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@#With potent biological activities, cellular growth factors are polypeptide factors that primarily stimulate cell growth and proliferation. They participate in the regulation of not only normal physiological functions such as human embryonic development and cell growth, but also neurorehabilitation and neuroplasticity in pathological processes such as nerve injury and recovery. Specifically, cellular growth factors have been shown to promote neuron survival, facilitate nerve regeneration and regulate synaptic plasticity, promote cell differentiation/vascular regeneration and modulate the microenvironment, promote nerve fiber myelination and improve nerve conduction. This review summarized current knowledge on the roles and various growth factors in neurorehabilitation and neuroplasticity, providing an update on potential clinical application of cellular growth factors in the field of neural rehabilitation.
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Photodynamic therapy (PDT), which uses photosensitizers to produce singlet oxygen to kill bacteria, was first discovered by scientists over 100 years ago and has been widely used in clinical treatment. Riboflavin is an endogenous and the most commonly used photosensitizer.A large number of studies have shown that riboflavin can produce singlet oxygen through photodynamic reaction(typeⅡ) after illumination.This method is currently widely used to kill pathogens such as bacteria and viruses in blood, and singlet oxygen is considered to be the key factor in the photodynamic effect.Singlet oxygen can induce cell apoptosis, necrosis and autophagy.At present, there are direct and indirect methods to detect singlet oxygen, but both with some limitations.This paper reviews production mechanism, action mechanism and detection of singlet oxygen produced by riboflavin during photodynamic therapy, which provides a basis for further application of photodynamic therapy in clinical practice and searching for a more suitable detection method for singlet oxygen.
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Objective To systematically evaluate the efficacy and safety of duloxetine and sertraline for Chinese depression patients.Methods The randomized controlled trials(RCTs)comparing the efficacy and safety of duloxetine and sertraline in the treatment of depression were retrieved from databases and the quality of literature was evaluated.Meta-analysis was performed with the software Revman 5.2.Results Eighteen RCTs involving 1 557 Chinese depression patients were included.The results of Meta-analysis showed that there were no significant differences in efficacy and cure rate between duloxetine and sertraline groups(OR=1.28, 95%CI:0.94 -1.73, P =0.11; OR =1.25,95%CI:0.97 -1.62,P =0.09, respectively).The Hamilton Depression Scale(HAMD)scores were significantly lower in duloxetine group than those in sertraline group at 1,2 weeks after treatment;however,there were no significant differences at 8-weeks after treatment between duloxetine and sertraline groups.The score of Medical Outcomes Study Pain Measures(MOSPM)in duloxetine group was significantly lower than that in sertraline group(P<0.01). The rate of insomnia in duloxetine group was significantly lower than that in sertraline group(RR=0.57, 95%CI:0.32 -1.00, P=0.04).There were no significant differences in other common side reactions between the two groups(P>0.05).Conclusions Duloxetine has similar long term treatment effect as sertraline,but it has a rapid-action profile.Duloxetine is more effective than sertraline in depression with painful physical symptoms;besides,duloxetine is less likely to induce insomnia.
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Objective To investigate the relationship between changes of cholinergic system and memory ability impairment in rats long-term exposed to hypoxia-hypercapnia.Methods Forty-eight SD rats were randomly divided into control group,2 weeks hypoxia-hypercapnia group and 4 weeks hypoxiahypercapnia group.The chronic hypoxia-hypercapnia rat model was set up.The memory ability was assessed by eight-arm radial maze.Morphological changes were observed by the HE staining and Nissl staining.Acetylcholine(ACh) content,choline acetyl-transferase (ChAT) activity and acetyl-cholinesterase (AChE) activity in the hippocampus were detected by spectrophotometry,while expression of α7 neuronal nicotinic acetylcholine receptor (α7 nAChR) protein by Western blot.Results Memory ability,especially the working memory was impaired in rats exposed to chronic hypoxia-hypercapnia.And the memory ability decreased more markedly in four weeks group.Compared with those of normoxic rats,the levels of ACh and the activities of AChE and ChAT in the hippocampus of the two weeks group were significantly decreased (ACh:(58.9 ±2.7) vs (47.4 ±3.2) μg/mg (protein) ; AChE:(0.326 ±0.019) vs (0.247 ±0.020) U/mg (protein) ; ChAT:(127.1 ±8.6) vs (90.4 ±6.9) U/g (tissue wet weight),t =7.674,8.139,9.408,all P ＜ 0.05).Compared with the two weeks group,those changes were more obvious in the four weeks group rats (ACh:(47.4 ±3.2) vs (32.5 ±3.2) μg/mg (protein); AChE:(0.247 ±0.020),(0.170±0.019) U/mg (protein); ChAT:(90.4 ±6.9),(55.6 ±6.0) U/g (tissue wet weight),t =9.279,8.036,10.781,all P ＜ 0.05).Compared with the normoxic rats,the expressions of α7 nAChR protein were significantly decreased in two weeks group rats (t =4.481,P ＜ 0.05).Moreover,the expressions of α7 nAChR protein were significantly decreased in four weeks group rats comparing with the two weeks group (t =4.965,P ＜ 0.05).Conclusions An impairment of rat' s memory ability may be induced by hypoxia-hypercapnia,and the injury degree is correlated with the exposure time.Cholinergic system dysfunctions may contribute to the memory function defects in chronic hypoxia-hypercapnia rats.