Dose-Response最新文献

Nanoparticles have shown promising potential for efficient drug delivery, circumventing biological interferences like immunological and renal clearance and mechanical and enzymatic destruction. However, a handful of research papers have questioned the biomedical use of metal-based nanoparticles like cadmium telluride quantum dots (CdTe-QDs) for their cytotoxic, genotoxic, and carcinogenic potential. Herein, we examined the effects of CdTe-QD NPs on gene expression profile of hepatocellular carcinoma (Huh-7) cell line. Huh-7 cells were treated with CdTe-QD NPs (10 μg/ml for 6, 12, and 24 hours, and 25 μg/ml for 6 and 12 hours), and transcriptomic analysis was performed using microarray to evaluate the global gene expression profile. Differential expressed genes (DEGs) were observed for both the doses (10 and 25 μg/ml) of CdTe-QD NPs at different time points. Gene ontology (GO) analysis revealed that genes involved in molecular function of cell cycle, organizational injury and abnormalities, cell death and survival, gene expression, cancer, organismal survival, and cellular development were differentially expressed. Overall, we have demonstrated differential expression of several genes, involved in maintaining cell survival, metabolism, and genome integrity. These findings were confirmed by RT-qPCR study for some canonical pathway genes signifying possible implication in NP toxicity-mediated cell survival and inhibition of cell death.

Previous research on "healing-with-intent" has reasonably demonstrated the validity of the phenomenon at least when a human healer is present and involved. However, in order for healing to be adopted into more conventional therapies, it must be able to be made scalable. The present study tests the effects of a scalable recording of the Bengston Healing Method on 3 cancer models. BalbC mice engrafted with 4T1 breast cancer cells, C57BL mice with melanoma B16 cells, and C3H mice with bladder MBT-2 wells were exposed to a recording of healing intent for 4 hours/day for approximately 1 month. In the breast cancer model, there was significant tumor suppression and a reduction of anemia marker HCT in treated vs control mice. In the melanoma model, there were no significant differences except for a reduction in platelet count among the treated mice. For unknown reasons, tumor growth never became evident in the bladder cancer model. While the effects of the recording seem to vary by model, there appears reason to pursue scalable delivery systems in multiple models and with multiple doses.

The dose due to photoneutron contamination outside the field of irradiation can be significant when using high-energy linear accelerators. The eye is a radiation-sensitive organ, and this risk increases when high linear energy transfer neutron radiation is involved. This study aimed to provide a fast method to estimate photoneutron dose to the eye during radiotherapy. A typical high-energy linear accelerator operating at 18 MV was simulated using the Monte Carlo N-Particle Transport Code System extended version (MCNPX 2.5.0). The latest International Atomic Energy Agency photonuclear data library release was integrated into the code, accounting for the most known elements and isotopes used in typical linear accelerator construction. The photoneutron flux from a 5 × 5 cm² field size was scored at the treatment table plane and used as a new source for estimating the absorbed dose in a high-resolution eye voxel anthropomorphic phantom. In addition, common shielding media were tested to reduce the photoneutron dose to the eye using common shielding materials. Introducing a 2 cm thickness of common neutron shielding medium reduced the total dose received in the eye voxel anthropomorphic phantom by 54%. In conclusion, individualized treatment based on photoneutron dose assessment is essential to better estimate the secondary dose inside or outside the field of irradiation.

Introduction: Hepatic inflammation is considered key driver of hepatic tissue impairment.We aimed to explore the interaction of Halamphora coffeaeformis (Amph.) with low dose ionizing γ radiation (γR) exposure against D-galactosamine (D-GaIN)-induced chronic hepatitis in Albino rats.

Methods: Chronic hepatitis was induced with single dose of D-GalN (400 mg/kg BW i.p.). Rats received 400 mg Amph/kg BW daily by gastric gavage concomitant with .25 Gy γ-R. Liver oxidative stress and inflammatory status were assessed. Gene expression levels of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NFKB) were estimated by q-PCR. D-Galactosamine injection significantly encouraged hepatic oxidative damage and inflammatory disturbance accompanied with improved intercellular adhesion molecule-1 level (ICAM-1).

Results: messenger RNA gene expression levels of STAT3 and NF-kB were expressively higher in D-GaIN-treated animals. Histopathological examination supported results. Interestingly, Amph treatment with γ-radiation (γ-R) subjection displayed significant improvement of oxidative and inflammatory status along with controlled signaling molecular factors which was supported by amended histological structure of induced liver hepatitis.

Conclusion: Results conclude the efficacious control of liver hepatitis progression by dual collaboration of Amph. with low dose γ-R via control of vital growth signaling factors linked with inflammation thru anti-inflammation, antioxidative and anti-proliferative activities.

Background: Polycystic ovarian syndrome (PCOS) is an endocrine metabolic disorder of women.

Purpose: This study aimed to explore the potential of aqueous extract of Garcinia cambogia Desr. (AEGC) in PCOS.

Methodology: The HPLC was used to determine the phytoconstituents present in Garcinia cambogia. Thirty adult female albino rats were divided into 6 groups: Normal control (NC) disease Control (PCOS; letrozole 1 mg/kg), plant extract (AEGC 100, 300, 500 mg/kg) and standard (metformin; 20 mg/kg). Disease was confirmed by vaginal smear cytology. After 10 weeks, animals were euthanized, ovaries dissected for histopathology, blood collected for hormonal and biochemical analysis.

Results: HPLC analysis showed the presence of phenolic contents; chlorogenic acid, gallic acid, coumaric acid while flavonoid contents were quercetin, kaempferol, and rutin. After treatment, there was dose dependent reduction of weight, ovarian cysts, improvement of follicle growth. DPPH radical scavenging percentage was 67.89%. Hormonal analysis showed a significant improvement (P < .05) in follicle stimulating hormone (FSH), estrogen, and progesterone while a reduction in testosterone, luteinizing hormone (LH) and insulin level. Antioxidant enzymatic markers were significantly (P < .05) increased. Lipid profile and LFTs were also improved.

Conclusions: The study validated the potential of Garcinia cambogia in the management of PCOS.

Radon exposure is significantly associated with lung cancer. Radon concentration is currently reduced mainly by physical methods, but there is a lack of protective drugs or biochemical reagents for radon damage. This study aimed to explore the protective effect of polydatin (PD) on the radon-exposed injury. The results showed that PD can significantly reduce ROS level, raise SOD activity, weaken the migration ability, increase E-cad, and decrease mesenchymal cell surface markers (FN1, Vimentin, N-cad, α-SMA, and Snail) in radon-exposed epithelial cells. In vivo, PD increased the mice weight, promoted SOD activity, and decreased MDA content, the number of bullae, pulmonary septum thickness, lung collagenous fibers, and mesenchymal cell surface markers. Furthermore, PD inhibited p-PI3K, p-AKT, and p-mTOR expression. Compared with directly adding PD on radon-exposed cells, adding PD before and after radon exposure could more obviously improve the adhesion of radon-exposed cells, significantly alleviate the migration ability, and more significantly reduce mesenchyme markers and p-AKT and p-mTOR. These results indicate that PD can reduce oxidative stress, weaken epithelial-mesenchymal transition (EMT) and lung fibrosis in radon-exposed cells/mice, and have good radiation protection against radon injury. The mechanism is related to the inhibition of the PI3K/AKT/mTOR pathway.