Brain control of humoral immune responses amenable to behavioural modulation.

It has been speculated that brain activities might directly control adaptive immune responses in lymphoid organs, although there is little evidence for this. Here we show that splenic denervation in mice specifically compromises the formation of plasma cells during a T cell-dependent but not T cell-independent immune response. Splenic nerve activity enhances plasma cell production in a manner that requires B-cell responsiveness to acetylcholine mediated by the α9 nicotinic receptor, and T cells that express choline acetyl transferase1,2 probably act as a relay between the noradrenergic nerve and acetylcholine-responding B cells. We show that neurons in the central nucleus of the amygdala (CeA) and the paraventricular nucleus (PVN) that express corticotropin-releasing hormone (CRH) are connected to the splenic nerve; ablation or pharmacogenetic inhibition of these neurons reduces plasma cell formation, whereas pharmacogenetic activation of these neurons increases plasma cell abundance after immunization. In a newly developed behaviour regimen, mice are made to stand on an elevated platform, leading to activation of CeA and PVN CRH neurons and increased plasma cell formation. In immunized mice, the elevated platform regimen induces an increase in antigen-specific IgG antibodies in a manner that depends on CRH neurons in the CeA and PVN, an intact splenic nerve, and B cell expression of the α9 acetylcholine receptor. By identifying a specific brain-spleen neural connection that autonomically enhances humoral responses and demonstrating immune stimulation by a bodily behaviour, our study reveals brain control of adaptive immunity and suggests the possibility to enhance immunocompetency by behavioural intervention.

Protective effects of curcumin on desipramine-induced islet ß-cell damage via AKAP150/PKA/PP2B complex.

Tricyclic antidepressants (TCAs) are widely used to treat depression and anxiety-related mood disorders. But evidence shows that TCAs elevate blood glucose levels and inhibit insulin secretion, suggesting that TCAs are a risk factor, particularly for individuals with diabetes. Curcumin is a bioactive molecule from the rhizome of the Curcuma longa plant, which has shown both antidepressant and anti-diabetic activities. In the present study, we investigated the protective effect of curcumin against desipramine-induced apoptosis in ß cells and the underlying molecular mechanisms. In the mouse forced swimming test (FST), we found that lower doses of desipramine (5 and 10 mg/kg) or curcumin (2.5 mg/kg) alone did not affect the immobility time, whereas combined treatment with curcumin (2.5 mg/kg) and desipramine (5, 10 mg/kg) significantly decreased the immobility time. Furthermore, desipramine dose-dependently inhibited insulin secretion and elevated blood glucose levels, whereas the combined treatment normalized insulin secretion and blood glucose levels. In RIN-m5F pancreatic ß-cells, desipramine (10 µM) significantly reduced the cell viability, whereas desipramine combined with curcumin dose-dependently prevented the desipramine-induced impairment in glucose-induced insulin release, most effectively with curcumin (1 and 10 µM). We demonstrated that desipramine treatment promoted the cleavage and activation of Caspase 3 in RIN-m5F cells. Curcumin treatment inhibited desipramine-induced apoptosis, increased mitochondrial membrane potential and Bcl-2/Bax ratio. Desipramine increased the generation of reactive oxygen species, which was reversed by curcumin treatment. Curcumin also inhibited the translocation of forkhead box protein O1 (FOXO1) from the cytoplasm to the nucleus and suppressed the binding of A-kinase anchor protein 150 (AKAP150) to protein phosphatase 2B (PP2B, known as calcineurin) that was induced by desipramine. These results suggest that curcumin protects RIN-m5F pancreatic ß-cells against desipramine-induced apoptosis by inhibiting the phosphoinositide 3-kinase/AKT/FOXO1 pathway and the AKAP150/PKA/PP2B interaction. This study suggests that curcumin may have therapeutic potential as an adjunct to antidepressant treatment.

Staggered Assembly of a Dimeric Au13 Cluster: Impacts on Coupling of Geometric Isomerism.

The specific states of aggregation of metal atoms in sub-nanometer-sized gold clusters are related to the different quantum confinement volumes of electrons, leading to novel optical and electronic properties. These volumes can be tuned by changing the relative positions of the gold atoms to generate isomers. Studying the isomeric gold core and the electron coupling between the basic units is fundamentally important for nanoelectronic devices and luminescence; however, appropriate cases are lacking. In this study, the structure of the first staggered di-superatomic Au25 -S was solved using single-crystal X-ray diffraction. The optical properties of Au25 -S were studied by comparing with eclipsed Au25 -E. From Au25 -E to Au25 -S, changes in the electronic structures occurred, resulting in significantly different optical absorptions originating from the coupling between the two Au13 modules. Au25 -S shows a longer electron decay lifetime of 307.7 ps before populating the lowest triplet emissive state, compared to 1.29 ps for Au25 -E. The experimental and theoretical results show that variations in the geometric isomerism lead to distinct photophysical processes owing to isomerism-dependent electronic coupling. This study offers new insights into the connection between the geometric isomerism of nanosized building blocks and the optical properties of their assemblies, opening new possibilities for constructing function-specific nanomaterials.

Comprehensive transcriptomic profiling and mutational landscape of primary gastric linitis plastica.

BACKGROUND: Primary gastric linitis plastica (GLP) is a distinct phenotype of gastric cancer with poor survival. Comprehensive molecular profiles and putative therapeutic targets of GLP remain undetermined. METHODS: We subjected 10 tumor-normal tissue pairs to whole exome sequencing (WES) and whole transcriptome sequencing (WTS). 10 tumor samples were all GLP which involves 100% of the gastric wall macroscopically. TCGA data were compared to generate the top mutated genes and the overexpressed genes in GLP. RESULTS: Our results reveal that GLP has distinctive genomic and transcriptomic features, dysfunction in the Hippo pathway is likely to be a key step during GLP development. 6 genes were identified as significantly highly mutated genes in GLP, including AOX1, ANKRD36C, CPXM1, PTPN14, RPAP1, and DCDC1). MUC6, as a previously identified gastric cancer driver gene, has a high mutation rate (20%) in GLP. 20% of patients in our GLP cohort had CDH1 mutations, while none had RHOA mutations. GLP exhibits high immunodeficiency and low AMPK pathway activity. Our WTS results showed that 3 PI3K-AKT pathway-related genes (PIK3R2, AKT3, and IGF1) were significantly up-regulated in GLP. Two genes were identified using immunohistochemistry (IHC), IGF2BP3 and MUC16, which specifically expressed in diffuse-type-related gastric cancer cell lines, and its knockdown inhibits PI3K-AKT pathway activity. CONCLUSIONS: We provide the first integrative genomic and transcriptomic profiles of GLP, which may facilitate its diagnosis, prognosis, and treatment.

Construction of a mouse model of Posner-Schlossman syndrome by anterior chamber infection with cytomegalovirus.

Accumulated clinical evidence has shown that Posner-Schlossman syndrome (PSS) is most likely the result of recurrent human cytomegalovirus (HCMV) infection in the anterior chamber (AC). Establishing an animal model is necessary to investigate the pathogenesis of PSS. In this study, we constructed a mouse model of (PSS) by injecting murine cytomegalovirus (MCMV) into the AC of BALB/c mice. Twenty-five BALB/c mice were divided into 5 groups. Smith strain MCMV expressing enhanced green fluorescent protein (EGFP) was passaged with mouse embryonic fibroblast (MEF). Right eyes in the 4 experiment groups received AC injection of 1 µL of virus solution with concentrations of 103,104,105,106 pfu/mL respectively, and the control group received only PBS. PSS-like signs (mutton-fat keratic precipitates (KP), pupil dilation, IOP elevation and corneal edema) were recorded 0-28 days post-injection (DPI). Sections of eyeballs from another 9 mice harvested on 0,10 and 28 DPI were examined to locate KP and the fluorescence signal of the virus. Reversible PSS-like signs except KP were observed in 20% and 60% mice of 104 and 105 groups while no PSS-like signs in the control and 103 group; 80% in the 106 group with partially unreversible signs till 28DPI. Much More fluorescent signals of virus in the iris and KP were found on 10DPI than 28 DPI, while no fluorescent signals and KP on 0DPI. The extent of PSS-like signs (pupil dilation, IOP elevation and corneal edema) was virus concentration-dependent (Spearman correlation coefficient, r = 0.830, = 0.475, = 0.662, p < 0.0001, <0.05, <0.001, respectively, n = 25). Success rate of PSS model (mice with PSS-like signs) was also virus concentration-dependent (Chi-square trend test, χ2 = 6.828, df = 1, p < 0.01, n = 25). Our results indicate that AC injection of 1 µL MEF passaged MCMV (Smith strain) of 104-106 pfu/mL in BALB/c mice can be used to construct a mouse model of PSS. MCMV can infect iris tissue and replicate in it and then establish latency. This might account for the recurrent and self-limited nature of PSS.

Organizational principles of amygdalar input-output neuronal circuits.

The amygdala, one of the most studied brain structures, integrates brain-wide heterogeneous inputs and governs multidimensional outputs to control diverse behaviors central to survival, yet how amygdalar input-output neuronal circuits are organized remains unclear. Using a simplified cell-type- and projection-specific retrograde transsynaptic tracing technique, we scrutinized brain-wide afferent inputs of four major output neuronal groups in the amygdalar basolateral complex (BLA) that project to the bed nucleus of the stria terminals (BNST), ventral hippocampus (vHPC), medial prefrontal cortex (mPFC) and nucleus accumbens (NAc), respectively. Brain-wide input-output quantitative analysis unveils that BLA efferent neurons receive a diverse array of afferents with varied input weights and predominant contextual representation. Notably, the afferents received by BNST-, vHPC-, mPFC- and NAc-projecting BLA neurons exhibit virtually identical origins and input weights. These results indicate that the organization of amygdalar BLA input-output neuronal circuits follows the input-dependent and output-independent principles, ideal for integrating brain-wide diverse afferent stimuli to control parallel efferent actions. The data provide the objective basis for improving the virtual reality exposure therapy for anxiety disorders and validate the simplified cell-type- and projection-specific retrograde transsynaptic tracing method.

Ultrathin In-Plane Heterostructures for Efficient CO2 Chemical Fixation.

Chemical fixation of carbon dioxide (CO2 ) into value-added organics is regarded as a competitive and viable method in large scale industrial production, during which the catalysts with promoting CO2 activation ability are needed. Herein, we proposed an in-plane heterostructure strategy to construct Lewis acid-base sites for efficient CO2 activation. By taking ultrathin in-plane Cu2 O/Cu heterostructures as a prototype, we show that Lewis acid-base sites on heterointerface can facilitate a mixed C and O dual coordination on surface, which not only strengthen CO2 adsorption, but also effectively activate the inert molecules. As revealed by in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) and quasi in situ X-ray photoelectron spectroscopy (XPS), Lewis acid-base sites could readily activate CO2 to . CO2 - species, which is the key intermediate radical for CO2 fixation. As a result, abundant Lewis acid-base sites endow Cu2 O/Cu nanosheets with excellent performances for dimethyl carbonate generation, a high conversion yield of 28 % with nearly 100 % selectivity under mild conditions. This study provides a model structure for CO2 fixation reactions.

Exciton-Mediated Energy Transfer in Heterojunction Enables Infrared Light Photocatalysis.

Although a few semiconductors can directly absorb infrared light, their intrinsic properties like improper band-edge position and strong electron-hole interaction restrict further photocatalytic applications. Herein, we propose an exciton-mediated energy transfer strategy for realizing efficient infrared light response in heterostructures. Using black phosphorous/polymeric carbon nitride (BP/CN) heterojunction, CN could be indirectly excited by infrared light with the aid of nonradiatively exciton-based energy transfer from BP. At the same time, excitons are dissociated into free charge carriers at the interface of BP/CN heterojunction, followed by hole injection to BP and electron retainment in CN. As a result of these unique photoexcitation processes, BP/CN heterojunction exhibits promoted conversion rate and selectivity in amine-amine oxidative coupling reaction even under infrared light irradiation. This study opens a new way for the design of efficient infrared light activating photocatalysts.

Sulfonic Groups Lined along Channels of Metal-Organic Frameworks (MOFs) for Super-Proton Conductor.

Designing high-performance proton-conducting metal-organic frameworks simultaneously having highly hydrothermal stability and a high-density proton carrier remains a great challenge. Fe-MIL-88B is a classic metal-organic framework (MOF) with a large-size one-dimensional (1D) channel lined with a high-density uncoordinated metal atom for postfunctionalization; however this MOF cannot act as a proton conductor due to the weak hydrothermal stability. Here, we prepared an ultrastable isostructure Cr-MIL-88B, which is subsequently functionalized by anchoring 3-pyridinesulfonic acid and 2-(4-pyridyl) ethanesulfonic acid on the naked Cr atoms exposed on the surface of the host-framework, producing two new MOFs, i.e. Cr-MIL-88B-pyridine sulfonic acid (abbreviated as Cr-MIL-88B-PSA) and Cr-MIL-88B-pyridine ethanesulfonic acid (abbreviated as Cr-MIL-88B-PESA). Thus, Cr atoms on the host framework were modified by functional sulfonic groups, which stick out toward the center of the channel forming ordered high-density sulfonic groups as proton donors along the open channel and achieving the highest proton conductivity of 4.50 × 10-2 S cm-1 for Cr-MIL-88B-PESA and 1.58 × 10-1 S cm-1 for Cr-MIL-88B-PSA, surpassing that of the Nafion membrane.

Excitonic Effects in Polymeric Photocatalysts.

Owing to the intrinsically low dielectric properties, robust Coulomb interactions between photoinduced electrons and holes lead to dramatically strong exciton effects in polymeric photocatalysts. Such effects endow polymeric matrixes with nontrivial photoexcitation processes determining photocatalytic energy utilization. In this Minireview, we describe recent progress in the investigation of the excitonic effect in polymeric photocatalysts. On the basis of the understanding of excitonic effects in polymeric systems, we outline the relationships between excitonic behaviors and photocatalytic performance. Advances in optimizing the excitonic effect for gaining high-efficiency polymer-based photocatalysis are summarized. We also discuss the challenges in the field and forecast the directions for future research.

Extra Silver Atom Triggers Room-Temperature Photoluminescence in Atomically Precise Radarlike Silver Clusters.

Luminescent metal clusters show promise for applications in imaging and sensing. However, promoting emission from metal clusters at room temperature is a challenging task owing to the lack of an efficient approach to suppress the nonradiative decay process in metal cores. We report herein that the addition of a silver atom into a metal interstice of the radarlike thiolated silver cluster [Ag27 (St Bu)14 (S)2 (CF3 COO)9 (DMAc)4 ]⋅DMAc (NC1, DMAc=dimethylacetamide), which is non-emissive under ambient conditions, produced another silver cluster [Ag28 (AdmS)14 (S)2 (CF3 COO)10 (H2 O)4 ] (NC2) that displayed bright green room-temperature photoluminescence aided by the new ligand 1-adamantanethiol (AdmSH). The 28th Ag atom, which hardly affects the geometrical and electronic structures of the Ag-S skeleton, triggered the emission of green light as a result of the rigidity of the cluster structure.

Corticosterone Signaling and a Lateral Habenula-Ventral Tegmental Area Circuit Modulate Compulsive Self-Injurious Behavior in a Rat Model.

Self-injurious behavior (SIB) is commonly observed in patients with neuropsychiatric disorders, as well as in nonclinical populations with stress-related mental-health problems. However, the exact circuitry mechanisms underlying SIB have remained poorly understood. Here, with bilateral injection of muscimol into the entopeduncular nucleus (EP), we established a rat model of SIB. Following the muscimol injection, the male rats exhibited in a dose-dependent manner stereotypic self-biting behavior that lasted for hours and often resulted in wounds of various severities. The SIB was associated with an elevated level of serum corticosterone and could be exacerbated by enhancing the corticosterone signaling and, conversely, alleviated by inhibiting the corticosterone signaling. Activity mapping using c-fos immunostaining, combined with connectivity mapping using herpes simplex virus-based anterograde tracing from the EP and pseudorabies virus-based retrograde tracing from the masseter muscle, revealed the potential involvement of many brain areas in SIB. In particular, the lateral habenula (LHb) and the ventral tegmental area (VTA), the two connected brain areas involved in stress response and reward processing, showed a significant increase in neuronal activation during SIB. Furthermore, suppressing the LHb activity or modulating the GABAergic transmission in the VTA could significantly reduce the occurrence of SIB. These results demonstrate the importance of stress hormone signaling and the LHb-VTA circuit in modulating SIB resulting from EP malfunction, and suggest potential targets for therapeutic intervention of SIB and related disorders.SIGNIFICANCE STATEMENT Self-injurious behavior (SIB) occurs in ∼4% of the general population, with substantially higher occurrence among adolescents and patients of neuropsychiatric disorders. Stress has been linked to the occurrence of SIB, yet the underlying mechanisms have remained unclear. Using a rat model of SIB induced by disruption of activity in the entopeduncular nucleus (EP), we found that the behavior is regulated by stress and linked to corticosterone signaling. Viral tracing and c-fos immunostaining revealed the involvement of various subcortical areas, especially the EP-lateral habenula (LHb)-ventral tegmental area (VTA) circuit, in SIB. Furthermore, regulating activity in the LHb or the VTA alleviates SIB. These results may have implications in the development of new strategies for treating SIB.

Enhanced Superoxide Generation on Defective Surfaces for Selective Photooxidation.

Photocatalytic selective oxidation reactions hold great promise for the design of high-value-added organic intermediates, but many of these reactions suffer from low conversion efficiency and selectivity due to uncontrollable oxidation processes. In view of using photogenerated reactive oxygen species as the key oxidant in a selective oxidation reaction, we propose that a highly selective oxidation reaction can be achieved by modulating the corresponding photocatalytic molecular oxygen (O2) activation processes. Using cubic indium sulfide (ß-In2S3) nanosheets as a model system, we show that the charge carriers involved in O2 activation can be optimized with the introduction of surface S vacancies. Benefiting from the enhanced charge separation and transfer processes, the In2S3 nanosheets with S vacancies could simultaneously activate O2 into superoxide radicals via electron transfer under visible-light irradiation to display outstanding activity for the selective oxidation of alcohols to aldehydes with high conversion and selectivity. This study offers a new strategy to optimize photocatalytic selective oxidation reactions.

Quantitative proteomics study of host response to virulent and attenuated pseudorabies virus infection in mouse brain.

Bartha, the pseudorabies virus (PRV) vaccine strain, is widely used in studies of neuronal circuit-tracing, due to its attenuated virulence and retrograde spreading. However, we know little regarding the molecular mechanisms of PRV infection and spreading between structurally connected neurons. In this study, we systematically analyzed the host brain proteomes after acute infection with PRV, attempting to identified the proteins involved in the processes. Mice were injected with PRV-Bartha and PRV-Becker (PRV-Bartha's wild-type parent strain) in the olfactory system, the proteomes of the brain and synaptosome were analyzed and compared at various infection intervals using mass spectrometry-based proteomics techniques. In all, we identified >100 PRV-infection regulated proteins at the whole-tissue level and the synaptosome level. While at whole-tissue level, bioinformatics analyses mapped most of the regulations to the inflammation pathways, at the synaptosome level, most of those to synaptic transmission, cargo transport and cytoskeleton organization. We established regulated protein networks demonstrating distinct cellular regulation pattern between the global and the synaptosome levels. Moreover, we identified a series of potentially PRV-strain-specific regulated proteins with diverse biological functions. This study may provide new clues for molecular mechanisms for PRV infection and spread.

Self-Assembly of a Stable Silver Thiolate Nanocluster Encapsulating a Lacunary Keggin Phosphotungstate Anion.

A polyoxometalate-templated silver(I) thiolate nanocluster has been synthesized by a one-pot reaction in high yield. This novel and stable nanocluster exhibits a core-shell structure with a Ag67S36 shell and two lacunary Keggin [PW9O34]9- cores, which is fully characterized by X-ray crystallography, X-ray photoelectron spectroscopy, UV-vis, powder X-ray diffraction, and cyclic voltammetry.

SRC2-1 is required in PcINF1-induced pepper immunity by acting as an interacting partner of PcINF1.

Elicitins are elicitors that can trigger hypersensitive cell death in most Nicotiana spp., but their underlying molecular mechanism is not well understood. The gene Phytophthora capsici INF1 (PcINF1) coding for an elicitin from P. capsici was characterized in this study. Transient overexpression of PcINF1 triggered cell death in pepper (Capsicum annuum L.) and was accompanied by upregulation of the hypersensitive response marker, Hypersensitive Induced Reaction gene 1 (HIR1), and the pathogenesis-related genes SAR82, DEF1, BPR1, and PO2. A putative PcINF1-interacting protein, SRC2-1, was isolated from a pepper cDNA library by yeast two-hybrid screening and was observed to target the plasma membrane. The interaction between PcINF1 and SRC2-1 was confirmed by bimolecular fluorescence complementation and co-immunoprecipitation. Simultaneous transient overexpression of SRC2-1 and PcINF1 in pepper plants triggered intensive cell death, whereas silencing of SRC2-1 by virus-induced gene silencing blocked the cell death induction of PcINF1 and increased the susceptibility of pepper plants to P. capsici infection. Additionally, membrane targeting of the PcINF1-SRC2-1 complex was required for cell death induction. The C2 domain of SRC2-1 was crucial for SRC2-1 plasma membrane targeting and the PcINF1-SRC2-1 interaction. These results suggest that SRC2-1 interacts with PcINF1 and is required in PcINF1-induced pepper immunity.

Antiproliferative and apoptosis-inducing activity of schisandrin B against human glioma cells.

BACKGROUND: Malignant glioma is the most devastating and aggressive tumour in the brain and is characterised by high morbidity, high mortality and extremely poor prognosis. The main purpose of the present study was to investigate the effects of schisandrin B (Sch B) on glioma cells both in vitro and in vivo and to explore the possible anticancer mechanism underlying Sch B-induced apoptosis and cell cycle arrest. METHODS: The anti-proliferative ability of Sch B on glioma cells were assessed by MTT and clony formation assays. Flow cytometric analysis was used to detect cell cycle changes. Apoptosis was determined by Hoechst 33342 staining and annexin V/PI double-staining assays. The mitochondrial membrane potential was detected by Rhodamine 123 staining. The in vivo efficacy of Sch B was measured using a U87 xenograft model in nude mice. The expressions of the apoptosis-related and cell cycle-related proteins were analysed by western blot. Student's t-test was used to compare differences between treated groups and their controls. RESULTS: We found that Sch B inhibited growth in a dose- and time-dependent manner as assessed by MTT assay. In U87 and U251 cells, the number of clones was strongly suppressed by Sch B. Flow cytometric analysis revealed that Sch B induced cell cycle arrest in glioma cells at the G0/G1 phase. In addition, Sch B induced glioma cell apoptosis and reduced mitochondrial membrane potential (ΔΨm) in a dose-dependent manner. Mechanically, western blot analysis indicated that Sch B induced apoptosis by caspase-3, caspase-9, PARP, and Bcl-2 activation. Moreover, Sch B significantly inhibited tumour growth in vivo following the subcutaneous inoculation of U87 cells in athymic nude mice. COCLUSIONS: In summary, Sch B can reduce cell proliferation and induce apoptosis in glioma cells and has potential as a novel anti-tumour therapy to treat gliomas.

Lateral entorhinal modulation of piriform cortical activity and fine odor discrimination.

The lateral entorhinal cortex (LEC) receives direct input from olfactory bulb mitral cells and piriform cortical pyramidal cells and is the gateway for olfactory input to the hippocampus. However, the LEC also projects back to the piriform cortex and olfactory bulb. Activity in the LEC is shaped by input from the perirhinal cortices, hippocampus, and amygdala, and thus could provide a rich contextual modulation of cortical odor processing. The present study further explored LEC feedback to anterior piriform cortex by examining how LEC top-down input modulates anterior piriform cortex odor evoked activity in rats. Retrograde viral tracing confirmed rich LEC projections to both the olfactory bulb and piriform cortices. In anesthetized rats, reversible lesions of the ipsilateral LEC increased anterior piriform cortical single-unit spontaneous activity. In awake animals performing an odor discrimination task, unilateral LEC reversible lesions enhanced ipsilateral piriform cortical local field potential oscillations during odor sampling, with minimal impact on contralateral activity. Bilateral LEC reversible lesions impaired discrimination performance on a well learned, difficult odor discrimination task, but had no impact on a well learned simple odor discrimination task. The simple discrimination task was impaired by bilateral reversible lesions of the anterior piriform cortex. Given the known function of LEC in working memory and multisensory integration, these results suggest it may serve as a powerful top-down modulator of olfactory cortical function and odor perception. Furthermore, the results provide potential insight into how neuropathology in the entorhinal cortex could contribute to early olfactory deficits seen in Alzheimer's disease.

Variations in energy metabolism along the pericardium meridian and its relationship with visceral function adjustments during electroacupuncture.

BACKGROUND: Electroacupuncture (EA) is a traditional Chinese medicine treatment guided by meridian theory. As it gradually gains more worldwide acceptance, a clarification of its mechanisms is extremely urgent. We observed variations in transcutaneous oxygen pressure/carbon dioxide pressure (tcpO2/tcpCO2) and microcirculation blood perfusion units (BPU) along the pericardium meridian, and cardiac function during EA at Neiguan (PC6) to explore variations in energy metabolism and its relationship with visceral function adjustments during EA. METHODS: Twenty-two healthy volunteers participated in this study. Three channel laser Doppler flowmetry and tcpO2/tcpCO2 detection systems were used to detect tcpO2/tcpCO2 and microcirculation BPU along the pericardium meridian. A hemodynamic monitor was used to detect cardiac function. RESULTS: In the normal state, the microcirculatory BPU along the pericardium meridian were significantly higher than that of their bilateral corresponding control points (p < 0.05). During EA at PC6, the values of the microcirculatory BPU along the pericardium meridian did not vary, and few increased. In the normal state, the values of tcpO2 along the pericardium meridian were significantly higher than those of their bilateral corresponding control points (p < 0.05). In addition, the values of tcpCO2 along the pericardium meridian were lower than those of their bilateral corresponding control points. In comparison with the normal state, EA could decrease tcpO2 along the meridian significantly (p < 0.05) and increase tcpCO2. During EA at PC6 in healthy volunteers treated by artificial acute mild hypoxia, cardiac output and cardiac index (p < 0.05) decreased and systemic vascular resistance increased significantly (p < 0.05). CONCLUSIONS: In the normal state, the values of microcirculatory BPU and tcpO2 along the pericardium meridian were both higher than those of their bilateral corresponding control points. Energy metabolism was vigorous along the meridian. During EA, the decrease in oxygen partial pressure along the pericardium meridian might be a result of strengthened energy metabolism of associated tissue and increased oxygen consumption. The variations in energy metabolism along the pericardium meridian during the course of EA had a close relationship with visceral function adjustments. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTRTRC13003193.