ABSTRACT
Background: In chronic kidney disease (CKD), renal regulatory mechanisms may be insufficient to balance intestinal magnesium absorption hence insufficient to maintain homeostasis. But related data are relatively sparse and not readily available, especially in Bangladesh context. Aim of the study: The aim of the study was to assess the pattern of serum magnesium level in different stages of CKD patients. Material & Methods: This descriptive cross-sectional study was conducted in the Department of Medicine and the Department of Nephrology, Dhaka Medical College Hospital (DMCH) for nine months’ period. Approval for the study was taken from the ethical review committee of DMC before the commencement of the study. Diagnosed patients of chronic kidney disease (CKD) were approached for the inclusion of the study. Informed written consent was taken from each patient. All patients were subjected to detailed history taking, physical examination, and relevant investigations. For the study purpose, serum magnesium was done for all patients. Results: After compiling data from all participants, statistical analysis was performed using the statistical package for social science (SPSS) version 22 for windows, and a p < 0.05 was considered statistically significant. Mean age of the patients was 53 years with male predominance (male 64% vs female 36%). Of all, 6.7% of cases had hypomagnesemia and 55.3% had hypermagnesemia. The mean serum magnesium level was 2.68±0.81 mg/dl. Assessment of serum magnesium in a different stages of CKD showed that hypermagnesemia is associated with higher staging (p<0.05), and there is a negative correlation between lower e-GFR with serum magnesium ((r=-0.753, p<0.01). Conclusion: Nearly two-third of CKD patients were found with altered magnesium level in the form of hypomagnesemia or hypermagnesemia in this study. Serum magnesium was found increased in higher stages of CKD. That means serum magnesium level increases along with higher stage of the disease. Urinary magnesium excretion also decreases when eGFR of patient decreased.
ABSTRACT
Reprogramming of energy metabolism is one of the basic characteristics of cancer and has been proved to be an important cancer treatment strategy. Isocitrate dehydrogenases (IDHs) are a class of key proteins in energy metabolism, including IDH1, IDH2, and IDH3, which are involved in the oxidative decarboxylation of isocitrate to yield α-ketoglutarate (α-KG). Mutants of IDH1 or IDH2 can produce d-2-hydroxyglutarate (D-2HG) with α-KG as the substrate, and then mediate the occurrence and development of cancer. At present, no IDH3 mutation has been reported. The results of pan-cancer research showed that IDH1 has a higher mutation frequency and involves more cancer types than IDH2, implying IDH1 as a promising anti-cancer target. Therefore, in this review, we summarized the regulatory mechanisms of IDH1 on cancer from four aspects: metabolic reprogramming, epigenetics, immune microenvironment, and phenotypic changes, which will provide guidance for the understanding of IDH1 and exploring leading-edge targeted treatment strategies. In addition, we also reviewed available IDH1 inhibitors so far. The detailed clinical trial results and diverse structures of preclinical candidates illustrated here will provide a deep insight into the research for the treatment of IDH1-related cancers.
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The liver has a complex cellular composition and a remarkable regenerative capacity. The primary cell types in the liver are two parenchymal cell populations, hepatocytes and cholangiocytes, that perform most of the functions of the liver and that are helped through interactions with non-parenchymal cell types comprising stellate cells, endothelia and various hemopoietic cell populations. The regulation of the cells in the liver is mediated by an insoluble complex of proteins and carbohydrates, the extracellular matrix, working synergistically with soluble paracrine and systemic signals. In recent years, with the rapid development of genetic sequencing technologies, research on the liver's cellular composition and its regulatory mechanisms during various conditions has been extensively explored. Meanwhile breakthroughs in strategies for cell transplantation are enabling a future in which there can be a rescue of patients with end-stage liver diseases, offering potential solutions to the chronic shortage of livers and alternatives to liver transplantation. This review will focus on the cellular mechanisms of liver homeostasis and how to select ideal sources of cells to be transplanted to achieve liver regeneration and repair. Recent advances are summarized for promoting the treatment of end-stage liver diseases by forms of cell transplantation that now include grafting strategies.
Subject(s)
Humans , Liver/surgery , Hepatocytes/transplantation , Stem Cells/metabolism , Liver Diseases/surgeryABSTRACT
Long noncoding RNAs (lncRNAs) are a class of RNA molecules that are greater than 200 nt in length and do not have protein-coding capabilities or encode micropeptides only. LncRNAs are involved in the regulation of cell proliferation, differentiation, apoptosis and other biological processes, and are closely associated with the occurrence, recurrence and metastasis of a variety of malignant hematologic diseases. This article summarizes the function, regulatory mechanism and potential clinical application of lncRNAs in leukemia. In general, lncRNAs regulate the occurrence and development of leukemia and the multi-drug resistance in chemotherapy through epigenetic modification, ribosomal RNA transcription, competitive binding with miRNA, modulating glucose metabolic pathway, and activating tumor-related signaling pathway. Studies on lncRNAs provide new references for understanding the pathogenesis of leukemia, uncovering new prognostic markers and potential therapeutic targets, and addressing the problems of drug resistance and post-treatment recurrence in patients in clinical treatment of leukemia.
Subject(s)
Humans , Cell Proliferation , Leukemia/genetics , MicroRNAs , Neoplasms , RNA, Long Noncoding/geneticsABSTRACT
With the constant change of global climate, plants are often affected by multiple abiotic stresses such as heat stress, drought stress, cold stress and saline-alkali stress. Heat shock transcription factors (HSFs) are a class of transcription factors widely existing in plants to respond to a variety of abiotic stresses. In this article, we review and summarize the structure, signal regulation mechanism of HSFs and some research in plants like Arabidopsis thaliana, tomato, rice and soybean, to provide reference for further elucidating the role of HSFs in the stress regulation network.
Subject(s)
Arabidopsis/metabolism , Droughts , Gene Expression Regulation, Plant , Heat Shock Transcription Factors/genetics , Plant Proteins/genetics , Stress, Physiological , Transcription Factors/metabolismABSTRACT
Cerebral hemorrhage, also known as hemorrhagic stroke, refers to non-traumatic intracerebral hemorrhage. Cerebral hemorrhage is a common and frequently-occurring disease in middle-aged and elderly people. It has the characteristics of high mortality and high disability rate. Most survivors have serious neurological deficits, which seriously threaten human health and quality of life.The pathological process of cerebral hemorrhage is more complicated, including the formation and expansion of hematoma, elevated intracranial pressure, destruction of blood-brain barrier, brain edema, neuronal apoptosis and neurological dysfunction.At present, the main methods for treating cerebral hemorrhage by western medicine include antiplatelet therapy, blood pressure reduction and hematoma surgery. However, it is usually accompanied by the risk of rebleeding caused by surgery, infection, nerve damage and insufficient effective perfusion pressure. Chinese medicine believes that blood stasis and endogenous fever are the most basic pathogenesis of acute cerebral hemorrhage. The previous studies found that many traditional Chinese medicine(TCM) can improve blood-brain barrier damage, brain edema, neuronal apoptosis and neurological dysfunction related to cerebral hemorrhage to reduce cerebral hemorrhage injury. Main signal transduction pathways regulated by TCM to treat cerebral hemorrhageinclude Aquaporin 4(AQP4)-related, phosphatidylinositol-3-kinase/protein kinase B(PI3K/Akt), nuclear factor kappa B(NF-κB),suppressor protein 53/Bcl-2-associated X protein/Caspase-3(p53/Bax/Caspase-3)molecular pathways, etc.In this paper, based on the current Chinese medicine to improve the brain damage caused by cerebral hemorrhage and the molecular pathway of intervention, it reviews the research progress published in foreign journals in the past ten years, in order to provide clues and reference for the treatment of hemorrhagic stroke diseases and and the further development of new drugs.
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Long non-coding RNA (lncRNA) is a group of non-coding RNA with length larger than 200 nucleotides. LncRNAs have limited or no protein-coding capacity due to lacking of open reading frame. Recent studies indicated that lncRNAs were involved in various cellular processes and their aberrant expression might lead to tumor development and progression. FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) was found to exhibit aberrant expression in various malignancies, and its dysregulation level was closely related with prognosis of cancer patients. The biological functions and molecular regulatory mechanisms of FOXD2-AS1 in tumors will be summarized in this paper.
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Bone marrow mesenchymal stem cells are the main progenitor cells of osteoblasts , and are regarded as the seed cells for bone repair and regeneration because of their osteogenic differentiation potential .Promoting the osteogenic differentiation and bone formation is feasible to treat osteoporosis .LncRNAs regulate gene expression at the transcriptional and post-transcriptional levels , influence fundamental biological processes including cell differentiation and organ development , and are closely associated with many diseases including osteoporosis .This paper reviews the research of lncRNA in regulating osteogenic differentiation to provide a new tar -get for bone formation and treatment of osteoporosis .
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Cardiopulmonary bypass (CPB) related lung injury is the most common complication in cardiac surgery .Ischemia reperfusion injury and systemic inflammatory reaction may be the important causes of CPB -related lung injury , but the specific mecha-nism is still to be elucidated.In recent years, apoptosis is paid increasing attention in the pathogenesis of CPB .Therefore, cell apopto-sis has been a hot spot in the research of CPB related lung injury .This article summarizes the latest researches on the characteristics , reasons and mechanisms of CPB-related pneumonocyte apoptosis .
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Aim Toexplorethemechanismofupregu-lation of osteopontin ( OPN ) expression induced by high glucose in human renal tubular epithelial cells (HK-2cells).Methods Afterstimulationwithhigh-glucose (25 mmol·L-1 ) culture medium, HK-2 cells were then treated with the specific inhibitors or siRNA to inhibit the activity of PI3K and/or mTOR. Subse-quently, Real-time PCR was used to investigate the mRNA level of OPN, and Western blot was performed to detect the protein expression of OPN, p-AKT, p-S6,RaptorandRictor.Results Theexpressionlevel of OPN was increased in a time-dependent manner in HK-2 cells followed by high-glucose stimulation. The mRNA level of OPN peaked at 48 h; while the protein expression of OPN reached the highest level at 72h. Meanwhile, high glucose activated the PI3K/AKT/mTOR signaling pathway. Moreover, inhibition of the PI3 K/AKT/mTOR pathway by LY294002 and/or rapa-mycin led to significant down-regulation of OPN. Addi-tionally, the treatment with Raptor siRNA, but not Rictor siRNA resulted in reduction of OPN expression. Conclusion Highglucoseincreasestheexpressionof OPN through the activation of PI3 K/AKT/mTORC1 signaling pathway in HK-2 cells.