Yashraj Srivastava

Mr. Yashraj Srivastava

orcid

Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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11 January 2025 in Journal of Clinical Medicine
Verified
Journal Article
Open access
PDF file
RBRiana Lo Bu
Riana Lo Bu
RFRose Fluss
Rose Fluss
YSYashraj Srivastava
Yashraj Srivastava
RRRafael De la Garza Ramos
Rafael De la Garza Ramos
SMSaikiran G. Murthy
Saikiran G. Murthy
YMYaroslav Gelfand MD
Yaroslav Gelfand MD
Bone mineral density (BMD) is an essential indicator of bone strength and plays a crucial role in the clinical management of various spinal pathologies. Hounsfield units (HUs) calculated from computed tomography (CT) scans are a well-established, effective, and non-invasive method to determine bone density in the lumbar spine when juxtaposed to dual-energy X-ray absorptiometry (DEXA) scans, the gold standard for assessing trabecular bone density. Only recently have studies begun to investigate and establish HUs as a reliable and valid alternative for bone quality assessment in the cervical spine as well. In addition, multiple recent studies have identified cervical HUs as an accurate predictor of cage subsidence, an undesired complication of anterior cervical discectomy and fusion (ACDF) of anterior cervical corpectomy and fusion (ACCF) procedures. Subsidence involves migration of the spinal fusion cage into vertebral bodies, causing a loss of disk space, negatively altering spine alignment, and possibly necessitating further unwanted surgical intervention. Using the PRISMA-ScR checklist and the registered scoping review protocol (INPLASY2024100126), this review explores the current research on the use of cervical spine HU measurements as both a determinant of BMD and as a prognosticator of postoperative subsidence following cervical spine procedures (i.e., ACDFs and ACCFs) with the aim of improving clinical and surgical outcomes.

YSYashraj Srivastava
Yashraj Srivastava
KHKorri Hershenhouse
Korri Hershenhouse
IFIsaac Faith
Isaac Faith
TNTanner Nelson
Tanner Nelson
BFBrandon Edward Ferrell
Brandon Edward Ferrell
Tadahisa SugiuraTadahisa Sugiura
Tadahisa Sugiura
Background: Immune dysregulation and clinical immunosuppression are biologically plausible contributors to thoracic aortic wall vulnerability through endothelial injury, protease-mediated extracellular matrix remodeling, vascular smooth muscle cell dysfunction, and impaired vascular repair. Yet, the clinical relevance of immunomodulated states to thoracic aortic aneurysm (TAA) incidence or growth and acute aortic syndromes remains undefined. Methods: This comprehensive review synthesizes clinical and translation evidence linking immunomodulated states in solid organ transplantation, autoimmune disease (predominantly systemic lupus erythematosus), HIV, and oncologic therapies to thoracic aortic dilation, aneurysmal progression, and acute aortic events. Principal Findings: Across transplant, autoimmune, and HIV cohorts, recurring themes include chronic immune dysregulation, endothelial dysfunction, proteolytic matrix remodeling, and impaired vascular repair capacity, although thoracic segment-specific longitudinal growth data remain limited and are often embedded within analyses of multiple vascular beds. In oncologic cohorts, aggregate analyses generally do not demonstrate uniform acceleration of aneurysm growth with malignancy or chemotherapy exposure, although agent-level models suggest that regimen-specific effects may be obscured in pooled estimates. Two studies most directly addressed our question in thoracic-relevant contexts reported (1) very low mean annual ascending aortic aneurysm growth (0.18 ± 0.64 mm/year) with no detectable association with chemotherapy or radiotherapy and (2) prior immunosuppressive/cytostatic chemotherapy exposure to be common in a proximal TAA surgical cohort (39.3%) without a clear difference in thoracic phenotype at presentation or postoperative outcomes. In HIV cohorts, available evidence supports modest but reproducible proximal aortic remodeling and a clinically meaningful aneurysm burden across vascular beds, yet definitive thoracic segment-specific natural history data remain limited. Conclusions: The available literature supports clinical vigilance and exposure-aware surveillance, while suggesting that thoracic aortic risk is unlikely to be uniform across immunosuppressive and cytotoxic therapies. Standardized, segment-specific longitudinal imaging with granular agent-level exposure characterization (dose, duration, sequencing, and combination regimens), consistent definitions of baseline diameter and growth, careful adjustment for key confounders, and prospective ascertainment of dissection/rupture and operative endpoints are needed to translate immunobiology into actionable risk stratification and long-term management strategies.