The results suggest that sleep quality may have an impact on several aspects of the quality of life of caregivers. Understanding the correlation between sleep quality and the quality of life of caregivers may assist health professionals in enhancing the sleep quality of caregivers and their ability to care for patients and themselves.
Danshen (salvia miltiorrhiza Bunge) is widely used in traditional Chinese medicine. However, it is definite clinical effort and mechanism on breast cancer is unclear. In our study, we used the real-world database to investigate in vivo protective effort of danshen in the breast cancer patients through using population-based data from the Taiwan National Health Insurance Research Database (NHIRD). In vitro, human breast cancer cells (MCF-7 cells and MDA-MB-231 cells) were used to investigate the effect and the underlying mechanism through XTT assay, flow cytometry, glutathione peroxidase (GPX) activity assay, GSH (reduced glutathione)/GSSG (oxidized glutathione), malondialdehyde (MDA), and western blot analysis. The in vivo effect was investigated through a xenograft nude mouse model. We found that dihydroisotanshinone I (DT), a pure compound present in danshen, can inhibit the growth of breast carcinoma cells, including MCF-7 cells and MDA-MB-231 cells. Moreover, DT induced apoptosis and ferroptosis in these breast cancer cells. DT also repressed the protein expression of GPX4 (Glutathione peroxidase 4). For in vivo study, DT treatment also significantly inhibited the final tumor volume without adverse effects in a xenograft nude mouse model. In conclusion, danshen has protective efforts in breast cancer patients, which could be attributed to DT through inducing apoptosis and ferroptosis of breast cancer cells.
Background: Numerous studies have revealed that statins have antitumor effects in vivo and in vitro. However, few studies have explored the relationship between statin use and the mortality of gastric cancer (GC) patients after treatments. This study examines the relationship between statin use and the overall survival (OS) of GC patients after surgery and adjuvant chemotherapy, using data from the nationwide cohort database of Taiwan. Methods: All patients newly diagnosed with GC from 1999 to 2008 in Taiwan were identified from the Registry of Catastrophic Illness Patients Database. Through propensity score matching, statin users were matched to statin non-users at a 1:4 ratio. The relationship between statin use and the OS of patients with GC was estimated through Cox regression models. Results: The study cohort included 1835 patients with GC who had received therapies during the study period. The death numbers among statin users (defined as those who used more than 28 cumulative defined daily doses (cDDDs)) and statin non-users were 138 and 895, respectively. A dose–response association was noted between statin use and the OS of patients with GC after treatments. The adjusted hazard ratios were 0.62 (95% confidence intervals (CI), 0.50–0.78) and 0.34 (95% CI, 0.26–0.45) for statin users administered 28–167 cDDDs and >168 cDDDs, respectively, compared with no statin use (<28 cDDDs). Conclusions: This study highlights that statin use may dose-dependently improve the OS of patients with GC after surgery and adjuvant chemotherapy in Taiwan. Additional studies are required to confirm the efficacy and safety of statin use.
Hypokalemic paralysis is rarely seen as the presenting feature in patients with Gitelman syndrome. We report a Chinese man who presented with periodic paralysis, in whom molecular analysis revealed compound heterozygous inheritance of three mutations of the thiazide-sensitive sodium chloride cotransporter. Family history revealed intrafamilial variation in phenotypes. Gitelman syndrome should be considered as a cause of hypokalemic paralysis, and molecular analysis may help establish the diagnosis.
A series of reactive fluorescent dyes were successfully synthesized and their structure was proven by IR spectra, NMR spectra, elemental analysis, and mass spectra. The fluorescence performance 6-amino-2(-3-phenyl-propyl)-benzo [de]isoquinoline-1,3-dione and 2-benzyl-6-hydroxy-benzo [de]isoquinoline-1,3-dione appears at around 276 and 437.4 nm, respectively, and their quantum yields are 0.662 and 0.562, respectively. It is important to indicate that the fluorescence performance is better for 6-amino-2(-3-phenyl-propyl)-benzo [de]isoquinoline-1,3-dione than for as a result of more electron donating groups linked to the 6-amino-2(-3-phenyl-propyl)-benzo [de]isoquinoline-1,3-dione molecule. These fluorescent dyes further react with toluene diisocyanate and other additives to form fluorescent dye based polyurethane (PU) ionomer molecules, and their structures are demonstracted by IR spectra. In aqueous solution, the fluorescence performance appears to be better for 6-amino-2(-3-phenyl-propyl)-benzo [de]isoquinoline-1,3-dione based PU ionomer than for 6-amino-2-phenyl-ethylbenzo [de]isoquinoline-1,3-dione based PU ionomer. For the fluorescent dye based PU ionomer molecule system, the number-average particle sizes of the fluorescent dye based PU ionomer molecules in water increase with increasing concentration of the fluorescent dye, as a result of the increased free volume of the ionomer molecule. This may be the result of increased intermolecular interactions between ionomer-molecules themselves.
We have previously reported a mouse Rnf33/Trim60 gene that is temporally expressed in the pre‐implantation embryo. The Rnf33 structural gene is composed of a short noncoding exon 1 and an intronless coding exon 2. In the present work, Rnf33 was shown to be expressed in the mouse testis and in the testicular cell lines TM3 and TM4. To elucidate Rnf33 transcriptional modulation, a 2.5‐kb Rnf33 sequence, inclusive of the upstream regulatory region, exon 1 and the associated intronic sequence, was dissected in transient transfection and luciferase assays. An initiator and an atypical TATA‐box were shown to act as the core promoter elements of the gene. Deletion and mutagenesis of the 2.5‐kb sequence in luciferase constructs further demonstrated that an intronic and palindromic kappa B (κB) sequence was an important cis element targeted by the nuclear factor‐κB (NF‐κB) subunits p65/RELA and p50/NFκB1, and also through modulation by tumor necrosis factor α. Transcriptional up‐regulation of Rnf33 by NF‐κB and tumor necrosis factor‐α was directly demonstrated in TM3 and TM4 cells by real‐time PCR quantification of the Rnf33 mRNA levels. Small interfering RNA knockdown of p65 and p50 confirmed Rnf33 down‐regulation by p65/p50. Spermatogenesis is regulated by a wide range of stimuli, including NF‐κB, which, in turn, is regulated by other signals. Hence, demonstration of NF‐κB‐regulated Rnf33 expression in testicular cells, particularly in Sertoli cells, implicates functional involvement of the putative RNF33 protein in spermatogenesis through association of the RNF33 protein with the microtubule via interaction with kinesin motor proteins, as previously demonstrated [Huang et al., submitted].
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