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Sleep plays an important role in energy balance. As reported， sleep disorder is an important risk factor for metabolic diseases. Controlling the relationship between energy metabolism and sleep can affect sleep homeostasis and body metabolic rate. Chinese medicine， with remarkable curative effects in the prevention and treatment of insomnia， has the characteristics of green， safety， and few side effects， and attracts extensive attention of scholars in the world. In recent years， remarkable progress has been made in the research on the mechanism of Chinese medicine in interfering with sleep. This paper reviewed the research progress of mind-tranquilizing Chinese medicines， such as compounds （pterostilbene）， Chinese medicinal drugs （Ziziphi Spinosae Semen）， and Chinese medicinal prescriptions （Jiaotaiwan， Suanzaoren tang， Tianwang Buxindan， Anmeidan， Banxia Houpotang， Qihuo decoction， Songyu Anshen prescriptions， and Shuxie Yihao prescriptions） in the treatment of sleep disorders by regulating energy metabolism. The findings revealed that Chinese medicine can intervene in the sleep deprivation model by affecting metabolism-related pathways such as material metabolism， mitochondrial function， oxidative stress and inflammatory response， appetite system， and biological clock system. In terms of frequency of use， the top drugs are Ziziphi Spinosae Semen， Poria， Schisandrae Chinensis Fructus， and Salviae Miltiorrhizae Radix et Rhizoma which affect heart and liver meridians to regulate blood circulation， ensure energy supply， and play the role of nourishing the heart and tranquilizing the mind. The present paper summarized the effects and mechanisms of Chinese medicine in the treatment of insomnia and other sleep disorders from the perspective of energy metabolism to provide references for further research and exploration of diseases in the future.
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ObjectiveTo investigate the effect of Anmeidan （AMD） on biological rhythm and related protein expression in sleep-deprived rats. MethodA total of 80 SD rats were randomized into control group （Ctrl， equivalent volume of saline）， model group （SD， equivalent volume of saline）， AMD group （9.09 g·kg-1·d-1）， and melatonin group （MT， 0.27 g·kg-1·d-1）. Insomnia was induced in rats by self-made sleep deprivation box （4 weeks）. Circadian rhythm of spontaneous activity was evaluated by spontaneous activity video analysis system. Morphology of hypothalamus was observed based on hematoxylin-eosin （HE） staining， and the histomorphology of hypothalamus neurons and the Nissl's bodies based on Nissl staining. Western blotting was employed to detect the expression of hypothalamic proteins in cAMP-response element binding protein （CREB）/clock gene period （Per） pathway， and immunohistochemistry the expression of brain and muscle ARNT-like protein 1 （Bmal1）， Clock， Per1， and cryptochrome circadian regulator 1 （Cry1）. ResultThe model group demonstrated circadian rhythm disorder， as manifested by the significant increase in activity time in 6 designated time periods compared with the control group， and the rise in the activity speed and frequency （P<0.01）. Moreover， model group showed decrease in number of neurons which were sparsely arranged with shrunken or fragmented nuclei， reduction in number and loss of Nissl's bodies with light color， and drop in the relative expression of p-CREB and Per1， and the positive rate of Bmal1， Clock， Per1， and Cry1 （P<0.01）. Compared with model group， AMD group demonstrated reduction in time， speed， and frequency of activity （P<0.01）. Moreover， the AMD group also showed alleviation of neuronal damage （P<0.01）， and increase in the number of neurons with clear nuclei and cytoplasm in some， and the number of Nissl's bodies. AMD raised the expression of p-CREB and Per1 proteins， and the positive rate of Bmal1， Clock， Per1， and Cry1 （P<0.01）. ConclusionAMD ameliorated spontaneous circadian rhythm of sleep-deprived rats by regulating CREB/Per signaling pathway and further increasing the expression of Bmal1， Clock， Per1， and Cry1.
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Adequate sleep is an important factor to ensure the healthy functioning of the body. A type of chronic sleep diseases characterized by insufficient sleep can be collectively referred to as sleep deprivation （SD）， which is divided into primary and secondary sources in terms of sources. As one of the most frequent types of diseases in recent years， SD has received more and more attention and attention from the whole society. SD can have a wide-ranging and far-reaching impact on cognitive behavior， such as decreased wakefulness， decreased alertness， and inattention， decreased sensory perception， decreased learning and memory capabilities， et al， involving the impact on multiple system functions of the human body， and It is closely related to the occurrence of many diseases， and may cause serious troubles to the normal life of patients and even their relatives and friends. The cognitive impairment caused by SD has been fully verified in clinical tests and various animal behavior experiments， mainly involving pathological damage such as changes in synaptic plasticity， enhanced endoplasmic reticulum stress， circadian rhythm disorders， and energy metabolism imbalance. Western medicine treatments for SD mostly have negative factors such as high side effect and strong addiction. However， Chinese medicine intervention focuses on the overall concept， has long-lasting effectiveness， significant effects， and mild side effects. It has also been widely recognized clinically for improving the complications of sleep disorders. This article reviews the current status and classification of SD research， its pathological mechanisms that lead to cognitive impairment and its molecular-level exploration directions and results. In recent 5 years， the therapeutic effect and experience of traditional Chinese medicine intervention therapy such as compound Chinese medicine， acupuncture and moxibustion as well as auxiliary therapy such as exercise and five sounds， in order to further summarize and clarify the interaction mechanism between SD and cognitive behavior， and provide a theoretical basis for the study of the pathological mechanism of SD disease and future clinical treatment.
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Objective:to explore the mechanism of modified Tianwang Buxindan in improving abnormal glucose and lipid metabolism in mice with chronic sleep deprivation from the signal pathway of orexin A/ orexin receptor 1（OX1R）. Method:The 50 6-week-old male C57BL/6 mice were randomly divided into blank group ， model group ， estazolam group and Tianwang Buxindan low and high dose groups ，for ten mice of each group. Except the blank group， rats were deprived of sleep for 8 weeks by the method of multi-platform water environment. In the last 4 weeks， Tianwang Buxindan （8.5，17 g·kg-1）and estazolam solution（9.1 mg·kg-1）were given to the stomach， and the blank group and the model group were fed with pure water of the same volume. The food intake and body weight of mice were measured twice a week， on the 49th day， blood samples were collected from the tail vein for glucose tolerance test （GTT），on the 52nd day for insulin tolerance test（ITT）， was used to detect the expression of total cholesterol （TCH）， triglyceride（TG）and free fatty acid（FFA）in serum， and enzyme-linked immunosorbent assay（ELISA）was used to detect the expression of orexin A in serum and hypothalamus. Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR）and Western blot were used to detect the mRNA and protein expression of OX1R in hypothalamus. Result:After administration， the food intake of mice in each group was different， compared with the blank group， the body weight of model group was significantly reduced（P<0.05）， the glucose tolerance was significantly abnormal， and the TCH， TG， FFA values were significantly increased（P<0.01）. The expression of orexin A in serum and hypothalamus increased significantly（P<0.01）， and the mRNA and protein expression levels of OX1R in hypothalamus increased significantly（P<0.01）. Compared with the model group， the body weight of each group of Tianwang Buxindan was significantly increased（P<0.05）， with better glucose tolerance and insulin sensitivity， TCH， TG， FFA values were significantly reduced（P<0.05，P<0.01）， accompanied by serum and the expression of orexin A in the hypothalamus was significantly decreased（P<0.05，P<0.01）， the mRNA and protein expression levels of OX1R were significantly decreased（P<0.05，P<0.01）. Conclusion:Tianwang Buxindan can protect mice from abnormal glucose and lipid metabolism induced by chronic sleep deprivation， and its mechanism may be related to the down-regulation of orexin A/OX1R signal expression.
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Objective:To detect the changes of functional expression profile of energy metabolism related differential genes in sleep deprived rats before and after intervention by Tianwang Buxindan by microarray sequencing technology， so as to provide possible ideas and theoretical basis for the prevention and treatment of sleep deprivation. Method:The rats were randomLy divided into two groups： the Tianwang Buxindan group and the model group. The Tianwang Buxindan group was given the decoction of Tianwang Buxindan at the dose of 20 g·kg-1， and the model group was given the pure water of equal volume for 14 days. Taking liver， heart and hypothalamus as samples， high-throughput sequencing was used to obtain differential genes. Gene Ontology（Go）classification and kyoto Encyclopedia of Genes and Genomes （KEGG）pathway enrichment analysis were used to construct a co expression network with lncrna. Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR）was used to detect the mRNA expression levels of neuropeptide Y（NPY）， bispecific phosphatase 1/mitogen-activated protein kinase phosphatase-1（DUSP1/MKP-1）and alpha-L-iduronidase（IDUA）， three key genes with significant differences in energy metabolism. Result:The 321 differentially expressed genes were obtained， 231 of which were up-regulated and 90 down regulated， which mainly promoted the process of lipid metabolism， glucose metabolism and protein metabolism， participated in the synthesis and expression of fibrinogen， vitamin B6 and mesencephalic astrocyte-derived neurotrophic factor（MANF）， and involved mitogen activated protein kinases（MAPK）， p53 gene（p53）， cyclic adenosine monophosphate（cAMP） and other signal pathways. Compared with the model group， the expression of IDUA significantly increased in the Tianwang Buxindan group （P<0.05）， but decreased significantly in NPY and DUSP1（P<0.01）. Conclusion:Tianwang Buxindan can interfere with the energy metabolism mechanism of sleep deprived rats in many ways. By down regulating the mRNA expression level of NPY and DUSP1 genes， it may activate the p38 MAPK signal pathway and affect the lipid metabolism.
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Objective:By studying the effects of Tianwang Buxindan on sleep quality， cognitive function， inflammatory factors and immune-related gene expression in sleep deprivation model rats， explore the effect of Tianwang Buxindan on the learning and memory process under sleep deprivation and its anti-inflammatory effects possible mechanism. Method:The 40 male SPF rats were used to simulate the sleep deprivation model by multi-platform water environment method， and were randomly divided into model group， Tianwang Buxindan group （20 g·kg-1） and estazolam group （0.1 mg·kg-1）， set up a normal group， 10 in each group. A total of 4 weeks of sleep deprivation modeling was performed， and drug intervention was performed 2 weeks later. The model group and the blank group were given equal volumes of pure water. Electroencephalogram （EEG） evaluation of modeling and analysis of sleep structure and quality of rats， Morris water maze positioning navigation and space exploration experiment analysis of learning and memory ability of rats， application of enzyme-linked immunosorbent assay （ELISA） was used to detect the serum inflammatory factor interleukin-1β （IL-1β）， tumor necrosis factor-α （TNF-α）， monocyte chemokine-1 （MCP-1） expression， Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA levels of EB virus inducible gene 3 （EBI3）， extracellular signal-regulated kinase 5 （ERK5）， and p21 activated protein kinase 4 （PAK4）. Result:The sleep deprivation model was successfully built. Compared with blank group， the total sleep time， total duration of slow wave sleep and the duration of the first and second phases of slow wave sleep in the model group were significantly shortened （P<0.01）. The incubation period on the upper platform， the total swimming distance and the time to reach the original platform for the first time increased significantly， while the number of times to cross the platform and the target quadrant significantly decreased （P<0.05，P<0.01）. The expression levels of IL-1β，TNF-α and MCP-1 increased significantly （P<0.01）， the mRNA expression levels of EBI3， ERK5 and PAK4 in the hypothalamus of the model group decreased significantly （P<0.01）. Compared with the model group， the sleep quality of the rats in the Tianwang Buxindan group was significantly improved. The total sleep time， the total duration of slow wave sleep and the duration of the first phase of slow wave sleep were significantly increased （P<0.01）. The incubation period on the platform， the total swimming distance and the time to reach the original platform for the first time are shortened， the number of times to cross the platform and the target quadrant time are extended （P<0.05，P<0.01）， IL-1β， TNF-α， MCP-1 expression levels were significantly reduced （P<0.05，P<0.01）， mRNA expression levels of EBI3， ERK5 and PAK4 in rat hypothalamus were significantly increased （P<0.05，P<0.01）. Conclusion:Tianwang Buxindan can improve the sleep quality and learning and memory ability of sleep deprivation model rats， which may be related to the increase of the expression level of related inflammatory factors and its anti-inflammatory effect.
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Objective:To explore the effect of Anmeidan （AMD） on the learning and memory levels of sleep deprived rats through mitochondrial mediated hippocampal neuronal apoptosis pathway. Method:Forty-eight SD rats were randomly divided into blank group， model group， low， medium， high-dose AMD groups （4.86， 9.72， 19.44 g·kg-1·d-1） and estazolam group （0.1 mg·kg-1·d-1）. Insomnia model was prepared by self-made sleep deprivation box for 14 days. Morris water maze was used to detect learning and memory levels， enzyme-linked immunosorbent assay （ELISA） was used to detect the expressions of cytochrome C （Cyt-C）， cysteine aspartic acid protease-3 （Caspase-3） in hippocampus. Transmission electron microscopy （TEM） was used to observe the morphological structure of mitochondria in hippocampus. Protein and mRNA expressions of Cyt-C， Caspase-3， Bcl-2， Bax were detected by immunofluorescence （IF） and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） respectively. Result:In the model group， the incubation period of the platform and the total distance of swimming and the time of first arriving platform were prolonged， the number of platform crossing and the time of target quadrant movement were reduced， protein and mRNA expressions of Bcl-2 dropped， protein and mRNA expressions of Bax increased （P<0.01）， and mitochondrial structure was abnormal with crista fracture， swelling and deformation. And protein and mRNA expressions of Cyt-C， Caspase-3 increased significantly （P<0.01）. Low， medium and high-dose AMD groups could improve levels of space exploration and navigation of SD rats （P<0.01）， increase protein and mRNA expressions of Bcl-2， decrease protein and mRNA expressions of Bax， improve the damage of mitochondria， and decrease the protein and mRNA expressions of Cyt-C， Caspase-3 （P<0.01）. Conclusion:AMD can improve the learning and memory levels of SD rats， the effect is related to the mitochondrial mediated hippocampal neuronal apoptosis pathway and decrease of Cyt-C and Caspase-3 expressions.
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Objective:To explore the mechanism of modified Tianwang Buxindan on oxidative damage of Trx system in parachlorophenylalanine (PCPA) insomnia model rats. Method:Sixty male SD rats were randomly divided into blank group and model group. Insomnia model was prepared through intraperitoneal injection with PCPA (150 mg·kg-1). The discontinuous injection lasted for 7 d. After successful modeling, the rats were divided into model group (the same volume of normal saline), low, medium, high-dose Tianwang Buxindan groups (8.8, 17.6, 35.2 g·kg-1·d-1) and estazolam group (0.1mg·kg-1·d-1), with 10 in each group. Autonomous activity video was used to detect circadian activity rhythm. Transmission electron microscopy (TEM) was used to observe supra chiasmatic nucleus (SCN) morphology and Organelle integrity. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expressions of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in serum. Expressions of Trx2, TrxR2 in SCN cells were detected by immunofluorescence (IF) and Western blot. Result:Compared with blank group, the activity rhythm of model group was irregular, the activity time increased (PPPPPPPPConclusion:The effect of modified Tianwang Buxindan on insomnia model rats is related to the regulation of Trx2 and TrxR2 protein expressions in Trx system.
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<p><b>Background</b>The pathogenesis of postural tachycardia syndrome (POTS) remains unclear. This study aimed to explore the changes and significance of sulfur dioxide (SO) in patients with POTS.</p><p><b>Methods</b>The study included 31 children with POTS and 27 healthy children from Peking University First Hospital between December 2013 and October 2015. A detailed medical history, physical examination results, and demographic characteristics were collected. Hemodynamics was recorded and the plasma SOwas determined.</p><p><b>Results</b>The plasma SOwas significantly higher in POTS children compared to healthy children (64.0 ± 20.8 μmol/L vs. 27.2 ± 9.6 μmol/L, respectively, P < 0.05). The symptom scores in POTS were positively correlated with plasma SOlevels (r = 0.398, P < 0.05). In all the study participants, the maximum heart rate (HR) was positively correlated with plasma levels of SO(r = 0.679, P < 0.01). The change in systolic blood pressure from the supine to upright (ΔSBP) in POTS group was smaller than that in the control group (P < 0.05). The ΔSBP was negatively correlated with baseline plasma SOlevels in all participants (r = -0.28, P < 0.05). In the control group, ΔSBP was positively correlated with the plasma levels of SO(r = 0.487, P < 0.01). The change in HR from the supine to upright in POTS was obvious compared to that of the control group. The area under curve was 0.967 (95% confidence interval: 0.928-1.000), and the cutoff value of plasma SOlevel >38.17 μmol/L yielded a sensitivity of 90.3% and a specificity of 92.6% for predicting the diagnosis of POTS.</p><p><b>Conclusions</b>Increased endogenous SOlevels might be involved in the pathogenesis of POTS.</p>
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Objective To investigate the effects of endogenous sulfur dioxide (SO2) on the oxidative stress induced by cobalt chloride (CoCl2) in the rat pulmonary artery smooth muscle cells (PASMCs).Methods Rat PASMCs were treated with 200 μ mol/L CoCl2 to mimic the hypoxia insult.Endogenous SO2 generating enzyme aspartate aminotransferase 1 (AAT1) expression was upregulated or downregulated (AAT1 sh) by transfection with lentivirus.Rat PASMCs were randomly divided into 8 groups:vehicle group,vehicle + CoCl2 group,AAT1 group,AAT1 + CoCl2 group,scramble group,scramble + SO2 group,AAT1 sh group and AAT1 sh + SO2 group.SO2 donor Na2 SO3/NaHSO3 at concentration of 100 μ mol/L were added in scramble + SO2 group and AAT1sh + SO2 group.The expressions of AAT1,superoxide dismutase 1 (SOD1) and SOD2 in PASMCs were detected by Western blot method.In situ SO2 content in PASMCs was detected by fluorescent probe.The superoxide anions in PASMCs were labeled by dihydroethidium (DHE) probe under fluorescent microscope.Results Compared with the vehicle group,the levels of SO2 and the expressions of AAT1 (0.221 ± 0.002 vs.0.446 ± 0.004),SOD1 (0.076 ± 0.028 vs.0.171 ± 0.019) and SOD2 (0.080 ± 0.031 vs.0.196 ± 0.018) significantly decreased (all P ＜ 0.01),and superoxide anion increased in rat PASMCs of vehicle + CoCl2 group.Meanwhile,compared with vehicle + CoCl2 group,the levels of SO2 and the expressions of AAT1 (0.839 ± 0.056 vs.0.221 ± 0.002),SOD1 (0.177 ± 0.020 vs.0.076 ± 0.028) and SOD2 (0.195 ±0.018 vs.0.080-± 0.031) markedly increased (all P ＜ 0.01),and superoxide anion decreased in rat PASMCs of AAT1 + CoCl2 group.On the contrary,compared with the scramble group,the levels of SO2 and the expressions of AAT1 (0.062 ±0.017 vs.0.354 ±0.034),SOD1 (0.054 ±0.029 vs.0.157 ±0.023) and SOD2(0.180 ±0.100 vs.0.586 ± 0.176)significantly decreased (all P ＜ 0.01),and superoxide anion increased in rat PASMCs of AAT1sh group.Furthermore,compared with the AAT1 sh group,the levels of SO2 and the expressions of SOD1 (0.155 ± 0.022vs.0.054 ± 0.029) and SOD2 (0.578 ± 0.200 vs.0.180 ± 0.100) significantly increased (all P ＜ 0.01),and superoxide anion decreased in rats PASMCs of AAT1sh + SO2 group.Conclusion Endogenous SO2/AAT1 inhibits CoCl2-induced oxidative stress in rat PASMCs.
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To study the pharmacokinetics characteristic of loganin, ferulic acid and stilbene glucoside in rat plasma after oral administration of Bushen Tongluo formula. The plasma samples were treated by using liquid-liquid extraction technique, the concentrations were determined by HPLC-UV. Johnson spherigel C18 column (4.6 mm x 250 mm, 5 μm) was adopted and eluted with the of mobile phase of methanol-water containing 0.01% glacial acetic acid in a gradient mode, with the flow rate at 1.0 mL x min(-1), column temperature at 30 degrees C and injection volume of 10 μL. According to the findings, loganin was determined at 235 nm, ferulic acid and stilbene glucoside were determined at 320 nm, with the sample size of 10 μL. The pharmacokinetic parameters of loganin, ferulic acid and stilbene glucoside were calculated by DAS 2. 0 software as follows: C(max) was (0.369 ± 0.042), (0.387 ± 0.071), (0.233 ± 0.044) mg x L(-1); t(max) was (0.226 ± 0.022), (0.282 ± 0.031), (0.233 ± 0.044) h; t(½β) was (6.89 ± 0.20), (10.73 ± 0.11), (6.93 ± 0.09) h; AUC(0-∞) was (1.91 ± 0.36), (3.22 ± 0.52), (1.52 ± 0.33) mg x h x L(-1); AUCO(0-t) was (1.62 ± 0.33), (2.58 ± 0.43), (1.30 ± 0.30) mg x h x L(-1); CL was (20.2 ± 4.0), (1.39 ± 0.23), (31.7 ± 6.9) L x h(-1) x kg(-1), respectively. The results showed that after the oral administration with Bushen Tongluo formula, loganin, ferulic acid and stilbene glucoside showed concentration-time curves in conformity with the two compartment model, with a rapid absorption, loganin and stilbene glucoside was excreted at a moderate speed, and ferulic acid was excreted slowly (but with the highest bioavailability). Bushen Tongluo formula can main maintain plasma concentration with three administrations everyday and so is suitable to be made into common oral preparation.
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Animals , Male , Rats , Administration, Oral , Biological Availability , Coumaric Acids , Blood , Pharmacokinetics , Drugs, Chinese Herbal , Pharmacokinetics , Glucosides , Blood , Pharmacokinetics , Iridoids , Blood , Pharmacokinetics , Rats, Sprague-Dawley , Stilbenes , Blood , PharmacokineticsABSTRACT
Objective To investigate the status and characteristics of physical activity of pregnant women during second pregnancy trimesters in Chengdu,and to provide the scientific evidence for developing rational movement of pregnant women.Methods 650 cases were recruited into this survey during August 2012 to March 2013,by convenience sampling method.A questionnaire survey was used to collect their physical activity information,advanced motion in pregnancy intentions,main physical activity ways and times during pregnancy,frequency and duration of physical activity.SPSS21.0 statistical software was conducted.Results Effective response rate was 95％(619/650).95.2％ (589/619)of them hold that physical activity during second trimesters was support and the main way for them to exercise was walk.The most of pregnant during second trimesters was engaged in low-density activity.There had significant difference between low-density and other density exercises,P＜0.01.Conclusion The physical activity forms of pregnant women in Chengdu is single and lack of knowledge.It is necessary to strengthen the health guidance for pregnant women and correct the bad habits of physical activity to ensure the safe of pregnant women and their children.
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Objective To study the change of the renal endogenous hydrogen sulfide (H2 S) pathway in the development of salt-sensitive hypertension in Dah1 rats.Methods Sixteen male Dah1 rats,in accordance with the random number table,were randomly divided into control group and high salt group fed with diet containing 80 g/kg NaCl.After 8 weeks,24 h urine sodium,24 h urinary protein,serum creatinine and serum urea were measured.The microstructural and ultrastructural changes in kidney were observed with light microscope and electronic microscope.The serum and kidney H2S contents were determined by using sulphur-sensitive electrode method.The mRNA levels of cystathionine β-synthase(CBS),cystathionine γ-lyase(CSE) and mercaptopyruvate sulfurtransferase(MPST) in renal tissue were determined by means of real-time polymerase chain reaction(RT-PCR).The protein expressions of CBS,CSE and MPST in renal tissue were detected by using Western blot.Results Compared with control group,high salt group rats had a significant rise in blood pressure,declined renal function,damaged renal structure,segmental glomerular sclero sis,small artery wall thickening,and occlusion of the lumen.Moreover,the endogenous H2S pathway in kidney of Dah1rats with high salt diet was downregulated markedly,demonstrated by the decreased serum and kidney H2S content,the reduced renal CBS,CSE and MPST mRNA expressions and CBS protein expression of kidney tissue.Conclusion The endogenous H2S/CBS pathway is downregulated during the development of salt-sensitive hypertension in Dah1 rats.
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<p><b>OBJECTIVE</b>To investigate the surgical outcomes of unilateral lumbar pedicle screw fixation and intervertebral body fusion in treating far lateral lumber disc herniation.</p><p><b>METHODS</b>From June 2007 to June 2009, 25 patients with far lateral lumbar disc herniation were treated with unilateral lumbar pedicle screw fixation and intervertebral body fusion. There were 12 males and 13 females,which ranged in age from 37 to 68, with an average of 54.6 years. The course of disease was from 3 to 36 months with an average of 8.8 months. All the patients had pain and/or numbness and/or soreness in front and/or the back of unilateral leg and buttocks; muscle strength, sensation and tendon reflexes had declined of different degrees. Lumbar CT or MRI showed far lateral lumbar disc herniation. Neurological function and lumbar function were respectively evaluated according to JOA 29 score system (including subjective, objective symptom and bladder function) and Oswestry disability index (ODI).</p><p><b>RESULTS</b>All the patients were followed-up from 12 to 36 months with an average of 24 months. Postoperative wound healed well and no perioperative complications and follow-up complications were found. Neurological function of patients obtain recovery of difference degrees. At final follow-up, JOA score and ODI improved compared with that of preoperative data (P < 0.01); the mean improvement rate of JOA score was 94.3%. All patients got good bone fusion and no recurrence cases were found.</p><p><b>CONCLUSION</b>Unilateral lumbar pedicle screw fixation and intervertebral body fusion could increase the initial stability after fusion, restore and maintain the intervertebral height, and elevate the improvement rate in treating far lateral lumber disc herniation. The surgical method is safe, effective and reliable, but need to strictly control indications.</p>
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Adult , Aged , Female , Humans , Male , Middle Aged , Bone Screws , Decompression, Surgical , Methods , Intervertebral Disc Displacement , General Surgery , Lumbar Vertebrae , General Surgery , Spinal Fusion , MethodsABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of acute heat stress on the expression patterns of heat shock protein 70 (HSP70) in the testis, epididymis and vas deferens of adult male mice.</p><p><b>METHODS</b>Thirty-two 8-week-old male mice were randomly divided into a control and 3 heat stress groups. After a week of pretreatment, the latter 3 groups were exposed to heat stress at (39 +/- 0.5) degrees C for 0.5, 1 and 3 hours, respectively, followed immediately by collection of the blood and determination of glutamic oxaloacetic transaminase (GOT) concentration. Sperm suspension was made from one epididymis for the detection of sperm concentration and abnormal acrosome rate, while the testis, epididymis and vas deferens on the other side were harvested for immunohistochemical analysis.</p><p><b>RESULTS</b>Heat stress induced different degrees of decrease in epididymis indexes and sperm concentration and a dramatic increase in GOT concentration (P < 0.01), but caused no significant changes in the body weight, testis indexes and abnormal acrosome rate in the mice (P > 0.05). There was a tendency of gradual descent in sperm concentration and ascent in abnormal acrosome rate with the increasing time of heat stress. The most decrease in body weight, testis indexes and epididymis indexes was observed in the 0.5 h group. Immunohistochemical results showed that HSP70 was expressed in the testis, epididymis and vas deferens, mildly in the Leydig cells of the testis and distributed in the nuclei of the Leydig cells, spermatoblasts and spermatocytes. In the epididymis, HSP70 was expressed mainly in the cytoplasm of principal and ciliated cells, but not in the basal and clear cells, while in the vas deferens, it was observed mainly in the cytoplasm of the basal cells, but not in the principal cells. With the increase of heating time, the HSP70 expression was markedly elevated in the testis and epididymis, but not so obviously in the vas deferens.</p><p><b>CONCLUSION</b>Acute heat stress was harmful to the reproductive system of adult male mice. The region- and cell-specific patterns of HSP70 expressions in the testis, epididymis and vas deferens suggested that HSP70 might play an important role in spermatogenesis and sperm maturation. The dramatic increase of HSP70 expression after heat stress might be responsible for the prevention of cells from high temperature.</p>
Subject(s)
Animals , Male , Mice , Epididymis , Metabolism , HSP70 Heat-Shock Proteins , Metabolism , Heat Stress Disorders , Metabolism , Mice, Inbred Strains , Testis , Metabolism , Vas Deferens , MetabolismABSTRACT
OBJECTIVE:To compare preventive effects of droperidol and tropisetron on nausea and vomiting after laparoscopic appendectomy.METHODS:60 patients with general anesthesia underwent elective laparoscopic appendectomy were randomly divided into group A,group B and group C (n=20).Before suture,group A received 0.9% sodium chloride injection 10 mL,group B droperidol 1.25 mg,group C tropisetron 5 mg.Patients were extubated as them became conscious.The occurrence of nausea and vomiting 24 h after operation were observed and recorded.RESULTS:The occurrence rate of postoperative nausea and vomiting in group B and group C were significantly lower than in group A (P0.05).CONCLUSION:Droperidol and tropisetron could significantly reduce the occurrence of nausea and vomiting after laparoscopic appendectomy.
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<p><b>OBJECTIVE</b>To identify the effect of interleukin-8 in cell progression and invasion of human breast cancer.</p><p><b>METHODS</b>Human cytokine antibody arrays were applied to screen a panel of cytokine expression from 11 human breast cancer cell lines, and the mechanism of identified key factors involved in breast cancer progression was studied.</p><p><b>RESULTS</b>Profiling of cytokine expression showed the expression of interleukin-8 was related to estrogen receptor status, metastasis and vimentin status in the 11 human breast cancer cell lines. Elevated expression of interleukin-8 in breast cancer cells had positive correlation with breast cancer invasion. Neutralization of antibody against interleukin-8 specifically blocked interleukin-8-mediated cell invasion. However, anti-interleukin-8 antibody did not influence the proliferation of breast cancer cells.</p><p><b>CONCLUSION</b>Interleukin-8 may be the key factor involved in human breast cancer progression and invasion, and play an important role in cell invasion of breast cancer.</p>