Parkinson's disease(PD)is a common neurological disorder that is defined by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta,eventually leading to striatal dopamine depletion.Restin...Parkinson's disease(PD)is a common neurological disorder that is defined by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta,eventually leading to striatal dopamine depletion.Resting tremors,rigid muscles,bradykinesia,and in rare circumstances,postural instability are symptoms of low dopamine levels.One to two percent of people over 65 worldwide is affected with PD,making it the second most common neurological illness in the world[1,2].Uncertainty about the cause and course of PD persists,as do the biological pathways that drive the disease[3].Mutations in the leucine-rich repeat kinase 2(LRRK2)gene are the most common cause of familial PD[4].LRRK2 missense mutations increase the risk of developing late-onset autosomal dominant PD,which is clinically comparable to sporadic PD[5,6].LRRK2 PD neuropathology is comparable to sporadic PD neuropathology,with LRRK2 patients experiencing progressive neurodegeneration of the nigrostriatal pathway,frequently resulting in alpha-Synuclein-positive Lewy bodies and brain tau pathology[5,7-9].While LRRK2 coding mutations are associated with sporadic PD,frequent non-coding variants at the LRRK2 locus are associated with an increased risk of developing PD[10-13].展开更多
Angiogenesis is known as a biological pathway that results in the formation of new capillary blood vessels originating from the pre-existing vascular system[1].The mechanism of angiogenesis is complicated because it i...Angiogenesis is known as a biological pathway that results in the formation of new capillary blood vessels originating from the pre-existing vascular system[1].The mechanism of angiogenesis is complicated because it is associated with multiple intricate interactions between various biological elements including different cells,soluble angiogenic agents,and extracellular molecules.It essentially comprises four discrete sequential stages:(1)Proteolytic enzymes degrade glycoproteins of the basement membrane and other extracellular matrix components which blood vessels are surrounded by them;(2)The activation and migration of endothelial cells;(3)The proliferation of endothelial cells.展开更多
Cystic fibrosis(CF)as the commonest inherited disorder in Caucasians can affect around 1 in every 2,500 live births.Which is due to the CF transmembrane conductance regulator(CFTR)dysfunction,located mainly at the api...Cystic fibrosis(CF)as the commonest inherited disorder in Caucasians can affect around 1 in every 2,500 live births.Which is due to the CF transmembrane conductance regulator(CFTR)dysfunction,located mainly at the apical surfaces of epithelial cells in the airways,pancreas,intestine,kidneys,sweat gland,and male reproductive tract,in which CFTR is vital for the transepithelial fluid homeostasis.CFTR malfunction may result in life-threatening disorders[1].The digestive problems are resulted in the forming abnormally thick mucus because of failure in chloride and water transport.In the gastrointestinal tract,such thick and sticky mucus can clog the ducts preventing digestive enzymes to enter the intestine.Nutritional insufficiency remains a big concern in CF patients and it accrues owing to the CFTR mutation which leads to the production of abnormally thick and sticky mucus affecting the food digestion and absorption,especially,fat and fat-soluble vitamins,and prohibiting digestive enzymes to be entered the intestine.Accordingly,foods are not digested or absorbed in good order,resulting in mal-digestion and malabsorption.Related complications are consist of exocrine pancreatic dysfunction,intestinal inflammation,enteric circular muscle impairment,bacterial overgrowth,and impaired bicarbonate and bile acid release[2].展开更多
文摘Parkinson's disease(PD)is a common neurological disorder that is defined by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta,eventually leading to striatal dopamine depletion.Resting tremors,rigid muscles,bradykinesia,and in rare circumstances,postural instability are symptoms of low dopamine levels.One to two percent of people over 65 worldwide is affected with PD,making it the second most common neurological illness in the world[1,2].Uncertainty about the cause and course of PD persists,as do the biological pathways that drive the disease[3].Mutations in the leucine-rich repeat kinase 2(LRRK2)gene are the most common cause of familial PD[4].LRRK2 missense mutations increase the risk of developing late-onset autosomal dominant PD,which is clinically comparable to sporadic PD[5,6].LRRK2 PD neuropathology is comparable to sporadic PD neuropathology,with LRRK2 patients experiencing progressive neurodegeneration of the nigrostriatal pathway,frequently resulting in alpha-Synuclein-positive Lewy bodies and brain tau pathology[5,7-9].While LRRK2 coding mutations are associated with sporadic PD,frequent non-coding variants at the LRRK2 locus are associated with an increased risk of developing PD[10-13].
文摘Angiogenesis is known as a biological pathway that results in the formation of new capillary blood vessels originating from the pre-existing vascular system[1].The mechanism of angiogenesis is complicated because it is associated with multiple intricate interactions between various biological elements including different cells,soluble angiogenic agents,and extracellular molecules.It essentially comprises four discrete sequential stages:(1)Proteolytic enzymes degrade glycoproteins of the basement membrane and other extracellular matrix components which blood vessels are surrounded by them;(2)The activation and migration of endothelial cells;(3)The proliferation of endothelial cells.
文摘Cystic fibrosis(CF)as the commonest inherited disorder in Caucasians can affect around 1 in every 2,500 live births.Which is due to the CF transmembrane conductance regulator(CFTR)dysfunction,located mainly at the apical surfaces of epithelial cells in the airways,pancreas,intestine,kidneys,sweat gland,and male reproductive tract,in which CFTR is vital for the transepithelial fluid homeostasis.CFTR malfunction may result in life-threatening disorders[1].The digestive problems are resulted in the forming abnormally thick mucus because of failure in chloride and water transport.In the gastrointestinal tract,such thick and sticky mucus can clog the ducts preventing digestive enzymes to enter the intestine.Nutritional insufficiency remains a big concern in CF patients and it accrues owing to the CFTR mutation which leads to the production of abnormally thick and sticky mucus affecting the food digestion and absorption,especially,fat and fat-soluble vitamins,and prohibiting digestive enzymes to be entered the intestine.Accordingly,foods are not digested or absorbed in good order,resulting in mal-digestion and malabsorption.Related complications are consist of exocrine pancreatic dysfunction,intestinal inflammation,enteric circular muscle impairment,bacterial overgrowth,and impaired bicarbonate and bile acid release[2].
