The major feature of spinal cord injury (SCI) was the damage of nervous tissue in spinal cord. The damaged spinal cord was difficult to be repaired and regenerated. MicroRNA-124 could play a role in the repairing and recovering the injured tissue. The BMSCs could participate in repairing
the damage. However, the regulatory effect of MicroRNA-124 on BMSCs and the inflammatory response of SCI was still not illustrated. These spinal cord nerve cells were assigned into group of mechanical damage, BMSCs and BMSCs with miR-124 overexpression followed by analysis of proliferation
of nerve cells by MTT assay, apoptotic activity, expression of miR-124, GFAP and BDNF by Real time PCR, levels of TNF-α and IL-6 by ELISA as well as MDH and SOD activity. miR-124 mimics transfection significantly promoted BMSCs proliferation and increased ALK activity and the
expression of GFAP and BDNF. In conclusion, the proliferation and differentiation of BMSCs could be regulated by miR-124. The inflammation and oxidative stress could be restrained so as to prompt the proliferation and repair of SCI cells and restrain apoptosis, indicating that it might be
beneficial to recover the SCI.
Dementia is an umbrella term for a collection of symptoms that are caused by disorders affecting the brain and impact on memory, thinking, behaviour and emotion. The most common is Alzheimer’s disease, which affects 50-60% of people with dementia. Other types of dementia include vascular dementia, Lewy body dementia and fronto-temporal dementia. Dementia can also sometimes affect people who are under the age of 65. This is known as young onset dementia. Our brains are made up of over 86 billion nerve cells – more than the stars in the Milky Way. Dementia damages nerve cells so they are no longer able to communicate effectively and this impacts on how our body functions.
Abstract Resveratrol, a natural polyphenol found in tempeh, has not been investigated especially in vitro as a neuroprotective agent against 2-methoxyethanol (2-ME)-induced beta-amyloid cytotoxicity. Beta amyloid peptides (Aβ) could initiate neurotoxic events and neuron-inflammatory response via microglial activation. However, it remains unknown whether the neurotoxic effect of beta-amyloid and/or associated with the potential of 2-ME to induce neurotoxic effects on primary culture of nerve cells induced by 2-ME. This study investigated potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid cytotoxicity on primary culture of nerve cells induced by 2-methoxyethanol. Biotium and MTT assays were used to analyze neurons, which were isolated from the cerebral cortex of fetal mice at gestation day 19 (GD-19). A standard solution of 2-methoxyethanol was dosed at 10 μL. The cultured cells were randomly divided into the following groups: (1) 2-ME group + resveratrol standard, (2) 2-ME group + resveratrol isolated from tempeh, (3) 2-ME group + resveratrol isolated from soybean seed coats, and (4) the control group, without the addition of either 2-ME or resveratrol. Exposure of the primary cortical neuron cells to beta-amyloid monoclonal antibody pre-incubated for 24 h with 10 µL of 4.2 µg/mL resveratrol and 7.5 mmol/l 2-methoxy-ethanol additions. Here, we report that the addition of 2-ME and resveratrol (standard and isolated from tempeh) of cell culture at concentrations of 1.4, 2.8 and 4.2 µg/mL showed that the majority of neurons grew well. In contrast, after exposure to 2-ME and Beta-amyloid, showed that glial activated. These findings demonstrate a role for resveratrol in neuroprotective-neurorescuing action.
The sense of smell provides people with valuable information about the biochemical environment and their own body. Olfactory disorders occur in pathologies of the nasal cavity, liver cirrhosis, psychological and endocrine diseases. Smell affects various psychological aspects of people's lives, forming positive and negative emotional memories associated with smells. With the dysfunction of the olfactory analyzer, a person will not do the analysis whether the food is good, will not be able to feel the presence of poisonous gases in the air, bad breath. This puts a person in an awkward position and increases the risk of social isolation. The purpose of the study was to highlight the components of the normal structure and functioning of the human olfactory analyzer. Identification of odors in the environment and from one's own body is provided by the olfactory analyzer. Primary odors as camphor, floral, fruity, spicy, tarry, burnt and putrid in different quantities form secondary odors. Aromas are composed of volatile molecules called odorants. The smallest amount of odorant that causes an odor sensation is called the odor threshold. In people with coronavirus disease the sense of smell temporarily disappears (anosmia); it is reduced (hyposmia) in liver cirrhosis and rhinitis, and in Alzheimer's disease and schizophrenia besides hyposmia there is olfactory hallucination (phantosmia). Olfactory dysfunction adversely affects children's cognitive abilities. Fragrances change emotions and behavior. Aromas are used to regulate the physical and psychological state of the patient. Volatile molecules of fragrances penetrate through the layer of mucus that covers the olfactory epithelium located in the olfactory region of the nasal mucosa. The olfactory epithelium consists of olfactory, supportive and basal epitheliocytes, as well as secretory cells of the olfactory glands. Olfactory cells are modified nerve cells that have a body, an axon, and a dendrite, which ends with a receptor in the form of olfactory cilia. Volatile molecules interact with the olfactory cilia and then with the receptor protein, which is located on the olfactory cell bodies. In humans, olfactory cells have 350 receptor proteins. One type of receptor can register molecules of several different odorants. Molecules of the same odorant can activate several different receptors simultaneously. The nerve impulse from the olfactory cells (bodies of I neurons) reaches the nerve cells (bodies of II neurons) of the olfactory bulbs via their central outgrowths (olfactory filaments). Axons of nerve cells of olfactory bulbs continue to bodies of III neurons, which are located in subcortical centers of the brain (almond-shaped body, nuclei of the transparent septum). In human, to analyze a particular odor, axons from bodies of III neurons continue to cortex, namely to the area of the uncus of the parahippocampal gyrus
AbstractDiabetes mellitus is a disorder characterized by elevated blood sugar levels, due to abnormalities in insulin secretion. This results in nerve cells edema and triggers the stimulation of various enzymes that can damage nerve cell through both metabolic and neurovascular factors. This condition will interfere with the supply of blood and oxsygen to the nerve cells, especially in the peripheral areas of the feet and hands. To prevent this, it is neccesary to do diabetic foot exsercises in people with diabetes mellitus. This scientific paper focused on two famillies with diabetes mellitus. the result stated applying diabetic food exercises for the patient is the efective and it could be done once a day. Furthermore, it also can help improve blood circulation in the legs. Through movements in diabetic food exercises, the muscles will contract so that it will increase the sensitivity of the feet in poeple with diabetes mellitus. Even if it is done routinely, it can prevent the occurrence of non-ulcer wounds or ulcers. Therefore, it is expected for the familly to support the patient in applying the exercises.Keywords: Diabetic Foot Exercises, Foot Sensitivity
Abstrakkadar gula dalam darah yang diakibatkan karena kelainan sekresi insulin akibatnya edema sel saraf serta memicu stimulasi berbagai enzim yang dapat merusak sel saraf baik melalui faktor metabolik maupun faktor neurovaskular, hal terdebut akan mengganggu suplai darah dan oksigen menuju sel saraf terutama di daerah perifer kaki dan tangan. Untuk mencegah akibat tersebut dilakukan senam kaki diabetik pada penderita Diabetes Mellitus. Fokus karya tulis ilmiah adalah 2 keluarga dengan Diabetes Mellitus Hasil penerapan senam kaki diabetik yang di lakukan untuk meningkatkan sensitivitas kaki pada penderita Diabetes Mellitus efektif untuk di terapkan pada penderita Diabetes Melitus bila dilakukan secara rutin satu kali sehari, senam kaki diabetik dapat membantu melancarkan sirkulasi darah pada kaki, melalui gerakan pada senam kaki diabetik otot-otot akan berkontraksi sehingga akan meningkatkan sensitivitas kaki pada penderita Diabetes Mellitus. Bahkan jika dilaukan secara rutin dapat mencegah terjadinya luka non ulkus ataupun luka ulkus. Di harapkan keluarga memberikan dukungan pada keluarga yang sakit dengan mendampingi saat melakukan latihan senam kaki diabetik.Kata kunci: Senam Kaki, Sensitivitas Kaki
Another advantage of Retro X Focus Nootropic Brain Booster is that it helps refresh your brain and provides nourishment to nerve cells. In general, a relaxed and stress-free conditions play a significant part in stimulating memory
Background: With the development of society, Neurodegenerative disease (ND), such as alzheimer's disease, is more and more important to the researchers. Metal iron may play a crucial role in this disease, so our research constructed the iron overloading model in nerve cells, induce the ferroptosis, simulate the state of the nerve in the body, and used the anesthesia Dexmedetomidine (Dex), and study whether the Dex can inhibit the ferroptosis and reduce the ND.Methods: Cell proliferation kit CCK8 and PI/Hoechst fluorescence double staining were used to detect the proliferation and apoptosis of HT22 cells. Western blot (WB) was used to detect the expression of PTGS2 and ACSL4, pathway proteins mTOR, TFR1. ROS content in HT22 cells was determined by DHE fluorescence probe. Lipid Peroxidation in nerve cells was detected by MDA Assay. Mito-ferrorange fluorescent probe was used to detect the level of ferrous ions in cells to demonstrate that ferroptosis occurred in nerve cells and Dex could protect nerve cells from ferroptosis.Results: Dex inhibits ferroptosis by regulating the mTOR-TFR1 pathway, reducing lipid peroxidation, intracellular reactive oxygen accumulation (ROS), reducing iron ions, and alleviating mitochondrial damage. mTOR is a well-known autophagy target and has been found to be closely related to ferroptosis. Dex activates the mTOR pathway, inhibits iron entry into the cell, reduces iron influx, and prevents ferroptosis by fenton reaction between excessive iron and lipids in the cell.Conclusion: Dex protects nerve cells from ferroptosis by regulating the mTOR-TFR1 pathway.