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The PTX and DOX microspheres not only exerted a synergistic effect, but also achieved a good sustained release effect. In vivo evaluation showed that the PPDM could effectively inhibit breast cancer recurrence and metastasis in mice with breast cancer. PPDM are expected to achieve postoperative chemotherapy for breast cancer and be highly efficient to prevent local breast cancer recurrence and metastasis.Hydrogels are soft materials consisting of a three-dimensional network of polymer chains. Over the years, hydrogels with different compositions have been developed as drug carriers for diverse biomedical applications, ranging from cancer therapy and wound care to the treatment of neurodegenerative and inflammatory diseases. Most of these carriers, however, are designed only to deliver single agents. Carriers based on hydrogels for co-delivery of multiple agents, with the release rate of each of the co-delivered agents tunable, are lacking. This study reports a one-pot method of fabricating alginate-based complex fibers with the Janus morphology, with carboxymethyl cellulose sodium functioning as a polymeric modifier of the properties of each of the fiber compartments. By using malachite green and minocycline hydrochloride as model drugs, the generated fibers demonstrate the capacity of enabling the release profile of each of the co-delivered drugs to be precisely controlled. Along with their negligible toxicity and the retention of the activity of the loaded drugs, the complex fibers reported in this study warrant further development and optimization for applications that involve co-delivery of multiple agents.There are several therapeutic approaches in type 2 diabetes mellitus (T2DM). When diet and exercise fail to control hyperglycemia, patients are forced to start therapy with antidiabetic agents. However, these drugs present several drawbacks that can affect the course of treatment. The major disadvantages of current oral modalities for the treatment of T2DM are mainly depicted in the low bioavailability and the immediate release of the drug, generating the need for an increase in frequency of dosing. In conjugation with the manifestation of adverse side effects, patient compliance to therapy is reduced. Over the past few years nanotechnology has found fertile ground in the development of novel delivery modalities that can potentially enhance anti-diabetic regimes efficacy. All efforts have been targeted towards two main vital steps (a) to protect the drug by encapsulating it into a nano-carrier system and (b) efficiently release the drug in a gradual as well as controllable manner. However, only a limited number of studies published in the literature used in vivo techniques in order to support findings. Here we discuss the current disadvantages of modern T2DM marketed drugs, and the nanotechnology advances supported by in vivo in mouse/rat models of glucose homeostasis. The generation of drug nanocarriers may increase bioavailability, prolong release and therefore reduce dosing and thus, improve patient compliance. This novel approach might substantially improve quality of life for diabetics. Application of metal nanoformulations as indirect hypoglycemic agents is also discussed.Fibrosis is a necessary process in the progression of chronic disease to cirrhosis or even cancer, which is a serious disease threatening human health. Recent studies have shown that the early treatment of fibrosis is turning point and particularly important. Therefore, how to reverse fibrosis has become the focus and research hotspot in recent years. So far, the considerable progress has been made in the development of effective anti-fibrosis drugs and targeted drug delivery. Moreover, the existing research results will lay the foundation for more breakthrough delivery systems to achieve better anti-fibrosis effects. Herein, this review summaries anti-fibrosis delivery systems focused on three major organ fibrotic diseases such as liver, pulmonary, and renal fibrosis accompanied by the elaboration of relevant pathological mechanisms, which will provide inspiration and guidance for the design of fibrosis drugs and therapeutic systems in the future.In the last decade, the use of nanotheranostics as emerging diagnostic and therapeutic tools for various diseases, especially cancer, is held great attention. Up to date, several approaches have been employed in order to develop smart nanotheranostics, which combine bioactive targeting on specific tissues as well as diagnostic properties. The nanotheranostics can deliver therapeutic agents by concomitantly monitor the therapy response in real-time. Consequently, the possibility of over- or under-dosing is decreased. Various non-invasive imaging techniques have been used to quantitatively monitor the drug delivery processes. Radiolabeling of nanomaterials is widely used as powerful diagnostic approach on nuclear medicine imaging. In fact, various radiolabeled nanomaterials have been designed and developed for imaging tumors and other lesions due to their efficient characteristics. Inorganic nanoparticles as gold, silver, silica based nanomaterials or organic nanoparticles as polymers, carbon based nanomaterials, liposomes have been reported as multifunctional nanotheranostics. In this review, the imaging modalities according to their use in various diseases are summarized, providing special details for radiolabeling. In further, the most current nanotheranostics categorized via the used nanomaterials are also summed up. To conclude, this review can be beneficial for medical and pharmaceutical society as well as material scientists who work in the field of nanotheranostics since they can use this research as guide for producing newer and more efficient nanotheranostics.In this comment, the opportunities of black phosphorus-based nano-drug delivery systems for cancer treatment are highlighted.Image, graphical abstract.Hepatocellular carcinoma (HCC) is one of the most common types of malignant tumor, and is the second highest cause of cancer-associated mortality, behind lung carcinoma. It is urgent to identify novel genes that can be used to confirm the diagnosis and prognosis of patients with HCC. The present study aimed to investigate the expression pattern of phosphatidylinositol glycan anchor biosynthesis class C (PIGC) in HCC and assess its clinical prognostic significance. Bioinformatics analyses were used to investigate PIGC mRNA expression levels in HCC and adjacent non-cancerous tissue samples. Furthermore, the present study detected the expression levels of PIGC protein in HCC and matched normal tissue samples via immunohistochemistry, and evaluated the prognostic significance of PIGC protein in HCC. The levels of PIGC mRNA and protein were found to be significantly higher in tissue from patients with HCC compared with non-cancerous liver tissue. The survival analysis showed that the expression levels of PIGC mRNA or protein were associated with the survival of patients with HCC. PIGC protein expression was significantly associated with Tumor-Node-Metastasis stage. A negative correlation between PIGC DNA methylation and mRNA expression was observed (Spearman r=-0.453). PIGC is an oncogene that is negatively regulated by DNA methylation, and high levels of PIGC mRNA or protein may predict an unfavorable prognosis in patients with HCC.Poor drug efficacy is a prominent cause of oral squamous cell carcinoma (OSCC) treatment failure. Although increased efforts in developing OSCC therapeutic strategies have been achieved in recent decades, the 5-year survival rate of patients with OSCC remains poor and effective drugs to treat OSCC are lacking. The aim of the present study was to investigate the apoptotic effect caused by lycorine hydrochloride (LH) and to identify its mechanism in the OSCC HSC-3 cell line. The findings demonstrated that LH effectively induced HSC-3 cell apoptosis and cell cycle arrest at the G0/G1 phase, resulting in the inhibition of cell proliferation. Furthermore, it was found that LH increased reactive oxygen species (ROS) production, triggered mitochondrial membrane potential (MMP) disorder, enhanced the protein expression levels of Bax, Bim, cleaved caspase-9, caspase-3 and poly(ADP-ribose) polymerase 1 and decreased Mcl-1 expression. The protein expression levels of important members of the JNK signaling pathway, including phosphorylated (p)-JNK, p-mitogen-activated protein kinase kinase 4 and p-c-Jun, were significantly increased in LH-treated cells, accompanied by an increase in ROS. However, N-acetyl cysteine (NAC), a potent antioxidant, reversed the upregulated mRNA expression of c-Jun, as well as the enhanced ROS production, the disorder of MMP and the apoptosis of HSC-3 cells induced by LH. These results suggested that LH may induce HSC-3 cell apoptosis via the ROS-mediated mitochondrial apoptotic pathway and the JNK signaling pathway, which indicated that LH may be a potential drug candidate for anti-OSCC therapy.Chemotherapy drug 5-fluorouracil (5-FU) is the first-line treatment for colorectal cancer (CRC); however, 5-FU resistance decreases CRC therapeutic efficiency. A previous study revealed that microRNA (miR)-9-5p serves an antitumor effect in CRC. However, the effect of miR-9-5p in CRC chemoresistance remains unknown. In the present study, two CRC cell lines, including HT-29 and HCT-116 cells, were used to investigate the impact of miR-9-5p in overcoming 5-FU resistance. The results revealed that treatment with 5-FU decreased CRC cell viability and upregulated miR-9-5p expression in both CRC cells. Knockdown of miR-9-5p decreased HCT-116 cell sensitivity to 5-FU and inhibited apoptosis. By contrast, miR-9-5p overexpression enhanced the sensitivity of HT-29 cells to 5-FU and induced apoptosis. Additionally, it was confirmed that miR-9-5p directly targeted high mobility group A2 (HMGA2). MRTX1257 HMGA2 overexpression reversed miR-9-5p-induced HT-29 apoptosis. The present study indicated that miR-9-5p enhanced the sensitivity of CRC cells to 5-FU via downregulating HMGA2 expression.The p53-upregulated modulator of apoptosis (PUMA) has been reported to be involved in various types of cancer. However, its potential biological role in gallbladder carcinoma (GBC) has not been fully elucidated. The present study aimed to determine the expression levels of PUMA and its biological effects on GBC. The mRNA and protein expression levels of PUMA in GBC tissues and cell lines were measured using reverse transcription-quantitative PCR and western blotting, respectively. The effects of PUMA overexpression on cell viability, proliferation and invasive ability were determined in vitro using the MTT, colony formation and Transwell invasion assays, respectively. The apoptotic rates were detected using the Annexin V-FITC apoptosis detection kit. Furthermore, follow-up of patients with GBC was performed to identify the association between PUMA expression levels and GBC prognosis. The results of the present study demonstrated that the expression levels of PUMA were significantly lower in the GBC tissues and cell lines compared with those in adjacent normal gallbladder tissues and normal gallbladder cells, respectively. Further experiments indicated that overexpression of PUMA inhibited the viability, proliferation and invasive ability of GBC cells compared with those in the control-transfected GBC cells. In addition, overexpression of PUMA significantly promoted apoptosis in GBC cells. Furthermore, overexpression of PUMA inhibited epithelial-mesenchymal transition, and promoted Bax upregulation and Bcl-2 downregulation compared with those in the control group. Low PUMA expression levels were associated with a short overall survival time in patients with GBC. In conclusions, PUMA may act as a tumor suppressor in GBC and may serve as a potential novel treatment target for human GBC.

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