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Osteoarthritis is not a peri-operative risk factor or indicator of poor clinical outcomes with surgical correction for thoracolumbar scoliosis
No full textBackground: Understanding peri-operative influences of patients' past medical history during spinal surgery is essential for promoting good clinical outcomes. A paucity of literature exists regarding the effect of common degenerative disorders like arthritis on spinal fusion outcomes. Methods: A retrospective review of a prospectively maintained database was utilized to examine patients undergoing spine fusion surgery at any spinal segment. Patients with a past medical history of arthritis were identified and analyzed for the following peri-operative events. Results: 532 patients met inclusion criteria, of which 192 suffered from comorbid osteoarthritis. Patients with arthritis were significantly older (P<00.1), had a higher BMI (P=0.0193), and were more likely to be former smokers (P<0.001). When examining intra-operative features, the arthritic cohort construct length was significantly longer (5.79 vs. 6.55, P=0.0112). There were no significant differences in rates of intra-operative complication. Post-operatively, there were no differences in complications, either in surgical site infection (P=0.89) or in the rate of venous thrombotic events (P=1). On follow-up, there were no significant differences in rate of instrumentation failure (P=0.11) or need for revision surgery (P=0.32). Multivariable analysis demonstrated the same trend for all intra-operative findings and all post-operative observations. Conclusion: Arthritis was not associated with increased incidence of intra-operative complications or increased need for fusion revision for our cohort. The presence of arthritis did yield an increased intra-operative blood loss without clear clinical significance. These results suggest that the presence of additional degenerative inflammatory disease does not intrinsically yield a greater incidence of peri-operative complications or failure rates.</p
Intraoperative Ultrasound-Based Displacement Mapping Through Deep Learning
No full textBrain shift during neurological surgery for brain tumors can be caused by factors such as retraction, resection, and osmotic changes and can undermine the reliability of preoperative image-based navigation. Intraoperative ultrasound (iUS) provides a low-cost, real-time imaging alternative, but current correction strategies rely on intraoperative MRI, limiting generalizability and spatial granularity. We present a deep learning framework that predicts voxel-wise brain deformation directly from paired iUS sweeps, allowing for localized brain shift compensation without relying on preoperative MRI.
Using the Brain Images of Tumor Evaluation data set of 13 patients with pre-resection and postresection 3-dimensional iUS and landmark annotations, we trained two 3-dimensional neural network architectures and their ensemble. Performance was measured using standard regression metrics at anatomic landmarks with leave-one-patient-out cross-validation.
The baseline model achieved the lowest average root median squared error [median: 1.45 (IQR: 0.39)], while the enhanced model had the best directional accuracy [median 69.33° (IQR: 44.45°)]. The ensemble balanced both metrics. Gradient-weighted Class Activation Mapping visualization helped identify regions more likely to deform in pre-resection scans. Landmark-wise error analysis showed consistency, with most patients below 2-mm median absolute error but one patient with atypical anatomy had higher error, suggesting challenges in generalizing large or nonuniform shifts with limited data.
Whereas most previous studies have focused on MRI-to-iUS or MRI-to-MRI deformation modeling, our study demonstrates the feasibility of estimating spatially resolved brain shift directly from iUS-to-iUS scans using deep learning. This approach provides dense, real-time deformation fields for better intraoperative adaptability. Future work should expand on data set diversity and size, and integrate multitask learning to distinguish deformation from parenchymal collapse
Data for benthic habitat changes in the Joulters cays and the North Abacos region, the Bahamas
No full textThe aim of this work is to understand how benthic habitat changes in the shallow water of the Bahamas in the last 80 years. Therefore, we compared the modern statellite images with historic images.
This dataset contains:
Data S1: original individual vintage image.
Data S2: assembled vintage image.
Data S3: ArcGIS file that interpret vintage/modern images.
Data S4: Interpreted habitat maps (shapefile).
Data S5: Spreadsheet containing area and perimeter statistics for individual patches.
Data S6: Spreadsheet containing tracking results.
Data S7: Input and output of STACKER model.
Readme: descriptions of these dataset in more details.
The code assoicated with Data S6, S7 is stored in: https://github.com/MindTheGap-ERC/TrackingHabitat.git
Single-dose genome editing therapy rescues auditory and vestibular functions in adult mice with DFNA41 deafness
No full textTargeting the APOM/S1P/S1PR4 AXIS in a Mouse Model of Glomerular Disease
No full textRenal lipid dysmetabolism is increasingly recognized as a key contributor to glomerular disease progression, including Alport Syndrome. We previously identified alterations in the apolipoprotein M (APOM), sphingosine-1-phosphate (S1P), and S1P receptor 4 (S1PR4) signaling axis in human glomerular disease. In this dissertation, we investigated whether this pathway is altered in Alport Syndrome and whether its modulation provides a therapeutic benefit. Glomeruli and podocytes from Col4a3-/- mice, a mouse model of Alport Syndrome exhibited reduced APOM and increased S1PR4 expression, mirroring the pattern observed in human disease. Treatment beginning at early disease stages with recombinant APOM or with CYM50358, a selective S1PR4 antagonist, prevented progression to renal failure and reduced neutral lipid accumulation in glomeruli and podocytes. S1PR4 antagonism enhanced autophagy and lysosomal clearance of lipid droplets, while APOM treatment increased cholesterol efflux, indicating that each treatment promotes distinct lipid clearance pathways. APOM knockdown or S1PR4 overexpression in podocytes were sufficient to induce cell death, although neither manipulation produced lipid droplet accumulation, suggesting that neutral lipid accumulation is an Alport Syndrome-specific phenotype not caused by these alterations alone. Together, these findings identify the APOM/S1PR4 axis as a therapeutically targetable pathway that modulates podocyte lipid handling and protects against renal injury in Alport Syndrome.</p
Serendipity, steroids and science
No full textThe androgen signaling pathway is probably the most important pathway in enabling prostate cancer progression but it also plays essential roles in numerous processes in normal physiology. Both testosterone and dihydrotestosterone are potent androgens that activate the androgen receptor (AR). The essentiality of the androgen pathway in prostate cancer is evidenced in part by the reactivation of AR in prostate cancer that becomes resistant to treatment by gonadal testosterone deprivation. Furthermore, steroid metabolic processes that allow the regeneration of potent androgens in prostate cancer tissues drive this treatment-resistant state, as is made clear by the survival benefit of blocking the synthesis of non-gonadal androgens, e.g., with abiraterone. Here, I narrate and review the process that led to a series of discoveries in androgen metabolism from our group. In this perspective and mechanistic narrative review, I give an honest description of the accidental nature of some of our initial findings, followed by data-driven hypothesis refinement and subsequent studies that illuminate elements of androgen metabolism, with a focus on metabolism of carbon 3, carbon 5 and carbon 17 of the steroid backbone
Inflammation-Associated Mechanisms of Blood–Brain Barrier Disruption and Depression Pathogenesis in People with and Without HIV
No full textDepression is the most common neuropsychiatric comorbidity in people with HIV (PWH), with a prevalence of 30–50%, nearly twice that of the general population. Depression is a major cause of disease burden worldwide associated with increased morbidity and mortality in both people with and without HIV. Converging lines of evidence indicate that chronic peripheral inflammation and neuroinflammation, blood–brain barrier (BBB) disruption, and neurocircuit-level changes interact to mediate depression pathogenesis, and that these processes may be especially relevant in PWH. HIV-associated chronic inflammation, which persists despite viral suppression with antiretroviral therapy, may contribute to depression pathogenesis in this population. BBB permeability has been hypothesized to serve as a key mediator for the interaction of peripheral inflammation with the central nervous system in depression pathogenesis. In this review, we will describe the structure and function of the BBB and how peripheral inflammation interacts with cells of the BBB and the mechanisms that lead to increased BBB permeability. We will discuss current research addressing how peripheral inflammation and BBB disruption contribute to depression pathogenesis in people with and without HIV. We will review current techniques for studying BBB permeability in in vitro, animal, and clinical models and outline future directions for ongoing research
Associations between neighborhood socioeconomic status and cardiometabolic health among Asian American residents of New York City
No full textAsian Americans represent the fastest-growing group in the United States. Yet the relationship between neighborhood socio-economic status (NSES) and cardiometabolic health has not been thoroughly examined. The study goal is to determine the association between NSES with obesity, hypertension, and diabetes among Asian American subgroups.
Data from 4,557 self-identified Chinese, Asians from the Indian sub-continent, or Other Asian participants of the 2017-2020 New York City Community Health Survey were analyzed. Each participant was geo-coded into one of 55 community districts and a NSES factor score was calculated and categorized into low, medium, or high NSES. Overweight/obesity, hypertension, and diabetes were self-reported. Hierarchical multivariable adjusted regression models were used to evaluate the association between NSES and cardiometabolic health.
Compared with high NSES, residing in a neighborhood of medium NSES was associated with higher odds of obesity (OR: 2.70, 95% CI: 1.43, 5.13) among Other Asians and higher odds of overweight/obesity among “All Asians” (OR: 1.41, 95% CI: 1.06, 1.89), Chinese (OR: 1.25, 95% CI: 1.01, 1.62), and “other Asians” (OR: 3.04, 95% CI: 1.39, 6.69).
Lower compared with higher NSES was associated with overweight/obesity among Asian Americans in NYC
Profiling Localized Immunomodulation and Drug Biodistribution within a Subcutaneous Vascularized Niche for Cell Transplantation
No full textSystemic immunosuppression remains essential for preventing allogeneic transplant rejection, but its chronic use causes substantial toxicity. Conceptually, local, site-specific immunomodulation offers a promising alternative, yet comparative mechanistic insight into how immunosuppressants behave when delivered directly to the graft is lacking. Here, we leveraged the Neovascularized Implantable Cell Homing and Encapsulation (NICHE) device, a subcutaneous, vascularized cell-encapsulation platform, as a spatially defined and reproducible model to study local immunomodulation in allogeneic islet transplantation. We systematically profiled the safety, local and systemic immunomodulatory effects, pharmacokinetics, and longitudinal biodistribution of five clinically relevant agents delivered locally at the graft site: CTLA4-Ig, anti-lymphocyte serum, anti-CD40L, anti-CD2, and anti-IL6. Sustained in situ exposure did not impair islet viability or function, and immunosuppressants were confined within the graft, with up to 100-fold lower systemic concentrations. Individual agents produced distinct immune signatures, spanning lymphocyte depletion and shifts in T-cell activation that can guide rational, mechanism-informed combinations for allogeneic cell transplantation. These findings provide a comparative framework for evaluating localized immunosuppression with the potential to transform immunoprotection in cell therapy
Treatment of Lipid Dysregulation in Diseases Through Orally Administrable Nanoparticle Mediated Treatment
No full textThe work presented here addresses the role of lipid dysregulation in disease models and how using advanced nanoparticle techniques, we can treat these diseases. Lipid dysregulation is a significant facet of several diseases including cancer, atherosclerosis and diabetes. By developing nanotherapeutic approaches to include existing drugs, or by creating their prodrugs we are able to increase their efficacy, particularly when used in conjunction with nanoparticle mediated drug delivery. Nanoparticles are emerging tools which can be fine tuned to deliver encapsulated and/or attached drugs to specific cell types or subcellular targets. Nanoparticles are particularly useful to facilitate the efficacy of drugs or prodrugs which are not readily soluble in water. By specifically targeting the lipid metabolism processes, we were able to achieve significant progress in treating these diseases. Throughout this work, we demonstrate that targeting lipid dysregulation in prostate cancer, hyperlipidemia due to atherosclerosis, and diabetic kidney disease, can have a considerable effect on the prognosis. By developing prodrugs which attack lipid metabolism in aggressive prostate cancer, or by developing nanoparticles which can clear excessive lipids deposited in blood vessels and tissue, we see that by correcting the dysregulated state of lipids, we can positively affect the therapeutic outcome. </p