A combination influenza mRNA vaccine candidate provided broad protection against diverse influenza virus challenge.

Influenza viruses present a significant threat to global health. The production of a universal vaccine is considered essential due to the ineffectiveness of current seasonal influenza vaccines against mutant strains. mRNA technology offers new prospects in vaccinology, with various candidates for different infectious diseases currently in development and testing phases. In this study, we encapsulated a universal influenza mRNA vaccine. The vaccine encoded influenza hemagglutinin (HA), nucleoprotein (NP), and three tandem repeats of matrix protein 2 (3M2e). Twice-vaccinated mice exhibited strong humoral and cell-mediated immune responses in vivo. Notably, these immune responses led to a significant reduction in viral load of the lungs in challenged mice, and also conferred protection against future wild-type H1N1, H3N2, or H5N1 influenza virus challenges. Our findings suggest that this mRNA-universal vaccine strategy for influenza virus may be instrumental in mitigating the impact of future influenza pandemics.

Enhanced NK cell activation via eEF2K-mediated potentiation of the cGAS-STING pathway in hepatocellular carcinoma.

BACKGROUND: Liver cancer, particularly hepatocellular carcinoma (HCC), is characterized by a high mortality rate, attributed primarily to the establishment of an immunosuppressive microenvironment. Within this context, we aimed to elucidate the pivotal role of eukaryotic elongation factor 2 kinase (eEF2K) in orchestrating the infiltration and activation of natural killer (NK) cells within the HCC tumor microenvironment. By shedding light on the immunomodulatory mechanisms at play, our findings should clarify HCC pathogenesis and help identify potential therapeutic intervention venues. METHODS: We performed a comprehensive bioinformatics analysis to determine the functions of eEF2K in the context of HCC. We initially used paired tumor and adjacent normal tissue samples from patients with HCC to measure eEF2K expression and its correlation with prognosis. Subsequently, we enrolled a cohort of patients with HCC undergoing immunotherapy to examine the ability of eEF2K to predict treatment efficacy. To delve deeper into the mechanistic aspects, we established an eEF2K-knockout cell line using CRISPR/Cas9 gene editing. This step was crucial for verifying activation of the cGAS-STING pathway and the subsequent secretion of cytokines. To further elucidate the role of eEF2K in NK cell function, we applied siRNA-based techniques to effectively suppress eEF2K expression in vitro. For in vivo validation, we developed a tumor-bearing mouse model that enabled us to compare the infiltration and activation of NK cells within the tumor microenvironment following various treatment strategies. RESULTS: We detected elevated eEF2K expression within HCC tissues, and this was correlated with an unfavorable prognosis (30.84 vs. 20.99 months, P = 0.033). In addition, co-culturing eEF2K-knockout HepG2 cells with dendritic cells led to activation of the cGAS-STING pathway and a subsequent increase in the secretion of IL-2 and CXCL9. Moreover, inhibiting eEF2K resulted in notable NK cell proliferation along with apoptosis reduction. Remarkably, after combining NH125 and PD-1 treatments, we found a significant increase in NK cell infiltration within HCC tumors in our murine model. Our flow cytometry analysis revealed reduced NKG2A expression and elevated NKG2D expression and secretion of granzyme B, TNF-α, and IFN-γ in NK cells. Immunohistochemical examination confirmed no evidence of damage to vital organs in the mice treated with the combination therapy. Additionally, we noted higher levels of glutathione peroxidase and lipid peroxidation in the peripheral blood serum of the treated mice. CONCLUSION: Targeted eEF2K blockade may result in cGAS-STING pathway activation, leading to enhanced infiltration and activity of NK cells within HCC tumors. The synergistic effect achieved by combining an eEF2K inhibitor with PD-1 antibody therapy represents a novel and promising approach for the treatment of HCC.

NLRP6 deficiency suppresses colorectal cancer liver metastasis growth by modulating M-MDSC-induced immunosuppressive microenvironment.

Colorectal cancer liver metastasis (CRLM) a profound influence on the prognosis of patients with colorectal cancer (CRC), prompting a comprehensive inquiry into its underlying mechanisms. Amidst the multifaceted tumor microenvironment, myeloid-derived suppressor cells (MDSCs) have emerged as pivotal orchestrators of immune modulation. However, their specific contributions to the CRLM have not been explored. The role of NLRP6, a member of the NOD-like receptor family, is of interest. Employing a liver metastasis model, our investigation revealed a heightened accumulation of monocytic MDSCs (M-MDSCs) within metastatic sites, culminating in an immunosuppressive milieu characterized by depleted CD8+ T cell populations. Remarkably, the absence of NLRP6 disrupts this intricate immunosuppressive network, highlighting its nuanced role in sculpting the trajectory of CRLM. This study elucidates the interplay between NLRP6 and MDSCs, potentially guiding novel therapeutic strategies to recalibrate the immune microenvironment in CRLM and enhance patient outcomes.

An Engineered Influenza a Virus Expressing the Co-Stimulator OX40L as an Oncolytic Agent Against Hepatocellular Carcinoma.

Background: Oncolytic virus (OV) therapy has emerged as a promising novel form of immunotherapy. Moreover, an increasing number of studies have shown that the therapeutic efficacy of OV can be further improved by arming OVs with immune-stimulating molecules. Methods: In this study, we used reverse genetics to produce a novel influenza A virus, termed IAV-OX40L, which contained the immune-stimulating molecule OX40L gene in the influenza virus nonstructural (NS1) protein gene. The oncolytic effect of IAV-OX40L was explored on hepatocellular carcinoma (HCC)HCC cells in vitro and in vivo. Results: Hemagglutination titers of the IAV-OX40L virus were stably 27-28 in specific-pathogen-free chicken embryos. The morphology and size distribution of IAV-OX40L are similar to those of the wild-type influenza. Expression of OX40L protein was confirmed by Western blot and immunofluorescence. MTS assays showed that the cytotoxicity of IAV-OX40L was higher in HCC cells (HepG2 and Huh7) than in normal liver cells (MIHA) in a time- and dose-dependent manner in vitro. We found that intratumoral injection of IAV-OX40L reduced tumor growth and increased the survival rate of mice compared with PR8-treated controls in vivo. In addition, the pathological results showed that IAV-OX40L selectively destroyed tumor tissues without harming liver and lung tissues. CD4+ and CD8+ T cells of the IAV-OX40L group were significantly increased in the splenic lymphocytes of mice. Further validation confirmed that IAV-OX40L enhanced the immune response mainly by activating Th1-dominant immune cells, releasing interferon-γ and interleukin-2. Conclusion: Taken together, our findings demonstrate the novel chimeric influenza OV could provide a potential therapeutic strategy for combating HCC and improve the effectiveness of virotherapy for cancer therapy.

A Recombinant Oncolytic Influenza Virus Carrying GV1001 Triggers an Antitumor Immune Response.

Oncolytic viruses are able to lyse tumor cells selectively in the liver without killing normal hepatocytes, in addition to activating the immune response. Oncolytic virus therapy is expected to revolutionize the treatment of liver cancer, including hepatocellular carcinoma (HCC), one of the most frequent and fatal malignancies. In this study, reverse genetics techniques were exploited to load NA fragments of the A/PuertoRico/8/34 virus (PR8) with GV1001 peptides derived from human telomerase reverse transcriptase. An in vitro assessment of the therapeutic effect of the recombinant oncolytic virus was followed by an in vivo study in mice with HCC. The recombinant virus was verified by sequencing of the recombinant viral gene sequence, and viral virulence was detected by hemagglutination assays and based on the 50% tissue culture infectious dose (TCID50). The morphological structure of the virus was observed by electron microscopy, and GV1001 peptide was localized by cellular immunofluorescence. The selective cytotoxicity of the recombinant oncolytic virus in vitro was demonstrated in cultured HCC cells and normal hepatocytes, as only the tumor cells were killed; the normal cells were not significantly altered. Consistent with the in vitro results, the recombinant oncolytic influenza virus significantly inhibited liver tumor growth in mice in vivo, in addition to inducing an antitumor immune response, including an increase in the number of CD4+ and CD8+ T lymphocytes and, in turn, improving survival. Our results suggest that oncolytic influenza virus carrying GV1001 is a promising immunotherapy in patients with HCC.

Three-dimensional chromatin landscapes in hepatocellular carcinoma associated with hepatitis B virus.

BACKGROUND: Three-dimensional (3D) chromatin architecture frequently altered in cancer. However, its changes during the pathogenesis of hepatocellular carcinoma (HCC) remained elusive. METHODS: Hi-C and RNA-seq were applied to study the 3D chromatin landscapes and gene expression of HCC and ANHT. Hi-C Pro was used to generate genome-wide raw interaction matrices, which were normalized via iterative correction (ICE). Moreover, the chromosomes were divided into different compartments according to the first principal component (E1). Furthermore, topologically associated domains (TADs) were visualized via WashU Epigenome Browser. Furthermore, differential expression analysis of ANHT and HCC was performed using the DESeq2 R package. Additionally, dysregulated genes associated with 3D genome architecture altered were confirmed using TCGA, qRT-PCR, immunohistochemistry (IHC), etc. RESULTS: First, the intrachromosomal interactions of chr1, chr2, chr5, and chr11 were significantly different, and the interchromosomal interactions of chr4-chr10, chr13-chr21, chr15-chr22, and chr16-chr19 are remarkably different between ANHT and HCC, which resulted in the up-regulation of TP53I3 and ZNF738 and the down-regulation of APOC3 and APOA5 in HCC. Second, 49 compartment regions on 18 chromosomes have significantly switched (A-B or B-A) during HCC tumorigenesis, contributing to up-regulation of RAP2A. Finally, a tumor-specific TAD boundary located on chr5: 6271000-6478000 and enhancer hijacking were identified in HCC tissues, potentially associated with the elevated expression of MED10, whose expression were associated with poor prognosis of HCC patients. CONCLUSION: This study demonstrates the crucial role of chromosomal structure variation in HCC oncogenesis and potential novel biomarkers of HCC, laying a foundation for cancer precision medicine development.

Mechanism of Bazhen decoction in the treatment of colorectal cancer based on network pharmacology, molecular docking, and experimental validation.

Objective: Bazhen Decoction (BZD) is a common adjuvant therapy drug for colorectal cancer (CRC), although its anti-tumor mechanism is unknown. This study aims to explore the core components, key targets, and potential mechanisms of BZD treatment for CRC. Methods: The Traditional Chinese Medicine Systems Pharmacology (TCMSP) was employed to acquire the BZD's active ingredient and targets. Meanwhile, the Drugbank, Therapeutic Target Database (TTD), DisGeNET, and GeneCards databases were used to retrieve pertinent targets for CRC. The Venn plot was used to obtain intersection targets. Cytoscape software was used to construct an "herb-ingredient-target" network and identify core targets. GO and KEGG pathway enrichment analyses were conducted using R language software. Molecular docking of key ingredients and core targets of drugs was accomplished using PyMol and Autodock Vina software. Cell and animal research confirmed Bazhen Decoction efficacy and mechanism in treating colorectal cancer. Results: BZD comprises 173 effective active ingredients. Using four databases, 761 targets related to CRC were identified. The intersection of BZD and CRC yielded 98 targets, which were utilized to construct the "herb-ingredient-target" network. The four key effector components with the most targets were quercetin, kaempferol, licochalcone A, and naringenin. Protein-protein interaction (PPI) analysis revealed that the core targets of BZD in treating CRC were AKT1, MYC, CASP3, ESR1, EGFR, HIF-1A, VEGFR, JUN, INS, and STAT3. The findings from molecular docking suggest that the core ingredient exhibits favorable binding potential with the core target. Furthermore, the GO and KEGG enrichment analysis demonstrates that BZD can modulate multiple signaling pathways related to CRC, like the T cell receptor, PI3K-Akt, apoptosis, P53, and VEGF signaling pathway. In vitro, studies have shown that BZD dose-dependently inhibits colon cancer cell growth and invasion and promotes apoptosis. Animal experiments have shown that BZD treatment can reverse abnormal expression of PI3K, AKT, MYC, EGFR, HIF-1A, VEGFR, JUN, STAT3, CASP3, and TP53 genes. BZD also increases the ratio of CD4+ T cells to CD8+ T cells in the spleen and tumor tissues, boosting IFN-γ expression, essential for anti-tumor immunity. Furthermore, BZD has the potential to downregulate the PD-1 expression on T cell surfaces, indicating its ability to effectively restore T cell function by inhibiting immune checkpoints. The results of HE staining suggest that BZD exhibits favorable safety profiles. Conclusion: BZD treats CRC through multiple components, targets, and metabolic pathways. BZD can reverse the abnormal expression of genes such as PI3K, AKT, MYC, EGFR, HIF-1A, VEGFR, JUN, STAT3, CASP3, and TP53, and suppresses the progression of colorectal cancer by regulating signaling pathways such as PI3K-AKT, P53, and VEGF. Furthermore, BZD can increase the number of T cells and promote T cell activation in tumor-bearing mice, enhancing the immune function against colorectal cancer. Among them, quercetin, kaempferol, licochalcone A, naringenin, and formaronetin are more highly predictive components related to the T cell activation in colorectal cancer mice. This study is of great significance for the development of novel anti-cancer drugs. It highlights the importance of network pharmacology-based approaches in studying complex traditional Chinese medicine formulations.

Spotlight on NLRP6 and Tumor Research Situation: A Potential Cancer Participant.

NOD-like receptor family pyrin domain containing 6 (NLRP6) is a new pattern recognition receptor in the mammalian innate immune system. Both the liver and the gut exhibit substantial levels of cytoplasmic expression. It can speed up cell response to endogenous danger signals or exogenous pathogen infection. NLRP6 can function in various ways as an inflammasome or a noninflammasome. The understanding of NLRP6 is steadily increasing thanks to ongoing investigations, but due to discrepancies in how those studies have described their link with tumors, the significance of NLRP6 in the emergence of cancer is still debatable as of this writing. This article will use the structure and function of NLRP6 as the pivotal point and thoroughly explain the present interactions between NLRP6 and tumors and any possible clinical benefits.

Data-independent acquisition mass spectrometry identification of extracellular vesicle biomarkers for gastric adenocarcinoma.

Early diagnosis of gastric adenocarcinoma (GAC) can effectively prevent the progression of the disease and significantly improve patient survival. Currently, protein markers in clinical practice barely meet patient needs; it is therefore imperative to develop new diagnostic biomarkers with high sensitivity and specificity. In this study, we extracted extracellular vesicles (EV) from the sera of 33 patients with GAC and 19 healthy controls, then applied data-independent acquisition (DIA) mass spectrometry to measure protein expression profiles. Differential protein expression analysis identified 23 proteins showing expression patterns across different cancer stages, from which 15 proteins were selected as candidate biomarkers for GAC diagnosis. From this subset of 15 proteins, up to 6 proteins were iteratively selected as features and logistic regression was used to distinguish patients from healthy controls. Furthermore, serum-derived EV from a new cohort of 12 patients with gastric cancer and 18 healthy controls were quantified using the same method. A classification panel consisting of GSN, HP, ORM1, PIGR, and TFRC showed the best performance, with a sensitivity and negative predictive value (NPV) of 0.83 and 0.82. The area under curve (AUC) of the receiver operating characteristic (ROC) is 0.80. Finally, to facilitate the diagnosis of advanced stage GAC, we identified a 3-protein panel consisting of LYZ, SAA1, and F12 that showed reasonably good performance with an AUC of 0.83 in the validation dataset. In conclusion, we identified new protein biomarker panels from serum EVs for early diagnosis of gastric cancer that worth further validation.

mRNA vaccines: A novel weapon to control infectious diseases.

Infectious diseases have always threatened human life, but with the development of vaccines, effective strategies for preventing and controlling these diseases have become available. The global outbreak of COVID-19 ushered in the advent of mRNA vaccine technologies, which quickly led to the introduction of mRNA vaccines effective against SARS-CoV-2. The success of this approach has stimulated research into the use of mRNA vaccines in the fight against other emerging as well as remerging infectious diseases. This review examines the constructive strategies and delivery systems used in mRNA vaccines and provides an overview of current clinical trials of those vaccines in the prevention of infectious diseases. The underlying mechanisms of mRNA vaccines are also discussed, including the double-edged sword of the innate immune response. Finally, the challenges but also the potential of mRNA vaccines are considered.

An OX40L mRNA vaccine inhibits the growth of hepatocellular carcinoma.

mRNA cancer vaccines show therapeutic potential for malignant tumors, including hepatocellular carcinoma (HCC). We optimized and synthesized stable mRNA encoding costimulator Oxford 40 ligand (OX40L). For systemic delivery, OX40L mRNAs were loaded into lipid nanoparticles (LNPs). The expression and costimulatory effects of OX40L were investigated in vitro. OX40L was expressed on the cell surface and costimulated T cells. In vivo, intratumoral injection of LNPs encapsulating OX40L mRNAs significantly reduced tumor growth and increased the survival of mice bearing H22 tumors. Importantly, CD4+ and CD8+ T cells were significantly increased in the OX40L mRNA group in vivo. Taken together, our findings provide a promising clinical strategy for immunotherapy for HCC using mRNA vaccines.

mRNA Vaccines: The Dawn of a New Era of Cancer Immunotherapy.

mRNA therapy is a novel anticancer strategy based on in vitro transcription (IVT), which has potential for the treatment of malignant tumors. The outbreak of the COVID-19 pandemic in the early 21st century has promoted the application of mRNA technologies in SARS-CoV-2 vaccines, and there has been a great deal of interest in the research and development of mRNA cancer vaccines. There has been progress in a number of key technologies, including mRNA production strategies, delivery systems, antitumor immune strategies, etc. These technologies have accelerated the progress and clinical applications of mRNA therapy, overcoming problems encountered in the past, such as instability, inefficient delivery, and weak immunogenicity of mRNA vaccines. This review provides a detailed overview of the production, delivery systems, immunological mechanisms, and antitumor immune response strategies for mRNA cancer vaccines. We list some mRNA cancer vaccines that are candidates for cancer treatment and discuss clinical trials in the field of tumor immunotherapy. In addition, we discuss the immunological mechanism of action by which mRNA vaccines destroy tumors as well as challenges and prospects for the future.

Proteomic analysis of lung cancer cells reveals a critical role of BCAT1 in cancer cell metastasis.

Metastasis is the major cause of high mortality in lung cancer. Exploring the underlying mechanisms of metastasis thus holds promise for identifying new therapeutic strategies that may enhance survival. Methods: We applied quantitative mass spectrometry to compare protein expression profiles between primary and metastatic lung cancer cells whilst investigating metastasis-related molecular features. Results: We discovered that BCAT1, the key enzyme in branched-chain amino acid metabolism, is overexpressed at the protein level in metastatic lung cancer cells, as well as in metastatic tissues from lung cancer patients. Analysis of transcriptomic data available in the TCGA database revealed that increased BCAT1 transcription is associated with poor overall survival of lung cancer patients. In accord with a critical role in metastasis, shRNA-mediated knockdown of BCAT1 expression reduced migration of metastatic cells in vitro and the metastasis of these cells to distal organs in nude mice. Mechanistically, high levels of BCAT1 depleted α-ketoglutarate (α-KG) and promoted expression of SOX2, a transcription factor regulating cancer cell stemness and metastasis. Conclusion: Our findings suggest that BCAT1 plays an important role in promoting lung cancer cell metastasis, and may define a novel pathway to target as an anti-metastatic therapy.

Role of miR-106-mediated mitogen-activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension.

We aim to investigate the role of miR-106-mediated mitogen-activated protein kinase (MAPK) signaling pathway in oxidative stress (OS) injury and inflammatory infiltration in the liver of the mouse with gestational hypertension (GH). Ninety specific pathogen-free mice (Kunming species) during middle to late gestation were selected for the study. Fifteen mice were used as control, while the rest were used for establishing the GH model. The mice were assigned to six groups: normal group (normal gestation), model group (GH model), negative control group (GH model, intravenously injected with negative control vector), miR-106a-mimic group (GH model, intravenously injected with vector overexpressing miR-106a, which mimics the overexpression of endogenous mature miR-106a), SB203580 group (GH model, intravenously injected with MAPK pathway inhibitor SB203580), and miR-106a-mimic+SB203580 group (GH model, intravenously injected with SB203580 and vector overexpressing miR-106a). Fourteen days after electrical stimulation, all the groups except for the normal group had elevated blood pressure vs those on day 0 and 7. Compared with the normal group, the other groups had lower levels of miR-106a expression, nitric oxide, nitric oxide synthase, catalase, superoxide dismutase, S cell ratio, and interleukin-4 (IL-4) and IL-10 in the serum and liver as opposed to increased levels of blood pressure, p38MAPK mRNA expression, p-p38MAPK positive expression rate, protein expressions of p-p38MAPK, p-ERK, and p-JNK, H2 O2 and malondialdehyde in liver, G0/G1 cell ratio, apoptosis rate, and IL-6, interferon-γ (IFN-γ), and IFN-α in the serum and liver (all P < .05). The miR-106 overexpression or inhibiting MAPK signaling pathway can attenuate OS injury and inflammatory response in the liver of the mouse with GH, and the effect can be even better if both miR-106a overexpression and inhibiting MAPK pathway are applied. In conclusion, miR-106a overexpression can inhibit OS injury and inflammatory infiltration in the liver of the mouse with GH by mediating MAPK signaling pathway.

Changes of Blood Flux at BL21 and Points along BL Meridian Resulted from Acupuncture or Moxibustion: Case Cross Design Study.

Acupuncture (Acup) and moxibustion (Moxi) are commonly used interventions in clinical practice. However, the difference between Acup and moxibustion mechanisms is unclear. In current study, blood perfusion responses resulted from Acup or Moxi at Weishu acupoint (BL21) and control points were explored, respectively. The time series of blood flux signals at BL21 and control points were transformed with Morlet wavelet, and the differences in each frequency interval were observed. The results suggested that acupoint response to different stimulation is a comprehensive process which related to all components of blood perfusion signals. Whereas the different response at control points was not observed, there has been significant difference coherence value between Acup and Moxi stimulation. The results suggested the influence of Acup and Moxi not only on the level of blood perfusion at local area; the intrinsic relevance after stimulation which can be evaluated by coherence analysis is also an appropriate index to distinguish different stimulations.

Response of Blood Perfusion at ST 36 Acupoint after Drinking Cold Glucose or Saline Injection.

Skin blood flux (SkBF) changes caused by drinking cold water are generally associated with vagal tone and osmotic factors in digestive system. According to acupuncture theory, change of SkBF at ST 36 might reflect the functional changes of digestive system. The aim of this study is to analyze the changes of SkBF after drinking 3°C 0.9% saline or 5% glucose injection by monitor blood flux at bilateral ST 36. The results indicated that, after drinking different cold water, the change ratio of SkBF at right side ST 36 has been different. Because all solutions have the same temperature (3°C) and both saline and glucose solution have the same osmolality, suggesting that the SkBF changes resulting from drinking cold water are not regulated just by the vagal tone and osmolality, there must have been other factors. These results have not been consistent with the frequency domain results of heart rate variability (HRV) analysis. Coherence analysis of blood flux signals at bilateral ST 36 indicated that there have been different coherence-frequency curves among different groups in special frequency bands, which suggested that coherence analysis might provide a potential tool to evaluate different status.

Is There Volume Transmission Along Extracellular Fluid Pathways Corresponding to the Acupuncture Meridians?

Volume transmission is a new major communication signaling via extracellular fluid (interstitial fluid) pathways. It was proposed by the current authors that such pathways can explain the meridian phenomena and acupuncture effects. To investigate whether meridian-like structures exist in fish body and operate via volume transmission in extracellular fluid pathways, we injected alcian blue (AB) under anesthesia into Gephyrocharax melanocheir, which has a translucent body. The migration of AB could be seen directly and was recorded by a digital camera. The fish was then embedded and cut transversely to observe the position of tracks in three dimensions. Eight longitudinal threadlike blue tracks were recognized on the fish. The positions of these threadlike tracks were similar to meridians on the human body. Transverse sections showed that these tracks distributed to different layers of distinct subcutaneous loose connective tissues and intermuscular septa. Lymphatic vessels were sometimes associated with the extracellular blue tracks where the migration of AB occurred. Extracellular fluid pathways were found on fish through their transport of AB. These pathways operating via volume transmission appeared to be similar in positions and functions to the acupuncture meridians in Chinese medicine.

[Color spectrum of cupping mark detected by hyperspectral camera:a preliminary observation].

OBJECTIVE: To perform quantitative observation on the color change of local skin after cupping, so as to explore objective and quantitative methods for skin response of cupping. METHODS: Seven health subjects were included. By quantitative meridian cupping instrument, cupping methods with four types of pressures were respectively performed on subjects for 5 min.The spectrum of cupping mark before and after the cupping was collected by hyperspectral camera, and the color change was recorded by digital camera. RESULTS: Before the cupping, the differences of back skin areas were not significant (P>0.05), and its average spectrum indicated two peaks at 540-550 nm and 580-590 nm. After cupping with different pressures, spectrum changes of skin were observed. For -0.02 MPa, the most significant reduction was observed at 550 nm (-12.1%, P<0.05); for -0.03 MPa, the most significant reduction was observed at 540 nm (-22.1%, P<0.05); for -0.04 MPa, the most significant reduction was observed at 610 nm (-26.7%, P<0.05); for -0.05 MPa, the most significant reduction was observed at several spectrums (all P<0.05). CONCLUSIONS: After cupping with different negative pressures, significant changes of spectrum are observed on skin; for different pressures, the spectrums of the most significant changes are different; the hyperspectral camera could be applied to perform quantitative observation on the color change of local skin.

Acupuncture regulates the heart rate variability.

Acupuncture is widely used in clinical practice. According to traditional acupuncture theory, the Neiguan acupoint (PC6) is one of the most commonly used acupoints and is indicated for treating cardiovascular-related disorders. We present the case of a 27-year-old female who had been diagnosed with ventricular septal defect and had undergone surgery to repair the defect at the age of 11 years. The patient had no obvious symptoms, such as palpitations and difficulty breathing. However, while performing electrocardiography (ECG), we found that she suffered from arrhythmia, and therefore, we treated her by acupuncture at the left PC6. An ECG monitor was used to record data during the entire acupuncture procedure, which was divided into the following three segments: prior to, during, and after acupuncture. Various indices of heart rate variability (HRV) were then determined and analyzed. The results indicate that acupuncture can regulate the HRV effectively; however, more studies are needed to confirm this finding.

Finding Blue Tracks in Gephyrocharax melanocheir Fish Similar to the Locations of Acupuncture Meridians after Injecting Alcian Blue.

This study investigated whether a meridian-like distribution of Alcian blue (AB) existed after it was injected into a fish's body and suggested a new animal model for meridian study. Twenty Gephyrocharax melanocheir fish with translucent bodies were injected with AB at a point near the spinal column or the dorsal fin. Distribution of AB was observed using a digital camera and a stereomicroscope. Three or more obvious blue tracks were found: one along the spinal column, another along the posterior margin of the abdomen extending to the superior margin of the anal fin, and a third along both sides of the dorsal fin. They were similar to the locations of the governor, conceptual vessel, and urinary bladder meridians, respectively, on the human body according to the classic theory of traditional Chinese medicine. A few other blue tracks were also found, which apparently did not correspond to any known meridians. The results show that the tracks of AB share important similarities with the locations of classically described meridians and that they are mainly distributed in the interstitial space around bones and blood vessels and inside muscular interstices. This study may provide a new experimental animal model for exploring acupuncture meridians.