China
Africa
Explore chapters and articles related to this topic
Anti-Hyperglycemic Property Of Medicinal Plants
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
Karanpreet Singh Bhatia, Arpita Roy, Navneeta Bhardavaj
Hyperglycemia or insulin independent hyperglycemia is relatively ubiquitous and related to obese and overweight individuals. With insulin independent hyperglycemia, pancreatic β cells usually lead to underproduction of insulin which due to which insulin is not capable to meet the body’s requirement or cells in the body shows resistance against insulin. Insulin resistance, or insensitivity, occurs primarily in liver, fat, and muscle cells. Incidence of insulin independent hyperglycemia has seen a tremendous increase in youth mainly due to lifestyle changes like more sedentary life and intake of junk food. Obesity has been cited as the major responsible factor for insulin resistance in the body and thus solely a plausible reason for insulin independent hyperglycemia (Ginsberg et al., 1975). Molecular Factors: Demographic genome wide association studies (GWAS) in United Kingdom, United States, China, Malaysia, Asian-Indian, and Africa have provided many genetic markers linked with insulin independent hyperglycemia. These are: CDKN2A/B, CDKAL1, SLC30A8, HHEX/IDE, IGFBP2, KCNQ1, TCF7L2 and CAPN10 (Horikawa et al., 2000; Dupuis et al., 2010).
Retinoic acid signaling is critical for generation of pancreatic progenitors from human embryonic stem cells
Published in Growth Factors, 2023
Niloufer P. Dumasia, Aparna P. Khanna, Prasad S. Pethe
We employed RA inhibition over 8 days and found that the critical transcription regulators such as HHEX, HNF4α, and PDX1 are controlled by RA signaling at early stages specifying a pancreatic fate from the DE during hESC differentiation. RA strongly induced HHEX expression at the PG tube and its expression remained high at the PF stage in our differentiating hESC culture. While RAR antagonist suppressed gene expression of HHEX with the cells displaying only low levels. Consistent with our results, gut spheroids derived from hPSCs showed downregulation of PDX1 and HHEX when treated with RAR antagonist BMS493 (Koike et al. 2019). In contrast, Molotkov, Molotkova, and Duester (2005) observed no effect of Raldh2 deletion on the expression of Hhex in the ventral (and not the dorsal endoderm) region of mice embryos. RA may, therefore, be required at the DE stage to pattern the gut tube in hESCs but not during mice development. An increase in HNF4α and PDX1 levels upon the addition of RA is consistent with the fact that these transcription factors are also upregulated in mESCs by RA (Micallef et al. 2005; Sui et al. 2012).
Trisomy 8 in acute myeloid leukemia
Published in Expert Review of Hematology, 2019
Anette Lodvir Hemsing, Randi Hovland, Galina Tsykunova, Håkon Reikvam
As describe in paragraph 2., there are recurrent concomitant gene mutations with trisomy 8, e.g. ASXL1, RUNX1, FLT3 and TET2 (Table 1). However, these mutations are not recommended by the ELN to be used as single MRD markers, because of frequent losses or gains of mutations and subclonal heterogeneity [116]. Then, it is not known if they might be surrogate markers for trisomy 8 MRD. A recent study by Salehzadeh et al., an Italian group, found that the presence of additional somatic mutations a baseline was a poor predictive factor in terms of response to induction (19% compared to 43% of those without additional mutations achieved CR), but neither OS or LFS were significantly conditioned by their presence or absence [125]. Saied et al. did another study, investigating the impact of trisomy 8 on the DNA methylation distribution. They identified methylation and repression of the HHEX gene in both diagnostic and relapsed trisomy 8 AML. Measurement of HHEX expression by RT-PCR was suggested in the paper as a potential diagnostic marker. As for MRD marker, the HHEX gene is not further investigated [100].
Research progress of nanocarriers for gene therapy targeting abnormal glucose and lipid metabolism in tumors
Published in Drug Delivery, 2021
Xianhu Zeng, Zhipeng Li, Chunrong Zhu, Lisa Xu, Yong Sun, Shangcong Han
Although abnormal expression of miR-130b has been detected in a variety of cancers (Yu et al. 2015; Mu et al. 2020), the mechanism of action of miR-130b has not been clearly elaborated until now. MiR-130b regulates the metabolism of nutrients and also participates in multiple growth processes of tumors. MiR-130b can regulate metabolism-related pathways, including fatty acid degradation, glycolipid metabolism, and other pathways (Assmann et al. 2020). It was found that Xiangsha Liujunzi decoction regulates cholesterol metabolism through long-chain non-coding miR-130b, which ultimately affects lipid accumulation. miR-130b regulates the cholesterol metabolism process mediated by PPAR gamma to decrease lipid deposition in the liver (Jiang et al. 2020; Liu et al. 2020). In addition, the miR-130 family is an important gene that regulates the progression of cancer. Several studies have shown that miR-130b is associated with the growth, blood vessel growth, metastasis, and proliferation of a variety of tumor cells. For example, miR-130b was found to act in a potential tumor network that negatively regulates hematopoietically-expressed homeobox protein (HHEX) expression. After downregulation of HHEX expression, metastasis, invasion, and proliferation of breast cancer cells was significantly higher than those of normal cell lines (Zhang et al. 2020). The same regulatory effect was also observed in cervical cancer, where the increase in miR-130b-5p (miR-130b-5p is a passenger strand of miR-130b) in cervical cancer stem cells downregulated ETS-like gene 1 (ELK1) expression. Enhancing miR-130b-5p or silencing ELK1 inhibited the self-renewal ability and tumor volume growth of cervical cancer stem cells, and promoted cell apoptosis (Huang & Luo 2021). However, opposite views exist. In lung adenocarcinoma tissues, the upregulation of miR-130b also promoted cell metastasis and invasion (Kim et al. 2021).