Determining a Cut-Off Point for Scores of the Breastfeeding Self-Efficacy Scale–Short Form: Secondary Data Analysis of an Intervention Study in Japan

Background

Breastfeeding self-efficacy can be measured with the Breastfeeding Self-Efficacy Scale-Short Form (BSES-SF). Mothers with low BSES-SF scores stop exclusive breastfeeding prematurely, but specific interventions can prevent that undesirable outcome. Because those interventions can be expensive, often one must decide which mothers will receive them. For that purpose, a cut-off BSES-SF score would be useful, but none is available. Therefore, we aimed to assess the overall accuracy of BSES-SF scores as predictors of not practicing post-discharge exclusive breastfeeding, and to choose an appropriate cut-off score for making that prediction.

Methods

This is a secondary data analysis of an intervention study. Data from 378 women in two non-Baby-Friendly Hospitals were analyzed. Participants were women in their third trimester who were 16 years of age or older, were able to read and write Japanese, were expected to have a singleton birth, and had completed the BSES-SF before discharge. BSES-SF scores were measured before discharge. Breastfeeding status was assessed 4 weeks and 12 weeks postpartum. Receiver Operating Characteristic (ROC) curves were used to assess the predictive ability of the BSES-SF and to inform the choice of a cut-off point.

Results

For both of the ROC curves (4 and 12 weeks postpartum) the area under the curve was 0.74. To obtain a high sensitivity, a cut-off score of 50 was chosen. With that cut-off score the sensitivity was 79% and the specificity was 52% 4 weeks postpartum, and they were 77% and 52%, respectively, 12 weeks postpartum.

Conclusion

In conclusion, the BSES-SF has moderate overall accuracy to distinguish women who will not practice exclusive breastfeeding after discharge from those who will. At non-Baby-Friendly hospitals in Japan, interventions to support exclusive breastfeeding might be considered for new mothers who have BSES-SF scores that are less than or equal to 50.     

Cryptococcus neoformans Infection in Mice Lacking Type I Interferon Signaling Leads to Increased Fungal Clearance and IL-4-Dependent Mucin Production in the Lungs

Type I interferons (IFNs) are secreted by many cell types upon stimulation via pattern recognition receptors and bind to IFN-α/β receptor (IFNAR), which is composed of IFNAR1 and IFNAR2. Although type I IFNs are well known as anti-viral cytokines, limited information is available on their role during fungal infection. In the present study, we addressed this issue by examining the effect of IFNAR1 defects on the host defense response to Cryptococcus neoformans. In IFNAR1KO mice, the number of live colonies was lower and the host immune response mediated not only by Th1 but also by Th2 and Th17-related cytokines was more accelerated in the infected lungs than in WT mice. In addition, mucin production by bronchoepithelial cells and expression of MUC5AC, a major core protein of mucin in the lungs, were significantly higher in IFNAR1KO mice than in WT mice. This increase in mucin and MUC5AC production was significantly inhibited by treatment with neutralizing anti-IL-4 mAb. In contrast, administration of recombinant IFN-αA/D significantly suppressed the production of IL-4, but not of IFN-γ and IL-17A, in the lungs of WT mice after cryptococcal infection. These results indicate that defects of IFNAR1 led to improved clearance of infection with C. neoformans and enhanced synthesis of IFN-γ and the IL-4-dependent production of mucin. They also suggest that type I IFNs may be involved in the negative regulation of early host defense to this infection.     

Baseline Serum Osteopontin Levels Predict the Clinical Effectiveness of Tocilizumab but Not Infliximab in Biologic-Na?ve Patients with Rheumatoid Arthritis: A Single-Center Prospective Study at 1 Year (the Keio First-Bio Cohort Study)

ObjectiveTo explore the baseline predictors of clinical effectiveness after tocilizumab or infliximab treatment in biologic-naïve rheumatoid arthritis patients.MethodsConsecutive biologic-naïve patients with rheumatoid arthritis initiating infliximab (n = 57) or tocilizumab (n = 70) treatment were included in our prospective cohort study. Our cohort started in February 2010, and the patients observed for at least 1 year as of April 2013 were analysed. We assessed baseline variables including patients'' characteristics (age, sex, disease duration, prednisolone dose, methotrexate dose, other disease-modifying antirheumatic drug use, Clinical Disease Activity Index [CDAI]) and serum biomarker levels (C-reactive protein, immunoglobulin M-rheumatoid factor, anti-cyclic citrullinated protein/peptide antibodies, interferon-γ, interleukin (IL)-1β, IL-2, IL-6, IL-8, IL-10, IL-17, tumor necrosis factor-α, soluble intercellular adhesion molecule-1, bone alkaline phosphatase, osteonectin, osteopontin) to extract factors associated with clinical remission (CDAI≤2.8) at 1 year using univariate analyses, and the extracted factors were entered into a multivariate logistic regression model. Similar analyses were also performed for Simplified Disease Activity Index (SDAI) remission (≤3.3) and Disease Activity Score with 28 joint counts, erythrocyte sedimentation rate (DAS28-ESR) remission (<2.6).ResultsThere were no significant differences in the baseline characteristics except for methotrexate use between the groups. In the multivariate analyses, the low baseline osteopontin levels (OR 0.9145, 95% CI 0.8399–0.9857) were identified as predictors of CDAI remission in the tocilizumab group, whereas no predictors of CDAI remission were found in the infliximab group. Similar results were obtained when using SDAI and DAS28-ESR remission criteria.ConclusionBaseline low serum osteopontin levels predict clinical remission 1 year after tocilizumab treatment and not infliximab treatment in biologic-naïve patients with rheumatoid arthritis. Our prediction model provided insights into how to optimize the choice of biologics and warrants external validation in other cohorts.     

Characterization of Piperacillin/Tazobactam-Resistant Klebsiella oxytoca Recovered from a Nosocomial Outbreak

We characterized 12 clinical isolates of Klebsiella oxytoca with the extended-spectrum β-lactamase (ESBL) phenotype (high minimum inhibitory concentration [MIC] values of ceftriaxone) recovered over 9 months at a university hospital in Japan. To determine the clonality of the isolates, we used pulsed-field gel electrophoresis (PFGE), multi-locus sequence typing (MLST), and PCR analyses to detect bla _RBI, which encodes the β-lactamase RbiA, OXY-2-4 with overproduce-type promoter. Moreover, we performed the isoelectric focusing (IEF) of β-lactamases, and the determination of the MICs of β-lactams including piperacillin/tazobactam for 12 clinical isolates and E. coli HB101 with pKOB23, which contains bla _RBI, by the agar dilution method. Finally, we performed the initial screening and phenotypic confirmatory tests for ESBLs. Each of the 12 clinical isolates had an identical PFGE pulsotype and MLST sequence type (ST9). All 12 clinical isolates harbored identical bla _RBI. The IEF revealed that the clinical isolate produced only one β-lactamase. E. coli HB101 (pKOB23) and all 12 isolates demonstrated equally resistance to piperacillin/tazobactam (MICs, >128 μg/ml). The phenotypic confirmatory test after the initial screening test for ESBLs can discriminate β-lactamase RbiA-producing K. oxytoca from β-lactamase CTX-M-producing K. oxytoca. Twelve clinical isolates of K. oxytoca, which were recovered from an outbreak at one university hospital, had identical genotypes and produced β-lactamase RbiA that conferred resistance to piperacillin/tazobactam. In order to detect K. oxytoca isolates that produce RbiA to promote research concerning β-lactamase RbiA-producing K. oxytoca, the phenotypic confirmatory test after the initial screening test for ESBLs would be useful.     

Effects of logging and recruitment on community phylogenetic structure in 32 permanent forest plots of Kampong Thom,Cambodia

Ecological communities including tropical rainforest are rapidly changing under various disturbances caused by increasing human activities. Recently in Cambodia, illegal logging and clear-felling for agriculture have been increasing. Here, we study the effects of logging, mortality and recruitment of plot trees on phylogenetic community structure in 32 plots in Kampong Thom, Cambodia. Each plot was 0.25 ha; 28 plots were established in primary evergreen forests and four were established in secondary dry deciduous forests. Measurements were made in 1998, 2000, 2004 and 2010, and logging, recruitment and mortality of each tree were recorded. We estimated phylogeny using rbcL and matK gene sequences and quantified phylogenetic α and β diversity. Within communities, logging decreased phylogenetic diversity, and increased overall phylogenetic clustering and terminal phylogenetic evenness. Between communities, logging increased phylogenetic similarity between evergreen and deciduous plots. On the other hand, recruitment had opposite effects both within and between communities. The observed patterns can be explained by environmental homogenization under logging. Logging is biased to particular species and larger diameter at breast height, and forest patrol has been effective in decreasing logging.     

Leucine-Rich Repeat Kinase 1 Regulates Autophagy through Turning On TBC1D2-Dependent Rab7 Inactivation

Autophagy is a conserved process that enables catabolic and degradative pathways. Rab family proteins, which are active in the GTP-bound form, regulate the transport and fusion of autophagosomes. However, it remains unclear how each cycle of Rab activation and inactivation is precisely regulated. Here, we show that leucine-rich repeat kinase 1 (LRRK1) regulates autophagic flux by controlling Rab7 activity in autolysosome formation. Upon induction of autophagy, LRRK1 was recruited via an association with VAMP7 to the autolysosome, where it activated the Rab7 GTPase-activating protein (GAP) TBC1D2, thereby switching off Rab7 signaling. Consistent with this model, LRRK1 deletion caused mice to be vulnerable to starvation and disrupted autolysosome formation, as evidenced by the accumulation of enlarged autolysosomes with undegraded LC3-II and persistently high levels of Rab7-GTP. This defect in autophagic flux was partially rescued by a mutant form of TBC1D2 with elevated Rab7-GAP activity. Thus, the spatiotemporal regulation of Rab7 activity during tunicamycin-induced autophagy is regulated by LRRK1.     

Genomic analysis identifies candidate pathogenic variants in 9 of 18 patients with unexplained West syndrome

West syndrome, which is narrowly defined as infantile spasms that occur in clusters and hypsarrhythmia on EEG, is the most common early-onset epileptic encephalopathy (EOEE). Patients with West syndrome may have clear etiologies, including perinatal events, infections, gross chromosomal abnormalities, or cases followed by other EOEEs. However, the genetic etiology of most cases of West syndrome remains unexplained. DNA from 18 patients with unexplained West syndrome was subjected to microarray-based comparative genomic hybridization (array CGH), followed by trio-based whole-exome sequencing in 14 unsolved families. We identified candidate pathogenic variants in 50 % of the patients (n = 9/18). The array CGH revealed candidate pathogenic copy number variations in four cases (22 %, 4/18), including an Xq28 duplication, a 16p11.2 deletion, a 16p13.1 deletion and a 19p13.2 deletion disrupting CACNA1A. Whole-exome sequencing identified candidate mutations in known epilepsy genes in five cases (36 %, 5/14). Three candidate de novo mutations were identified in three cases, with two mutations occurring in two new candidate genes (NR2F1 and CACNA2D1) (21 %, 3/14). Hemizygous candidate mutations in ALG13 and BRWD3 were identified in the other two cases (14 %, 2/14). Evaluating a panel of 67 known EOEE genes failed to identify significant mutations. Despite the heterogeneity of unexplained West syndrome, the combination of array CGH and whole-exome sequencing is an effective means of evaluating the genetic background in unexplained West syndrome. We provide additional evidence for NR2F1 as a causative gene and for CACNA2D1 and BRWD3 as candidate genes for West syndrome.     

Worldwide core collections of tea (Camellia sinensis) based on SSR markers

Tea (Camellia sinensis (L.) O. Kuntze) is the world’s most popular beverage crop. However, to date, no core collection has been selected from worldwide germplasm resources on the basis of genotype data. In this study, we analyzed 788 tea germplasm accessions using 23 simple sequence repeat (SSR) markers. Our population structure analysis divided the germplasms into a Japanese group and an exotic group. The latter could be divided into var. sinensis and var. assamica. The genetic diversity was higher in germplasms from China, Taiwan, India, and Sri Lanka than in those from other countries, and low in germplasms from Japan. Using the number of SSR alleles as a measure of genetic diversity, we developed a core collection consisting of 192 accessions and three subcore collections with 96, 48, and 24 accessions. Although the results might be affected by marker-selection bias, the core 192 collection adequately covered the range of variation of the 788 accessions in floral morphology, and the chemical composition of first-flush leaves. These collections will be powerful tools for breeding and genetic research in tea.