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51.
Lars Burdorf Christopher T. Laird Donald G. Harris Margaret R. Connolly Zahra Habibabady Emily Redding Natalie A. O'Neill Arielle Cimeno Dawn Parsell Carol Phelps David Ayares Agnes M. Azimzadeh Richard N. Pierson 《American journal of transplantation》2022,22(1):28-45
Galactosyl transferase knock-out pig lungs fail rapidly in baboons. Based on previously identified lung xenograft injury mechanisms, additional expression of human complement and coagulation pathway regulatory proteins, anti-inflammatory enzymes and self-recognition receptors, and knock-down of the β4Gal xenoantigen were tested in various combinations. Transient life-supporting GalTKO.hCD46 lung function was consistently observed in association with either hEPCR (n = 15), hTBM (n = 4), or hEPCR.hTFPI (n = 11), but the loss of vascular barrier function in the xenograft and systemic inflammation in the recipient typically occurred within 24 h. Co-expression of hEPCR and hTBM (n = 11) and additionally blocking multiple pro-inflammatory innate and adaptive immune mechanisms was more consistently associated with survival >1 day, with one recipient surviving for 31 days. Combining targeted genetic modifications to the lung xenograft with selective innate and adaptive immune suppression enables prolonged initial life-supporting lung function and extends lung xenograft recipient survival, and illustrates residual barriers and candidate treatment strategies that may enable the clinical application of other organ xenografts. 相似文献
52.
Anshu Khanna Eric M Sturgis Kristina R Dahlstrom Li Xu Qingyi Wei Guojun Li Neil D Gross 《American journal of cancer research》2021,11(5):2343
Smoking and alcohol exposure continue to be the dominant risk factors for the development of head and neck squamous cell carcinoma (SCCHN) worldwide. Moreover, human papillomavirus (HPV) is associated with SCCHN, particularly SCC of the oropharynx (SCCOP). Body mass index (BMI) has been reported as a possible risk factor for SCCHN, yet the data available so far about the relationship between BMI and SCCHN risk have been mixed. We sought to clarify this relationship. BMI and demographic, clinical, and epidemiological information at diagnosis were collected from 2310 SCCHN cases and 1915 controls (who were cancer-free) from October 2001 through May 2013. The odds ratios (ORs) and 95 percent confidence intervals (95% CI) were determined using the logistic regression process. Multivariable models were used to evaluate the strength of the relation between BMI and SCCHN risk. At diagnosis, 64 (2.8%) of the cases were underweight (BMI <18.5 kg/m2), 661 (28.6%) were normal weight (BMI 18.5<25 kg/m2), 833 (36.1%) were overweight (BMI 25<30 kg/m2), and 752 (32.6%) were obese (BMI ≥30 kg/m2). Comparatively, the ORs (95% CIs) for SCCHN associated with being underweight, overweight, and obese were 2.6 (1.54.7), 0.7 (0.6-0.8), and 0.8 (0.7-0.9), respectively, after adjusting for age, gender, race/ethnicity, smoking, and alcohol consumption. On analysis stratified by tumor sites, the risk of SCCOP among patients seropositive for HPVE6 and/or HPVE7 was higher among the overweight (OR, 5.4, 95% CI, 1.3-23.1) and obese patients (OR, 2.4, 95% CI, 1.1-7.6) compared to the normal weight patients. These findings suggest that pretreatment BMI could be a major risk factor for SCCHN, and the association between BMI and HPV may increase the risk of SCCOP. 相似文献
53.
Bruce L. Jacobs MD MPH Devin Rogers BS Jonathan G. Yabes PhD Jathin Bandari MD Omar M. Ayyash MD MPH Avinash Maganty MD Kody M. Armann BS Hermoon A. Worku BS Natalie M. Pace BS Anup Shah MD Kelly R. Pekala MD MS Michelle Yu MD Jacques E. Chelly MD PhD MBA Liam C. Macleod MD MPH Benjamin J. Davies MD 《Cancer》2021,127(2):257-265
54.
Douglas E. Holt Susan M. Hiniker John A. Kalapurakal John C. Breneman Jay C. Shiao Nicole Boik Benjamin T. Cooper Paige L. Dorn Matthew D. Hall Natalie Logie John T. Lucas Iain J. MacEwan Adam C. Olson Joshua D. Palmer Samir Patel Luke E. Pater Stephanie Surgener Derek S. Tsang Sarah A. Milgrom 《International journal of radiation oncology, biology, physics》2021,109(2):505-514
55.
Fredenburg Kristianna M. Whitlock Joan Morris Christopher Kirwan Jessica Silver Natalie L. Ragin Camille Parker Alexander Mendenhall William M. 《Cancer causes & control : CCC》2021,32(11):1269-1278
Cancer Causes & Control - Disparate clinical outcomes for pharyngeal squamous cell carcinoma (PSCC) of the oropharynx (OPSCC) and hypopharynx (HPSCC) have been observed in Black compared with... 相似文献
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Falardeau J Chung WC Beenken A Raivio T Plummer L Sidis Y Jacobson-Dickman EE Eliseenkova AV Ma J Dwyer A Quinton R Na S Hall JE Huot C Alois N Pearce SH Cole LW Hughes V Mohammadi M Tsai P Pitteloud N 《The Journal of clinical investigation》2008,118(8):2822-2831
Idiopathic hypogonadotropic hypogonadism (IHH) with anosmia (Kallmann syndrome; KS) or with a normal sense of smell (normosmic IHH; nIHH) are heterogeneous genetic disorders associated with deficiency of gonadotropin-releasing hormone (GnRH). While loss-of-function mutations in FGF receptor 1 (FGFR1) cause human GnRH deficiency, to date no specific ligand for FGFR1 has been identified in GnRH neuron ontogeny. Using a candidate gene approach, we identified 6 missense mutations in FGF8 in IHH probands with variable olfactory phenotypes. These patients exhibited varied degrees of GnRH deficiency, including the rare adult-onset form of hypogonadotropic hypogonadism. Four mutations affected all 4 FGF8 splice isoforms (FGF8a, FGF8b, FGF8e, and FGF8f), while 2 mutations affected FGF8e and FGF8f isoforms only. The mutant FGF8b and FGF8f ligands exhibited decreased biological activity in vitro. Furthermore, mice homozygous for a hypomorphic Fgf8 allele lacked GnRH neurons in the hypothalamus, while heterozygous mice showed substantial decreases in the number of GnRH neurons and hypothalamic GnRH peptide concentration. In conclusion, we identified FGF8 as a gene implicated in GnRH deficiency in both humans and mice and demonstrated an exquisite sensitivity of GnRH neuron development to reductions in FGF8 signaling. 相似文献