Additionally, by classifying sputum samples of patients suffering from chronic obstructive pulmonary disease, we showed that adding genomes of genomospecies to a reference database offers higher taxonomic resolution for taxonomic profiling. Finally, we show how our genomospecies database is able to identify correctly a clinical stool sample from a patient with a streptococcal infection, proving that genomospecies provide better taxonomic coverage for metagenomic analyses.Patients with triple-negative breast cancer have few therapeutic strategy options. In this study, we investigated the effect of isoliquiritigenin (ISL) on the proliferation of triple-negative breast cancer cells. We found that treatment with ISL inhibited triple-negative breast cancer cell line (MDA-MB-231) cell growth and increased cytotoxicity. ISL reduced cell cycle progression through the reduction of cyclin D1 protein expression and increased the sub-G1 phase population. The ISL-induced apoptotic cell population was observed by flow cytometry analysis. The expression of Bcl-2 protein was reduced by ISL treatment, whereas the Bax protein level increased; subsequently, the downstream signaling molecules caspase-3 and poly ADP-ribose polymerase (PARP) were activated. Moreover, ISL reduced the expression of total and phosphorylated mammalian target of rapamycin (mTOR), ULK1, and cathepsin B, whereas the expression of autophagic-associated proteins p62, Beclin1, and LC3 was increased. The decreased cathepsin B cause the p62 accumulation to induce caspase-8 mediated apoptosis. In vivo studies further showed that preventive treatment with ISL could inhibit breast cancer growth and induce apoptotic and autophagic-mediated apoptosis cell death. Taken together, ISL exerts an effect on the inhibition of triple-negative MDA-MB-231 breast cancer cell growth through autophagy-mediated apoptosis. Therefore, future studies of ISL as a supplement or alternative therapeutic agent for clinical trials against breast cancer are warranted.Photonic crystals (PhC) are spatially ordered structures with lattice parameters comparable to the wavelength of propagating light. Their geometrical and refractive index features lead to an energy band structure for photons, which may allow or forbid the propagation of electromagnetic waves in a limited frequency range. These unique properties have attracted much attention for both theoretical and applied research. Devices such as high-reflection omnidirectional mirrors, low-loss waveguides, and high- and low-reflection coatings have been demonstrated, and several application areas have been explored, from optical communications and color displays to energy harvest and sensors. In this latter area, photonic crystal fibers (PCF) have proven to be very suitable for the development of highly performing sensors, but one-dimensional (1D), two-dimensional (2D) and three-dimensional (3D) PhCs have been successfully employed, too. The working principle of most PhC sensors is based on the fact that any physical phenomenon which affects the periodicity and the refractive index of the PhC structure induces changes in the intensity and spectral characteristics of the reflected, transmitted or diffracted light; thus, optical measurements allow one to sense, for instance, temperature, pressure, strain, chemical parameters, like pH and ionic strength, and the presence of chemical or biological elements. In the present article, after a brief general introduction, we present a review of the state of the art of PhC sensors, with particular reference to our own results in the field of mechanochromic sensors. We believe that PhC sensors based on changes of structural color and mechanochromic effect are able to provide a promising, technologically simple, low-cost platform for further developing devices and functionalities.Senescent cells are generally characterized by permanent cell cycle arrest, metabolic alteration and activation, and apoptotic resistance in multiple organs due to various stressors. Excessive accumulation of senescent cells in numerous tissues leads to multiple chronic diseases, tissue dysfunction, age-related diseases and organ ageing. Immune cells can remove senescent cells. Immunaging or impaired innate and adaptive immune responses by senescent cells result in persistent accumulation of various senescent cells. Although senolytics-drugs that selectively remove senescent cells by inducing their apoptosis-are recent hot topics and are making significant research progress, senescence immunotherapies using immune cell-mediated clearance of senescent cells are emerging and promising strategies to fight ageing and multiple chronic diseases. This short review provides an overview of the research progress to date concerning senescent cell-caused chronic diseases and tissue ageing, as well as the regulation of senescence by small-molecule drugs in clinical trials and different roles and regulation of immune cells in the elimination of senescent cells. ABBV-CLS-484 phosphatase inhibitor Mounting evidence indicates that immunotherapy targeting senescent cells combats ageing and chronic diseases and subsequently extends the healthy lifespan.Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common cause of chronic kidney disease in children. The search for genetic causes of CAKUT has led to genetic diagnosis in approximately 5-20 % of CAKUT patients from Western countries. In this study, genetic causes of CAKUT in Korean children were sought using targeted exome sequencing (TES) of 60 genes reported to cause CAKUT in human or murine models. We identified genetic causes in 13.8% of the 94 recruited patients. Pathogenic single nucleotide variants of five known disease-causing genes, HNF1B, PAX2, EYA1, UPK3A, and FRAS1 were found in 7 cases. Pathogenic copy number variations of 6 patients were found in HNF1B, EYA1, and CHD1L. Genetic abnormality types did not significantly differ according to CAKUT phenotypes. Patients with pathogenic variants of targeted genes had syndromic features more frequently than those without (p less then 0.001). This is the first genetic analysis study of Korean patients with CAKUT. Only one-seventh of patients were found to have pathogenic mutations in known CAKUT-related genes, indicating that there are more CAKUT-causing genes or environmental factors to discover.