Michael D. Swartz

Michael D. Swartz

The University of Texas Health Science Center at Houston, School of Public Health, Houston, Texas, USA

Research Focus & Metrics

Academic Career Length

33Years (1994-Present)

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

Representative Publications

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23 April 2014 in The Oncologist
Verified
Journal Article
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DHDavid Hui
David Hui
RSRenata dos Santos
Renata dos Santos
GCGary Chisholm
Gary Chisholm
SBSwati Bansal
Swati Bansal
TSThiago Buosi Silva
Thiago Buosi Silva
EBEduardo Bruera
Eduardo Bruera
Background.: The physical signs of impending death have not been well characterized in cancer patients. A better understanding of these signs may improve the ability of clinicians to diagnose impending death. We examined the frequency and onset of 10 bedside physical signs and their diagnostic performance for impending death. Methods.: We systematically documented 10 physical signs every 12 hours from admission to death or discharge in 357 consecutive patients with advanced cancer admitted to two acute palliative care units. We examined the frequency and median onset of each sign from death backward and calculated their likelihood ratios (LRs) associated with death within 3 days. Results.: In total, 203 of 357 patients (52 of 151 in the U.S., 151 of 206 in Brazil) died. Decreased level of consciousness, Palliative Performance Scale ≤20%, and dysphagia of liquids appeared at high frequency and >3 days before death and had low specificity (<90%) and positive LR (95%) and positive LRs for death within 3 days, including pulselessness of radial artery (positive LR: 15.6; 95% confidence interval [CI]: 13.7–17.4), respiration with mandibular movement (positive LR: 10; 95% CI: 9.1–10.9), decreased urine output (positive LR: 15.2; 95% CI: 13.4–17.1), Cheyne-Stokes breathing (positive LR: 12.4; 95% CI: 10.8–13.9), and death rattle (positive LR: 9; 95% CI: 8.1–9.8). Conclusion.: We identified highly specific physical signs associated with death within 3 days among cancer patients.

1 May 2012 in Cancer Epidemiology, Biomarkers & Prevention
Verified
Journal Article
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LCLee Cheng
Lee Cheng
MSMichael D. Swartz
Michael D. Swartz
HZHui Zhao
Hui Zhao
AKAsha S. Kapadia
Asha S. Kapadia
DLDejian Lai
Dejian Lai
SGSharon H. Giordano
Sharon H. Giordano
Background: Few studies have used SEER-Medicare data to describe recurrence of breast cancer after primary treatment for U.S. women. Methods: We used SEER-Medicare data to estimate the annual hazard rate (HR) of recurrence for women with breast cancer between 1991 and 1997 with 10 years of follow-up. The Kaplan–Meier method was used to derive the HR. Multivariate Cox proportional hazards model was used to estimate the relative hazard of the recurrence-associated prognostic factors. Results: Of 20,027 women, 36.8% had recurrence within 10 years, with most of these recurrences (81.9%) occurring within 5 years after diagnosis. Women with stage III cancer showed the highest HR peak and largest magnitude than women with stage I or II disease (both P < 0.01) within the first 5 years. Women with negative tumor hormone receptor status had a higher peak hazard of developing recurrence within the first 5 years (P < 0.01), but the hazards were remarkably lower beyond 5 years of follow-up than in women with positive or unknown hormone receptor status (P > 0.05). Women with poorly differentiated histologic grade tumors showed higher HR in the first 5 years than women with other grades after primary treatment (both P < 0.01). The increased risk of recurrence of breast cancer was associated with advanced stage, moderate and poorly differently grades, and negative hormone receptor status (all P < 0.01). Conclusion: The HRs of the recurrence are dynamic over 10 years and are markedly determined by prognostic factors at diagnosis. Impact: Our study suggests that the optimal follow-up may differ among women. Cancer Epidemiol Biomarkers Prev; 21(5); 800–9. ©2012 AACR.

11 May 2016 in PLOS Pathogens
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Journal Article
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JBJustin Bahl
Justin Bahl
TPTruc T. Pham
Truc T. Pham
NHNichola J. Hill
Nichola J. Hill
IHIslam T. M. Hussein
Islam T. M. Hussein
EMEric J. Ma
Eric J. Ma
JRJonathan A. Runstadler
Jonathan A. Runstadler
Despite evidence for avian influenza A virus (AIV) transmission between wild and domestic ecosystems, the roles of bird migration and poultry trade in the spread of viruses remain enigmatic. In this study, we integrate ecosystem interactions into a phylogeographic model to assess the contribution of wild and domestic hosts to AIV distribution and persistence. Analysis of globally sampled AIV datasets shows frequent two-way transmission between wild and domestic ecosystems. In general, viral flow from domestic to wild bird populations was restricted to within a geographic region. In contrast, spillover from wild to domestic populations occurred both within and between regions. Wild birds mediated long-distance dispersal at intercontinental scales whereas viral spread among poultry populations was a major driver of regional spread. Viral spread between poultry flocks frequently originated from persistent lineages circulating in regions of intensive poultry production. Our analysis of long-term surveillance data demonstrates that meaningful insights can be inferred from integrating ecosystem into phylogeographic reconstructions that may be consequential for pandemic preparedness and livestock protection. It is assumed that AIV outbreaks in poultry are introduced from wild birds. To test this, we incorporated ecosystem and location of isolation into a comparative genetic analysis. We show high rates of viral transmission from domestic to wild birds within a region and, that wild birds could transmit AIV to poultry between regions. However, the highest rates of viral flow between regions was among domestic populations, indicating poultry trade may play a major role in spreading viral populations. We demonstrate that interactions between migratory birds and animal productions systems contribute to the emergence of AIV. The assumption of unidirectional viral flow from wild birds to domestic poultry provides an incomplete picture of influenza ecology and may confound control efforts.

1 October 2009 in Cancer Epidemiology, Biomarkers & Prevention
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Journal Article
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CRCielito C. Reyes-Gibby
Cielito C. Reyes-Gibby
MSMargaret R. Spitz
Margaret R. Spitz
SYSriram Yennurajalingam
Sriram Yennurajalingam
MSMichael D. Swartz
Michael D. Swartz
JGJian Gu
Jian Gu
SSSanjay Shete
Sanjay Shete
Many of the same inflammatory factors that promote tumor growth are also hypothesized to function as pain modulators. There is substantial interindividual variation in pain severity in cancer patients. Therefore, we evaluated 59 single nucleotide polymorphisms in 37 inflammation genes in newly diagnosed non-Hispanic Caucasian lung cancer patients (n = 667) and assessed their association with pain severity. Patients rated their pain “during the past week” on an 11-point numeric scale (0 = “no pain” and 10 = “pain as bad as you can imagine”) at presentation before initiating cancer therapy. Reported analgesic use was abstracted from charts and converted to morphine equivalent daily dose. Results showed that 16% of the patients reported severe pain (score ≥7). Advanced stage of disease [odds ratio (OR), 2.34; 95% confidence interval (95% CI), 1.50-3.65; P = 0.001], age ≤50 years (OR, 2.10; 95% CI, 1.32-3.30; P = 0.002), reports of depressed mood (OR, 3.68; 95% CI, 1.96-6.93; P = 0.001), fatigue (OR, 3.72; 95% CI, 2.36-5.87; P = 0.001), and morphine equivalent daily dose (OR, 1.02; 95% CI, 1.01-1.03) were significantly correlated with severe pain. Controlling for these nongenetic covariates, we found that patients with CC genotypes for PTGS2 exon10+837T>C (rs5275) were at lower risk for severe pain (OR, 0.33; 95% CI, 0.11-0.97) and an additive model for TNFα −308GA (rs1800629; OR, 1.67; 95% CI, 1.08-2.58) and NFKBIA Ex6+50C>T (rs8904) was predictive of severe pain (OR, 0.64; 95% CI, 0.43-0.93). In a multigene analysis, we found a gene-dose effect, with each protective genotype reducing the risk for severe pain by as much as 38%. This study suggests the importance of inflammation gene polymorphisms in modulating pain severity. Additional studies are needed to validate our findings. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2636–42)

1 February 2019 in The American Journal of Surgery
Verified
Journal Article
Closed access
RLRoy Lei
Roy Lei
MSMichael D. Swartz
Michael D. Swartz
JHJohn A. Harvin
John A. Harvin
BCBryan A. Cotton
Bryan A. Cotton
JHJohn B. Holcomb
John B. Holcomb
SASasha D. Adams
Sasha D. Adams

6 May 2022 in The Journal of Infectious Diseases
Verified
Journal Article
Open access
PDF file
MSMichael D. Swartz
Michael D. Swartz
SDStacia M DeSantis
Stacia M DeSantis
AYAshraf Yaseen
Ashraf Yaseen
FBFrances A Brito
Frances A Brito
MVMelissa A Valerio-Shewmaker
Melissa A Valerio-Shewmaker
EBEric Boerwinkle
Eric Boerwinkle
Understanding the duration of antibodies to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus that causes COVID-19 is important to controlling the current pandemic. Participants from the Texas Coronavirus Antibody Response Survey (Texas CARES) with at least 1 nucleocapsid protein antibody test were selected for a longitudinal analysis of antibody duration. A linear mixed model was fit to data from participants (n = 4553) with 1 to 3 antibody tests over 11 months (1 October 2020 to 16 September 2021), and models fit showed that expected antibody response after COVID-19 infection robustly increases for 100 days postinfection, and predicts individuals may remain antibody positive from natural infection beyond 500 days depending on age, body mass index, smoking or vaping use, and disease severity (hospitalized or not; symptomatic or not).