LHPP, a risk factor for major depressive disorder, regulates stress-induced depression-like behaviors through its histidine phosphatase activity.

Histidine phosphorylation (pHis), occurring on the histidine of substrate proteins, is a hidden phosphoproteome that is poorly characterized in mammals. LHPP (phospholysine phosphohistidine inorganic pyrophosphate phosphatase) is one of the histidine phosphatases and its encoding gene was recently identified as a susceptibility gene for major depressive disorder (MDD). However, little is known about how LHPP or pHis contributes to depression. Here, by using integrative approaches of genetics, behavior and electrophysiology, we observed that LHPP in the medial prefrontal cortex (mPFC) was essential in preventing stress-induced depression-like behaviors. While genetic deletion of LHPP per se failed to affect the mice's depression-like behaviors, it markedly augmented the behaviors upon chronic social defeat stress (CSDS). This augmentation could be recapitulated by the local deletion of LHPP in mPFC. By contrast, overexpressing LHPP in mPFC increased the mice's resilience against CSDS, suggesting a critical role of mPFC LHPP in stress-induced depression. We further found that LHPP deficiency increased the levels of histidine kinases (NME1/2) and global pHis in the cortex, and decreased glutamatergic transmission in mPFC upon CSDS. NME1/2 served as substrates of LHPP, with the Aspartic acid 17 (D17), Threonine 54 (T54), or D214 residue within LHPP being critical for its phosphatase activity. Finally, reintroducing LHPP, but not LHPP phosphatase-dead mutants, into the mPFC of LHPP-deficient mice reversed their behavioral and synaptic deficits upon CSDS. Together, these results demonstrate a critical role of LHPP in regulating stress-related depression and provide novel insight into the pathogenesis of MDD.

DSCAM Deficiency Leads to Premature Spine Maturation and Autism-like Behaviors.

Mutations in some cell adhesion molecules (CAMs) cause abnormal synapse formation and maturation, and serve as one of the potential mechanisms of autism spectrum disorders (ASDs). Recently, DSCAM (Down syndrome cell adhesion molecule) was found to be a high-risk gene for autism. However, it is still unclear how DSCAM contributes to ASD. Here, we show that DSCAM expression was downregulated following synapse maturation, and that DSCAM deficiency caused accelerated dendritic spine maturation during early postnatal development. Mechanistically, the extracellular domain of DSCAM interacts with neuroligin1 (NLGN1) to block the NLGN1-neurexin1ß (NRXN1ß) interaction. DSCAM extracellular domain was able to rescue spine overmaturation in DSCAM knockdown neurons. Precocious spines in DSCAM-deficient mice showed increased glutamatergic transmission in the developing cortex and induced autism-like behaviors, such as social novelty deficits and repetitive behaviors. Thus, DSCAM might be a repressor that prevents premature spine maturation and excessive glutamatergic transmission, and its deficiency could lead to autism-like behaviors. Our study provides new insight into the potential pathophysiological mechanisms of ASDs.SIGNIFICANCE STATEMENTDSCAM is not only associated with Down syndrome but is also a strong autism risk gene based on large-scale sequencing analysis. However, it remains unknown exactly how DSCAM contributes to autism. In mice, either neuron- and astrocyte-specific or pyramidal neuron-specific DSCAM deficiencies resulted in autism-like behaviors and enhanced spatial memory. In addition, DSCAM knockout or knockdown in pyramidal neurons led to increased dendritic spine maturation. Mechanistically, the extracellular domain of DSCAM binds to NLGN1 and inhibits NLGN1-NRXN1ß interaction, which can rescue abnormal spine maturation induced by DSCAM deficiency. Our research demonstrates that DSCAM negatively modulates spine maturation, and that DSCAM deficiency leads to excessive spine maturation and autism-like behaviors, thus providing new insight into a potential pathophysiological mechanism of autism.

Increasing LRP4 diminishes neuromuscular deficits in a mouse model of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular disease characterized by progressive wasting of skeletal muscles. The neuromuscular junction (NMJ) is a synapse between motor neurons and skeletal muscle fibers, critical for the control of muscle contraction. The NMJ decline is observed in DMD patients, but the mechanism is unclear. LRP4 serves as a receptor for agrin, a proteoglycan secreted by motor neurons to induce NMJ, and plays a critical role in NMJ formation and maintenance. Interestingly, we found that protein levels of LRP4 were reduced both in muscles of the DMD patients and DMD model mdx mice. We explored whether increasing LRP4 is beneficial for DMD and crossed muscle-specific LRP4 transgenic mice with mdx mice (mdx; HSA-LRP4). The LRP4 transgene increased muscle strength, together with improved neuromuscular transmission in mdx mice. Furthermore, we found the LRP4 expression mitigated NMJ fragments and denervation in mdx mice. Mechanically, we showed that overexpression of LRP4 increased the activity of MuSK and expression of dystrophin-associated glycoprotein complex proteins in the mdx mice. Overall, our findings suggest that increasing LRP4 improves both function and structure of NMJ in the mdx mice and Agrin signaling might serve as a new therapeutic strategy in DMD.

Over-expression of DEC1 inhibits myogenic differentiation by modulating MyoG activity in bovine satellite cell.

Differentiated embryo chondrocyte 1 (DEC1), a member of basic-helix-loop-helix transcription factor Bhlhe40, also called stimulated by retinoic acid 13, STRA13, plays an important role in the regulation of adipogenesis, tumorigenesis, peripheral circadian output, response to hypoxia, and development of metabolic syndrome. Previous studies suggested that DEC1 was involved in skeletal muscle development; however, its precise role in myoblast differentiation has not been determined. In the present study, we showed that DEC1 expressed ubiquitously in different bovine tissues and was down-regulated in differentiated bovine satellite cells. Expression of muscle specific transcription factors (Myf5, MyoD, MyoG, and MHC) was significantly down-regulated when DEC1 was over-expressed by both CoCl2 -simulated hypoxia and Adenovirus-mediated transduction in bovine satellite cells. Consistent with that, promoter analyses via luciferase reporter assay also revealed that overexpression of bovine DEC1 could inhibit MyoG promoter activity. In conclusion, overexpression of DEC1 blocked myogenesis by inhibiting MyoG promoter activity in bovine. Our results provided a new mechanism for the muscle growth, which would contribute to increase cattle meat productivity.

Performance Analysis of Evolutionary Algorithms for Steiner Tree Problems.

The Steiner tree problem (STP) aims to determine some Steiner nodes such that the minimum spanning tree over these Steiner nodes and a given set of special nodes has the minimum weight, which is NP-hard. STP includes several important cases. The Steiner tree problem in graphs (GSTP) is one of them. Many heuristics have been proposed for STP, and some of them have proved to be performance guarantee approximation algorithms for this problem. Since evolutionary algorithms (EAs) are general and popular randomized heuristics, it is significant to investigate the performance of EAs for STP. Several empirical investigations have shown that EAs are efficient for STP. However, up to now, there is no theoretical work on the performance of EAs for STP. In this article, we reveal that the (1+1) EA achieves 3/2-approximation ratio for STP in a special class of quasi-bipartite graphs in expected runtime [Formula: see text], where [Formula: see text], [Formula: see text], and [Formula: see text] are, respectively, the number of Steiner nodes, the number of special nodes, and the largest weight among all edges in the input graph. We also show that the (1+1) EA is better than two other heuristics on two GSTP instances, and the (1+1) EA may be inefficient on a constructed GSTP instance.

Cerebral activation effects of acupuncture using Zusanli (ST36) and Yanglingquan (GB34) points based on Regional Homogeneity indices: A resting-state fMRI study.

OBJECTIVE: This study aimed to observe the cerebral activation effects of acupuncturing the Zusanli (ST36) plusYanglingquan (GB34) points in young healthy volunteers based on Regional Homogeneity (ReHo) indices. METHODS: Ten healthy volunteers were enrolled, including 4 males and 6 females between the ages 20 and 34 years with a median age of 23 years. Magnetic resonance imaging (GE Signa HDxt 3.0T) was performed in four groups: Before acupuncture (Control Group), after acupuncture at Zusanli (ST36 Group), after acupuncture at Yanglingquan (GB34 Group) and after acupuncture at both Zusanli and Yanglingquan (Compatibility Group). Differences in the brain ReHo indices of the 4 groups were analyzed by statistical parametric mapping (SPM8) and ReHo data processing methods. The significantly different brain regions were obtained using a false discovery rate correction (FDR-Corrected). RESULTS: The ReHo indices revealed that the main significant effect was in the Compatibility Group. Compared with the resting state of the Control Group, the ReHo values of the Compatibility Group increased in the right middle frontal gyrus (BA8, 9), left superior temporal areas (BA22), ventral anterior cingulate area (BA24) and right inferior parietal lobe (BA40); in contrast, the ReHo values decreased in the left thalamus, right insular cortex (BA13), left inferior frontal lobe (BA9) and right dorsal anterior cingulate area (BA32). Our analysis showed that the Compatibility Group had higher ReHo values than the left inferior parietal lobule (BA40) and right frontal cortex (BA6) of the ST36 Group and the posterior lobe of the right cerebellum, dorsal anterior cingulate (BA32), left and right middle frontal gyrus (BA46, BA9), left precuneus (BA7), right inferior parietal love (BA40) of the GB34 Group. CONCLUSION: The results of our neuroimaging study suggest that the combination of acupoints could more widely activate areas of the brain compared to a single acupoint. Additionally, the combination of acupoints can activate some new brain areas and generate new curative effects.

Hypoxia promotes satellite cell self-renewal and enhances the efficiency of myoblast transplantation.

Microenvironmental oxygen (O(2)) regulates stem cell activity, and a hypoxic niche with low oxygen levels has been reported in multiple stem cell types. Satellite cells are muscle-resident stem cells that maintain the homeostasis and mediate the regeneration of skeletal muscles. We demonstrate here that hypoxic culture conditions favor the quiescence of satellite cell-derived primary myoblasts by upregulating Pax7, a key regulator of satellite cell self-renewal, and downregulating MyoD and myogenin. During myoblast division, hypoxia promotes asymmetric self-renewal divisions and inhibits asymmetric differentiation divisions without affecting the overall rate of proliferation. Mechanistic studies reveal that hypoxia activates the Notch signaling pathway, which subsequently represses the expression of miR-1 and miR-206 through canonical Hes/Hey proteins, leading to increased levels of Pax7. More importantly, hypoxia conditioning enhances the efficiency of myoblast transplantation and the self-renewal of implanted cells. Given the robust effects of hypoxia on maintaining the quiescence and promoting the self-renewal of cultured myoblasts, we predict that oxygen levels in the satellite cell niche play a central role in precisely balancing quiescence versus activation, and self-renewal versus differentiation, in muscle stem cells in vivo.

Adenosine as a probing tool for the mechanistic study of acupuncture treatment.

To date, acupuncture has been widely used despite a lack of solid clinical evidence in the East and West. However, there are few validated in vitro models for the mechanistic studies of acupuncture. We hypothesized that adenosine could be used as a probing tool in the mechanistic studies of acupuncture because of its critical role in the action of acupuncture. Subsequently, we tested this hypothesis using both in vitro and in vivo experiments. First, we found that adenosine stimulation mimicked the effect of acupuncture on microRNA profiling (including miR-339, miR-145 and miR-451) and protein level (including Sirt2) in nerve growth factor-induced differentiated PC12 cells. These miRNA and proteins have been found to be regulated by acupuncture treatment in the brain of spontaneously hypertensive rats. Next, we found that adenosine stimulation downregulated miR-339 expression through adenosine A1 receptor-mediated pathway. Finally, we showed that the concentration of adenosine was actually decreased in the brain of spontaneously hypertensive rats after acupuncture treatment at Taichong acupoint. Taken together, these findings suggest that adenosine could be used as a useful probing tool for acupuncture mechanistic studies, while more validation studies are certainly warranted.

Brain areas involved in the acupuncture treatment of AD model rats: a PET study.

BACKGROUND: Acupuncture may effectively treat certain symptoms of Alzheimer's disease (AD). Although several studies have used functional brain imaging to investigate the mechanisms of acupuncture treatment on AD, these mechanisms are still poorly understood. We therefore further explored the mechanism by which needling at ST36 may have a therapeutic effect in a rat AD model. METHODS: A total of 80 healthy Wistar rats were divided into healthy control (n = 15) and pre-model (n = 65) groups. After inducing AD-like disease, a total of 45 AD model rats were randomly divided into three groups: the model group (n = 15), the sham-point group (n = 15), and the ST36 group (n = 15). The above three groups underwent PET scanning. PET images were processed with SPM2. RESULTS: The brain areas that were activated in the sham-point group relative to the model group were primarily centred on the bilateral limbic system, the right frontal lobe, and the striatum, whereas the activated areas in the ST36 group were primarily centred on the bilateral limbic system (pyriform cortex), the bilateral temporal lobe (olfactory cortex), the right amygdala and the right hippocampus. Compared with the sham-point group, the ST36 group showed greater activation in the bilateral amygdalae and the left temporal lobe. CONCLUSION: We concluded that needling at a sham point or ST36 can increase blood perfusion and glycol metabolism in certain brain areas, and thus may have a positive influence on the cognition of AD patients.

Tongue feature recognition to monitor rehabilitation: deep neural network with visual attention mechanism.

Objective: We endeavor to develop a novel deep learning architecture tailored specifically for the analysis and classification of tongue features, including color, shape, and coating. Unlike conventional methods based on architectures like VGG or ResNet, our proposed method aims to address the challenges arising from their extensive size, thereby mitigating the overfitting problem. Through this research, we aim to contribute to the advancement of techniques in tongue feature recognition, ultimately leading to more precise diagnoses and better patient rehabilitation in Traditional Chinese Medicine (TCM). Methods: In this study, we introduce TGANet (Tongue Feature Attention Network) to enhance model performance. TGANet utilizes the initial five convolutional blocks of pre-trained VGG16 as the backbone and integrates an attention mechanism into this backbone. The integration of the attention mechanism aims to mimic human cognitive attention, emphasizing model weights on pivotal regions of the image. During the learning process, the allocation of attention weights facilitates the interpretation of causal relationships in the model's decision-making. Results: Experimental results demonstrate that TGANet outperforms baseline models, including VGG16, ResNet18, and TSC-WNet, in terms of accuracy, precision, F1 score, and AUC metrics. Additionally, TGANet provides a more intuitive and meaningful understanding of tongue feature classification models through the visualization of attention weights. Conclusion: In conclusion, TGANet presents an effective approach to tongue feature classification, addressing challenges associated with model size and overfitting. By leveraging the attention mechanism and pre-trained VGG16 backbone, TGANet achieves superior performance metrics and enhances the interpretability of the model's decision-making process. The visualization of attention weights contributes to a more intuitive understanding of the classification process, making TGANet a promising tool in tongue diagnosis and rehabilitation.

The central mechanisms of electroacupuncture at LR3 in the treatment of spontaneous hypertension: a PET and mRNA transcriptome study.

Objective: To reveal the efficacy and potential mechanisms of electroacupuncture (EA) in treating hypertension. Methods: Male spontaneously hypertensive rats (SHRs) were randomly assigned to the SHR group, EA group, and Sham-EA group, with Wistar-Kyoto rats (WKY) as the normal control group. SHRs in the EA group received electroacupuncture at the bilateral Taichong (LR3) acupoints for 7 consecutive days. Evaluation of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR) was conducted. Positron emission tomography-computed tomography (PET-CT) was employed to explore the active brain regions associated with acupuncture-induced blood pressure reduction. Furthermore, mRNA expression profiling was analyzed in the active brain regions to identify differentially expressed genes, and quantitative polymerase chain reaction (qPCR) was used to validate the mRNA expression of differentially expressed genes in the active brain region. Results: EA reduced elevated SBP, DBP, MAP and HR in SHR. PET-CT revealed that EA decreased glucose metabolism in the hypothalamus. Genomic analysis suggested that, compared to the SHR group, the differentially expressed genes in the hypothalamus of the EA group included Nr4a1, Sirt1, Trh, GPR88, Cck, and Th. EA downregulated the mRNA expression of Th, Trh, Gpr88, and Nr4a1, while upregulating the expression of Sirt1 and Cck at the mRNA level. Conclusion: EA may exert a unique antihypertensive effect in the hypothalamus of SHR, involving the modulation of sympathetic nerve activity, neuroinflammation, and oxidative stress response.

Deficiency of skeletal muscle Agrin contributes to the pathogenesis of age-related sarcopenia in mice.

Sarcopenia, a progressive and prevalent neuromuscular disorder, is characterized by age-related muscle wasting and weakening. Despite its widespread occurrence, the molecular underpinnings of this disease remain poorly understood. Herein, we report that levels of Agrin, an extracellular matrix (ECM) protein critical for neuromuscular formation, were decreased with age in the skeletal muscles of mice. The conditional loss of Agrin in myogenic progenitors and satellite cells (SCs) (Pax7 Cre:: Agrin flox/flox) causes premature muscle aging, manifesting a distinct sarcopenic phenotype in mice. Conversely, the elevation of a miniaturized form of Agrin in skeletal muscle through adenovirus-mediated gene transfer induces enhanced muscle capacity in aged mice. Mechanistic investigations suggest that Agrin-mediated improvement in muscle function occurs through the stimulation of Yap signaling and the concurrent upregulation of dystroglycan expression. Collectively, our findings underscore the pivotal role of Agrin in the aging process of skeletal muscles and propose Agrin as a potential therapeutic target for addressing sarcopenia.

Quantitative proteome of medulla oblongata in spontaneously hypertensive rats.

We performed an extensive quantitative proteomic analysis on the pooled medulla sample of the 11-week-old spontaneously hypertensive rats (SHR) compared to age-matched normotensive Wistar rats, using iTRAQ technology coupled with nano two-dimentional liquid chromatography followed by high resolution mass spectrometric abundance indexes techniques. Many differentially expressed proteins identified were involved in energy metabolism, such as mitochondrial part, pyruvate dehydrogenase complex, and respiratory chain. These proteins were included in citrate cycle (TCA cycle), pyruvate metabolism and oxidative phosphorylation. The proteomic analysis and subsequent Western blotting on two independent cohorts of animials indicated that the dysregulation of energy metabolism existed in the medulla of the SHR rats. The differentially expressed proteins in the dysregulation of energy metabolism in the medulla of SHR rats included down-regulated ATP6V1D, ATP6VOA1, ATP5L, DLD proteins and up-regulated AK1 protein. MAO-A protein also exhibited decreased regulation, as well as the other 3 above-mentioned energy-relative proteins (ATP6V1D, ATP5L and DLD proteins) belonging to the heterocycle metabolic process. A receiver operating characteristic curve (ROC) analysis on 4 of the differentially expressed proteins respectively resulted in an area under the receiver operating characteristic curve (AUC) of 0.95, 0.90, 0.92, and 0.81 for differentiating the SHR rats from the normotensive rats. This dysfunction in energy metabolism localizes to the medulla, the lower part of brain stem, and is, therefore, likely to contribute to the development, as well as to pathophysiological complications of hypertension.

Intramuscular adipose is derived from a non-Pax3 lineage and required for efficient regeneration of skeletal muscles.

Ectopic accumulation of adipose in the skeletal muscle is associated with muscle wasting, insulin resistance and diabetes. However, the developmental origin of postnatal intramuscular adipose and its interaction with muscle tissue are unclear. We report here that compared to the fast EDL muscles, slow SOL muscles are more enriched with adipogenic progenitors and have higher propensity to form adipose. Using Cre/LoxP mediated lineage tracing in mice, we show that intramuscular adipose in both EDL and SOL muscles is exclusively derived from a Pax3(-) non-myogenic lineage. In contrast, inter-scapular brown adipose is derived from the Pax3(+) lineage. To dissect the interaction between adipose and skeletal muscle tissues, we used Myf5-Cre and aP2-Cre mice in combination with ROSA26-iDTR mice to genetically ablate myogenic and adipogenic cell lineages, respectively. Whereas ablation of the myogenic cell lineage facilitated adipogenic differentiation, ablation of the adipogenic cell lineage surprisingly impaired the regeneration of acutely injured skeletal muscles. These results reveal striking heterogeneity of tissue-specific adipose and a previously unappreciated role of intramuscular adipose in skeletal muscle regeneration.

Haplotype combination of polymorphisms in the ADIPOQ gene promoter is associated with growth traits in Qinchuan cattle.

Adiponectin modulates lipid and glucose metabolism in adipose tissues and is also related to bone metabolism. Polymorphisms in the ADIPOQ gene likely have an impact on growth traits in cattle. In this study, we examined the relationship between ADIPOQ polymorphisms and body measurement parameters in Chinese beef cattle. First, we sequenced ADIPOQ and 1.2 kb of DNA upstream of its promoter, and we found 14 polymorphisms. With the luciferase reporter assay, we showed that the two polymorphisms SNP PR_-135 A>G and PR_-68 G>C, which are located in the core region of promoter, influence promoter activity of ADIPOQ. Second, we identified three haplotypes involved in these two polymorphic sites: A (A-135/C-68), B (A-135/G-68), and C (G-135/G-68). Haplotypes B and C are major haplotypes in five Chinese populations of cattle (Qinchuan, Nanyang, Jiaxian, Hazakh, and Chinese Holstein). We studied the effects of these three haplotypes on body measurements, gene expression, and promoter activity, and we found that the genotypes are associated with body measurement parameters in Qinchuan cattle. Individuals with genotype BC (AG/GG) had significantly higher body height and heart girth than others, and this result may be interpreted by the following two observations. The promoter activity with haplotype B (A/G) is significantly higher than those with A (A/C) and C (G/G) in driving reporter gene transcription; the ADIPOQ mRNA level in cattle with genotype BC (AG/GG) is relatively lower than that in cattle with genotype BB (AA/GG).

SIRT1 gene polymorphisms are associated with growth traits in Nanyang cattle.

Growth is under complex genetic control and uncovering the molecular mechanisms how the genes and polymorphisms affect economic growth traits, are important for successful marker-assisted selection and more efficient management strategies in commercial cattle populations. SIRT1 is a NAD(+)-dependent deacetylase that belongs to the class III histone deacetylases. It plays an important role in numerous fundamental cellular processes including gene silencing, DNA repair, and metabolic regulation. In addition, SIRT1 acts as an inhibitor of adipogenesis and has been associated with body weight regulation. The objective of the present study was to identify single nucleotide polymorphisms (SNPs) of bovine SIRT1 using 1255 animals representing the five main Chinese breeds and to determine if these SNPs are associated with economically important traits in Nanyang cattle. The approach consisted of resequencing SIRT1 using a panel of DNA from unrelated animals of five different breeds and the process revealed five novel SNPs. SNPs g.17324T>C and g.17491G>A exhibited a high degree of linkage disequilibrium in all tested breeds. Seven major haplotypes accounting for 91.2% of the alleles were observed and the haplotype 'GCCGA' was the most common haplotype in NY, QC, LX and JX breeds. An association analysis was performed between the five SNPs and six performance traits. SNP g.-274C>G was demonstrated to have a strong effect on 24-months-old body weight and g.17379A>G polymorphism was related to 6 and 12-months-old body weight in NY population, although these effects did not remained significant after the Bonferroni correction. Our results provide evidence that polymorphisms in SIRT1 are associated with growth efficiency traits, and may be used for marker-assisted selection and management in feedlot cattle.

mRNA expression pattern and association study with growth traits of bovine vaspin gene.

Visceral adipose tissue-derived serine protease inhibitor (vaspin) is an interesting novel adipocytokine with insulin-sensitizing effects. Some studies have suggested that vaspin could play an important role in the development of obesity and metabolic disorders. However, the tissue expression patterns in cattle and impact of vaspin gene variants on the growth traits has not been determined yet. Herein, we firstly investigated the tissue expression patterns of vaspin gene in new born and adult cattle. The results showed that vaspin was ubiquitously expressed in most tissues and strongly expressed in the heart, skeletal muscle and fat. Then, genetic variants within bovine vaspin gene were screened in 1235 individuals from five Chinese indigenous cattle breeds. Two novel mutations in coding region (NW_001494061: g.1124477 G>A and g.1118561 T>C) of bovine vaspin gene were identified using MspI PCR-RFLP and HhaI ACRS PCR-RFLP detection. Association analysis revealed both two mutations were significantly associated with bodyweight and chest girth at 24 months in cattle (P < 0.05). Therefore, the MspI and HhaI genetic variants of bovine vaspin gene were recommended as DNA markers related to growth traits through marker-assisted selection for genetics and breeding in cattle.

[Effect of needling at waiguan (SJ5) on brain glucose metabolism in patients with cerebral infarction].

OBJECTIVE: To observe changes of brain glucose metabolism by needling at Waiguan (SJ5) in cerebral infraction (CI) patients using 18F-fluorodeoxyglucose (FDG) positron-emission computer tomography (PET/CT), thus exploring its effect and mechanisms. METHODS: A total of 21 patients with CI were recruited in this study. The location of lesion was limited to the left basal ganglia by CT or MRI scan. All patients were randomly assigned to three groups. i.e., the acupoint group (Group A), the non-acupoint group (Group B), the blank control group (Group C), 7 in each group. Patients in Group A were needled at right Waiguan (SJ5). Those in Group B were needled at non-acupoint [10 mm beside Waiguan (SJ5)], whereas those in Group C did not receive any treatment. All patients underwent PET/CT head scan. All data were statistically analyzed using SPSS 13.0 Software and SPM8 Software. RESULTS: Compared with Group C, glucose metabolism increased in bilateral superior temporal gyrus (BA38), right superior frontal gyrus (BA9), left cingulate gyrus (BA24), left culmen and pyramid of cerebellum, and right cerebellar tonsil of cerebellum in Group A. Compared with Group C, glucose metabolism increased in bilateral superior frontal gyrus (BA6, BA9, BA10), bilateral middle frontal gyrus (BA6, BA10), left middle frontal gyrus (BA4), bilateral uncus of limbic lobe (BA36, BA38), left cingulate gyrus (BA24, BA31), left posterior cingulate gyrus (BA30), left precuneus (BA7), left inferior parietal lobule (BA4), and left lingual gyrus of occipital lobe (BA18) in Group B. Compared with Group B, glucose metabolism increased in bilateral superior temporal gyrus (BA22, BA38), right inferior frontal gyrus (BA47), left culmen and cerebellar tonsil of cerebellum in Group A. Activated encephalic regions of needling at Waiguan (SJ5) were mainly dominated in the healthy side, bilateral superior temporal gyrus, and right inferior frontal gyrus. Activated encephalic regions of cerebellum were located at the left cerebellar hemisphere, left culmen of anterior cerebella lobe, and bilateral cerebellar tonsil of posterior cerebella lobe. CONCLUSIONS: Needling at Waiguan (SJ5) of CI patients induced increased glucose metabolism in local cerebral regions. Functional neuroimaging using PET/CT could directly reflect changes of brain glucose metabolism by acupuncture.

The role of Rapsyn in neuromuscular junction and congenital myasthenic syndrome.

Rapsyn, an intracellular scaffolding protein associated with the postsynaptic membranes in the neuromuscular junction (NMJ), is critical for nicotinic acetylcholine receptor clustering and maintenance. Therefore, Rapsyn is essential to the NMJ formation and maintenance, and Rapsyn mutant is one of the reasons causing the pathogenies of congenital myasthenic syndrome (CMS). In addition, there is little research on Rapsyn in the central nervous system (CNS). In this review, the role of Rapsyn in the NMJ formation and the mutation of Rapsyn leading to CMS will be reviewed separately and sequentially. Finally, the potential function of Rapsyn is prospected.