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Context: Hospice utilization in New York State (NYS) is low compared to the rest of the U.S., Objectives: The first part of a mixed-methods study elicited information from New York State stakeholders and identified 54 hospice-related barriers in nine categories, some specific to NYS. This second part used national data to examine the differences between NYS and the rest of the country by evaluating the variables associated with low NYS hospice utilization., Methods: Ten Medicare or publicly available datasets provided data from the year prior to death for all traditional Medicare-insured patients dying in 2018. Multivariate analyses identified variables independently associated with differences in hospice enrollment or length of stay between NYS and the rest of the country., Results: The NYS population was relatively older, included more women and minorities, had higher socioeconomic status (SES), and saw more physicians during the last two years of life. NYS had more physicians, more skilled nursing facility (SNF) beds, and fewer for-profit hospitals, SNFs, home care agencies, and hospice agencies. In multivariate analyses, lower NYS hospice utilization was associated with higher SES; more physicians seen during the last two years of life; more SNF beds and fewer for-profit SNF facilities; and fewer hospice agencies., Conclusion: NYS's low hospice utilization is independently associated with diverse factors, including those related to the health care system. Combined with information from stakeholders, these findings may help target, and inform initiatives to improve hospice utilization., Competing Interests: Declaration of Interests No competing interests declared., (Copyright © 2021 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.)

Study Objectives: To characterize respiratory abnormalities in a convenience sample of ironworkers exposed at the World Trade Center (WTC) disaster site for varying lengths of time between September 11, 2001, and February 8, 2002., Design: Cross-sectional study., Setting: The Mount Sinai Medical Center, a large tertiary hospital., Participants: Ninety-six ironworkers engaged in rescue and recovery with exposure onset between September 11, 2001, and September 15, 2001, who responded to an invitation to undergo respiratory evaluation., Measurements: Medical and exposure history, physical examination, spirometry, forced oscillation (FO), and chest radiographs. The relationships of prevalence of respiratory symptoms and presence of obstructive physiology to smoking, exposure on September 11, duration of exposure, and type of respiratory protection were examined using univariate and linear and logistic regression analyses., Results: Seventy-four of 96 workers (77%) had one or more respiratory symptoms (similar in smokers [49 of 63 subjects, 78%] and nonsmokers [25 of 33 subjects, 76%]). Cough was the most common symptom (62 of 96 subjects, 65%), and was associated with exposure on September 11. Chest examination and radiograph findings were abnormal in 10 subjects (10%) and 19 subjects (20%), respectively. FO revealed dysfunction in 34 of 64 subjects tested (53%), while spirometry suggested obstruction in only 11 subjects (17%). Lack of a respirator with canister was a risk factor for large airway dysfunction, and cigarette smoking was a risk factor for small airway dysfunction. No other relationships reached statistical significance., Conclusions: Respiratory symptoms occurred in the majority of ironworkers at the WTC disaster site and were not attributable to smoking. Exposure on September 11 was associated with a greater prevalence of cough. Objective evidence of lung disease was less common. Spirometry underestimated the prevalence of lung function abnormalities in comparison to FO. Continuing evaluation of symptoms, chest radiographs, and airway dysfunction should determine whether long-term clinical sequelae will exist.

HFE is a nonclassical class I molecule that associates with beta 2-microglobulin (beta 2m) and with the transferrin receptor. HFE accumulates in transferrin-containing endosomes, and its overexpression in human cell lines correlates with decreased transferrin receptor (TFR)-mediated iron uptake and decreased intracellular iron pools. A mutation that interferes with proper folding and assembly of HFE complexes results in a severe iron-overload disease hereditary hemochromatosis. We previously suggested that viruses could also interfere with iron metabolism through the production of proteins that inactivate HFE, similarly to classical class I proteins. In particular, we demonstrated in a transient expression system that human cytomegalovirus (HCMV) US2 targeted HFE for proteasomal degradation. Here we demonstrate that the stable expression of HCMV US2 in HEK 293 cells constitutively expressing HFE leads to loss of HFE expression both intracellularly and on the cell surface, and the significant reduction of classical class I expression. Both HFE and classical class I molecules are targeted to degradation via a similar pathway. This HCMV US2-mediated degradation of HFE leads to increased intracellular iron pools as indicated by reduced synthesis of TfR and increased ferritin synthesis. Whether this interference with regulation of iron metabolism potentiates viral replication and/or promotes damage of HCMV-infected tissues remains to be determined. Nevertheless, the deleterious effect of US2 on the expression of HFE and classical class I major histo-compatibility complexes (MHC) provides HCMV with an efficient tool for altering cellular metabolic functions, as well as supporting the escape of virus-infected cells from cytotoxic T lymphocyte (CTL)-mediated immune responses.

Antigen processing and presentation by class I MHC molecules generally require assembly with peptide epitopes generated by the proteasome and transported into the ER by the transporters associated with antigen presentation (TAP). Recently, TAP-independent pathways supporting class I MHC-mediated presentation of exogenous antigens, as well as of endogenously synthesized viral antigens, were described. We now characterize a TAP-independent pathway that is operative in both TAP1- and TAP2-deficient Adenovirus (Ad)-transformed fibroblast cell lines. To the best of our knowledge, this is the first time that the existence of such a pathway has been described in non-infected cells that do not belong to the hematopoietic lineage. We show that this pathway is proteasome-independent and chloroquine-sensitive. Cell surface expression of these TAP-independent class I complexes is modulated by tapasin levels and is enhanced by IFN-gamma. The data imply that IFN-gamma increases the relative level of TAP-independent high affinity class I complexes that exit the ER on their way to the cell surface and to vacuolar compartments where peptide cleavage/exchange might take place before recycling to the cell surface. Since both TAP and tapasin expression are altered in numerous tumors and in virus-infected cells, TAP-independent class I complexes may be a valuable target source for immune responses.

Study Objective: To determine the relationship between the degree of immune deficiency and the risk of Pneumocystis carinii pneumonia (PCP) among HIV-infected patients receiving inhaled pentamidine prophylaxis., Design: Retrospective chart review., Setting: AIDS clinic of inner-city hospital., Patients: Patients attending inhaled pentamidine clinic between 1989 and 1991., Intervention: Review of medical records of patients receiving inhaled pentamidine, 300 mg/month, via nebulizer (Respirgard II) as primary or secondary prophylaxis of PCP. Statistical analysis of lymphocyte subset results and selected clinical data., Results: Ten of 57 patients developed PCP during the period of analysis. Patients with CD4 counts less than 60/mm3 were significantly more likely to develop PCP (p = 0.01; Fisher's exact test) with a relative risk of 7.55 compared to patients with CD4 lymphocyte counts greater than 60/mm3., Conclusion: Failure of inhaled pentamidine prophylaxis is seen almost exclusively among patients with CD4 lymphocyte counts below 60/mm3.

Despite the recent passage of coverage for Papanicolaou test screening under Medicare, several aspects of the natural history of cervical cancer in the elderly remain uncertain. This article reviews what we know about cervical cancer in elderly women to provide clinicians with the background necessary for assessments of screening recommendations, integration of new data into practice, and development of consensus approaches to screening in the elderly. Two central questions that affect a screening program for the elderly are how long the neoplastic process takes from preinvasive disease to the development of invasive cancer, and how likely is it that a given neoplastic state observed in an elderly woman will, in fact, progress to a more severe state. The ultimate success of the new Medicare benefit will also be affected by the use of Papanicolaou testing, the technique of obtaining the smear, and the adequacy of reporting and follow-up. The expansion of Medicare benefits to include early cervical cancer detection has the potential to improve the quality and the duration of older women's lives.