Perceived discrimination and physical activity mediate the associations between receiving a survivorship care plan and cancer pain

BackgroundSurvivorship care plan helps improve the continuity of care and manage ongoing pain that affects up to 46% of cancer survivors by promoting health behaviors, including physical activity. However, perceived discrimination may decrease the likelihood of cancer survivors participating in physical activities and negatively influence their pain status. Thus, this study aimed to examine the mediating role of physical activity and perceived discrimination in the relationship between receiving a survivorship care plan and cancer pain.MethodsThis cross-sectional, correlational study utilized data from the 2012–2019 Behavioral Risk Factor Surveillance System. Analyses accounted for the complex survey design. Logistic regression was utilized to analyze the association among survivorship care plans, discrimination, physical activity, and pain. Generalized structural equation modeling was conducted to test a hypothesized model in which survivorship care plans and discrimination affect physical activity, and subsequently influence pain status.ResultsForty-two and 81% of survivors reported receiving treatment summaries and follow-up care plans, respectively, and 8% experienced cancer pain. After controlling for covariates, the highest discrimination quintile was three times more likely to report cancer pain than the lowest quintile. While receiving follow-up care plans was positively related to cancer pain, respondents in the third- to fifth- quintiles were less likely to report cancer pain when receiving follow-up care plans than the first quintile respondents. Physical activity mediated the association between discrimination and cancer pain.ConclusionsReverse relationships between receiving follow-up care plans and cancer pain existed; however, discrimination and physical activity mediated these relationships.     

Association of dietary risks,behavioural and lifestyle factors,and the magnitude of disability burden among Australian cancer patients: An observational epidemiology study

BackgroundCancer patients are confronted with a variety of other health-related issues, including physical disability, poor quality of life, and psychological challenges. This study aims to quantify the association of dietary, behavioural and lifestyle risk factors and comorbidities on the magnitude and distribution of disability burden among cancer patients in Australia.MethodsThis study comprised a sample of 2283 cancer patients drawn from the latest nationwide Australian National Health Survey conducted in 2017–18. Negative binomial regression models were used to estimate the incidence rate ratio (IRR) of the number of disabilities and its associations.ResultsForty-five percent of cancer patients experienced at least one disability. The magnitude of disability was significantly associated with sugar-sweetened drink consumption ≥ 3 days per week (IRR= 1.12, 95% CI: 1.02–1.26), a lack of physical activity (IRR = 1.69, 1.38–2.07), frequent or regular alcohol consumption (IRR = 1.95, 1.84–2.08), poor health status (IRR = 1.99, 1.78–2.24) and the presence of five or more chronic comorbid conditions (IRR = 3.59, 2.90–4.46). Cancer patients who consumed vegetables at least two or more times per day had a 10% lower risk of disability burden (IRR = 0.90, 0.82–0.99).ConclusionsThis study shows the association of diet, behavioural, and lifestyle risk factors on the degree of disability burden among cancer patients, highlighting the need for bold and effective policies. The findings will inform the implementation of evidence-based lifestyle interventions and offer a foundation for evaluating their influence on cancer survivors’ health.     

Patterns and predictors of referral to the specialized chronic lymphocytic leukemia clinic in Manitoba,Canada

BackgroundBetter CLL patient survival has been reported for specialized CLL clinics/hematologists (compared to other CLL patients). It is possible that improved survival is driven by a better prognosis of referred patients.MethodsWe used logistic regression to calculate the odds ratios (ORs) and 95 % confidence intervals 95 %CIs) of the association between patient characteristics and CLL referral of all persons diagnosed in 2005–2016 with a pathologically-confirmed CLL or SLL.ResultsTwo-thirds of 1293 patients were referred to the CLL clinic. Referred patients were younger (16 % vs 44 % were 80 +) and in better health (47 % vs 56 % with a chronic diseases) than non-referred patients. Referral increased over time: in 2005–2010, about 60 % of patients were referred; in 2011–2016, this increased to 76 %. Gender did not affect referral (the OR for females is 1.0, 95 %CI 0.8–1.2), but age played a major role; CLL patients diagnosed at age 80 + were less likely to be referred than patients diagnosed < 60, 0.2 (0.1–0.3).ConclusionBecause referral to Manitoba’s specialized CLL clinic is associated with age and the patient’s overall health before referral, one should be careful in interpreting differences in outcomes between CLL patients based on referral status alone.     

淋巴瘤幸存者复发恐惧的影响因素及认知行为干预对患者生活质量和心理状态的影响

摘要 目的：分析淋巴瘤幸存者复发恐惧（FCR）的影响因素,并分析认知行为干预对患者生活质量和心理状态的影响。方法：本次研究为回顾性调查研究,选取2018年7月~2021年6月期间我院收治的淋巴瘤患者80例,根据病历资料获取患者婚姻状况、疾病分期、工作状况、年龄、治愈时间、文化程度、疾病类型、性别、医疗费用承担情况、家庭人均月收入。采用多因素Logistic回归分析淋巴瘤幸存者FCR的影响因素。将80例淋巴瘤患者分为对照组和干预组,各为40例。对照组给予常规处理,干预组在此基础上接受认知行为干预,对比两组生活质量和心理状态变化。结果：淋巴瘤幸存者FCR总分为（86.90±5.96）分。不同婚姻状况、年龄、疾病分期、家庭人均月收入的患者FCR总分对比差异有统计学意义（P<0.05）。多因素Logistic回归分析显示家庭人均月收入、婚姻状况、疾病分期、年龄是淋巴瘤幸存者FCR的影响因素（P<0.05）。干预后,两组生理职能、躯体疼痛、精神健康、生理功能、总体健康、情感职能、活力、社会功能维度评分均较干预前升高,且干预组高于对照组（P<0.05）。干预组干预后的恐惧疾病进展简化量表（FoP-Q-SF）评分低于对照组（P<0.05）。结论：淋巴瘤幸存者的FCR应得到重视,尤其针对年龄偏低、婚姻状况为离异/未婚/丧偶、家庭人均月收入偏低、疾病分期高的人群,给予认知行为干预后,可提高患者的生活质量和心理状态。     

Altered Pattern of Immunoglobulin Hypermutation in Mice Deficient in Slip-GC Protein

We recently identified a novel germinal center GTPase, SLIP-GC, that localizes to replication factories in B cells and that, when reduced, induces DNA breaks in lymphoma B cell lines in an activation-induced deaminase (AID)-dependent manner. Herein, we generated mice deficient in SLIP-GC and examined the impact of SLIP-GC deficiency in immunoglobulin hypermutation and class switch recombination, both AID-dependent mechanisms. SLIP-GC-deficient mice experienced a substantial increase in mutations at G:C base pairs at the region downstream of JH4 in the immunoglobulin heavy chain locus. This change was reflected in the overall mutation frequency, and it was associated with an increase in transitions from G:C base pairs, a hallmark of AID-mediated deamination during replication. In addition, G:C transitions at non-immunoglobulin loci also increased in these mice. Given the intracellular localization of SLIP-GC to sites of replicating DNA, these results suggest that SLIP-GC protects replicating DNA from AID-mediated deamination of cytosines in both strands.     

Primary mediastinal large B-cell lymphoma in HIV: report of two cases

Primary mediastinal large B cell lymphoma (PMLBCL) is a subtype of diffuse large B cell lymphoma arising in the mediastinum with distinctive clinical and morphological features. Though diffuse large B cell lymphoma is one of the most common non-Hodgkin lymphoma associated with AIDS, there are no data available regarding the association of HIV and PMLBCL. We report here two cases of PMLBCL arising in AIDS patients. In both cases, PMLBCL presented in a setting of low CD4 T-cell count as rapidly enlarging mediastinal mass. The morphologic and immunophenotypic findings are characteristic of PMLBCL. One of the two patients, a 25-year-old woman who had localized disease and evidence of Epstein–Barr virus in lymphoma cells, did not respond to chemotherapy and died of disease progression 5 months after diagnosis. The second patient, a 38-year-old male with disseminated disease, responded to therapy and is disease-free after 9 months of follow-up.     

Apoptosis-inducing factor plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells

It has been proposed that continuously generated hydrogen peroxide (H₂O₂) inhibits typical apoptosis and instead initiates an alternate, apoptosis-inducing factor (AIF)-dependent process. Aside from the role of AIF, however, the detailed morphological characterization of H₂O₂-induced cell death is not complete. This study examined the cellular mechanism(s) by which the continuous presence of H₂O₂ induces cell death. We also further analyzed the precise role of AIF by inhibiting its expression with siRNA. Exposure of cells to H₂O₂ generated by glucose oxidase caused mitochondrion-mediated, caspase-independent cell death. In addition, H₂O₂ exposure resulted in cell shrinkage and chromatin condensation without nuclear fragmentation, indicating that H₂O₂ stimulates a pyknotic cell death. Further analysis of AIF-transfected cells clearly demonstrated that nuclear translocation of AIF is the most important event required for nuclear condensation, phosphatidyl serine translocation, and ultimately cell death in H₂O₂-exposed cells. Furthermore, ATP was rapidly and severely depleted in cells exposed to H₂O₂ generated by glucose oxidase but not by H₂O₂ added as a bolus. Suppression of the H₂O₂-mediated ATP depletion by 3-aminobenzamide led to a significant increase of nuclear fragmentation in glucose oxidase-exposed cells. Collectively, these findings suggest that an acute energy reduction by H₂O₂ causes caspase-independent and AIF-dependent cell death.     

Relative risks of radiation-associated cancer: comparison of second cancer in therapeutically irradiated populations with the Japanese atomic bomb survivors

In this paper the radiation-associated relative risks of second primary cancer incidence in groups treated for first primary cancer by radiotherapy are compared with radiation-associated relative risk estimates in the Japanese atomic bomb survivor cancer incidence data. For four cancer sites, namely lung cancer, bone cancer, ovarian cancer and leukaemia, the relative risks in the comparable (age at exposure, time since exposure, sex matched) subsets of the Japanese data are significantly greater than those in the majority of second cancer studies. Even when the differences between the relative risks in the Japanese atomic bomb survivors and the medical series do not approach conventional levels of statistical significance, relative risks tend to be higher in the Japanese data than in the second cancer studies. At least for leukaemia, the discrepancy between the Japanese and second cancer risks can be largely explained by cell- sterilisation effects. There are few indications of modification of radiation-associated second cancer relative risk among those treated with adjuvant chemotherapy, nor are there strong indications of modification of radiation- associated relative risk by heritable genetic factors. If anything, there is evidence that second cancer relative excess risks are lower among those patients with cancer-prone disorders than among non-susceptible patients. However, the higher underlying cancer risk in some of these medically exposed populations should also be considered, in particular for those with cancer-prone conditions, so that the absolute excess risk is sometimes higher than in the Japanese data. Received: 14 May 1999 / Accepted in revised form: 17 September 1999     

A stochastic carcinogenesis model incorporating genomic instability fitted to colon cancer data

A generalization of the two-mutation stochastic carcinogenesis model of Moolgavkar, Venzon and Knudson and certain models constructed by Little is developed; the model incorporates progressive genomic instability and an arbitrary number of mutational stages. This model is shown to have the property that, at least in the case when the parameters of the model are eventually constant, the excess relative and absolute cancer rates following changes in any of the parameters will eventually tend to zero. It is also shown that when the parameters governing the processes of cell division, death, or additional mutation (whether of the normal sort or that resulting in genomic destabilization) at the penultimate stage are subject to perturbations, there are relatively large fluctuations in the hazard function for the model, which start almost as soon as the parameters are changed. The model is fitted to US Caucasian colon cancer incidence data. A model with five stages and two levels of genomic destabilization fits the data well. Comparison with patterns of excess risk in the Japanese atomic bomb survivor colon cancer incidence data indicate that radiation might act on early mutation rates in the model; a major role for radiation in initiating genomic destabilization is less likely.     

The chemical bases of the various AIDS epidemics: Recreational drugs,anti-viral chemotherapy and malnutrition

In 1981 a new epidemic of about two-dozen heterogeneous diseases began to strike non-randomly growing numbers of male homosexuals and mostly male intravenous drug users in the US and Europe. Assuming immunodeficiency as the common denominator the US Centers for Disease Control (CDC) termed the epidemic, AIDS, for acquired immunodeficiency syndrome. From 1981-1984 leading researchers including those from the CDC proposed that recreational drug use was the cause of AIDS, because of exact correlations and of drug-specific diseases. However, in 1984 US government researchers proposed that a virus, now termed human immunodeficiency virus (HIV), is the cause of the non-random epidemics of the US and Europe but also of a new, sexually random epidemic in Africa. The virus-AIDS hypothesis was instantly accepted, but it is burdened with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS patients, only antibodies against it? Why would HIV take 10 years from infection to AIDS? Why is AIDS not self-limiting via antiviral immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and Europe not random like other viral epidemics? Why did AIDS not rise and then decline exponentially owing to antiviral immunity like all other viral epidemics? Why is AIDS not contagious? Why would only HIV carriers get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition? Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs 7–9%, but that of all (mostly untreated) HIV-positives globally is only 1–4%? Here we propose that AIDS is a collection of chemical epidemics, caused by recreational drugs, anti-HIV drugs, and malnutrition. According to this hypothesis AIDS is not contagious, not immunogenic, not treatable by vaccines or antiviral drugs, and HIV is just a passenger virus. The hypothesis explains why AIDS epidemics strike non-randomly if caused by drugs and randomly if caused by malnutrition, why they manifest in drug- and malnutrition-specific diseases, and why they are not self-limiting via anti-viral immunity. The hypothesis predicts AIDS prevention by adequate nutrition and abstaining from drugs, and even cures by treating AIDS diseases with proven medications.