Common community acquired infections and subsequent risk of chronic lymphocytic leukaemia

Emerging evidence supports a role for immune-related factors in the causation of chronic lymphocytic leukemia (CLL). Using the population-based U.S. SEER-Medicare database, we identified 10,171 elderly CLL patients and 122,531 frequency-matched controls to evaluate several community acquired infections associated with subsequent CLL risk. Odds ratios (ORs) were adjusted for gender, age, race, calendar year, and number of physician claims. We found increased CLL risk following Medicare claims for sinusitis (OR=1.11; 95%CI=1.05–1.17), pharyngitis (OR=1.15; 1.08–1.22), bronchitis (OR=1.14; 1.08–1.19), pneumonia (OR=1.17; 1.11–1.24), influenza (OR=1.10; 1.01–1.19), cellulitis (OR=1.08; 1.02–1.14), and herpes zoster (OR=1.26; 1.15–1.37). Associations with pneumonia and cellulitis remained significant when the 5-year period before diagnosis/control was excluded. CLL risk increased with increasing severity/frequency of pneumonia (p=0.005), cellulitis (p<0.001), and herpes zoster (p<0.001). Our findings suggest that common infections may play a role in CLL etiology. Alternatively, the associations might reflect an underlying immune disturbance present several years prior to CLL diagnosis

Cancer-Specific Mortality, Cure Fraction, and Noncancer Causes of Death Among Diffuse Large B-cell Lymphoma Patients in the Immunochemotherapy Era.

BACKGROUND Survival after the diagnosis of diffuse large B-cell lymphoma (DLBCL) has been increasing since 2002 because of improved therapies; however, long-term outcomes for these patients in the modern treatment era are still unknown. METHODS Using Surveillance, Epidemiology, and End Results data, this study first assessed factors associated with DLBCL-specific mortality during 2002-2012. An epidemiologic risk profile, based on clinical and demographic characteristics, was used to stratify DLBCL cases into low-, medium-, and high-risk groups. The proportions of DLBCL cases that might be considered cured in these 3 risk groups was estimated. Risks of death due to various noncancer causes among DLBCL cases versus the general population were also calculated with standardized mortality ratios (SMRs). RESULTS Overall, 8274 deaths were recorded among 18,047 DLBCL cases; 76% of the total deaths were attributed to DLBCL, and 24% were attributed to noncancer causes. The 10-year survival rates for the low-, medium-, and high-risk groups were 80%, 60%, and 36%, respectively. The estimated cure proportions for the low-, medium-, and high-risk groups were 73%, 49%, and 27%, respectively; however, these cure estimates were uncertain because of the need to extrapolate the survival curves beyond the follow-up time. Mortality risks calculated with SMRs were elevated for conditions including vascular diseases (SMR, 1.3), infections (SMR, 3.1), gastrointestinal diseases (SMR, 2.5), and blood diseases (SMR, 4.6). These mortality risks were especially high within the initial 5 years after the diagnosis and declined after 5 years. CONCLUSIONS Some DLBCL patients may be cured of their cancer, but they continue to experience excess mortality from lymphoma and other noncancer causes. Cancer 2017. © 2017 American Cancer Society

Asymptotic Behavior of the Correlator for Polyakov Loops

The asymptotic behavior of the correlator for Polyakov loop operators separated by a large distance $R$ is determined for high temperature QCD. It is dominated by nonperturbative effects related to the exchange of magnetostatic gluons. To analyze the asymptotic behavior, the problem is formulated in terms of the effective field theory of QCD in 3 space dimensions. The Polyakov loop operator is expanded in terms of local gauge-invariant operators constructed out of the magnetostatic gauge field, with coefficients that can be calculated using resummed perturbation theory. The asymptotic behavior of the correlator is $\exp(-MR)/R$, where $M$ is the mass of the lowest-lying glueball in $(2+1)$-dimensional QCD. This result implies that existing lattice calculations of the Polyakov loop correlator at the highest temperatures available do not probe the true asymptotic region in $R$.Comment: 10 pages, NUHEP-TH-94-2

Demographics and survival of AIDS cases with cancer, Washington, DC, 1996-2006

Background Washington, DC (DC) has one of the highest HIV/AIDS rates in the U.S and cancer is the second leading cause of death among DC residents. This study sought to examine the demographic characteristics and survival of persons with AIDS defining cancers (ADCs) compared to those with non-AIDS defining cancers (NADCs) between the early HAART era (1996-2001) and the late HAART era (2002-2006) in DC. Methods Cases reported from 1996-2006 to the DC Cancer Registry and the AIDS Surveillance Registry were linked using a probabilistic matching algorithm. Cases were included if the cancer occurred from 4 months to 60 months post-AIDS diagnosis and were stratified into ADCs and NADCs for analyses. Cancer diagnoses were stratified into the early and late HAART eras to compare the availability of HAART on the distribution of cancer type. Kaplan-Meier survival analysis and adjusted Cox proportional hazards regression were used to assess survival time and risk of death by cancer type. Results From 1996-2006, among 8,800 AIDS cases, 300 (3.4%) cases had a cancer diagnosis. NADCs accounted for 51% of cancers and were significantly more likely to be diagnosed with AIDS (p\u3c0.0001) and cancer (p\u3c0.0001) at 40 years or older and had a significantly longer median time from AIDS to cancer diagnosis (2.46 vs. 1.75 years, p=0.01) compared to ADCs. The most common ADCs were Kaposi sarcoma (40%) and non-Hodgkin lymphoma (NHL) (44%); the most common NADC cases were lung (20%), Hodgkin lymphoma (8%) and anal (8%) cancer. ADCs accounted for 56% of cancer cases in the late-HAART as compared to the early-HAART period (45%). Mortality within the first year of cancer diagnosis was similar (ADC 41% vs. NADC 37%) and no statistical difference in survival time was observed. In the adjusted model, NHL and lung cases were significantly more likely to die as compared to other cancers (NHL HR=3.06; Lung HR=3.44). Conclusions In DC, despite high HIV/AIDS and cancer prevalence, only a small proportion of AIDS cases also develop cancer with ADCs and NADCs being equally common. HAART availability does not seem to have altered survival among ADCs and NADCs. Survival among NHL cases was relatively low reflecting the need for increased access to care among HIV+ persons. NADC cases are most likely developing cancers related to advancing age with higher proportions of lung cancers being observed. Public health efforts should focus on lung cancer prevention and continued monitoring of HIV-infected persons for cancers

Driving Bose-Einstein Condensate Vorticity with a Rotating Normal Cloud

We have developed an evaporative cooling technique that accelerates the rotation of an ultracold ⁸⁷Rb gas, confined in a static harmonic potential. As a normal gas is evaporatively spun up and cooled below quantum degeneracy, it is found to nucleate vorticity in a Bose-Einstein condensate. Measurements of the condensate’s aspect ratio and surface-wave excitations are consistent with effective rigid-body rotation. Rotation rates of up to 94% of the centrifugal limit are inferred. A threshold in the normal cloud’s rotation is observed for the intrinsic nucleation of the first vortex. The threshold value lies below the prediction for a nucleation mechanism involving the excitation of surface waves of the condensate

Oral leukoplakia and risk of progression to oral cancer: A population-based cohort study

BACKGROUND: The optimal clinical management of oral precancer remains uncertain. We investigated the natural history of oral leukoplakia, the most common oral precancerous lesion, to estimate the relative and absolute risks of progression to cancer, the predictive accuracy of a clinician\u27s decision to biopsy a leukoplakia vis-à-vis progression, and histopathologic predictors of progression. METHODS: We conducted a retrospective cohort study (1996-2012) of patients with oral leukoplakia (n = 4886), identified using electronic medical records within Kaiser Permanente Northern California. Among patients with leukoplakia who received a biopsy (n = 1888), we conducted a case-cohort study to investigate histopathologic predictors of progression. Analyses included indirect standardization and unweighted or weighted Cox regression. RESULTS: Compared with the overall Kaiser Permanente Northern California population, oral cancer incidence was substantially elevated in oral leukoplakia patients (standardized incidence ratio = 40.8, 95% confidence interval [CI] = 34.8 to 47.6; n = 161 cancers over 22 582 person-years). Biopsied leukoplakias had a higher oral cancer risk compared with those that were not biopsied (adjusted hazard ratio = 2.38, 95% CI = 1.73 to 3.28). However, to identify a prevalent or incident oral cancer, the biopsy decision had low sensitivity (59.6%), low specificity (62.1%), and moderate positive-predictive value (5.1%). Risk of progression to oral cancer statistically significantly increased with the grade of dysplasia; 5-year competing risk-adjusted absolute risks were: leukoplakia overall = 3.3%, 95% CI = 2.7% to 3.9%; no dysplasia = 2.2%, 95% CI = 1.5% to 3.1%; mild-dysplasia = 11.9%, 95% CI = 7.1% to 18.1%; moderate-dysplasia = 8.7%, 95% CI = 3.2% to 17.9%; and severe dysplasia = 32.2%, 95% CI = 8.1%-60.0%. Yet 39.6% of cancers arose from biopsied leukoplakias without dysplasia. CONCLUSIONS: The modest accuracy of the decision to biopsy a leukoplakia vis-à-vis presence or eventual development of oral cancer highlights the need for routine biopsy of all leukoplakias regardless of visual or clinical impression. Leukoplakia patients, particularly those with dysplasia, need to be closely monitored for signs of early cancer