United States

Objective:
This is an observational descriptive epidemiological study. We aim to examine global patterns and trends in brain and CNS cancer incidence and mortality using GLOBOCAN 2022 data, analyzing how socioeconomic development, measured by the Human Development Index (HDI), influences these rates and identifying potential mediating factors that explain this association.

Background:
Brain and central nervous system (CNS) cancers pose a significant and complex global health challenge, despite accounting for less than 2% of all cancer diagnoses worldwide. These malignancies are particularly notable for their devastating impact, characterized by high mortality rates and significant challenges in treatment and patient care. Emerging epidemiological research suggests a compelling connection between economic development and brain cancer incidence and mortality, prompting a deeper investigation into the underlying factors, such as healthcare capacity, environmental exposures, and population health that influence these patterns.

Methods:
We obtained brain and CNS cancer incidence and mortality data for 193 countries from GLOBOCAN 2022 and classified countries according to their Human Development Index rankings from lowest to highest development levels. Analysis confirmed that countries with higher HDI scores demonstrated significantly greater brain cancer incidence and mortality rates compared to less developed nations. We hypothesized that several factors might explain this pattern, including better diagnostic capabilities, healthcare infrastructure, population health characteristics, and environmental exposures. We collected data on healthcare workforce density (neurosurgeons, pathologists), diagnostic technology availability (MRI scanners), health system factors (universal coverage, number of clinical trials, radiotherapy availability), population metrics (life expectancy, obesity prevalence, height), and environmental variables (air pollution, radon exposure). Statistical regression models were used to identify which factors best account for the observed relationship between development level and brain cancer burden.

Results:
Higher HDI rankings demonstrated significant positive correlations with both brain and CNS cancer incidence and mortality rates. Among all variables analyzed, population height, life expectancy at birth, and pathologist density showed the strongest positive correlations with both incidence and mortality of brain and CNS tumors. Healthcare system factors, including radiotherapy availability, universal health coverage, and neurosurgeon density, also demonstrated significant associations, though with slightly lower correlation strength. MRI availability was significantly correlated, but less strongly than other healthcare capacity measures. In contrast, the number of clinical trials for brain malignancies and national radon activity showed no significant correlation with incidence or mortality, and air pollution levels were weakly negatively correlated, suggesting limited relevance in this global dataset. These results suggest that both population-level demographic factors and health system capacity help explain the observed link between higher socioeconomic development and greater reported brain tumor burden, while some environmental exposures and research activity appear to play a minimal mediating role in this relationship.

Conclusion:
Healthcare infrastructure and population health indicators substantially explain the higher brain cancer burden observed in more developed countries. These findings suggest that the relationship between socioeconomic development and brain cancer incidence reflects complex interactions between diagnostic capacity, healthcare access, and population-level health characteristics rather than solely representing differences in disease occurrence.

AMA Research Challenge 2025 

Understanding Longitudinal Incidence &amp; Mortality of Malignant Brain Tumors Through the Lens of Socioeconomic Development: A Global Analysis

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Understanding Longitudinal Incidence & Mortality of Malignant Brain Tumors Through the Lens of Socioeconomic Development: A Global Analysis

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Background
Beta-globinopathies, including beta-thalassemia and sickle cell disease (SCD), result from defective adult hemoglobin for which current treatments, including hydroxyurea and gene therapies, have variable efficacy, safety concerns, or limited accessibility. The transcription factor ZBTB7A represses gamma-globin expression, limiting fetal hemoglobin (HbF) production. Historically, transcription factors have been considered “undruggable.” We hypothesize that pharmacological degradation of ZBTB7A with SH6, a novel small-molecule degrader, could increase HbF, potentially serving as a treatment for beta-globinopathies.

Methods
In vitro, CD34+ cells from healthy donors and patients with SCD or beta-thalassemia were isolated and differentiated into erythroid lineage, and treated with SH6 at varying concentrations. HbF levels, ZBTB7A protein expression, and cell viability were assessed by high-performance liquid chromatography (HPLC), flow cytometry, immunoblotting, and cell counting.

In vivo, immunodeficient NBSGW mice transplanted with human CD34+ hematopoietic stem and progenitor cells from healthy donors were randomized to SH6 (2.5 or 5 mg/kg) or vehicle for 21 days. Peripheral blood was monitored for engraftment. At endpoint, bone marrow and peripheral blood cells were analyzed for viability, lineage markers, and HbF levels using intracellular staining and cation-exchange HPLC. Toxicity was evaluated via complete blood counts, serum chemistries, organ weights, and histopathology.

Results
In vitro, SH6 treatment of erythroid cultures from healthy donor CD34+ cells significantly increased gamma-globin expression and raised HbF levels from 11% to 34.7% by HPLC, with similar increases detected by flow cytometry, without affecting differentiation markers or cell expansion. In SCD and β-thalassemia patient-derived CD34+ cells, SH6 at 0.05 μM significantly increased HbF levels from 11% to 19% and from 26% to 36%, respectively, as reflected in flow cytometry analyses. SH6 elevated gamma-globin expression in patient-derived erythroid cells, including hydroxyurea-resistant lines.

In vivo, SH6 induced a significant, dose-dependent increase in HbF in human CD235a+ bone marrow cells within humanized mice, raising HbF from 2.5% in vehicle controls to 5% at 5 mg/kg, a level consistent with initial therapeutic thresholds reported in preclinical studies. SH6 also reduced ZBTB7A protein levels, confirming target engagement. Human hematopoietic engraftment remained stable, with preservation of erythroid differentiation markers and ability to reconstitute multiple lineages. SH6 was well tolerated, with normal serum chemistries, organ weights, and tissue histology.

Conclusion
SH6 effectively elevates HbF in vitro and in vivo through ZBTB7A degradation, without impairing hematopoiesis or causing significant toxicity. These findings highlight SH6 as a potential novel therapy for beta-globinopathies.

A Small-Molecule Approach to Overcome ZBTB7A-Mediated Fetal Hemoglobin Repression in Beta-Globinopathies

Introduction:
Mental health stigma remains one of the most persistent barriers to care, especially within religious communities where faith, culture, and social norms strongly shape perceptions of mental illness. Many individuals experience shame, fear of judgment, or the belief that seeking therapy reflects weak faith, all of which delay open conversations and treatment. Mental illness is frequently framed as a test of devotion or moral failing rather than a legitimate medical condition requiring professional intervention. Understanding how religious identity influences stigma and support is critical for developing culturally responsive approaches to care.
Methods:
An anonymous Qualtrics survey was distributed from March to June 2025 across diverse religious communities in Ohio to assess perceived stigma, support, and attitudes toward professional mental health services. Recruitment occurred through campus email lists, word of mouth, QR codes in community spaces, and outreach at The Ohio State University, libraries, and gyms. Religious leaders further assisted by promoting the survey through bulletin boards and newsletters. The instrument included demographic items, Likert-scale statements, and limited open-ended questions designed to capture both quantitative and qualitative perspectives on mental health beliefs and barriers.
Results:
A total of 316 responses were collected, of which 248 were complete and analyzable. Participants were 54% female, 44% male, and 2% identifying as other, with the majority aged 18–24. Most respondents identified as Muslim (75%), followed by Christian (14%), Jewish (6%), Other (4%), Buddhist (1%), and Hindu (<1%). The most frequently cited barriers to care were fear of judgment or gossip (94%), lack of awareness (72%), cultural or religious misconceptions (71%), feeling misunderstood by the community (63%), limited access to culturally sensitive professionals (56%), and belief that spirituality alone is sufficient (51%). These findings highlight stigma and misinformation as dominant obstacles, even among younger adults.
Conclusion:
Stigma continues to shape mental health attitudes in Ohio’s religious communities. Despite widespread belief that faith supports seeking help, misconceptions and fear of judgment persist. Addressing these issues requires community education, stronger partnerships between providers and faith leaders, and expansion of culturally competent mental health resources to bridge the gap between religious identity and professional care.

Religious Influence on Mental Health Attitudes and Stigma: Findings from a Community-Based Survey

Background:
Venous malformations (VMs) are congenital slow flow malformations that produce a wide spectrum of disease, from asymptomatic nodules to large painful lesions that cause coagulopathy or death. Current interventions are palliative and recurrence is common; there are no FDA-approved treatments. Discovery of PIK3CA variants in VMs have identified a role for PI3K/AKT/mTOR hyperactivation in VM pathophysiology and led to the repurposing of drugs that inhibit the PI3K pathway. Further development of therapeutics is limited by an incomplete understanding of the mechanism by which PI3K hyperactivation causes VM pathology. Previous work with endothelial cells isolated from patient VMs (VMECs) has shown proteostasis defects, abnormal cell morphology, and hyperproliferation consistent with the clinical presentation of VMs. We hypothesize that protein homeostasis defects in VMECs are downstream of PI3K hyperactivation and that distinct variants affect phenotypic severity.

Methods:
Human umbilical vein endothelial cells (HUVECs) were engineered to express empty plasmid or H1047R, E545K, or E542K pathogenic variants of PIK3CA using a lentiviral system. The resulting cells lines were stained by immunofluorescence for pAKT, CD31, and VECADHERIN and imaged using fluorescence microscopy. Quantification was performed using ImageJ. Statistical analysis was performed using one-way ANOVA with post-hoc Tukey t-test.

Results:
All three PIK3CA variants significantly increased the levels of activated AKT (ANOVA, p<0.0001) confirming effective transduction and function of the transgenes. All three variants led to significantly increased cell size (ANOVA, p<0.0001). The H1047R variant also showed significantly increased number of multi-nucleated cells (post-hoc Tukey t-test, p<0.0001). Abnormal cytoplasmic accumulation of CD31 and VECADHERIN was seen in all three cell variants. Quantification of protein levels showed that H1047R and E542K variants had significantly increased CD31 expression (post-hoc Tukey t-test, p< 0.05 and p<0.005). Only the H1047R and E545K variants had significantly increased VECADHERIN expression (post-hoc Tukey t-test, p<0.005). These changes in protein expression mimic changes observed in patient derived VMECs.

Conclusion:
The introduction of PIK3CA variants that hyperactivate PI3K signaling recapitulated cell morphology and proteostasis defects seen in patient VMECs. The H1047R variant demonstrated the most severe phenotype, which correlates with published clinical data. Disparities between variants may be relevant to understanding both the clinical heterogeneity of VM patients and their differential response to treatment. These data provide compelling evidence that VMEC phenotypes are downstream of PI3K/AKT/mTOR signaling. Future studies of how PI3K hyperactivation causes VMEC dysfunction may uncover novel avenues for therapeutic treatment.

PI3K Activation Drives Protein Homeostasis Pathology in Venous Malformations

Introduction: With increases in antimicrobial resistance, stewardship is essential in antibiotic decisions. Infectious diarrhea is a common reason for antibiotic usage. The Gastrointestinal PCR Panel (GPP) is a rapid multiplex molecular test detecting common pathogens causes of infectious diarrhea. Unfortunately, current medical literature contains limited guidance on incorporating GPP results into stewardship decisions. This study investigates the appropriateness of antimicrobial selection in patients with bacterial or parasitic causes of infectious diarrhea. 

Methods: We retrospectively analyzed all positive bacterial or parasitic GPP results from adults (≥18 years) in the Prisma Health Medical System in 2023, excluding patients with concurrent diagnosed infections. We assessed each patient for appropriateness of antimicrobial selection, including antibiotic choices, doses, and durations before and after GPP results. Inappropriate was defined as receiving an ineffective antibiotic, receiving more antibiotics than indicated, indicating but not prescribing treatment, and inappropriate duration of antimicrobial course based on the pathogen, patient’s risk factors, and overall clinical condition.

Results: Of 283 patients, 111 (39.2%) had an inappropriate antimicrobial selection or duration, 29 of which never received an effective antimicrobial despite being warranted. Of the 111, 91 (82.0%) received an inappropriate duration of therapy. Sixty-three patients (56.8%) had an inappropriate antibiotic selection with many receiving unneeded metronidazole. Inappropriate antimicrobial selection or duration occurred frequently in all medical settings: outpatient 7/21 (33.3%), emergency department not admitted 29/68 (42.6%), ED admitted 39/110 (35.5%), and inpatient 36/84 (42.8%). Nineteen of 54 immunocompromised patients (35.2%) received an insufficient duration of therapy. Immunocompromised individuals with Campylobacter (8/8, 100%) and Enteropathogenic E. coli EPEC (4/9, 44.4%) were frequently undertreated. Additionally, patients with Shigella and HIV frequently received an inappropriately short course (5/9, 55.5%). In contrast, immunocompetent individuals frequently received inappropriately long antibiotic courses to treat mild cases of Shigella (4/9, 44.4%), Campylobacter (4/10, 40%), EPEC (5/16, 31.3%), and Enteroaggregative E. coli (EAEC) (2/10, 20%).

Conclusion: Inappropriate antimicrobial therapy for infectious diarrhea was very common in all medical settings. Frequently immunocompromised patients were undertreated while mild infections in immunocompetent patients were overtreated. Many patients received multiple antibiotics when only one antibiotic was indicated.

Future studies:We plan to develop and implement a Prisma Health-specific GPP interpretation guideline to support stewardship via the Prisma Health Stewardship mobile application, with future studies evaluating its impact on prescribing patterns.

Opportunities for antimicrobial stewardship interventions based on Gastrointestinal Pathogen Panel Rapid Diagnostics

Background
Percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) in post-coronary artery bypass grafting (CABG) patients is particularly challenging due to complex anatomy, comorbidities, and limited collateral channels. Hybrid strategies and advanced intravascular imaging are often needed for procedural success.

Case Presentation
A 76-year-old Portuguese male with CAD status post CABG (LIMA-LAD, SVG-OM), type B aortic dissection, AVNRT (s/p ablation), hypertension, hyperlipidemia, thrombocytopenia, and anemia on GDMT presented with exertional angina. Workup revealed inferior wall ischemia secondary to a right coronary artery (RCA) CTO. An initial antegrade PCI in December 2024 achieved proximal RCA stenting but failed to cross the distal CTO, despite subintimal tracking and the use of a Stingray reentry device, limited by the available contrast volume. On January 22, 2025, IVUS-guided PCI of the mid-distal RCA CTO was completed via bilateral femoral access using a Gaia Next 3 wire for true lumen crossing, sequential ballooning, and Synergy XD stent placement. Optimal stent expansion and TIMI III flow were achieved without complications. The patient was discharged on dual antiplatelet therapy and aggressive risk factor modification. Follow-up noted marked symptomatic improvement.

Discussion
This case illustrates the technical complexity of CTO PCI in post-CABG patients, emphasizing the importance of meticulous planning, intravascular imaging, and hybrid strategies. IVUS guidance was critical in achieving optimal outcomes, underscoring its growing role in complex PCI cases.

IVUS-Guided CTO in post-CABG patient using a hybrid approach

Abstract Title: Vagus Nerve Stimulation Ameliorates Inflammatory Skin Diseases through Systemic Anti-Inflammatory Pathways: Evidence from Murine Models of Psoriasis and Atopic Dermatitis
William J. Nahm,1 Ki Joong Kim,2 Eui Namgung,3 Vincent Falanga,4

1) New York University Grossman School of Medicine, New York, NY, USA
2) Department of Oriental Medicine, Daejeon University, Daejeon, ROK
3) Department of Physics, University of California, San Diego, La Jolla, CA, USA
4) Department of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, USA

Background: The cholinergic anti-inflammatory pathway, activated through vagus nerve stimulation (VNS), plays a crucial role in immune response regulation. Although the skin lacks direct vagal nerve (VN) innervation, VNS may influence cutaneous inflammatory disorders through indirect mechanisms. In recent years, VNS has shown promise in modulating rheumatoid arthritis, inflammatory bowel disease, and other conditions, such as cardiovascular disease. This study investigated whether VNS could improve inflammatory skin diseases by modulating systemic inflammatory responses and local inflammatory cytokines.

Methods: Two distinct murine models were employed: C57/BL6 mice with imiquimod-induced psoriasis lesions and NC/Nga mice with dinitrochlorobenzene (DNCB)-induced atopic dermatitis. In the imiquimod model, psoriasis-like lesions were induced by applying imiquimod 5% cream to shaved dorsal skin for seven consecutive days, followed by every other day for six days. The DNCB model involved sensitization with 1% DNCB for seven days, followed by 0.3% DNCB for three days, resulting in marked scaling, crusting, and exudate formation. Cervical VNS (5V/5mA/5Hz/5ms/5min) was administered at 6- and 24-hour pre-sacrifice in the imiquimod model, and 24 hours pre-sacrifice in the DNCB model. Outcomes were assessed through clinical evaluation, histological analysis, immunofluorescence staining, western blotting, and cytokine measurement in plasma and splenic tissue.

Results: The application of imiquimod and DNCB produced psoriatic and eczematous-type clinical inflammation, accompanied by markedly increased epidermal thickening. VNS significantly reduced epidermal thickening and attenuated clinical manifestations in both models. In the imiquimod model, VNS produced a moderate reduction of erythema, scaling, and crusting. The DNCB-induced dermatitis was dramatically ameliorated following VNS treatment. Both models demonstrated significant reduction in pro-inflammatory cytokine expression (TNF-α, IL-6, IL-1β) and decreased CD11b-positive cutaneous macrophage infiltration. Immunofluorescence confirmed decreased epidermal TNF-α expression post-VNS. A single VNS application in DNCB-treated mice resulted in a 32% reduction in plasma TNF-α concentrations (p < 0.01). Notably, the protein levels of TNF-α and IL-1β, which were elevated in splenic tissue in both inflammatory models, were subsequently downregulated by VNS treatment.

Conclusion: These findings establish VNS as a promising therapeutic approach for inflammatory skin diseases. The therapeutic effects appear to be mediated through the modulation of systemic and subsequently local inflammation. These findings suggest that cutaneous inflammatory disorders may be linked to systemic inflammatory processes, providing mechanistic insights into the anti-inflammatory effects of VNS in dermatological conditions. Additionally, VN dysregulation emerges as a potential unifying mechanism underlying the well-established association between inflammatory skin diseases and their systemic comorbidities.

Vagus Nerve Stimulation Ameliorates Inflammatory Skin Diseases through Systemic Anti-Inflammatory Pathways: Evidence from Murine Models of Psoriasis and Atopic Dermatitis

Background: Glaucoma is characterized by the insidious degeneration of Retinal Ganglion Cells (RGCs). Such degeneration can be monitored with the Combined Structure Function Index (CSFI), which can generate an estimated RGC count (eRGCC) to identify early glaucomatous change. In this study, we examine the relationship between enlargement of the Foveal Avascular Zone, a capillary free region of the macula, with decreasing eRGCC, to investigate loss of microvascular integrity as a potential etiology for eRGCC decline.

Methods: Five subjects (9 eyes) underwent comprehensive eye exam, OCT for eRGCC calculation, and OCT-A for FAZ area calculation. Pearson correlation and linear regression were used.

Results: Subjects averaged 55±15 years old, with a mean eRGCC of 892,514± 2,222. A significant negative correlation was found between FAZ and eRGCC (r2 = -0.915, p=0.01). in a linear regression model, FAZ as a predictor explained 5.1% of variance in eRGCC (p=0.010), while age, hypertension, and diabetes account for 93.9% (p=0.002). Every 0.01mm2 rise in FAZ was associated with a 327 eRGCC loss.

Conclusion: Increase in FAZ correlates with eRGCC loss in Glaucoma Suspects, implicating a vascular etiology of Glaucoma.

Increased Foveal Avascular Zone Area Predicts Decreased Estimated Retinal Ganglion Cell Count in Glaucoma Suspects: A Pilot Study

Background
Research has shown that dismissal of pain and medical gaslighting remain prevalent issues in healthcare. The current medical education system has increasingly emphasized cultural competence, communication skills and empathy training. Medical gaslighting and dismissal of symptoms have been shown to be associated with decreased trust in healthcare providers, which can subsequently lead to poorer health outcomes.
The objective of this narrative review is to explore the systemic factors that contribute to dismissal of pain in adolescents and young adults and the impact caused by those factors.
Methods
A narrative review of recent literature (2005-2025) was conducted.
Inclusion criteria were: 
Peer-reviewed original research articles, systematic reviews or graduate theses.
Studies that focus on adolescents or young adults based on the World Health Organization (WHO) definition (ages 10 to 30).
Articles addressing patient experience of pain or dismissal of pain by healthcare professionals, parents or other caregivers.
Exclusion criteria were:
Studies limited to the adult population over the age of 30
Articles not in English or not available in full text
Themes from the included studies were synthesized and investigated to identify key contributors to dismissal of pain in adolescents and young adults and to identify any associated outcomes.

Results
Studies have found that between 10% and 54% of adolescents and young adults report having experienced at least one instance of dismissal of pain. Studies also report female gender, identifying as Black and neurodiversity status are associated with reporting more instances of dismissal of pain. 
Conclusion
Our review revealed that dismissal of pain is common among adolescents and young adults with a disproportionately higher prevalence among female, Black and neurodivergent patients. These findings mirror broader patterns reported in the general adult population. Pain dismissal is associated with negative psychosocial outcomes such as the feeling of anger, hostility, self-doubt and isolation. It may also cause strains in the physician-patient relationships and loss of trust in the healthcare providers. 
Given the relational consequences of pain dismissal, there is a need to further investigate possible long-term mental health impacts of pain dismissal in adolescence and young adulthood.
Currently, there is a lack of standard tools for assessing pain dismissal. Developing such tools would enable more accurate measurement and monitoring of pain dismissal. Moreover, developing strategies such as healthcare provider education on pain dismissal to improve communication and validation of patient experiences may reduce potential negative clinical outcomes.


Prevalence and Outcomes of Systemic Dismissal of Pain in Adolescents and Young Adults



Abstract Title: Lung Cancer Screening Among Medicaid Older Adults in New Jersey, 2017-2022 



Background: Routine lung cancer screenings (LCS) were disrupted during the COVID-19 pandemic due to safety restrictions and the diversion of resources for COVID-19 diagnoses. Though the literature has reviewed differences in lung cancer screening rates among distinct groups depending on racial or ethnic minorities or socioeconomic factors, little is known about the impact of the disruption on vulnerable patient populations, particularly the Medicaid population following peak pandemic years. The study objective is to examine LCS rates for pre and post pandemic among New Jersey Medicaid enrollees. This is important because the Medicaid population often have higher risk factors for lung cancer such as smoking and face greater barriers to healthcare, so this enables us to better understand if screening initiatives are working and how they can be improved. 



Methods: This descriptive analysis uses secondary data from the Medicaid Management Information System to estimate the LCS rate among Medicaid enrollees ages 50-75 in New Jersey, 2017-2022. LCSs were identified using the low-dose CT claims code. Results were stratified by socioeconomic factors. Bivariate analysis was performed to assess within-group differences. 



Results*: During the 6-year period, April 2020 had the lowest LCS rate. Rates rebounded and surpassed pre-pandemic levels by August 2020. Comparing 2019 to 2022, the annual screening rate almost doubled, with rate increases across all demographic and regional variables. Key findings were: (1) The younger group (50-64 years old) consistently had higher screening rates than the older (65-75); (2) Non-Hispanic Black enrollees had the greatest increase in rates; (3) The dually eligible (Medicare and Medicaid) screening rate tripled; and (4) Screening rate varied by geographic region, with the Shore region being the highest. 



* In accordance with the project Data Use Agreement, analyses (e.g., rates) are subject to review and comment by the New Jersey Medicaid agency. The analyses are currently under review, and the point estimates will be available for public release prior to the September AMA symposium. 



Conclusion: This study demonstrates success in one state to surpass previous LCS rates. There remains work to be done, however, as LCS is still underutilized compared to other routine cancer screenings. Health organizations can capitalize on the recent increased interest in lung health due to the pandemic and USPTSF lung cancer screening guideline expansion to encourage the use of LCS to reduce cancer mortality. 



Medicaid Lung Cancer Screenings in New Jersey, 2017-2022

Background: Our work describes the clinical course of a patient who developed disseminated coccidiomycosis infection of the central nervous system, resulting in swelling of the central cord at the level of the cervical spine. This, combined with craniocervical adhesions, was observed to block the flow of cerebrospinal fluid (CSF) such that intrathecal antifungals delivered via an intracranial Ommaya reservoir proved insufficient for the treatment of extracranial disease. 

Observations: As the first-ever reported case of an Ommaya reservoir placed in the lumbar spine for treatment of central nervous system coccidiomycosis, this 48-year-old male demonstrated dramatic improvement in upper and lower extremity function after only a few weeks of intrathecal antifungal therapy. With rates of coccidiomycosis infection skyrocketing over the past decade, our clinical study demonstrates the utility of this critical method of drug delivery, previously untapped for the treatment of disseminated coccidiomycosis. 

Lessons: Several months after placement, the lumbar Ommaya and catheter remain patent and functional, despite initial concern that the catheter would become clogged due to the high protein content of CSF from coccidioides infection, as well as subsequent treatment. This clinical study proves intrathecal antifungals delivered via lumbar Ommaya are a viable treatment method to help combat the increasing number of central nervous system cases.

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A Small-Molecule Approach to Overcome ZBTB7A-Mediated Fetal Hemoglobin Repression in Beta-Globinopathies

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