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As the fertility rate declines, it becomes increasingly necessary for governments to guide power companies in introducing preferential tariffs to encourage nuclear families to have children. However, traditional household statistics for residential households are time-consuming and insufficient for enterprises seeking to adopt intelligent marketing schemes for different types of households. To address these issues, this paper proposes a nuclear family type identification method for residential electricity consumption based on a deep forest algorithm. The method first classifies nuclear households according to the number of children in them. Then, features are selected by combining the daily 48-point load and prior knowledge of nuclear families. The Pearson correlation coefficient and random forest importance ranking are used to remove features with low correlation and low importance. Additionally, features are classified based on their importance, and the number of features is balanced by stratified sampling to optimize the multi-granularity scan results and improve the model’s generalization. Finally, the improved cascade forest with feature input replacement base learner is trained, and the model is evaluated using accuracy evaluation metrics.The experimental results demonstrate that the proposed model accurately recognizes the number of children in different nuclear families and can be used in power companies to improve lean management. The results show that the improved method is effective in improving recognition com-pared to the original deep forest method, with recognition accuracy 5.1% higher than the random forest method and 0.7% higher than the deep forest method, reaching 94%.

We report the complete mitochondrial genome of Okuno 1994. The mitogenome was found to contain 16158 bp with 13 protein-coding genes (PCGs), 22 tRNA genes (tRNAs), 2 rRNA genes (rRNAs), and 1 putative control region. Phylogenetic analysis indicated that was sister to (PP= 1), of the same family Rhynchocinetidae. These results are helpful for research on the phylogenetic and evolutionary studies of this group.

Semisulcospiridae is a family of freshwater gastropods with over 100 species, primarily distributed in East Asia and North America. They play crucial ecological roles and are of medical importance as intermediate hosts for parasites. However, their phylogenetic relationship remains unclear. Most previous studies, which focused on fewer molecular markers (e.g., , , ), have shown limitations in resolving relationships with low resolution. Mitochondrial genomes, with their richer phylogenetic information, offer a promising tool to infer the evolutionary relationships within this family. This study sequenced, assembled, and annotated the complete mitochondrial genomes of three Semisulcospiridae species from China: , , and . Phylogenetic analyses were conducted using Maximum Likelihood (ML) and Bayesian Inference (BI) methods on five distinct datasets derived from the mitochondrial genomes, including nucleotide sequences of protein-coding genes (with and without third codon positions), amino acid sequences, and combinations with two ribosomal RNA genes. The complete (or near-complete) mitochondrial genomes of , , and were 15,474 bp, 15,660 bp, and 15,744 bp in length, respectively, showing typical gene content and an A+T bias. The gene order was highly conserved. Phylogenetic analyses consistently recovered the family Semisulcospiridae as monophyletic and revealed three well-supported, distinct clades corresponding to the genera , , and . While the overall tree topologies were robust for Semisulcospiridae, some incongruences were observed in the placements of other cerithioidean families depending on the dataset used. Evolutionary rate analysis (Ka/Ks) indicated strong purifying selection across all protein-coding genes, with being the most conserved. This study provided three new mitochondrial genomes for Semisulcospiridae: , , and Phylogenetic analysis based on mitochondrial genome datasets offers new evidence that supports the monophyly of the three Asian genera of Semisulcospiridae. Future research should include broader taxonomic sampling, particularly of the North American genus and the atypical Japanese lineages, to achieve a comprehensive phylogenetic framework.

ABSTRACTBackgroundWhether Inuit in Canada experience disparities in lung cancer survival remains unknown. When requiring investigation and treatment for lung cancer, all residents of Nunavik, the Inuit homeland in Quebec, are sent to the McGill University Health Centre (MUHC), in Montréal. We sought to compare survival among patients with lung cancer at the MUHC, who were residents of Nunavik and Montréal, Quebec, respectively. MethodsWe conducted a retrospective cohort study. Using lung cancer registry data, we identified Nunavik residents with histologically confirmed lung cancer diagnosed between 2005 and 2017. We aimed to match 2 Montréal residents to each Nunavik resident on sex, age, calendar year of diagnosis, and histology (non–small cell lung cancer v. small cell lung cancer). We reviewed medical records for data on additional patient characteristics and treatment, and obtained vital status from a provincial registry. We compared survival using Kaplan–Meier analysis and Cox proportional hazards regression. ResultsWe included 95 residents of Nunavik and 185 residents of Montréal. For non–small cell lung cancer, median survival times were 321 (95% confidence interval [CI] 184–626) days for Nunavik ( n = 71) and 720 (95% CI 536–1208) days for Montréal residents ( n = 141). For small cell lung cancer, median survival times were 190 (95% CI 159–308) days for Nunavik ( n = 24) and 270 (95% CI 194–766) days for Montréal residents ( n = 44). Adjusting for matching variables, stage, performance status, and comorbidity, Nunavik residents had a higher hazard of death (hazard ratio 1.68, 95% CI 1.17–2.41). InterpretationNunavik residents experience disparities in survival after lung cancer diagnosis. Although studies in other Inuit Nunangat regions are needed, our findings point to an urgent need to ensure that interventions aimed at improving lung cancer survival, including lung cancer screening, are accessible to Inuit Nunangat residents.

Melanoma is among the most aggressive cancers due to its tendency to metastasize early. Phenotype switching between a proliferative and an invasive state has been suggested as a critical process for metastasis, though the mechanisms that regulate state transitions are complex and remain poorly understood. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcriptional modulator that becomes aberrantly expressed in melanoma. Yet, the role of BORIS in melanoma remains elusive. Here, we show that BORIS is involved in melanoma phenotype switching. Genetic modification of BORIS expression in melanoma cells combined with whole-transcriptome analysis indicated that BORIS expression contributes to an invasion-associated transcriptome. In line with these findings, inducible BORIS overexpression in melanoma cells reduced proliferation and increased migration and invasion, demonstrating that the transcriptional switch is accompanied by a phenotypic switch. Mechanistically, we reveal that BORIS binds near the promoter of transforming growth factor-beta 1 (TFGB1), a well-recognized factor involved in the transition towards an invasive state, which coincided with increased expression of TGFB1. Overall, our study indicates a pro-invasive role for BORIS in melanoma via transcriptional reprogramming.

Two morphotypes of Plectropomus leopardus have been identified; morphometric and meristic analyses show that there is no diagnostic difference between them. A difference in color pattern was the most appropriate phenotypic character with which to distinguish between the two morphotypes. Complete mitochondrialDNA sequencing, however, indicated a clear difference between the two morphotypes. Barcoding analysis revealed no significant difference ( P >0.05) in CO1 or ND2 divergence among intramorphotypic individuals, even between geographically separated populations, whereas the intermorphotypic CO1 and ND2 divergences were large enough (averaging 0.95% for CO1 and 1.37% for ND2) to clearly discriminate between the two morphotypes. The color pattern difference, geographical distribution, together with the mtDNA and barcode sequencing data, suggest that the two morphotypes should be of two subspecies or even two species.

By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-beta and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-beta partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-beta release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.

Different clones, protocol conditions, instruments, and scoring/readout methods may pose challenges in introducing different PD-L1 assays for immunotherapy. The diagnostic accuracy of using different PD-L1 assays interchangeably for various purposes is unknown. The primary objective of this meta-analysis was to address PD-L1 assay interchangeability based on assay diagnostic accuracy for established clinical uses/purposes. A systematic search of the MEDLINE database using PubMed platform was conducted using “PD-L1” as a search term for 01/01/2015 to 31/08/2018, with limitations “English” and “human”. 2,515 abstracts were reviewed to select for original contributions only. 57 studies on comparison of two or more PD-L1 assays were fully reviewed. 22 publications were selected for meta-analysis. Additional data were requested from authors of 20/22 studies in order to enable the meta-analysis. Modified GRADE and QUADAS-2 criteria were used for grading published evidence and designing data abstraction templates for extraction by reviewers. PRISMA was used to guide reporting of systematic review and meta-analysis and STARD 2015 for reporting diagnostic accuracy study. CLSI EP12-A2 was used to guide test comparisons. Data were pooled using random-effects model. The main outcome measure was diagnostic accuracy of various PD-L1 assays. The 22 included studies provided 376 2×2 contingency tables for analyses. Results of our study suggest that, when the testing laboratory is not able to use an Food and Drug Administration-approved companion diagnostic(s) for PD-L1 assessment for its specific clinical purpose(s), it is better to develop a properly validated laboratory developed test for the same purpose(s) as the original PD-L1 Food and Drug Administration-approved immunohistochemistry companion diagnostic, than to replace the original PD-L1 Food and Drug Administration-approved immunohistochemistry companion diagnostic with a another PD-L1 Food and Drug Administration-approved companion diagnostic that was developed for a different purpose.

Pulmonary large cell neuroendocrine carcinoma (LCNEC) is a highly aggressive malignancy, which was recently found to comprise three major genomic subsets: small cell carcinoma-like, non-small cell carcinoma (predominantly adenocarcinoma)-like, and carcinoid-like. To further characterize adenocarcinoma-like subset, here we analyzed the expression of exocrine marker napsin A, along with TTF-1, in a large series of LCNECs ( n =112), and performed detailed clinicopathologic and genomic analysis of napsin A-positive cases. For comparison, we analyzed napsin A expression in other lung neuroendocrine neoplasms (177 carcinoids, 37 small cell carcinomas) and 60 lung adenocarcinomas. We found that napsin A was expressed in 15% of LCNEC (17/112), whereas all carcinoids and small cell carcinomas were consistently negative. Napsin A reactivity in LCNEC was focal in 12/17 cases, and weak or moderate in intensity in all cases, which was significantly lower in the extent and intensity than seen in adenocarcinomas ( P <0.0001). The combination of TTF-1-diffuse/napsin A-negative or focal was typical of LCNEC but was rare in adenocarcinoma, and could thus serve as a helpful diagnostic clue. The diagnosis of napsin A-positive LCNECs was confirmed by classic morphology, diffuse labeling for at least one neuroendocrine marker, most consistently synaptophysin, and the lack of distinct adenocarcinoma component. Genomic analysis of 14 napsin A-positive LCNECs revealed the presence of mutations typical of lung adenocarcinoma ( KRAS and/or STK11 ) in 11 cases. In conclusion, LCNECs are unique among lung neuroendocrine neoplasms in that some of these tumors exhibit low-level expression of exocrine marker napsin A, and harbor genomic alterations typical of adenocarcinoma. Despite the apparent close biological relationship, designation of adeno-like LCNEC as a separate entity from adenocarcinoma is supported by their distinctive morphology, typically diffuse expression of neuroendocrine marker(s) and aggressive behavior. Further studies are warranted to assess the clinical utility and optimal method of identifying adenocarcinoma-like and other subsets of LCNEC in routine practice.

Therapies that mitigate the fibrotic process may be able to slow progressive loss of function in many lung diseases. Because cyclic adenosine monophosphate is known to regulate fibroblasts, the current study was designed to evaluate the activity of selective phosphodiesterase (PDE) inhibitors on two in vitro fibroblast responses: chemotaxis and contraction of three-dimensional collagen gels. Selective PDE4 inhibitors, rolipram and cilomilast, each inhibited the chemotaxis of human fetal lung fibroblasts (HFL-1) toward fibronectin in the blindwell assay system (control: 100% versus cilomilast [10 microM]: 40.5 +/- 7.3% versus rolipram: [10 microM] 32.1 +/- 2.7% cells/5 high-power fields; P < 0.05, both comparisons). These PDE4 inhibitors also inhibited contraction of three-dimensional collagen gels (control: 100% versus cilomilast: 167.7 +/- 6.9% versus rolipram: 129.9 +/- 1.9% of initial size; P < 0.05, both comparisons). Amrinone, a PDE3 inhibitor, and zaprinast, a PDE5 inhibitor, had no effect in either system. Prostaglandin E(2) (PGE(2)) inhibited both chemotaxis and gel contraction, and the PDE4 inhibitors shifted the PGE(2) concentration-dependence curve to the left in both systems. The inhibition of endogenous PGE(2) production by indomethacin diminished the effects of the PDE4 inhibitors in both chemotaxis and gel contraction, consistent with the concept that the PDE4 inhibitory effects on fibroblasts are related to the presence of cyclic adenosine monophosphate in the cells. In summary, these in vitro results suggest that PDE4 inhibitors may be able to suppress fibroblast activity and, thus, have the potential to block the development of progressive fibrosis.