Weight-loss behaviors before pregnancy associate with increased risk of postpartum depression from the Japan Environment and Children's Study.

No studies showed the association between weight-loss behaviors before pregnancy and postpartum depression (PPD). We analyzed data from the nation-wide birth cohort study, the Japan Environment and Children's Study. Self-administrated questionnaires answered by 62,446 women was analyzed using logistic regression analysis. PPD was assessed using the Edinburgh Postnatal Depression Scale at 1 month after delivery. Women using at least one weight-loss method had higher risk of PPD than women using no weight-loss methods [women without antenatal psychological distress according to Kessler 6-Item Psychological Distress score: adjusted odds ratio (aOR) 1.318, 95% confidence interval (CI) 1.246-1.394; women with antenatal psychological distress: aOR 1.250, 95% CI 0.999-1.565]. Using extremely unhealthy weight-loss methods was associated with PPD compared with no use of each weight-loss method (vomiting after eating: aOR 1.743, 95% CI 1.465-2.065; smoking: aOR 1.432, 95% CI 1.287-1.591; taking diet pills: aOR 1.308, 95% CI 1.122-1.520). The association between weight-loss behaviors and PPD varied according to pre-pregnancy BMI. In normal-weight women, the weight-loss method score, which indicates the degree of weight-loss method use, was associated with PPD. These results indicate using weight-loss methods before pregnancy is associated with an increased risk of PPD in Japanese women.

An attempt to analyze the longitudinal psychological state of cancer patients in the active treatment stage.

The psychological state and changes over time of cancer patients in the active treatment stage were classified into emotions by the speech and behavior of the patient described in the medical record article of the cancer psychological interview record, and the analysis of the "emotional state map" was attempted. In all cases, positive / negative emotions were mixed and appeared with variation, but a relatively large number of positive emotions, including , , and , were manifested, and the same was true in patients who experienced stressful treatment events. In the background, the existence of appropriate support from medical professionals and psychological characteristics peculiar to the stage of active treatment was inferred, such as the active treatment of the target patient, the hospitalization environment in which mental and physical pain promptly appealed to medical professionals, and the influence of psychological interviews. Cancer patients during active treatment perceived and expressed changes in the body and pain caused by the disease, and after responses from medical professionals and family members, they were conscious of their physical condition and emotions. It is suggested that this analysis method helps to objectively understand and explain the invisible and ever-changing psychological state of cancer patients in the active treatment stage. J. Med. Invest. 68 : 148-153, February, 2021.

Curvature-sensitive trans-assembly of human Atg8-family proteins in autophagy-related membrane tethering.

In macroautophagy, de novo formation of the double membrane-bound organelles, termed autophagosomes, is essential for engulfing and sequestering the cytoplasmic contents to be degraded in the lytic compartments such as vacuoles and lysosomes. Atg8-family proteins have been known to be responsible for autophagosome formation via membrane tethering and fusion events of precursor membrane structures. Nevertheless, how Atg8 proteins act directly upon autophagosome formation still remains enigmatic. Here, to further gain molecular insights into Atg8-mediated autophagic membrane dynamics, we study the two representative human Atg8 orthologs, LC3B and GATE-16, by quantitatively evaluating their intrinsic potency to physically tether lipid membranes in a chemically defined reconstitution system using purified Atg8 proteins and synthetic liposomes. Both LC3B and GATE-16 retained the capacities to trigger efficient membrane tethering at the protein-to-lipid molar ratios ranging from 1:100 to 1:5,000. These human Atg8-mediated membrane-tethering reactions require trans-assembly between the membrane-anchored forms of LC3B and GATE-16 and can be reversibly and strictly controlled by the membrane attachment and detachment cycles. Strikingly, we further uncovered distinct membrane curvature dependences of LC3B- and GATE-16-mediated membrane tethering reactions: LC3B can drive tethering more efficiently than GATE-16 for highly curved small vesicles (e.g., 50 nm in diameter), although GATE-16 turns out to be a more potent tether than LC3B for flatter large vesicles (e.g., 200 and 400 nm in diameter). Our findings establish curvature-sensitive trans-assembly of human Atg8-family proteins in reconstituted membrane tethering, which recapitulates an essential subreaction of the biogenesis of autophagosomes in vivo.

Traumatic Events Among Cancer Patients That Lead to Compassion Fatigue in Nurses: A Qualitative Study.

CONTEXT: Cancer care nurses are frequently exposed to patients' traumatic experiences and are at high risk of compassion fatigue. OBJECTIVES: To describe the components and frequencies of traumatic events experienced by patients with cancer, which give rise to nurse compassion fatigue. METHODS: This study is a supplementary analysis of data from a previous qualitative study. Semistructured interviews were conducted with 30 Japanese nurses, with at least two years of experience in cancer care and a history of compassion fatigue. Content analysis and constant comparison was used to identify relevant subcategories and categories. The frequencies of these subcategories and categories were then evaluated. RESULTS: Eleven subcategories and four categories were identified. The kappa coefficient of these subcategories, determined by two independent raters, was 0.89. Subcategories with the highest frequencies among participants were as follows: having symptoms of cancer progression (n = 20; 67%), suffering because of insufficient pain control (n = 11; 37%), and being informed about getting cancer (n = 10; 33%). The four categories were as follows: worsening of physical condition (n = 20; 67%), bad news from doctors (n = 19; 63%), difficulty in treatment (n = 18; 60%), and emotional conflict with family (n = 6; 20%). CONCLUSION: This study identified the components and frequencies of traumatic events among patients with cancer that lead to the onset of nurse compassion fatigue. Such information will aid in understanding the triggers of compassion fatigue, allowing for possible preparation to reduce the risk of this occupational hazard.

Escherichia coli CrfC Protein, a Nucleoid Partition Factor, Localizes to Nucleoid Poles via the Activities of Specific Nucleoid-Associated Proteins.

The Escherichia coli CrfC protein is an important regulator of nucleoid positioning and equipartition. Previously we revealed that CrfC homo-oligomers bind the clamp, a DNA-binding subunit of the DNA polymerase III holoenzyme, promoting colocalization of the sister replication forks, which ensures the nucleoid equipartition. In addition, CrfC localizes at the cell pole-proximal loci via an unknown mechanism. Here, we demonstrate that CrfC localizes to the distinct subnucleoid structures termed nucleoid poles (the cell pole-proximal nucleoid-edges) even in elongated cells as well as in wild-type cells. Systematic analysis of the nucleoid-associated proteins (NAPs) and related proteins revealed that HU, the most abundant NAP, and SlmA, the nucleoid occlusion factor regulating the localization of cell division apparatus, promote the specific localization of CrfC foci. When the replication initiator DnaA was inactivated, SlmA and HU were required for formation of CrfC foci. In contrast, when the replication initiation was inhibited with a specific mutant of the helicase-loader DnaC, CrfC foci were sustained independently of SlmA and HU. H-NS, which forms clusters on AT-rich DNA regions, promotes formation of CrfC foci as well as transcriptional regulation of crfC. In addition, MukB, the chromosomal structure mainetanice protein, and SeqA, a hemimethylated nascent DNA region-binding protein, moderately stimulated formation of CrfC foci. However, IHF, a structural homolog of HU, MatP, the replication terminus-binding protein, Dps, a stress-response factor, and FtsZ, an SlmA-interacting factor in cell division apparatus, little or only slightly affected CrfC foci formation and localization. Taken together, these findings suggest a novel and unique mechanism that CrfC localizes to the nucleoid poles in two steps, assembly and recruitment, dependent upon HU, MukB, SeqA, and SlmA, which is stimulated directly or indirectly by H-NS and DnaA. These factors might concordantly affect specific nucleoid substructures. Also, these nucleoid dynamics might be significant in the role for CrfC in chromosome partition.

Daunorubicin can eliminate iPS-derived cancer stem cells via ICAD/CAD-independent DNA fragmentation.

Aim: To identify a drug that can effectively eliminate these cancer stem cells (CSCs) and determine its mode of action. Methods: CSCs were obtained from mouse induced pluripotent stem cells (miPSCs) using cancer cell-conditioned media. Drug screening was performed on these cells or after transplantation into mice. Apoptosis was analyzed by flow cytometry and western blotting. Results: Drug screening studies showed that daunorubicin, a topoisomerase II inhibitor, is specifically cytotoxic to miPS-CSCs. Daunorubicin-induced apoptosis was found to be associated with p53 accumulation, activation of the caspase cascade, and oligonucleosomal DNA fragmentation. Treatment with the caspase inhibitor abolished daunorubicin-induced DNA fragmentation and was therefore considered to act downstream of caspase activation. This was also suppressed by treatment with a Ca2+-specific chelator, which suggested that CAD endonuclease does not contribute. Moreover, no obvious ICAD reduction/degradation was detected. Conclusion: Daunorubicin effectively eliminated CSCs, which are dependent on the p53/caspase signaling cascade. The current findings provided the basis for further studies on CSC-targeted drugs for the development of cancer treatment strategies.

Cognitive reactions of nurses exposed to cancer patients' traumatic experiences: A qualitative study to identify triggers of the onset of compassion fatigue.

OBJECTIVE: Nurses in cancer care are considered to be at risk for compassion fatigue because they are frequently exposed to patients' traumatic experiences. However, only a few effective empirical studies have been conducted in this field, and cognitive factors in particular have not been sufficiently studied. This study aims to describe the components of nurses' cognitive reactions from their exposure to cancer patients' traumatic experience to the onset of compassion fatigue. METHODS: In this qualitative study, 30 nurses in cancer care were purposively selected. Data were collected through semistructured interviews and analyzed by using content analysis and the constant comparative method. RESULTS: Forty attributes were identified from 613 statements and classified into 11 categories: sense of professional inadequacy, compassion for patients and their families, desire to support patients and their families, rumination on oneself or one's family, sense of professional mission, dissatisfaction with medical staff, desire to integrate with colleagues, desire to avoid one's duties, conflict between one's belief and reality, reconsideration of the meaning of life, and sense of powerlessness over cancer. CONCLUSIONS: This study identified important components of cognitive reactions of nurses who encounter the traumatic experiences of cancer patients in Japan. This information can contribute to the understanding of the onset of compassion fatigue and provide the foundation for nurses in cancer care to avoid and recover from compassion fatigue.

Expression of a Vibrio parahaemolyticus toxin in Escherichia coli results in chromosomal DNA degradation.

A toxin-antitoxin system, vp1842/vp1843, locates within a superintegron on the Vibrio parahaemolyticus genome chromosome I whose toxin gene vp1843 encodes a DNA nicking endonuclease. We found that the vp1843 expression in Escherichia coli cells strongly induced chromosomal DNA degradation. On the basis of these observations, we discuss a possible physiological role of vp1842/vp1843 in V. parahaemolyticus.