There is a lack of research on health care providers' use of and perspectives on expedited partner therapy in a state where expedited partner therapy is not prohibited or explicitly allowed. The aim ...of our study was to understand if and how health care providers use expedited partner therapy, if specific demographic factors and knowledge contribute to increased use of expedited partner therapy, and to describe barriers and facilitators to the use of expedited partner therapy in Pittsburgh, Pennsylvania. A convenience sample of 112 health care providers from diverse disciplines who treat young women at risk for chlamydia completed an online survey. About 11% of health care providers used expedited partner therapy consistently. Those who self-reported that they were knowledgeable about expedited partner therapy were more likely to use expedited partner therapy (73% vs. 49%, p = .009) as were those who said no or were unsure about their institution's guidelines for expedited partner therapy (35% vs. 22%, p = 0.01) (62% vs. 57%, p = 0.01). The most commonly reported facilitator of expedited partner therapy was having clear legal guidelines (86%). This study finds that in a setting where expedited partner therapy is not expressly permitted, health care providers still use the practice but also experience barriers that limit uptake. Legislation expressly endorsing expedited partner therapy in the state and in medical institutions is needed to increase expedited partner therapy use.
We present a new analysis of previously published SuperCDMS data using a profile likelihood framework to search for sub-GeV dark matter (DM) particles through two inelastic scattering channels: ...bremsstrahlung radiation and the Migdal effect. By considering these possible inelastic scattering channels, experimental sensitivity can be extended to DM masses that are undetectable through the DM-nucleon elastic scattering channel, given the energy threshold of current experiments. We exclude DM masses down to 220 MeV/c2 at 2.7 x 10-30 cm2 via the bremsstrahlung channel. The Migdal channel search provides overall considerably more stringent limits and excludes DM masses down to 30 MeV/ c2 at 5.0 x 10-30 cm2.
Glycogen storage disease type Ia (GSDIa) is an inborn error of carbohydrate metabolism caused by pathogenic variants in the G6PC1 gene, and is associated with hepatocellular adenoma (HCA) formation. ...Data on risk factors for HCA occurrence in GSDIa are scarce. We investigated HCA development in relation to sex, G6PC1 genotype, and serum triglyceride concentration (TG).
An observational study of genetically confirmed GSDIa patients ≥12 years was performed. Patients were categorized for sex, presence of 2, 1, or zero predicted severe G6PC1 variants (PSV), and median TG during childhood (<12 years; stratified for above/below 5.65 mmol/L, i.e., 500 mg/dL).
Fifty-three patients (23 females) were included, of which 26 patients developed HCA at a median (interquartile range) age of 21 (17-25) years. At the age of 25 years 48% of females and 30% of males had developed HCA (Log-Rank p=0.045). Two-thirds of GSDIa patients carried 2 PSV, 20% one, and 13% none. Neither the number of PSV, nor any specific G6PC1 variants were associated with HCA occurrence. Childhood TG was 3.4 (3.0-4.2) mmol/L in males vs. 5.6 (4.0-7.9) mmol/L in females (p=0.026). Childhood TG >5.65 mmol/L was associated with HCA development at younger age, compared to patients with childhood TG <5.65 mmol/L (18 vs. 33 years; Log-Rank p=0.001). Cox-regression analysis including TG, sex, and TG-sex interaction correction revealed childhood TG >5.65 mmol/L as an independent risk factor for HCA development (HR 6.0, 95% CI 1.2-29.8; p=0.028).
In GSDIa patients, high childhood TG concentration was associated with an increased risk of HCA, and earlier onset of HCA development, independent of sex-associated hypertriglyceridemia, and G6PC1 genotype.
Glycogen storage disease type Ia (GSDIa) is a rare, inherited metabolic disease, that can be complicated by liver tumors (hepatocellular adenomas), which in turn may cause bleeding or progress to liver cancer. Risk factors associated with hepatocellular adenoma formation in GSDIa patients are largely unknown. In our study, we found that high serum triglyceride concentrations during childhood, but not specific genetic variants, were associated with increased risk of hepatocellular adenoma diagnosis later in life.
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•Glycogen storage disease Ia (GSDIa) is a metabolic disease caused by G6PC1 mutation•GSDIa patients often form hepatocellular adenoma (HCA), with unclear risk factors•Metabolic control in GSDIa is commonly evaluated through serum triglycerides (TG)•GSDIa patients with high childhood TG had increased risk and earlier onset of HCA•Sex-associated hypertriglyceridemia and G6PC1 genotype were not associated with HCA
Inhaled diesel exhaust particles (DEP) exert proinflammatory effects in the respiratory tract. This effect is related to the particle content of redox cycling chemicals and is involved in the ...adjuvant effects of DEP in atopic sensitization. We demonstrate that organic chemicals extracted from DEP induce oxidative stress in normal and transformed bronchial epithelial cells, leading to the expression of heme oxygenase 1, activation of the c-Jun N-terminal kinase cascade, IL-8 production, as well as induction of cytotoxicity. Among these effects, heme oxygenase 1 expression is the most sensitive marker for oxidative stress, while c-Jun N-terminal kinase activation and induction of apoptosis-necrosis require incremental amounts of the organic chemicals and increased levels of oxidative stress. While a macrophage cell line (THP-1) responded in similar fashion, epithelial cells produced more superoxide radicals and were more susceptible to cytotoxic effects than macrophages. Cytotoxicity is the result of mitochondrial damage, which manifests as ultramicroscopic changes in organelle morphology, a decrease in the mitochondrial membrane potential, superoxide production, and ATP depletion. Epithelial cells also differ from macrophages in not being protected by a thiol antioxidant, N-acetylcysteine, which effectively protects macrophages against cytotoxic DEP chemicals. These findings show that epithelial cells exhibit a hierarchical oxidative stress response that differs from that of macrophages by more rapid transition from cytoprotective to cytotoxic responses. Moreover, epithelial cells are not able to convert N-acetylcysteine to cytoprotective glutathione.
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