Publications by authors named "E C HAMMOND"

Objective: This study sought to: (1) evaluate hospital-level variation in infections following cardiac surgery and (2) develop and evaluate a 180-day infection quality metric.

Methods: This study evaluated Medicare claims that were merged with institutional Society of Thoracic Surgeons Adult Cardiac Surgery Database files among patients undergoing cardiac surgery across 33 Michigan centers. The primary outcome was an infection within 180 days of surgery.

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Hypoxia is a common feature of solid tumors that has previously been linked to resistance to radiotherapy and chemotherapy, and more recently to immunotherapy. In particular, hypoxic tumors exclude T cells and inhibit their activity, suggesting that tumor cells acquire a mechanism to evade T-cell recognition and killing. Our analysis of hypoxic tumors indicates that hypoxia downregulates the expression of MHC class I and its bound peptides (i.

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Apoptosis is a fundamental process of all mammalian cells but exactly how it is regulated in different primary cells remains less explored. In most contexts, apoptosis is engaged to eliminate cells. However, postmitotic cells such as neurons must efficiently balance the need for developmental apoptosis versus the physiological needs for their long-term survival.

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Article Synopsis
  • The study aimed to investigate the relationship between subregional NaF-SUV values, T-T measurements, and vertical ground reaction forces in patients with isolated patellofemoral-joint-osteoarthritis (PFJ-OA).
  • Thirty-five PFJ-OA patients underwent advanced imaging scans to assess their knee conditions and calculate loading rates during walking trials.
  • Results revealed complex associations between bone and cartilage measurements, highlighting a notable link between increased bone uptake and gait characteristics, suggesting important clinical implications for PFJ-OA management.
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Hypoxia-inducible factor 1 (HIF-1), recognized as a master transcription factor for adaptation to hypoxia, is associated with malignant characteristics and therapy resistance in cancers. It has become clear that cofactors such as ZBTB2 are critical for the full activation of HIF-1; however, the mechanisms downregulating the ZBTB2-HIF-1 axis remain poorly understood. In this study, we identified ZBTB7A as a negative regulator of ZBTB2 by analyzing protein sequences and structures.

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