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and in the food packaging industry and its future application. Thus, the review aims to focus on the benefits and new dimensions provided by nanomaterials and nanotechnology in health sectors by improving treatment strategies and quality of life.This study explored the design of supersaturable self-microemulsifying drug delivery systems (S-SMEDDS) to address poor solubility and oral bioavailability of a novel benzimidazole derivative anticancer drug (BI). Firstly, self-microemulsifying drug delivery systems SMEDDS made of Miglyol® 812, Kolliphor® RH40, Transcutol® HP, and ethanol were prepared and loaded with the BI drug. Upon dispersion, the systems formed neutrally charged droplets of around 20 nm. However, drug precipitation was observed following incubation with simulated gastric fluid (pH 1.2). Aiming at reducing this precipitation and enhancing drug payload, supersaturable systems were then prepared by adding 1% hydroxypropyl cellulose as precipitation inhibitor. Supersaturable systems maintained a higher amount of drug in a supersaturated state in gastric medium compared with conventional formulations and were stable in simulated intestinal medium (pH 6.8). In vitro cell studies using Caco-2 cell line showed that these formulations reduced in a transient manner the transepithelial electrical resistance of the monolayers without toxicity. Accordingly, confocal images revealed that the systems accumulated at tight junctions after a 2 h exposure. In vivo pharmacokinetic studies carried out following oral administration of BI-loaded S-SMEDDS, SMEDDS, and free drug to healthy mice showed that supersaturable systems promoted drug absorption compared with the other formulations. Overall, these data highlight the potential of using the supersaturable approach as an alternative to conventional SMEDDS for improving oral systemic absorption of lipophilic drugs.Global influence of male infertility is increasing in recent decades. Proper understanding of genetics, anatomy, physiology and the intricate interrelation of male reproductive system are much needed for explaining the etiology of male infertility; and a detailed study on the epigenetics, indeed, will reveal the molecular mechanism behind its etiology. Sirtuins, the molecular sensors, are NAD+ dependent histone deacetylases and ADP- ribosyl transferases, participate in the chief events of epigenetics. In mammals, sirtuin family comprises seven members (SIRT1-SIRT7), and they all possess a conserved NAD+ binding catalytic domain, termed the sirtuin core domain which is imperative for their activity. Sirtuins exert a pivotal role in cellular homeostasis, energy metabolism, apoptosis, age-related disorders and male reproductive system. However, their exact role in male reproduction is still obscure. This article specifically reviews the role of mammalian sirtuins in male reproductive function, thereby, prompting further research to discover the restorative methods and its implementation in reproductive medicine.Acute myeloid leukemia (AML) is a malignant cancer of the hematopoietic system. Although the effectiveness of arsenic compounds has been recognized and applied clinically, some patients are still found resistant to this chemotherapy. In this study, we investigated that a synthetic thyroid hormone analog (TA), 2-iodo-4-nitro-1-(o-tolyloxy) benzene, had a strong apoptosis effect on U937 cells. U937 cells were treated with TA, and examinted the generation of reactive oxygen species (ROS), dysfunction of mitochondria, expression of pro-apoptosis and anti-apoptosis, and cleavage of caspase-3 and Poly (ADP-ribose) polymerase (PARP). Further, it is also evaluated that insight molecular mechanism and signaling pathways involved in the study. It is found that TA significantly induced apoptosis in U937 cells through production of ROS, dysfunction of mitochondria, and activation of caspase cascade. It was also observed that MAPK signaling pathway including ERK, JNK, and P38 signals are involved in the induction of apoptosis. Moreover, marked activation of autophagy and ER stress markers such as LC3, P62, Beclin1 and GRP78, CHOP were observed, respectively. selleck products Pretreatment with ER stress inhibitor tauroursodeoxycholic acid (TUDCA) and autophagy inhibitor 3-Methyladenine (3-MA) have successfully attenuated and aggravated TA-induced apoptosis, respectively. We further confirmed the active involvement of ER stress and autophagy signals. In conclusion, TA induced apoptosis through ER stress and activation of autophagy, and the latter is not conducive to TA-induced cell death. Our results may provide a new insight into the strategic development of novel therapy for the treatment of AML.Hepatocellular carcinoma (HCC) is a malignant tumor with high mortality and severe complication in China. Numerous studies have shown that long noncoding RNAs (lncRNAs) are involved in the regulation of various processes in cancer cells. Our research aimed to investigate the underlying mechanism of the lncRNA small nucleolar RNA host gene 7 (SNHG7) in HCC development. The expression of SNHG7, microRNA-122-5p (miR-122-5p), and Forkhead box K2 (FOXK2) was assessed via quantitative real-time polymerase chain reaction. 3-(4,5) -dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) and transwell assays were performed to measure cell viability, migration, and invasion, respectively. The relative protein levels were detected by Western blot. The relationships between miR-122-5p and SNHG7 or FOXK2 were predicted by online software and then confirmed by dual-luciferase reporter assay. Animal experiments were conducted to clarify the effects of SNHG7 on proliferation in vivo. To begin with, SNHG7 was upregulated, while miR-122-5p was downregulated in HCC tissues and cells. Downregulation of SNHG7 inhibited cell growth and metastasis. Interestingly, SNHG7 could abolish the effects of miR-122-5p on HCC cells. Furthermore, miR-122-5p targeted FOXK2 and miR-122-5p recovered the effects of FOXK2 downregulation on cell growth and metastasis in HCC cells. Besides, SNHG7 facilitated HCC tumor growth in vivo through the miR-122-5p/FOXK2 axis. The lncRNA SNHG7 boosted the development of HCC by regulating FOXK2 through sponging miR-122-5p.