Exploration of the experiences of working stressors and coping strategies associated with menstrual symptoms among nurses with shifting schedules: a Q methodology investigation.

BACKGROUND: The essence and workload of nursing can easily lead to burdens associated with female nurses' menstrual symptoms, and consequently, result in decreased working performance. Without effective support this can lead to resignation due to maladaptation. This study adopted Q methodology to explore the experience of working stressors and coping strategies associated with menstrual symptoms among nurses with shifting schedules. METHODS: Data were collected in two stages. First, in-depth interviews were conducted to collect nurses' experiences. Sentences that best fit the study's purpose were extracted for the construction of Q statements. Second, nurses were allowed to subjectively rank these Q statements by using Q-sorts. A total of 90 participants ranked the designed Q statements. The Q factor analysis revealed a five-factor solution that accounted for 48.90% of the total variance. RESULTS: The five evident factors included: menstrual symptoms interfering in collaboration with colleagues, deficiency of professional function and stress due to symptoms burden, diverse experiences without a clear pattern, adapted self-management with and without medication use, and stress due to symptoms burden and using medication for self-management. CONCLUSIONS: The identification of these five groups may facilitate the development of responsive strategies to meet nurses' preferences. Furthermore, identifying workplace factors that are associated with the adverse effects of menstrual symptoms on nurses will be helpful for nursing supervisors and hospital managers. Additionally, strategies that can be implemented to create supportive work environments are discussed.

The skin microbiome of wound scars and unaffected skin in patients with moderate to severe burns in the subacute phase.

Although studies on skin microbiome of acute and chronic wounds abound, evidence on newly built microbial communities of subacute wounds remains scant. To characterize the skin microbiome of recently healed (scarred) burn wounds in relation to unaffected skin surfaces, we collected weekly swabs from patients with moderate to severe burns in the 3rd postburn month for 4 weeks in 2015. We performed skin type (moist, dry, and oily)-matched comparisons within six burn patients (43 pairs of swabs) and with 13 skin-healthy, control patients (22 pairs of samples) using 16S ribosomal RNA gene sequencing results. Results of comparative microbiome analysis showed that, there were no substantial variations in the microbial abundance (all p > 0.05) or composition (all p > 0.01, adjusted for multiple comparisons) between samples obtained from wound scars and those from unaffected surfaces of burn patients. Nor did we find significant temporal dynamics in microbial richness or diversity in burn samples (all p ≥ 0.05). However, samples from burn patients harbored more Firmicutes (median: 25.6%, interquartile range [IQR]: 14.3%-52.8%) than those of control patients (14.9%, IQR: 6.7%-27.0%; p: 0.016), even after adjusting for host age, sex, and skin type-matching (p: 0.026). The number of observed bacterial operational taxonomic units at the genus level was reduced in burn patients (median: 62, IRQ: 32-85) as compared to control patients (median: 128, IQR: 112-136; age-, skin type-adjusted p < 0.01). Meanwhile, estimates of community diversity and evenness for surveyed body sites of burn patients were higher than those of control patients (all adjusted p ≤ 0.05). With a much-reduced bacterial burden and a relative overgrowth of Staphylococcus spp., the skin microbiota of burn patients remained dysbiotic in the subacute phase as compared to that of skin-normal patients.

Influence of oxyR on Growth, Biofilm Formation, and Mobility of Vibrio parahaemolyticus.

Vibrio parahaemolyticus is a common marine food-borne enteropathogen. In this study, we examined the antioxidative activity, growth, biofilm formation, and cell mobility of an oxyR deletion mutant and its genetically complementary strain of V. parahaemolyticus. oxyR is the regulator of catalase and ahpC genes. Protection against extrinsic H2O2 and against the organic peroxides cumene hydroperoxide and tert-butyl hydroperoxide was weaker in the deletion mutant than in its parent strain. Expression of the major functional antioxidative genes, ahpC1 and VPA1418, was markedly decreased in the oxyR mutant. Growth of this mutant on agar medium was significantly inhibited by autoclaved 0.25% glucose and by 0.25% dipotassium hydrogen phosphate, 0.5% monosaccharides (glucose, galactose, xylose, and arabinose), or 114.8 mM phosphates. The inhibition of the growth of this oxyR mutant by extrinsic peroxides, autoclaved sugars, and phosphates was eliminated by the complementary oxyR gene or by the addition of catalase to the autoclaved medium, while no inhibition of growth was observed when filter-sterilized sugars were used. The formation of biofilm and swimming mobility were significantly inhibited in the oxyR mutant relative to that in the wild-type strain. This investigation demonstrates the antioxidative function of oxyR in V. parahaemolyticus and its possible roles in biofilm formation, cell mobility, and the protection of growth in heated rich medium.

Functions of VPA1418 and VPA0305 Catalase Genes in Growth of Vibrio parahaemolyticus under Oxidative Stress.

The marine foodborne enteropathogen Vibrio parahaemolyticus has four putative catalase genes. The functions of two katE-homologous genes, katE1 (VPA1418) and katE2 (VPA0305), in the growth of this bacterium were examined using gene deletion mutants with or without complementary genes. The growth of the mutant strains in static or shaken cultures in a rich medium at 37°C or at low temperatures (12 and 4°C), with or without competition from Escherichia coli, did not differ from that of the parent strain. When 175 µM extrinsic H2O2 was added to the culture medium, bacterial growth of the ΔkatE1 strain was delayed and growth of the ΔkatE1 ΔkatE2 and ΔkatE1 ΔahpC1 double mutant strains was completely inhibited at 37°C for 8 h. The sensitivity of the ΔkatE1 strain to the inhibition of growth by H2O2 was higher at low incubation temperatures (12 and 22°C) than at 37°C. The determined gene expression of these catalase and ahpC genes revealed that katE1 was highly expressed in the wild-type strain at 22°C under H2O2 stress, while the katE2 and ahpC genes may play an alternate or compensatory role in the ΔkatE1 strain. This study demonstrated that katE1 encodes the chief functional catalase for detoxifying extrinsic H2O2 during logarithmic growth and that the function of these genes was influenced by incubation temperature.

Nursing Students' Perceptions of Menstrual Distress during Clinical Practice: A Q-Methodology Study.

This study aimed to explore the cluster patterns of female nursing students' perceptions of the effects of menstrual distress during clinical practice. This study adopted the Q-methodology study design. We recruited female nursing students from a college in northern Taiwan. Forty-seven Q-statements were constructed to explore participants' experiences of the impact of menstrual distress on clinical learning. In total, 58 participants subjectively ranked Q-statements concerning menstrual distress experiences during clinical practice and were classified. After Q-sorting, the subjective ranking process PQ Method (version 2.35, Schmolck, Emmendingen, Germany) was employed for factor analysis. Four patterns of shared perspectives, accounting for 46.6% of the total variance, were identified: (a) influencing clinical learning and making good use of painkillers; (b) responsible attitudes and diversified relief of discomfort; (c) seeking peer support and effect on mood; (d) negative impact on learning ability and conservative self-care. Clinical practice is a major component of nursing education; menstrual distress affects female nursing students' clinical learning and performance. The exploration of clustering different nursing students' perceptions may facilitate customized strategies to enable more appropriate assistance.

Dipyridamole suppresses high glucose-induced osteopontin secretion and mRNA expression in rat aortic smooth muscle cells.

BACKGROUND: Diabetic patients are frequently afflicted with medial artery calcification, a predictor of cardiovascular mortality. Diabetes induced the expression of osteopontin in arterial vasculature, which is an indicator of disease progression in artery calcification and vascular stiffness. Signal transduction and strategies that suppress high glucose-induced osteopontin expression in arterial vascular smooth muscle cells is investigated. METHODS AND RESULTS: The incubation of rat aortic smooth muscle cells under high glucose concentration increased osteopontin protein secretion and mRNA expression. Treatment with dipyridamole decreased high glucose-induced osteopontin expression and secretion. Dipyridamole decreased glucose-induced osteopontin through inhibition of phosphodiesterase, thereby increasing intracellular levels of adenosine-3',5'-cyclic monophosphate (cAMP) and guanosine-3',5'-cyclic monophosphate (cGMP), and increased thioredoxin expression to inhibit the reactive oxygen species (ROS) system. Induction of osteopontin was reversed when cells were pretreated with N-[2-bromocinnamyl(amino)ethyl]-5-isoquinolinesulfonamide (H89, cAMP-dependent protein kinase inhibitor), KT5823 (cGMP-dependent protein kinase inhibitor), or dinitrochlorobenzene (thioredoxin reductase inhibitor). The antioxidant, N-acetyl-L-cysteine, suppressed glucose-induced osteopontin expression by decreasing ROS concentration. Both H89 and KT5823 downregulated thioredoxin expression. CONCLUSIONS: These results suggest a novel effect for dipyridamole to suppress high glucose-induced osteopontin protein secretion and mRNA expression. Dipyridamole has antioxidant properties and a phosphodiesterase inhibitor activity, which might be useful to ameliorate diabetic vasculopathy and its cardiovascular complications.

SOX4 activates CXCL12 in hepatocellular carcinoma cells to modulate endothelial cell migration and angiogenesis in vivo.

The overexpression of SOX4 in various kinds of cancer cells was associated with poor prognosis for patients. The role of SOX4 in angiogenesis and tumor microenvironment modulation was recently documented in breast cancer but remains unclear in hepatocellular carcinoma (HCC). In our study, the clinical relevance of SOX4 overexpression in HCC and its role in the tumor microenvironment were investigated. The overexpression of SOX4 (SOX4high) in tumor lesions was associated with higher microvessel density (P = 0.012), tumor thrombosis formation (P = 0.012), distant metastasis (P < 0.001), and an independent prognostic factor for disease-free survival in HCC patients (P = 0.048). Endogenous SOX4 knockout in Hep3B cells by the CRISPR/cas9 system reduced the expression of CXCL12, which, in turn, attenuated chemotaxis in human umbilical vein endothelial cells, tube formation in vitro, reduced tumor growth, reticular fiber production, and angiogenesis in vivo in a xenograft mouse model. Treatment with an antagonist targeting CXCR4 (AMD3100), a receptor of CXCL12, inhibited chemotaxis and tube formation in endothelial cells in vitro. The CXCL12 promoter was activated by ectopic expression of a Flag-tagged SOX4 plasmid, endogenous SOX4 knockdown abolished promoter activity of CXCL12 as shown by luciferase assays, and an association with the CXCL12 promoter was identified via chromatin immunoprecipitation in HCC cells. In conclusion, SOX4 modulates the CXCL12 promoter in HCC cells. The secretory CXCL12, in turn, modulates CXCR4 in endothelial cells, reticular fibers to regulate the tumor microenvironment and modulate neovascularization, which might contribute to the distant metastasis of tumors.

Protective roles of katG-homologous genes against extrinsic peroxides in Vibrio parahaemolyticus.

The marine foodborne enteropathogen, Vibrio parahaemolyticus, has four putative catalase genes. Function of the katG-homologous genes, katG1(VPA0768) and katG2(VPA0453), was examined using gene deletion mutants, and compared with those of the katE-homologous genes, katE1(VPA1418) and katE2(VPA0305). Bacterial growth of ΔkatG1 was significantly delayed in the presence of 200-300 µM H2O2, and such inhibition was enhanced when incubation temperature was lowered from 37°C to 22°C. In the stationary phase, the ΔkatG1 strain was more susceptible to the lethal dosage of H2O2 than the ΔkatE1 strain. The minimum inhibitory concentrations and minimum bactericidal concentrations revealed that ΔkatE1/ΔkatE2 strains were more susceptible to H2O2 than the ΔkatG1/ΔkatG2 strains in exponential phase, while ΔkatG1 was more susceptible than the ΔkatE1/ΔkatE2 strains in the starved culture. This study demonstrated the chief antioxidative role of katG1 in the stationary phase and starved culture of V. parahaemolyticus, while katG1 and katG2 were also responsive to H2O2 and cumene hydroperoxide in the exponential phase.

Lily ASR protein-conferred cold and freezing resistance in Arabidopsis.

The lily LLA23 protein is a member of the abscisic acid, stress and ripening-induced (ASR) protein family. Constitutive overexpression of LLA23 under the cauliflower mosaic virus 35S promoter confers cold and freezing tolerance in Arabidopsis. The phenotypical growth and survival percentage of the two transgenic 35S::LLA23 plants showed higher resistance to cold and freezing conditions than those of wild-type (WT) plants. The electrolyte leakage in WT leaves increased by approximately fourfold at -2 °C relative to that at 22 °C whereas both transgenic leaves showed little ion leakage under the same conditions. A microarray analysis of LLA23-overexpressing transgenic line, 35S::LLA23E, under normal growing conditions was previously conducted by Yang et al. (Protoplasma, 2008, 233:241-254). Microarray analysis showed that 12 cold-responsive genes are upregulated and 25 cold-responsive genes are downregulated by lily ASR. Many ASR-regulated genes encode proteins involved in the classes of defense/stress-related, transcription, and metabolism. Quantitative polymerase chain reaction analysis confirms the changes in mRNA levels observed in the microarray analysis. Thus, our results provide in vivo evidence implying that LLA23 mediates cold/freezing stress-responsive signaling. To gain further insight into the functions of LLA23 protein, an in vitro enzyme protection assay was used in which lactate dehydrogenase and malate dehydrogenase were subjected to unfavorable conditions. The assay revealed that both enzyme activities were significantly retained with the addition of LLA23, which was superior to either trehalose or BSA, suggesting that the LLA23 protein can protect enzymatic activities against freeze-thaw cycles. The 35S::LLA23 seedlings also exhibited enzyme activity superior to WT at -4 °C. These results suggest that LLA23 may act as an osmoprotectant as well as a transcription factor to confer 35S::LLA23 plants enhanced cold and freezing resistance.

Dipyridamole inhibits cobalt chloride-induced osteopontin expression in NRK52E cells.

Osteopontin plays a pivotal role in the progression of interstitial fibrosis in renal ischemia. In the present study, rat renal tubular NRK52E cells treated with hypoxia mimetic cobalt chloride (CoCl(2)) increased osteopontin production, and are associated with increased phosphorylation of Akt/PKB (protein kinase B) and p38 mitogen-activated protein kinase (p38MAPK). Furthermore, pretreatment of cells with l-N-acetylcysteine (an antioxidant) inhibited CoCl(2)-stimulated osteopontin protein expression and p38MAPK phosphorylation, but not Akt/PKB phosphorylation. Pretreatment of cells with anti-inflammatory agents celecoxib, tanshinone IIA, and dipyridamole inhibited CoCl(2)-induced osteopontin production paralleled by heme oxygenase-1 (HO-1) induction. Pretreatment of cells with tin protoporphyrin (a HO-1 inhibitor) or hemoglobin (a carbon monoxide scavenging agent) reversed dipyridamole inhibition of osteopontin expression. Moreover, transfection of HO-1 small interfering RNA (siRNA) reduced dipyridamole-stimulated mitogen-activated protein kinase phosphatase-1 (MKP-1) phosphorylation. Conversely, MKP-1 knockdown reversed dipyridamole inhibition of osteopontin expression. Taken together, these data suggest that dipyridamole may inhibit CoCl(2)-induced osteopontin expression through HO-1 induction. Increased HO-1 may catalyze the conversion of heme into carbon monoxide, in turn carbon monoxide activates MKP-1. MKP-1 activation inhibits the p38MAPK signaling pathway that mediates CoCl(2)-induced osteopontin production.

RNA interference prevents lipopolysaccharide-induced preprotachykinin gene expression.

We showed previously that lipopolysaccharide (LPS) induces noncholinergic airway hyperreactivity to capsaicin via an upregulation of tachykinin synthesis. This study was designed to test whether double-stranded preprotachykinin (ds PPT) RNA, RNA interference (RNAi), prevents the LPS-induced alterations. First, cultured primary nodose ganglial cells of newborn Brown-Norway rats were divided into four groups: control; LPS; LPS+RNAi; and LPS+RNAi+liposome. Second, young Brown-Norway rats for the in vivo study were divided into three groups (control; LPS; and LPS+RNAi), and ds PPT RNA was microinjected bilaterally into the nodose ganglia in the LPS+RNAi group. Then, ganglial cells were collected from the culture whereas the nodose ganglia and lungs were sampled from the animals, and PPT mRNA and substance P (SP) levels were analyzed. Also, airway reactivity to capsaicin was performed in vivo. LPS induced significant increases in PPT mRNA and SP levels in vitro and in vivo and an increase in airway reactivity to capsaicin in vivo. However, ds PPT RNA, but not scrambled RNA, prevented all LPS-induced alterations. The effect of ds PPT RNA was not enhanced by liposome in vitro. Therefore, we demonstrated that the local application of RNAi prevents effectively the activation of the noncholinergic system modulating the lungs/airways.