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The authors have obtained rotationally resolved vacuum ultraviolet pulsed field ionization-photoelectron (vuv-PFI-PE) spectrum of HD in the photon energy range of 15.29–18.11 eV, covering the ionization transitions HD+(X 2Σg+,v+=0–21,N+)←HD(X 1Σg+,v″=0,J″). The assignment of rotational transitions resolved in the vuv-PFI-PE vibrational bands for HD+(X 2Σg+,v+=0–20) and their simulation using the Buckingham-Orr-Sichel (BOS) model are presented. Rotational branches corresponding to the ΔN=N+-J″=0, ±1, ±2, ±3, and ±4 transitions are observed in the vuv-PFI-PE spectrum of HD. The BOS simulation shows that the perturbation of vuv-PFI-PE rotational line intensities due to near resonance autoionization is very minor at v+>=5 and decreases as v+ is increased. Thus, the rotationally resolved PFI-PE bands for HD+(v+>=5) presented here provide reliable estimates of state-to-state cross sections for direct photoionization of HD, while the rotationally resolved PFI-PE bands for HD+(v+<5) are useful data for fundamental understanding of the near resonance autoionizing mechanism. On the basis of the rovibrational assignment of the vuv-PFI-PE bands, the ionization energies for the formation of HD+(X 2Σg+,v+=0–20,N+) from HD(X 1Σg+,v″=0,J″) and the vibrational constants (ωe, ωeχe, ωeye, and ωeze), the rotational constants (Be and αe), the vibrational energy spacings, and the dissociation energy for HD+(X 2Σg+) are determined. As expected, these values are found to be in excellent agreement with high level theoretical predictions. [ABSTRACT FROM AUTHOR]

Reports on the acquisition of rotationally resolved pulsed field ionization photoelectron spectra of oxygen covering the ionization transitions of O[sup +][sub 2](B [sup 2]Sigma[sup -][sub g], v[sup +]=0-7,N[sup +]...O[sub 2](X [sup 3]Sigma[sup -][sub g], v''=0,N''). Pulsed field ionization photoelectron measurements; Measurements of lifetimes for high-n Rydberg states.

Examines the pulsed field ionization photoelectron spectrum (PFI-PE) of oxygen gas. Observation on the rotational branches; Estimation of the rotational linewidths; Determination of the predissociation lifetimes; Calculation of equilibrium bond distances; Measurement of nominal lifetimes for Rydberg states.

Examines the collision-induced dissociation (CID) reaction of chloro compounds. Measurement of the absolute total cross sections produced by the CID reaction in the center-of-mass collision energy; Validity of the energy randomization of chloro compounds; Promotion of couplings or energy flow among the vibrational modes.

Presents a theoretical study of the vacuum ultraviolet pulsed field ionization photoelectron band for carbonyl sulphide. Correlation between the experimental and theoretical Renner-Teller calculations of the vibronic states; Factors attributing the symmetry of geometry-dependent electronic transition dipole operator components.

Improves a newly developed experimental scheme for high resolution pulsed field ionization photoelectron (PFI-PE) studies of oxygen using the high resolution monochromatized multibunch undulator synchroton of the chemical dynamics beamline at the advanced light source. Advantage of the scheme for PFI-PE measurements to have no contamination by background electrons.

The vacuum ultraviolet pulsed field ionization-photoelectron (PFI-PE) spectra for CO[sub 2] have been measured in the energy range of 13.6-14.7 eV, revealing complex vibronic structures for the ground CO[sub 2][sup +](X [sup 2]Π[sub g]) state. Many vibronic bands for CO[sub 2][sup +](X [sup 2]Π[sub g]), which were not resolved in previous photoelectron studies, are identified in the present measurement based on comparison with available optical data and theoretical predictions. As observed in the HeI photoelectron spectrum of CO[sub 2], the PFI-PE spectrum is dominated by the symmetry allowed ν[sub 1][sup +] (symmetric stretch) vibrational progression for CO[sub 2][sup +](X [sup 2]Π[sub g]). However, PFI-PE vibronic bands due to excitation of the symmetry disallowed ν[sub 2][sup +] (bending) and ν[sub 3][sup +] (asymmetric stretch) modes with both odd quanta, together with the symmetry allowed even quanta excitations, are clearly discernible. The simulation of rotational contours resolved in PFI-PE vibronic bands associated with excitation to the (ν[sub 1][sup +]=0-1, ν[sub 2][sup +]=0-2, ν[sub 3][sup +]=0) vibrational levels has yielded accurate ionization energies for the formation of these vibronic states from CO[sub 2](X [sup 1]Σ[sub g][sup +]). © 2000 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Objective: We analyzed the pooled case-control data from the International Head and Neck Cancer Epidemiology (INHANCE) consortium to compare cigarette smoking and alcohol consumption risk factors for head and neck cancer between less developed and more developed countries., Subjects and Methods: The location of each study was categorized as either a less developed or more developed country. We compared the risk of overall head and neck cancer and cancer of specific anatomic subsites associated with cigarette smoking and alcohol consumption. Additionally, age and sex distribution between categories was compared., Results: The odds ratios for head and neck cancer sites associated with smoking duration differed between less developed and more developed countries. Smoking greater than 20 years conferred a higher risk for oral cavity and laryngeal cancer in more developed countries, whereas the risk was greater for oropharynx and hypopharynx cancer in less developed countries. Alcohol consumed for more than 20 years conferred a higher risk for oropharynx, hypopharynx, and larynx cancer in less developed countries. The proportion of cases that were young (<45 years) or female differed by country type for some HNC subsites., Conclusion: These findings suggest the degree of industrialization and economic development affects the relationship between smoking and alcohol with head and neck cancer., (© 2022 Wiley Periodicals LLC.)

The American Cancer Society predicted more than 52 000 new cases of thyroid cancer in 2020, making it the most prevalent endocrine malignancy. Due to the approximately threefold higher incidence of thyroid cancer in women, we hypothesize that androgens and/or androgen receptors play a protective role and that thyroid cancer in men represents an escape from androgen-mediated cell regulation. The analysis of androgen receptor (AR) expression in patient tissue samples identified a 2.7-fold reduction in AR expression (p < 0.005) in papillary thyroid cancer compared with matched, normal tissue. An in vitro cell model was developed by stably transfecting AR into 8505C undifferentiated thyroid cancer cells (resulting in clone 84E7). The addition of DHT to the clone 84E7 resulted in AR translocation into the nucleus and a 70% reduction in proliferation, with a shift in the cell cycle toward G1 arrest. RNASeq analysis revealed significant changes in mRNA levels associated with proliferation, cell cycle, and cell cycle regulation. Furthermore, androgen significantly decreased the levels of the G1-associated cell cycle progression proteins cdc25a CDK6 CDK4 and CDK2 as well as increased the levels of the cell cycle inhibitors, p27 and p21. The data strongly suggest that DHT induces a G1 arrest in androgen-responsive thyroid cancer cells. Together, these data support our hypothesis that AR/androgen may play a protective, antiproliferative role and are consistent with younger men having a lower incidence of thyroid cancer than women., (© 2021 Wiley Periodicals LLC.)

Background: Alcohol is a well-established risk factor for head and neck cancer (HNC). This study aims to explore the effect of alcohol intensity and duration, as joint continuous exposures, on HNC risk., Methods: Data from 26 case-control studies in the INHANCE Consortium were used, including never and current drinkers who drunk ≤10 drinks/day for ≤54 years (24234 controls, 4085 oral cavity, 3359 oropharyngeal, 983 hypopharyngeal and 3340 laryngeal cancers). The dose-response relationship between the risk and the joint exposure to drinking intensity and duration was investigated through bivariate regression spline models, adjusting for potential confounders, including tobacco smoking., Results: For all subsites, cancer risk steeply increased with increasing drinks/day, with no appreciable threshold effect at lower intensities. For each intensity level, the risk of oral cavity, hypopharyngeal and laryngeal cancers did not vary according to years of drinking, suggesting no effect of duration. For oropharyngeal cancer, the risk increased with durations up to 28 years, flattening thereafter. The risk peaked at the higher levels of intensity and duration for all subsites (odds ratio = 7.95 for oral cavity, 12.86 for oropharynx, 24.96 for hypopharynx and 6.60 for larynx)., Conclusions: Present results further encourage the reduction of alcohol intensity to mitigate HNC risk.

Head and neck cancer (HNC) risk prediction models based on risk factor profiles have not yet been developed. We took advantage of the large database of the International Head and Neck Cancer Epidemiology (INHANCE) Consortium, including 14 US studies from 1981-2010, to develop HNC risk prediction models. Seventy percent of the data were used to develop the risk prediction models; the remaining 30% were used to validate the models. We used competing-risk models to calculate absolute risks. The predictors included age, sex, education, race/ethnicity, alcohol drinking intensity, cigarette smoking duration and intensity, and/or family history of HNC. The 20-year absolute risk of HNC was 7.61% for a 60-year-old woman who smoked more than 20 cigarettes per day for over 20 years, consumed 3 or more alcoholic drinks per day, was a high school graduate, had a family history of HNC, and was non-Hispanic white. The 20-year risk for men with a similar profile was 6.85%. The absolute risks of oropharyngeal and hypopharyngeal cancers were generally lower than those of oral cavity and laryngeal cancers. Statistics for the area under the receiver operating characteristic curve (AUC) were 0.70 or higher, except for oropharyngeal cancer in men. This HNC risk prediction model may be useful in promoting healthier behaviors such as smoking cessation or in aiding persons with a family history of HNC to evaluate their risks., (© The Author(s) 2019. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

High dietary glycaemic index (GI) and glycaemic load (GL) may increase cancer risk. However, limited information was available on GI and/or GL and head and neck cancer (HNC) risk. We conducted a pooled analysis on 8 case-control studies (4081 HNC cases; 7407 controls) from the International Head and Neck Cancer Epidemiology (INHANCE) consortium. We estimated the odds ratios (ORs) and 95% confidence intervals (CIs) of HNC, and its subsites, from fixed- or mixed-effects logistic models including centre-specific quartiles of GI or GL. GI, but not GL, had a weak positive association with HNC (OR Q4 vs. Q1  = 1.16; 95% CI = 1.02-1.31). In subsites, we found a positive association between GI and laryngeal cancer (OR Q4 vs. Q1  = 1.60; 95% CI = 1.30-1.96) and an inverse association between GL and oropharyngeal cancer (OR Q4 vs. Q1  = 0.78; 95% CI = 0.63-0.97). This pooled analysis indicates a modest positive association between GI and HNC, mainly driven by laryngeal cancer.

Background: Tobacco use is a well-established risk factor for head and neck cancer (HNC). However, less is known about the potential impact of exposure to tobacco at an early age on HNC risk., Methods: We analyzed individual-level data on ever tobacco smokers from 27 case-control studies (17,146 HNC cases and 17,449 controls) in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using random-effects logistic regression models., Results: Without adjusting for tobacco packyears, we observed that younger age at starting tobacco use was associated with an increased HNC risk for ever smokers (OR <10 years vs. ≥30 years : 1.64, 95% CI: 1.35, 1.97). However, the observed association between age at starting tobacco use and HNC risk became null after adjusting for tobacco packyears (OR <10 years vs. ≥30 years : 0.97, 95% CI: 0.80, 1.19). In the stratified analyses on HNC subsites by tobacco packyears or years since quitting, no difference in the association between age at start and HNC risk was observed., Conclusions: Results from this pooled analysis suggest that increased HNC risks observed with earlier age at starting tobacco smoking are largely due to longer duration and higher cumulative tobacco exposures., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Objectives: This study aimed at re-evaluating the strength and shape of the dose-response relationship between the combined (or joint) effect of intensity and duration of cigarette smoking and the risk of head and neck cancer (HNC). We explored this issue considering bivariate spline models, where smoking intensity and duration were treated as interacting continuous exposures., Materials and Methods: We pooled individual-level data from 33 case-control studies (18,260 HNC cases and 29,844 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. In bivariate regression spline models, exposures to cigarette smoking intensity and duration (compared with never smokers) were modeled as a linear piecewise function within a logistic regression also including potential confounders. We jointly estimated the optimal knot locations and regression parameters within the Bayesian framework., Results: For oral-cavity/pharyngeal (OCP) cancers, an odds ratio (OR) >5 was reached after 30 years in current smokers of ∼20 or more cigarettes/day. Patterns of OCP cancer risk in current smokers differed across strata of alcohol intensity. For laryngeal cancer, ORs >20 were found for current smokers of ≥20 cigarettes/day for ≥30  years. In former smokers who quit ≥10  years ago, the ORs were approximately halved for OCP cancers, and ∼1/3 for laryngeal cancer, as compared to the same levels of intensity and duration in current smokers., Conclusion: Referring to bivariate spline models, this study better quantified the joint effect of intensity and duration of cigarette smoking on HNC risk, further stressing the need of smoking cessation policies., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: Thyroid cancer is the most common endocrine malignancy worldwide, with the predominant form papillary thyroid carcinoma (PTC) representing approximately 80% of cases., Objective: This study was addressed to identify potential genes and pathways involved in the pathogenesis of PTC and potential novel biomarkers for this disease., Methods: Gene expression profiling was carried out by DNA microarray technology. Validation of microarray data by qRT-PCR, western blot, and enzyme linked immunosorbent assay was also performed in a selected set of genes and gene products, with the potential to be used as diagnostic or prognostic biomarkers, such as those associated with cell adhesion, extracellular matrix (ECM) remodeling and immune/inflammatory response., Results: In this study we found that upregulation of extracellular activities, such as proteoglycans, ECM-receptor interaction, and cell adhesion molecules, were the most prominent feature of PTC. Significantly over-expressed genes included SDC1 (syndecan 1), SDC4 (syndecan 4), KLK7 (kallikrein-related peptidase 7), KLK10 (kallikrein-related peptidase 10), SLPI (secretory leukocyte peptidase inhibitor), GDF15 (growth/differentiation factor-15), ALOX5 (arachidonate 5-lipoxygenase), SFRP2 (secreted Frizzled-related protein 2), among others. Further, elevated KLK10 levels were detected in patients with PTC. Many of these genes belong to KEGG pathway "Proteoglycans in cancer"., Conclusions: Using DNA microarray analysis allowed the identification of genes and pathways with known important roles in malignant transformation, and also the discovery of novel genes that may be potential biomarkers for PTC.

There have been few published studies on differences between Blacks and Whites in the estimated effects of alcohol and tobacco use on the incidence of head and neck cancer (HNC) in the United States. Previous studies have been limited by small numbers of Blacks. Using pooled data from 13 US case-control studies of oral, pharyngeal, and laryngeal cancers in the International Head and Neck Cancer Epidemiology Consortium, this study comprised a large number of Black HNC cases (n = 975). Logistic regression was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI) for several tobacco and alcohol consumption characteristics. Blacks were found to have consistently stronger associations than Whites for the majority of tobacco consumption variables. For example, compared to never smokers, Blacks who smoked cigarettes for > 30 years had an OR 4.53 (95% CI 3.22-6.39), which was larger than that observed in Whites (OR 3.01, 95% CI 2.73-3.33; p interaction  < 0.0001). The ORs for alcohol use were also larger among Blacks compared to Whites. Exclusion of oropharyngeal cases attenuated the racial differences in tobacco use associations but not alcohol use associations. These findings suggest modest racial differences exist in the association of HNC risk with tobacco and alcohol consumption.

The possible role of dietary fiber in the etiology of head neck cancers (HNCs) is unclear. We used individual-level pooled data from ten case-control studies (5959 cases and 12,248 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium, to examine the association between fiber intake and cancer of the oral cavity/pharynx and larynx. Odds Ratios (ORs) and their 95% Confidence Intervals (CIs) were estimated using unconditional multiple logistic regression applied to quintile categories of non-alcohol energy-adjusted fiber intake and adjusted for tobacco and alcohol use and other known or putative confounders. Fiber intake was inversely associated with oral and pharyngeal cancer combined (OR for 5th vs. 1st quintile category = 0.49, 95% CI: 0.40-0.59; p for trend <0.001) and with laryngeal cancer (OR = 0.66, 95% CI: 0.54-0.82, p for trend <0.001). There was, however, appreciable heterogeneity of the estimated effect across studies for oral and pharyngeal cancer combined. Nonetheless, inverse associations were consistently observed for the subsites of oral and pharyngeal cancers and within most strata of the considered covariates, for both cancer sites. Our findings from a multicenter large-scale pooled analysis suggest that, although in the presence of between-study heterogeneity, a greater intake of fiber may lower HNC risk., (© 2017 UICC.)