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1.
Public Health ; 224: 45-50, 2023 Sep 14.
Article in English | MEDLINE | ID: mdl-37716175

ABSTRACT

OBJECTIVES: We aimed to examine potential relationships and gender differences between cardiovascular disease (CVD), diabetes, obesity, respiratory-related disorders, and gambling disorder (GD). We hypothesized that (1) GD patients would be more likely than controls to have CVD, diabetes, obesity, and respiratory-related diseases; and (2) females with GD would be more likely than men with GD to have CVD, diabetes, obesity, and respiratory-related diseases. STUDY DESIGN: National retrospective case-control study. METHODS: We used data from the Swedish National Board of Health and Welfare between 2005 and 2019. A total of 10,766 patients were included, and 3592 of them had GD. Every GD patient was matched with two age- and gender-matched controls. Patient data, including the history of medical diagnoses, were extracted. Descriptive statistics, Chi-squared and Fisher's exact tests were used to compare GD patients and controls. RESULTS: GD patients had a higher prevalence of CVD and respiratory-related disorders than controls. Diabetes rates were 5% for GD patients and 2% for controls; CVD (18% vs 12%); respiratory-related disease (7% vs 4%); and obesity (7% vs 3%). Women with a diagnosis of GD have a higher prevalence of obesity and somatic comorbidities other than diabetes compared to men. CONCLUSIONS: This is the largest case-control study conducted to date showing GD patients have a higher prevalence of CVD, diabetes, obesity, and respiratory-related disorders than controls. Women with GD appear to be more susceptible than men to CVD, obesity, and respiratory-related disorders; however, this may be partially explained by differences in help-seeking behavior. Thus, our findings highlight the importance of early identification of GD patients who may also have somatic conditions requiring treatment. This can be accomplished by implementing a screening program for GD, CVD, diabetes, obesity, and respiratory-related disorders, and by including healthy lifestyle management strategies.

2.
Blood ; 75(4): 951-7, 1990 Feb 15.
Article in English | MEDLINE | ID: mdl-2302462

ABSTRACT

Recently, low-molecular-weight B-cell growth factor (LMW-BCGF) has been reported to stimulate growth of leukemic cells from B-cell precursor-acute lymphoblastic leukemia (BCP-ALL). We further investigated the effects of LMW-BCGF on proliferation of leukemic clonogenic (progenitor) and nonclonogenic (progeny) cells from children with BCP-ALL (28 patients) and B-cell ALL (two patients). Patients were either at diagnosis (n = 18) or in relapse (n = 12). Response of leukemic progenitor cells was determined by culturing cells (10(5) cells/mL) in methylcellulose with 0.1 U/mL LMW-BCGF. Colonies (greater than 20 cells) were counted at day 7. The response of the leukemic progeny population was determined by DNA synthesis studies using tritiated-thymidine and by DNA quantitation with propidiumiodide for determination of cell-cycle status. LMW-BCGF supported growth of leukemic progenitor cells from 20 of 28 (71%) BCP-ALL and two of two B-cell ALL patients. Colony numbers ranged from 7 to 2,400 (mean 145, median 45). A dose-response effect in colony growth was noted, with an apparent plateau at approximately 2.0 U/mL LMW-BCGF. Colony cells were primarily of leukemic phenotype (CD19+/CD10+/-). LMW-BCGF also induced significant increases in leukemic progeny cell proliferation as measured by both thymidine incorporation (stimulation indexes of 1.6 to 34) and by cell-cycle assay (percentage S+ G2/M stimulation indexes of 1.6 to 6). LMW-BCGF was more effective in stimulating leukemic proliferation than three recombinant interleukins (rIL-2, rIL-3, rIL-4), although rIL-3 was able to support colony growth in 4 of 11 patients. These results indicate that LMW-BCGF and, to a lesser degree rIL-3, are able to stimulate proliferation of BCP-ALL progenitor and progeny cells, whereas rIL-2 and rIL-4 do not support progenitor cell proliferation and have only marginal effects on leukemic progeny cell proliferation.


Subject(s)
Burkitt Lymphoma/blood , Cell Transformation, Neoplastic/drug effects , Lymphokines/pharmacology , Bone Marrow/drug effects , Bone Marrow Cells , Burkitt Lymphoma/metabolism , Burkitt Lymphoma/pathology , Cell Cycle/drug effects , DNA/metabolism , Humans , Interleukin-2/pharmacology , Interleukin-3/pharmacology , Interleukin-4/pharmacology , Lymphokines/physiology , Stem Cells/drug effects , Thymidine/metabolism
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