford from March 2020 to February 2021. Study participants were seen for in-person visits at diagnosis and every 1-3 months for up to 1 year after diagnosis; they completed symptom surveys and underwent blood draws and nasal swab collections at each visit.RESULTSOur cohort (n = 617) ranged from asymptomatic to critical COVID-19 infections. In total, 40% of participants reported at least 1 symptom associated with COVID-19 six months after diagnosis. Median time from diagnosis to first resolution of all symptoms was 44 days; median time from diagnosis to sustained symptom resolution with no recurring symptoms for 1 month or longer was 214 days. Anti-nucleocapsid IgG level in the first week after positive RT-PCR test and history of lung disease were associated with time to sustained symptom resolution. COVID-19 disease severity, ethnicity, age, sex, and remdesivir use did not affect time to sustained symptom resolution.CONCLUSIONWe found that all disease severities had a similar risk of developing post-COVID-19 syndrome in an ethnically diverse population. Comorbid lung disease and lower levels of initial IgG response to SARS-CoV-2 nucleocapsid antigen were associated with longer symptom duration.TRIAL REGISTRATIONClinicalTrials.gov, NCT04373148.FUNDINGNIH UL1TR003142 CTSA grant, NIH U54CA260517 grant, NIEHS R21 ES03304901, Sean N Parker Center for Allergy and Asthma Research at Stanford University, Chan Zuckerberg Biohub, Chan Zuckerberg Initiative, Sunshine Foundation, Crown Foundation, and Parker Foundation.

View details for DOI 10.1172/jci.insight.156713

View details for PubMedID 35801588

Diagnostic programs and second opinion clinics have grown and evolved in the recent years to help patients with rare, puzzling, and complex conditions who often suffer prolonged diagnostic journeys, but there is a paucity of literature on the clinical characteristics of these patients and the efficacy of these diagnostic programs. This study aims to characterize the diagnostic journey, case features, and diagnostic outcomes of patients referred to a team-based second opinion clinic at Stanford.Retrospective chart review was performed for 237 patients evaluated for diagnostic second opinion in the Stanford Consultative Medicine Clinic over a 5 year period. Descriptive case features and diagnostic outcomes were assessed, and correlation between the two was analyzed.Sixty-three percent of our patients were women. 49% of patients had a potential precipitating event within about a month prior to the start of their illness, such as medication change, infection, or medical procedure. A single clear diagnosis was determined in 33% of cases, whereas the remaining cases were assessed to have multifactorial contributors/diagnoses (20%) or remained unclear despite extensive evaluation (47%). Shorter duration of illness, fewer prior specialties seen, and single chief symptom were associated with higher likelihood of achieving a single clear diagnosis.A single-site academic consultative service can offer additional diagnostic insights for about half of all patients evaluated for puzzling conditions. Better understanding of the clinical patterns and patient experiences gained from this study helps inform strategies to shorten their diagnostic odysseys.

View details for DOI 10.1515/dx-2022-0029

View details for PubMedID 35596123

Background: In primary care clinics, time constraints and lack of exposure to highly complex cases may limit the breadth and depth of learning for internal medicine residents. To address these issues, we piloted a novel experience for residents to evaluate patients with puzzling symptoms referred by another clinician.Objective: To increase internal medicine residents' exposure to patients with perplexing presentations and foster a team-based approach to solving diagnostically challenging cases.Methods: During the academic year 2020-2021, residents participating in their 2-week primary care "block" rotation were given protected time to evaluate 1-2 patients from the Stanford Consultative Medicine clinic, an internist-led diagnostic second opinion service, and present their patients at the case conference. We assessed the educational value of the program with resident surveys including 5-point Lickert scale and open-ended questions.Results: 21 residents participated in the pilot with a survey response rate of 66.6% (14/21). Both the educational value and overall quality of the experience were rated as 4.8 out of 5 (SD 0.4, range 4-5; 1:"very poor"; 5:"excellent"). Residents learned about new diagnostic tools as well as how to approach complex presentations and diagnostic dilemmas. Residents valued the increased time devoted to patient care, the team-based approach to tackling difficult cases, and the intellectual challenge of these cases. Barriers to implementation include patient case volume, time, and faculty engagement.Conclusions: Evaluation of diagnostically challenging cases in a structured format is a highly valuable experience that offers a framework to enhance outpatient training in internal medicine.

View details for DOI 10.1177/23821205221091036

View details for PubMedID 35372696

Background: Autonomic dysfunction is a known complication of post-acute sequelae of SARS-CoV-2 (PASC)/long COVID, however prevalence and severity are unknown.Objective: To assess the frequency, severity, and risk factors of autonomic dysfunction in PASC, and to determine whether severity of acute SARS-CoV-2 infection is associated with severity of autonomic dysfunction.Design: Cross-sectional online survey of adults with PASC recruited through long COVID support groups between October 2020 and August 2021.Participants: 2,413 adults ages 18-64 years with PASC including patients who had a confirmed positive test for COVID-19 (test-confirmed) and participants who were diagnosed with COVID-19 based on clinical symptoms alone.Main measures: The main outcome measure was the Composite Autonomic Symptom 31 (COMPASS-31) total score, used to assess global autonomic dysfunction. Test-confirmed hospitalized vs. test-confirmed non-hospitalized participants were compared to determine if the severity of acute SARS-CoV-2 infection was associated with the severity autonomic dysfunction.Key results: Sixty-six percent of PASC patients had a COMPASS-31 score >20, suggestive of moderate to severe autonomic dysfunction. COMPASS-31 scores did not differ between test-confirmed hospitalized and test-confirmed non-hospitalized participants [28.95 (15.62, 46.60) vs. 26.4 (13.75, 42.10); p = 0.06].Conclusions: Evidence of moderate to severe autonomic dysfunction was seen in 66% of PASC patients in our study, independent of hospitalization status, suggesting that autonomic dysfunction is highly prevalent in the PASC population and independent of the severity of acute COVID-19 illness.

View details for DOI 10.3389/fneur.2022.1012668

View details for PubMedID 36353127

View details for DOI 10.1056/NEJMms2111017

View details for PubMedID 34936744

View details for DOI 10.23937/2643-4466/1710013

It is well recognised that medical training globally and at all levels lacks sufficient incorporation of genetics and genomics education to keep up with the rapid advances and growing application of genomics to clinical care. However, the best strategy to implement these desired changes into postgraduate medical training and engage learners is still unclear. We developed a novel elective rotation in 'Genomic Medicine and Undiagnosed Diseases' for categorical Internal Medicine Residents to address this educational gap and serve as an adaptable model for training that can be applied broadly across different specialties and at other institutions. Key curriculum goals achieved include increased understanding about genetic testing modalities and tools available for diagnosis and risk analysis, the role of genetics-trained allied health professionals, and indications and limitations of genetic and genomic testing in both rare and common conditions.

View details for DOI 10.1136/postgradmedj-2018-136355

View details for PubMedID 31439813

The protozoan parasite Toxoplasma gondii triggers severe small intestinal immunopathology characterized by IFN-γ- and intestinal microbiota-mediated inflammation, Paneth cell loss, and bacterial dysbiosis. Paneth cells are a prominent secretory epithelial cell type that resides at the base of intestinal crypts and releases antimicrobial peptides. We demonstrate that the microbiota triggers basal Paneth cell-specific autophagy via induction of IFN-γ, a known trigger of autophagy, to maintain intestinal homeostasis. Deletion of the autophagy protein Atg5 specifically in Paneth cells results in exaggerated intestinal inflammation characterized by complete destruction of the intestinal crypts resembling that seen in pan-epithelial Atg5-deficient mice. Additionally, lack of functional autophagy in Paneth cells within intestinal organoids and T. gondii-infected mice causes increased sensitivity to the proinflammatory cytokine TNF along with increased intestinal permeability, leading to exaggerated microbiota- and IFN-γ-dependent intestinal immunopathology. Thus, Atg5 expression in Paneth cells is essential for tissue protection against cytokine-mediated immunopathology during acute gastrointestinal infection.

View details for DOI 10.1016/j.chom.2018.01.001

View details for PubMedID 29358083

View details for PubMedCentralID PMC6179445

COMMD1 deficiency results in defective copper homeostasis, but the mechanism for this has remained elusive. Here we report that COMMD1 is directly linked to early endosomes through its interaction with a protein complex containing CCDC22, CCDC93, and C16orf62. This COMMD/CCDC22/CCDC93 (CCC) complex interacts with the multisubunit WASH complex, an evolutionarily conserved system, which is required for endosomal deposition of F-actin and cargo trafficking in conjunction with the retromer. Interactions between the WASH complex subunit FAM21, and the carboxyl-terminal ends of CCDC22 and CCDC93 are responsible for CCC complex recruitment to endosomes. We show that depletion of CCC complex components leads to lack of copper-dependent movement of the copper transporter ATP7A from endosomes, resulting in intracellular copper accumulation and modest alterations in copper homeostasis in humans with CCDC22 mutations. This work provides a mechanistic explanation for the role of COMMD1 in copper homeostasis and uncovers additional genes involved in the regulation of copper transporter recycling.

View details for DOI 10.1091/mbc.E14-06-1073

View details for PubMedID 25355947

View details for PubMedCentralID PMC4279232

A 40-year-old Chinese man was admitted for haemoptysis and progressive deep vein thrombosis involving the inferior vena cava (IVC) despite anticoagulation. An IVC filter had been placed earlier at an outside hospital. CT angiography revealed two pulmonary artery aneurysms. The patient was found to have a history of oral and genital ulcers, uveitis and erythema nodosum, thus meeting criteria for Behçet's disease. Other causes of the haemoptysis and thrombophilia were excluded. He underwent successful coil embolisation of the pulmonary artery aneurysms and responded well to immunosuppressive therapy with cyclophosphamide and steroids. Anticoagulation was cautiously continued to limit the long-term risk of secondary thrombosis from his IVC filter. The patient remains well 5 months after initiation of immunosuppressive therapy. Making a diagnosis of Behçet's disease in the setting of thrombosis is crucial, as treatment must include immunosuppression, and, thus, fundamentally differs from the management of most other thrombotic disorders.

View details for DOI 10.1136/bcr-2013-200893

View details for PubMedID 24214153

View details for PubMedCentralID PMC3830209

The human double-homeodomain retrogene DUX4 is expressed in the testis and epigenetically repressed in somatic tissues. Facioscapulohumeral muscular dystrophy (FSHD) is caused by mutations that decrease the epigenetic repression of DUX4 in somatic tissues and result in mis-expression of this transcription factor in skeletal muscle. DUX4 binds sites in the human genome that contain a double-homeobox sequence motif, including sites in unique regions of the genome as well as many sites in repetitive elements. Using ChIP-seq and RNA-seq on myoblasts transduced with DUX4 we show that DUX4 binds and activates transcription of mammalian apparent LTR-retrotransposons (MaLRs), endogenous retrovirus (ERVL and ERVK) elements, and pericentromeric satellite HSATII sequences. Some DUX4-activated MaLR and ERV elements create novel promoters for genes, long non-coding RNAs, and antisense transcripts. Many of these novel transcripts are expressed in FSHD muscle cells but not control cells, and thus might contribute to FSHD pathology. For example, HEY1, a repressor of myogenesis, is activated by DUX4 through a MaLR promoter. DUX4-bound motifs, including those in repetitive elements, show evolutionary conservation and some repeat-initiated transcripts are expressed in healthy testis, the normal expression site of DUX4, but more rarely in other somatic tissues. Testis expression patterns are known to have evolved rapidly in mammals, but the mechanisms behind this rapid change have not yet been identified: our results suggest that mobilization of MaLR and ERV elements during mammalian evolution altered germline gene expression patterns through transcriptional activation by DUX4. Our findings demonstrate a role for DUX4 and repetitive elements in mammalian germline evolution and in FSHD muscular dystrophy.

View details for DOI 10.1371/journal.pgen.1003947

View details for PubMedID 24278031

View details for PubMedCentralID PMC3836709

Generation of skeletal muscles with forms adapted to their function is essential for normal movement. Muscle shape is patterned by the coordinated polarity of collectively migrating myoblasts. Constitutive inactivation of the protocadherin gene Fat1 uncoupled individual myoblast polarity within chains, altering the shape of selective groups of muscles in the shoulder and face. These shape abnormalities were followed by early onset regionalised muscle defects in adult Fat1-deficient mice. Tissue-specific ablation of Fat1 driven by Pax3-cre reproduced muscle shape defects in limb but not face muscles, indicating a cell-autonomous contribution of Fat1 in migrating muscle precursors. Strikingly, the topography of muscle abnormalities caused by Fat1 loss-of-function resembles that of human patients with facioscapulohumeral dystrophy (FSHD). FAT1 lies near the critical locus involved in causing FSHD, and Fat1 mutant mice also show retinal vasculopathy, mimicking another symptom of FSHD, and showed abnormal inner ear patterning, predictive of deafness, reminiscent of another burden of FSHD. Muscle-specific reduction of FAT1 expression and promoter silencing was observed in foetal FSHD1 cases. CGH array-based studies identified deletion polymorphisms within a putative regulatory enhancer of FAT1, predictive of tissue-specific depletion of FAT1 expression, which preferentially segregate with FSHD. Our study identifies FAT1 as a critical determinant of muscle form, misregulation of which associates with FSHD.

View details for DOI 10.1371/journal.pgen.1003550

View details for PubMedID 23785297

View details for PubMedCentralID PMC3681729

In most cases facioscapulohumeral muscular dystrophy (FSHD) is caused by contraction of the D4Z4 repeat in the 4q subtelomere. This contraction is associated with local chromatin decondensation and derepression of the DUX4 retrogene. Its complex genetic and epigenetic cause and high clinical variability in disease severity complicate investigations on the pathogenic mechanism underlying FSHD. A validated cellular model bypassing the considerable heterogeneity would facilitate mechanistic and therapeutic studies of FSHD. Taking advantage of the high incidence of somatic mosaicism for D4Z4 repeat contraction in de novo FSHD, we have established a clonal myogenic cell model from a mosaic patient. Individual clones are genetically identical except for the size of the D4Z4 repeat array, being either normal or FSHD sized. These clones retain their myogenic characteristics, and D4Z4 contracted clones differ from the noncontracted clones by the bursts of expression of DUX4 in sporadic nuclei, showing that this burst-like phenomenon is a locus-intrinsic feature. Consequently, downstream effects of DUX4 expression can be observed in D4Z4 contracted clones, like differential expression of DUX4 target genes. We also show their participation to in vivo regeneration with immunodeficient mice, further expanding the potential of these clones for mechanistic and therapeutic studies. These cell lines will facilitate pairwise comparisons to identify FSHD-specific differences and are expected to create new opportunities for high-throughput drug screens.

View details for DOI 10.1016/j.ajpath.2012.07.007

View details for PubMedID 22871573

View details for PubMedCentralID PMC3463638

Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited muscular dystrophies. The causative gene remains controversial and the mechanism of pathophysiology unknown. Here we identify genes associated with germline and early stem cell development as targets of the DUX4 transcription factor, a leading candidate gene for FSHD. The genes regulated by DUX4 are reliably detected in FSHD muscle but not in controls, providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD. Additionally, we show that DUX4 binds and activates LTR elements from a class of MaLR endogenous primate retrotransposons and suppresses the innate immune response to viral infection, at least in part through the activation of DEFB103, a human defensin that can inhibit muscle differentiation. These findings suggest specific mechanisms of FSHD pathology and identify candidate biomarkers for disease diagnosis and progression.

View details for DOI 10.1016/j.devcel.2011.11.013

View details for PubMedID 22209328

View details for PubMedCentralID PMC3264808

Double homeobox 4 (DUX4) is a candidate disease gene for facioscapulohumeral dystrophy (FSHD), one of the most common muscular dystrophies characterized by progressive skeletal muscle degeneration. Despite great strides in understanding precise genetics of FSHD, the molecular pathophysiology of the disease remains unclear. One of the major limitations has been the availability of appropriate molecular tools to study DUX4 protein. In the present study, we report the development of five new monoclonal antibodies targeted against the N- and C-termini of human DUX4, and characterize their reactivity using Western blot and immunofluorescence staining. Additionally, we show that expression of the canonical full coding DUX4 induces cell death in human primary muscle cells, whereas the expression of a shorter splice form of DUX4 results in no such toxicity. Immunostaining with these new antibodies reveals a differential effect of two DUX4 isoforms on human muscle cells. These antibodies will provide an excellent tool for investigating the role of DUX4 in FSHD pathogenesis.

View details for DOI 10.1089/hyb.2010.0094

View details for PubMedID 21529284

View details for PubMedCentralID PMC3132944

Each unit of the D4Z4 macrosatellite repeat contains a retrotransposed gene encoding the DUX4 double-homeobox transcription factor. Facioscapulohumeral dystrophy (FSHD) is caused by deletion of a subset of the D4Z4 units in the subtelomeric region of chromosome 4. Although it has been reported that the deletion of D4Z4 units induces the pathological expression of DUX4 mRNA, the association of DUX4 mRNA expression with FSHD has not been rigorously investigated, nor has any human tissue been identified that normally expresses DUX4 mRNA or protein. We show that FSHD muscle expresses a different splice form of DUX4 mRNA compared to control muscle. Control muscle produces low amounts of a splice form of DUX4 encoding only the amino-terminal portion of DUX4. FSHD muscle produces low amounts of a DUX4 mRNA that encodes the full-length DUX4 protein. The low abundance of full-length DUX4 mRNA in FSHD muscle cells represents a small subset of nuclei producing a relatively high abundance of DUX4 mRNA and protein. In contrast to control skeletal muscle and most other somatic tissues, full-length DUX4 transcript and protein is expressed at relatively abundant levels in human testis, most likely in the germ-line cells. Induced pluripotent (iPS) cells also express full-length DUX4 and differentiation of control iPS cells to embryoid bodies suppresses expression of full-length DUX4, whereas expression of full-length DUX4 persists in differentiated FSHD iPS cells. Together, these findings indicate that full-length DUX4 is normally expressed at specific developmental stages and is suppressed in most somatic tissues. The contraction of the D4Z4 repeat in FSHD results in a less efficient suppression of the full-length DUX4 mRNA in skeletal muscle cells. Therefore, FSHD represents the first human disease to be associated with the incomplete developmental silencing of a retrogene array normally expressed early in development.

View details for DOI 10.1371/journal.pgen.1001181

View details for PubMedID 21060811

View details for PubMedCentralID PMC2965761

Inhibitors of 5alpha-reductase (SRD5A) that lower intraprostatic levels of dihydrotestosterone (DHT) reduce the overall incidence of prostate cancer (PCa), but there is significant variation in chemopreventive activity between individual men. In seeking molecular alterations that might underlie this variation, we compared gene expression patterns in patients with localized PCa who were randomized to prostatectomy alone versus treatment with two different doses of the SRD5A inhibitor dutasteride. Prostatic levels of DHT were decreased by >90% in both dutasteride-treated patient groups versus the untreated patient group. Despite significant and uniform suppression of tissue DHT, unsupervised clustering based on prostatic gene expression did not discriminate these groups. However, subjects could be resolved into distinct cohorts characterized by high or low expression of genes regulated by the androgen receptor (AR), based solely on AR transcript expression. The higher-dose dutasteride treatment group was found to include significantly fewer cancers with TMPRSS2-ERG genetic fusions. Dutasteride treatment was associated with highly variable alterations in benign epithelial gene expression. Segregating subjects based on expression of AR and androgen-regulated genes revealed that patients are differentially sensitive to SRD5A inhibition. Our findings suggest that AR levels may predict the chemopreventive efficacy of SRD5A inhibitors.

View details for DOI 10.1158/0008-5472.CAN-09-2509

View details for Web of Science ID 000278485700003

View details for PubMedID 20124490

View details for PubMedCentralID PMC2822890

DNA methylation might have a significant role in preventing normal differentiation in pediatric cancers. We used a genomewide method for detecting regions of CpG methylation on the basis of the increased melting temperature of methylated DNA, termed denaturation analysis of methylation differences (DAMD). Using the DAMD assay, we find common regions of cancer-specific methylation changes in primary medulloblastomas in critical developmental regulatory pathways, including Sonic hedgehog (Shh), Wingless (Wnt), retinoic acid receptor (RAR), and bone morphogenetic protein (BMP). One of the commonly methylated loci is the PTCH1-1C promoter, a negative regulator of the Shh pathway that is methylated in both primary patient samples and human medulloblastoma cell lines. Treatment with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increases the expression of PTCH1 and other methylated loci. Whereas genetic mutations in PTCH1 have previously been shown to lead to medulloblastoma, our study indicates that epigenetic silencing of PTCH1, and other critical developmental loci, by DNA methylation is a fundamental process of pediatric medulloblastoma formation. This finding warrants strong consideration for DNA demethylating agents in future clinical trials for children with this disease.

View details for DOI 10.1073/pnas.0907606106

View details for PubMedID 19966297

View details for PubMedCentralID PMC2806770

Deletion of a subset of the D4Z4 macrosatellite repeats in the subtelomeric region of chromosome 4q causes facioscapulohumeral muscular dystrophy (FSHD) when occurring on a specific haplotype of 4qter (4qA161). Several genes have been examined as candidates for causing FSHD, including the DUX4 homeobox gene in the D4Z4 repeat, but none have been definitively shown to cause the disease, nor has the full extent of transcripts from the D4Z4 region been carefully characterized. Using strand-specific RT-PCR, we have identified several sense and antisense transcripts originating from the 4q D4Z4 units in wild-type and FSHD muscle cells. Consistent with prior reports, we find that the DUX4 transcript from the last (most telomeric) D4Z4 unit is polyadenylated and has two introns in its 3-prime untranslated region. In addition, we show that this transcript generates (i) small si/miRNA-sized fragments, (ii) uncapped, polyadenylated 3-prime fragments that encode the conserved C-terminal portion of DUX4 and (iii) capped and polyadenylated mRNAs that contain the double-homeobox domain of DUX4 but splice-out the C-terminal portion. Transfection studies demonstrate that translation initiation at an internal methionine can produce the C-terminal polypeptide and developmental studies show that this peptide inhibits myogenesis at a step between MyoD transcription and the activation of MyoD target genes. Together, we have identified new sense and anti-sense RNA transcripts, novel mRNAs and mi/siRNA-sized RNA fragments generated from the D4Z4 units that are new candidates for the pathophysiology of FSHD.

View details for DOI 10.1093/hmg/ddp180

View details for PubMedID 19359275

View details for PubMedCentralID PMC2694690

Cardiovascular disease, largely because of disruption of atherosclerotic lesions, accounts for the majority of deaths in people with type 1 diabetes. Recent mouse models have provided insights into the accelerated atherosclerotic lesion initiation in diabetes, but it is unknown whether diabetes directly worsens more clinically relevant advanced lesions. We therefore used an LDL receptor-deficient mouse model, in which type 1 diabetes can be induced at will, to investigate the effects of diabetes on preexisting lesions. Advanced lesions were induced by feeding mice a high-fat diet for 16 weeks before induction of diabetes. Diabetes, independently of lesion size, increased intraplaque hemorrhage and plaque disruption in the brachiocephalic artery of mice fed low-fat or high-fat diets for an additional 14 weeks. Hyperglycemia was not sufficient to induce plaque disruption. Furthermore, diabetes resulted in increased accumulation of monocytic cells positive for S100A9, a proinflammatory biomarker for cardiovascular events, and for a macrophage marker protein, without increasing lesion macrophage content. S100A9 immunoreactivity correlated with intraplaque hemorrhage. Aggressive lowering primarily of triglyceride-rich lipoproteins prevented both plaque disruption and the increased S100A9 in diabetic atherosclerotic lesions. Conversely, oleate promoted macrophage differentiation into an S100A9-positive population in vitro, thereby mimicking the effects of diabetes. Thus, diabetes increases plaque disruption, independently of effects on plaque initiation, through a mechanism that requires triglyceride-rich lipoproteins and is associated with an increased accumulation of S100A9-positive monocytic cells. These findings indicate an important link between diabetes, plaque disruption, and the innate immune system.

View details for DOI 10.1073/pnas.0709958105

View details for PubMedID 18252823

View details for PubMedCentralID PMC2538884

In vivo, replicative DNA polymerases are made more processive by their interactions with accessory proteins at the replication fork. Single-stranded DNA binding protein (SSB) is an essential protein that binds tightly and cooperatively to single-stranded DNA during replication to remove adventitious secondary structures and protect the exposed DNA from endogenous nucleases. Using information from high resolution structures and biochemical data, we have engineered a functional chimeric enzyme of the bacteriophage RB69 DNA polymerase and SSB with substantially increased processivity. Fusion of RB69 DNA polymerase with its cognate SSB via a short six amino acid linker increases affinity for primer-template DNA by sixfold and subsequently increases processivity by sevenfold while maintaining fidelity. The crystal structure of this fusion protein was solved by a combination of multiwavelength anomalous diffraction and molecular replacement to 3.2 A resolution and shows that RB69 SSB is positioned proximal to the N-terminal domain of RB69 DNA polymerase near the template strand channel. The structural and biochemical data suggest that SSB interactions with DNA polymerase are transient and flexible, consistent with models of a dynamic replisome during elongation.

View details for DOI 10.1002/prot.21088

View details for PubMedID 16881051

The conformation of a constrained peptide mimicking the putative first intracellular domain (iLP1) of thromboxane A(2) receptor (TP) was determined by (1)H 2D NMR spectroscopy. Through completed assignments of TOCSY, DQF-COSY, and NOESY spectra, a NMR structure of the peptide showed a beta-turn in residues 56-59 and a short helical structure in the residues 63-66. It suggests that residues 63-66 may be part of the second transmembrane domain (TM), and that Arg60, in an exposed position on the outer surface of the loop, may be involved in signaling through charge contact with Gq protein. The sequence alignment of Lys residue in the same position of other prostanoid receptors mediates different G protein couplings, suggesting that the chemical properties of Arg and Lys may also affect the receptor signaling activity. These hypotheses were supported by mutagenesis studies, in which the mutant of Arg60Leu completely lost activity in increasing intracellular calcium level through Gq coupling, and the mutant of Arg60Lys retained only about 35% signaling activity. The difference between the side chain functions of Lys and Arg in effecting the signaling was discussed.

View details for DOI 10.1016/j.abb.2004.01.001

View details for Web of Science ID 000220164100003

View details for PubMedID 15001390

Learn together with your colleagues

Participants report that enrolling in a program with colleagues fosters collaborative learning and amplifies their impact.

Please provide your details to get more information about the group-enrollment pricing.

The benefit of learning together with your friend is that you keep each other accountable and have meaningful discussions about what you're learning.

Congratulations!

Based on the information you provided, your team is eligible for a special discount, for Sustainability Strategies starting on June 20, 2024 .

We’ve sent you an email with enrollment next steps. If you’re ready to enroll now, click the button below.

Sustainability Strategies: Develop Initiatives to Transform Your Business

Get your brochure, last day to enroll.

8 weeks, online 4–6 hours per week

PROGRAM FEE

US$2,800 and get US$280 off with a referral

For Your Team

Enroll your team and learn with your peers

Sustainability Leadership Starts with You

A survey of recent headlines and research reports reveals the ways that consumers, employees, investors, and other stakeholders are using their influence to demand solutions to our global climate crisis. The majority of business leaders have sustainability on their radar, but what do sustainability initiatives look like in practice, and how can we make progress when the challenges seem insurmountable?

of S&P 500 organizations publish ESG reports in some form, as do approximately 70 percent of Russell 1000 organizations.

(SOURCE: MCKINSEY SUSTAINABILITY) August, 2022

of millennials consider an organization’s social and environmental commitments when deciding where to work.

(SOURCE: DELOITTE) May, 2022

of global consumers are willing to pay higher-than-average prices for products made with sustainable materials, and demand for sustainable products is expected to grow exponentially in emerging markets.

Key Takeaways

• Develop an understanding of the impacts and root causes of climate change to communicate the value of sustainable business practices to key stakeholders.
• Learn to identify business opportunities that arise by transitioning to an environmentally sustainable organization.
• Understand the interdependence between innovation and sustainability as a guiding force for developing your own sustainability initiatives.
• Develop a proactive mindset to lead change effectively, with an eye toward positioning the organization as an agent of change.

This Program Is Ideal for Professionals and Leaders Who Are:

Building strategies that move the needle on sustainability efforts within their organizations or industries

Developing and communicating the vision and value of a sustainable business future

Striving to be on the leading edge of environmental sustainability or transitioning from a legacy business model to a more innovative approach to business

Driving strategies at the business unit or organizational level, where maintaining a competitive advantage is critical

Program modules.

• Develop your understanding of the climate challenges at hand and key terminology, including the carbon cycle, energy buildup, tipping points, and cumulative emissions.
• Reflect on how climate change is impacting your organization and what you can learn from your competitors.
• Make a pitch for sustainability as part of a communication exercise.
• Understand the components of a business model using the business model architecture framework.
• Examine Tesla’s business model as part of a case study deep dive.
• Explore where your business model intersects with sustainability issues and identify opportunities.
• Learn how Little’s law—a numerical theorem—is applied to understanding circular economies and their relationship to the value chain. Map your organization’s value chain in relation to sustainability.
• Propose short and long-term actions that impact your organization's value chain as it relates to climate change.
• Identify opportunities to lead sustainability change at any level of your organization and learn how to become an agent of change.
• Understand how leadership can be leveraged to support and grow sustainability goals across the organization.
• Explore the interdependency between innovation and accomplishing sustainability goals.
• Understand the role of leadership in managing the risks associated with change.
• Examine several use cases, including Toyota Prius, Boeing 787, and Tesla, using the DICE framework—a unified framework for business model innovation.
• Analyze the impacts of political risks from private political groups, such as nongovernmental organizations, individual activists, and the media, using Citigroup's case study as a practical example.
• Investigate the influence of location-based political risks on business decision making through Tata Motors' case.
• Apply practical tools to mitigate and manage political risks in various business contexts.
• Utilize a structured framework to systematically assess the responses of various interest groups to environmental policies.
• Examine the intricacies of global environmental policy development and implementation and evaluate an organization's existing sustainability strategy.
• Use the triple bottom line framework to measure, evaluate, and communicate sustainability performance for your organization.
• Analyze sustainability-related strategic performance and how it relates to your organization’s value creation activities and create your action plan for sustainability.

Program Walk-Through

Access to Stanford Graduate School of Business proprietary strategy tools and frameworks

Manageable time investment (four to six hours/week)

Live sessions with faculty

Assignments for you to apply learnings to your own role or industry

Networking with global peers

Featured case study and cross-industry examples

Feedback on assignments to ensure the relevance of the program material

Certificate of completion from Stanford Graduate School of Business

Featured Program Elements

Capstone project designed to jump-start your sustainability efforts

Create an action plan that will positively impact sustainability in your organization. Using your weekly workbook exercises, you will identify your priorities based on where you can make an immediate difference for your organization.

Original strategic frameworks and tools from Stanford faculty

The proprietary frameworks are tools that help leaders support an organization's value chain and become efficient in leading sustainability initiatives and driving business change.

Featured case studies

Gain insights from Tesla, Lego, General Motors, and Citigroup’s business models and other successful businesses through case studies.

Testimonials

“I appreciated the way each module was shown as part of a bigger theme and how the concepts built on top of and across each other to provide a wide understanding of sustainability from different angles. The required workbooks and the capstone project helped put everything together.” — Nadia Szeinbaum, Innovation Scientist at Beyond Meat

“The program content was taught by faculty with impressive expertise and a diversity of teaching methods that helped us to learn new concepts and immediately put them into practice.” — Marco Luchsinger, MBA Candidate

“The module workbooks really forced me to think deeply about my organization.” — Andrea Wong, board member at Liberty Media

Meet the Faculty

William Barnett

The Thomas M. Siebel Professor of Business Leadership, Strategy, and Organizations

Chris Field

The Perry L. McCarty Director of the Stanford Woods Institute for the Environment and the Melvin and Joan Lane Professor for Interdisciplinary Environmental Studies at Stanford University

Saumitra Jha

Associate Professor of Political Economy

Haim Mendelson

The Kleiner Perkins Caufield & Byers Professor of Electronic Business and Commerce, and Management

Joseph Piotroski

The Robert K. Jaedicke Professor of Accounting

Erica Plambeck

The Charles A. Holloway Professor of Operations, Information and Technology

Stefanos Zenios

The Investment Group of Santa Barbara Professor of Entrepreneurship and Professor of Operations, Information & Technology

William Barnett The Thomas M. Siebel Professor of Business Leadership, Strategy, and Organizations

Chris Field The Perry L. McCarty Director of the Stanford Woods Institute for the Environment and the Melvin and Joan Lane Professor for Interdisciplinary Environmental Studies at Stanford University

Saumitra Jha Associate Professor of Political Economy

Haim Mendelson The Kleiner Perkins Caufield & Byers Professor of Electronic Business and Commerce, and Management

Joseph Piotroski The Robert K. Jaedicke Professor of Accounting

Erica Plambeck The Charles A. Holloway Professor of Operations, Information and Technology

Stefanos Zenios The Investment Group of Santa Barbara Professor of Entrepreneurship and Professor of Operations, Information & Technology

Certificate

Upon completion of this program, you will receive a certificate of completion from Stanford Graduate School of Business that you can share with your professional network.

How do I know if this program is right for me?

After reviewing the information on the program landing page, we recommend that you submit the short form above to gain access to the program brochure, which includes more in-depth information. If you still have questions on whether this program is a good fit for you, please email [email protected] , and a dedicated program advisor will follow up with you very shortly.

Are there any prerequisites for this program?

Participants must be 18 years old or above to apply to this program. Some programs do have prerequisites, particularly the more technical ones. This information will be noted on the program landing page and in the program brochure. If you are uncertain about program prerequisites and your capabilities, please email us at [email protected] for assistance.

Note that, unless otherwise stated on the program web page, all programs are taught in English, and proficiency in English is required..

What is the typical class profile?

More than 50 percent of our participants are from outside the United States. Class profiles vary from one cohort to the next, but, generally, our online certificates draw a highly diverse audience in terms of professional experience, industry, and geography—leading to a very rich peer learning and networking experience.

At what other dates will this program be offered in the future?

Check back to this program web page or email us at [email protected] to inquire whether future program dates or the timeline for future offerings has been confirmed.

How much time is required each week?

Each program includes an estimated learner effort per week. This is referenced at the top of the program landing page under the Duration section as well as in the program brochure, which you can obtain by submitting the short form at the top of this web page.

How will my time be spent?

We have designed this program to fit into your current working life as efficiently as possible. Time will be spent among a variety of activities, including:

• Engaging with recorded video lectures from faculty
• Attending webinars and office hours as per the specific program schedule
• Reading or engaging with examples of core topics
• Completing knowledge checks/quizzes and required activities
• Engaging in moderated discussion groups with your peers
• Completing your final project, if required

The program is designed to be highly interactive while also allowing time for self-reflection and demonstrating an understanding of the core topics through various active learning exercises. Please contact us at [email protected] if you need further clarification on program activities.

A dedicated program support team is available 24/5 (Monday to Friday) to answer questions about the learning platform, technical issues, or anything else that may affect your learning experience.

How do I interact with other program participants?

Peer learning adds substantially to the overall learning experience and is an important part of the program. You can connect and communicate with other participants through our learning platform.

What are the requirements to earn the certificate?

Each program includes an estimated learner effort per week, so you can gauge what will be required before you enroll. This is referenced at the top of the program landing page under the Duration section as well as in the program brochure, which you can obtain by submitting the short form at the top of this web page. All programs are designed to fit into your working life. This program is scored as a pass or no pass; participants must complete the required activities to pass and obtain the certificate of completion. Some programs include a final project submission or other assignments to obtain passing status. This information will be noted in the program brochure. Please contact us at [email protected] if you need further clarification on any specific program requirements.

What type of certificate will I receive?

Upon successful completion of the program, you will receive a smart digital certificate. The smart digital certificate can be shared with friends, family, schools, or potential employers. You can use it on your cover letter or resume or display it on your LinkedIn profile. The digital certificate will be sent approximately two weeks after the program end date, once grading is complete.

Can I get a the hard copy of the certificate?

No, only verified digital certificates will be issued upon successful completion. This allows you to share your credentials on social platforms, such as LinkedIn, Facebook, and Twitter.

Do I receive alumni status after completing this program?

No, there is no alumni status granted for this program. In some cases, there are credits that count toward a higher level of certification. This information will be clearly noted in the program brochure.

How long will I have access to the learning materials?

You will have access to the online learning platform and all the videos and program materials for 12 months following the program start date . Access to the learning platform is restricted to registered participants as per the terms of the agreement.

What equipment or technical requirements are there for this program?

Participants will need the latest version of their preferred browser to access the learning platform. In addition, Microsoft Office and a PDF viewer are required to access documents, spreadsheets, presentations, PDF files, and transcripts.

Do I need to be online to access the program content?

Yes, the learning platform is accessed via the internet, and video content is not available for download. However, you can download files of video transcripts, assignment templates, readings, etc. For maximum flexibility, you can access program content from a desktop, laptop, tablet, or mobile device. Video lectures must be streamed via the internet, and any live stream webinars and office hours will require an internet connection as well. However, these sessions are always recorded, so you may view them later.

Can I still register if the registration deadline has passed?

Yes, you can register up to seven days after the published start date of the program without missing any of the core program material or learnings.

What is the program fee, and what forms of payment do you accept?

The program fee is noted at the top of this program web page and is usually referenced in the program brochure as well. Flexible payment options are available (see details below as well as at the top of this program web page next to FEE).

What if I don’t have a credit card? Is there another method of payment accepted?

Yes, you can do a bank remittance in the program currency via wire transfer or debit card. Please contact your program advisor or email us at [email protected] for details.

I was not able to use the discount code provided. Can you help?

Yes! Please email us at [email protected] with the details of the program you are interested in, and we will assist you.

How can I obtain an invoice for payment?

Please email [email protected] with your invoicing requirements and the specific program you’re interested in enrolling in.

Is there an option to make flexible payments for this program?

Yes, the flexible payment option allows participants to pay the program fee in installments. This option is made available on the payment page and should be selected before submitting the payment.

How can I obtain a W9 form?

Please email us at [email protected] for assistance.

Who will be collecting the payment for the program?

Emeritus collects all program payments, provides learner enrollment and program support, and manages learning platform services.

Are there any restrictions on the types of funding that can be used to pay for the program?

Program fees for Emeritus programs with Stanford Graduate School of Business Executive Education may not be paid for with (a) funds from the GI Bill, the Post-9/11 Educational Assistance Act of 2008, or similar types of military education funding benefits or (b) Title IV financial aid funds.

What is the program refund and deferral policy?

For the program refund and deferral policy, please click the link here .

Didn't find what you were looking for? Write to us at [email protected] or Schedule a call with one of our Program Advisors or call us at +1 401 443 9709   (US) / +44 127 959 8043  (UK) / +65 3129 4367 (SG)

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Continue exploring available programs.

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The first week is an orientation module only, there is no teaching, and it is recorded. Join the online program now and don't delay the impact that the program will have on your career.

83 years later, 105-year-old finally earns master's from Stanford

Virginia Hislop has spent a lifetime trying to increase access to education, and now, at 105 years old, she appears to have completed her own schooling.

On Sunday, Hislop celebrated Stanford University's conference of a master of art's degree in education — 83 years after having left campus just shy of the degree. Her son-in-law had contacted the institution and discovered a final thesis, her unfulfilled obligation, was no longer required.

“I’ve been doing this work for years and it’s nice to be recognized with this degree,” Hislop told Stanford for a story about her nearly lifelong journey to a stage on campus , where a diploma in a Cardinal-red cover was placed in her hand.

In 1941, on the eve of the United States' direct involvement in World War II, and as her fiance was preparing to be called to serve, Hislop skipped out on the thesis.

Her Stanford days, starting in 1936, were nonetheless fruitful, and she earned an undergraduate education degree before moving directly to postgraduate studies.

She wanted to go to law school, Hislop has said, but her father wouldn't pay for it, so she opted for the briefer time required for teaching.

Hislop had completed coursework for a master's and needed only to turn in the final version of her thesis, she has said. Instead, she told NBC Bay Area, she skipped town and had a honeymoon in Oklahoma near her husband's Army post at Fort Sill.

"Not my idea of a place for a honeymoon," she told the station, "but I had no choice in the matter."

At the time, such a sacrifice — trading her career for marriage and a future family — was seen as a way to support the war effort. It was a sacrifice for America.

She had grown up in Los Angeles, but after the war the California girl found herself with husband George in Yakima, Washington, where George took part in the family business of ranching.

They raised two children, which put Hislop's focus on a passion stoked during her days in Palo Alto: education.

"I didn’t return to teaching, but I feel I put my teaching certificate to good use serving in committees and on boards and trying to improve the educational opportunities every chance I got," she told the Yakima Herald-Republic in 2018.

She opposed middle school curricula that required home economics but not advanced English for her daughter, so she ran for the Yakima School District Board of Directors and won, according to the publication.

Hislop also successfully lobbied for independent community college districts in Washington state at a time when Yakima's two-year college was under the otherwise K-12 district.

She was eventually recruited to raise funds for what would become Heritage University, a women-founded, women-led institution about 20 miles south of Yakima.

She launched the school's annual Bounty of the Valley Scholarship Dinner, which by 2018 had raised nearly $6 million to help students attend the institution. Hislop is listed by the school as a board member emerita.

At Pacific Northwest University, a medical and health sciences school in Yakima, a scholarship, the Virginia Hislop Emergency Fund , bares her name.

Her interest in broad access to education may have been inspired by an aunt who was the principal of a public school in West Los Angeles' Sawtelle Japantown neighborhood when Hislop grew up in L.A.

Sawtelle is an area originally anchored by a housing and care facility for disabled veterans of the Civil War, but it evolved into a community populated by Japanese Americans and Latinos.

Hislop said she was moved by her aunt’s experience seeing education change lives on L.A.’s Westside, according to the Yakima Herald-Republic.

“Aunt Nora would tell us about some of the Hispanic students in her school and how they were doing and the difference that education made for them,” she told the publication. “It seemed to me that without an education, your future was limited and with an education it was unlimited.”

Her new degree is punctuation for a life spent advocating for public education for the masses.

On Sunday, Daniel Schwartz, dean of Stanford’s Graduate School of Education, handed Hislop her master’s diploma with a broad smile, describing her as “a fierce advocate for equity and the opportunity to learn."

Dennis Romero is a breaking news reporter for NBC News Digital. 

Doctoral Program

The Ph.D. program is a full time program leading to a Doctoral Degree in Economics.  Students specialize in various fields within Economics by enrolling in field courses and attending field specific lunches and seminars.  Students gain economic breadth by taking additional distribution courses outside of their selected fields of interest.

General requirements

Students  are required to complete 1 quarter of teaching experience. Teaching experience includes teaching assistantships within the Economics department or another department .

University's residency requirement

135 units of full-tuition residency are required for PhD students. After that, a student should have completed all course work and must request Terminal Graduate Registration (TGR) status.

Department degree requirements and student checklist

1. core course requirement.

Required: Core Microeconomics (202-203-204) Core Macroeconomics (210-211-212) Econometrics (270-271-272).  The Business School graduate microeconomics class series may be substituted for the Econ Micro Core.  Students wishing to waive out of any of the first year core, based on previous coverage of at least 90% of the material,  must submit a waiver request to the DGS at least two weeks prior to the start of the quarter.  A separate waiver request must be submitted for each course you are requesting to waive.  The waiver request must include a transcript and a syllabus from the prior course(s) taken.  

2.  Field Requirements

Required:  Two of the Following Fields Chosen as Major Fields (click on link for specific field requirements).  Field sequences must be passed with an overall grade average of B or better.  Individual courses require a letter grade of B- or better to pass unless otherwise noted.

Research fields and field requirements :

• Behavioral & Experimental
• Development Economics
• Econometric Methods with Causal Inference
• Econometrics
• Economic History
• Environmental, Resource and Energy Economics
• Industrial Organization
• International Trade & Finance
• Labor Economics
• Market Design
• Microeconomic Theory
• Macroeconomics
• Political Economy
• Public Economics

3.  Distribution

Required:  Four other graduate-level courses must be completed. One of these must be from the area of economic history (unless that field has already been selected above). These courses must be distributed in such a way that at least two fields not selected above are represented.  Distribution courses must be passed with a grade of B or better.

4.  Field Seminars/Workshops

Required:  Three quarters of two different field seminars or six quarters of the same field seminar from the list below.   

Programs and Specialties

Innovation and transformation.

The mission of the Stanford Department of Emergency Medicine is to transform healthcare for all by leading in the advancement of emergency medicine through innovation and scientific discovery.

Research and practice in targeted areas of specialization ensure Stanford leads the transformation of emergency medicine and makes our vision of a healthier world a reality.

PEDIATRIC EM

Learn more about Pediatric EM

CRITICAL CARE

Learn more about Critical Care

Learn more about EMS

Learn more about Global EM

Learn more about Ultrasound

BIOSECURITY

Learn more about Biosecurity

SOCIAL EM & POPULATION HEALTH

Learn more about Social EM

WILDERNESS EM

Learn more about Wilderness Medicine

Stanford Department of Emergency Medicine strives to bring expertise and new ideas to all aspects of the practice of emergency medicine - within the ED, around the globe, and many points in between.

PhD Program

More information and a full list of requirements for the PhD program in Mathematics can be found in the University Bulletin .

During their first year in the program, students typically engage in coursework and seminars which prepare them for the  Qualifying Examinations .  Currently, these two exams test the student’s breadth of knowledge in algebra and real analysis. 

Starting in Autumn 2023, students will choose 2 out of 4 qualifying exam topics: 

• real analysis
• geometry and topology
• applied mathematics

Course Requirements for students starting prior to Autumn 2023

To qualify for candidacy, the student must have successfully completed 27 units of Math graduate courses numbered between 200 and 297.

Within the 27 units, students must satisfactorily complete a course sequence. This can be fulfilled in one of the following ways:

• Math 215A, B, & C: Algebraic Topology, Differential Topology, and Differential Geometry
• Math 216A, B, & C: Introduction to Algebraic Geometry
• Math 230A, B, & C: Theory of Probability
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How the Apparel Industry Could Refashion Itself with Sustainability in Mind

From disposable styles to fossil-fueled fabrics, our clothes are ready for a makeover.

June 27, 2024

Textile recycling and buying secondhand can keep fabric waste and used clothes out of landfills. | iStock/undrey

A bit of retail therapy can feel like harmless fun. Yet getting a great deal on a new shirt or pair of shoes may come with a hidden price tag: greenhouse gas emissions, resource depletion, and the mistreatment of workers and animals. The average cotton T-shirt, for example, requires about 700 gallons of water to make. A fast-fashion polyester top is made from petroleum, sheds microfibers, and may spend decades decomposing in a landfill.

And the apparel industry’s footprint has been expanding. Global fiber production has more than doubled since 2000, and consumers are buying more clothes as fast-fashion brands churn out inexpensive looks. To mitigate the environmental and social issues associated with the apparel industry, companies and consumers alike must shift toward sustainability, says Barchi Gillai , the associate director of the Value Chain Innovation Initiative (VCII) at Stanford Graduate School of Business. “It’s a responsibility that all of us share,” she says.

In a new white paper , Gillai and her colleagues examine the production processes behind three essential everyday materials: polyester, cotton, and leather. Coauthored by Hau Lee , VCII’s faculty codirector and a professor emeritus of operations, information, and technology; Jessica Landzberg , MBA ’23; and Nina Sabharwal , MBA ’23, the paper explores each material’s unique impacts and details potential solutions.

Polyester is a durable, lightweight material composed of fibers made from polyethylene terephthalate (PET), which is derived from fossil fuels. The production of polyester and other synthetic fibers requires large amounts of energy, accounting for about 1.35% of global oil consumption. This results in greenhouse gas emissions that contribute to global warming. Possible solutions to these problems include switching to renewable energy and substituting virgin polyester with alternative materials such as biosynthetics and fibers that utilize carbon dioxide waste.

The cotton supply chain starts on a farm instead of a factory, but it also has a unique set of environmental impacts. Cotton cultivation often involves a variety of pesticides that can cause serious health issues in farm workers and contaminate freshwater systems, soil, and animal habitats. Cotton also consumes large amounts of water. To address these issues, cotton growers can implement non-chemical methods of pest control such as crop rotation and conserve water through drip irrigation.

Leather production has also grown over the past three decades. One of the primary concerns surrounding leather goods is animal cruelty. To ensure ethical sourcing of raw hides, brands can utilize certification programs that verify the humane treatment of farm animals. However, acquiring raw materials is only the first step in leather production. Transforming these raw hides into wearable fabrics requires several chemical-heavy processes, many of them relying on toxic materials. Moreover, 30%-45% of the toxic chromium used in the tanning process is not absorbed in the leather, and can potentially contaminate the environment when it is discarded. Finally, as much as 75% of the leather that enters the production process of leather goods does not end up in the finished product. Rather, these scraps and leftovers will likely be sent to landfills or incinerated.

Slowing Down Fast Fashion

A garment’s impact continues even after it has been sold. Used garments often wind up in landfills or incinerators, wasting potentially valuable and non-renewable resources, and releasing greenhouse gases as they decay. The paper offers a range of strategies that clothing brands can adopt to increase the lifespans of garments and improve their reusability and recyclability. For instance, high-quality garments with timeless designs may be enjoyed for many years. Switching to single-material composition can make fabrics easier to recycle. And garments made from 100% natural materials are more suitable for composting.

Quote Slowing down the rate of production doesn’t have to come at the expense of profitability. Attribution Barchi Gillai

Unfortunately, some of the available solutions that address a problem in one part of a product’s life cycle might lead to unwanted consequences later on. For example, while producing polyester from recycled PET uses less oil, fabrics made from these materials tend to release more microfibers into the environment. “We’ve seen quite a few of those solutions that are helpful in one respect, but also have some drawbacks to them,” Gillai says. “It’s therefore important to figure out the total environmental impact of any solution we consider implementing.” The paper recommends that manufacturers use life-cycle assessments to help them choose solutions that offer the most positive impact throughout a garment’s lifespan.

While some companies have taken steps in the right direction, the apparel industry as a whole is showing no signs of becoming more sustainable. This is largely due to the popularity of “fast fashion”: low-quality garments with frequently-changing designs that are mass produced for little cost and viewed by consumers as almost disposable. The rise of fast fashion has fueled a surge in garment production, leading to an increase in textile waste.

The paper encourages companies to find new ways to generate revenue without producing more garments. One option is to start garment collection or buyback programs in conjunction with opening secondhand stores where consumers can purchase pre-owned items at a discount. “Slowing down the rate of production doesn’t have to come at the expense of profitability,” Gillai says.

Gillai also highlights the importance of textile-to-textile recycling. “Such closed-loop, garment-to-garment recycling solutions not only keep textile waste out of landfills, but also reduce the amount of resources that we use to make clothes, as well as the pollution associated with these production processes.”

While much of the paper describes how companies can practice sustainability, it ends with a discussion of the important role played by consumers. “To achieve meaningful results it is crucial for consumers to take a part in this effort,” Gillai says. “Try to donate items that are still wearable. Consider buying secondhand clothes. And think of renting items needed for a special occasion,” she advises. “If we embrace the need for change and if our shopping habits reflect this understanding, then we can help drive change in this industry.”

For media inquiries, visit the Newsroom .

Explore More

It takes a village: using game theory to get farmers to fight deforestation, replacing the “take-make-waste” model with sustainable supply chains, everlane takes on fashion’s plastic problem, editor’s picks.

Material Selection to Improve Sustainability in the Apparel Industry Barchi Gillai Jessica Landzberg Nina Sabharwal Hau L. Lee

July 18, 2022 Replacing the “Take-Make-Waste” Model with Sustainable Supply Chains The switch to a circular economy could protect the environment while helping companies generate more value.

June 28, 2021 Making Supply Chains Deliver More Than Just Faster, Cheaper Products Hau Lee envisions a system that benefits buyers, consumers, workers, and the environment.

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