Acupuncture improves immunity and fatigue after chemotherapy in breast cancer patients by inhibiting the Leptin/AMPK signaling pathway.

OBJECTIVE: Acupuncture has become a popular complementary treatment in oncology. This study is based on RNA-Seq transcriptome sequencing technology to investigate the molecular mechanisms underlying the effect of acupuncture-mediated regulation of the Leptin/AMPK signaling pathway on mitochondrial dysfunction-induced fatigue in breast cancer patients after chemotherapy. METHODS: Peripheral blood samples from 10 patients with post-operative chemotherapy for breast cancer were selected for transcriptome sequencing to screen the key molecular pathways involved in fatigue after chemotherapy in breast cancer patients. Besides, peripheral blood samples were collected from 138 post-operative chemotherapy patients with breast cancer to study the composite fatigue and quality of life scores. Flow cytometry was used to detect T lymphocyte subsets in peripheral blood-specific immune cells. In addition, a blood cell analyzer was used to measure peripheral blood leukocyte counts, and MSP-PCR was used to detect mitochondrial DNA mutations in peripheral blood leukocytes. RESULTS: Transcriptome bioinformatics analysis screened 147 up-regulated mRNAs and 160 down-regulated mRNAs. Leptin protein was confirmed as the key factor. Leptin was significantly higher in the peripheral blood of breast cancer patients who developed fatigue after chemotherapy. Acupuncture treatment effectively improved post-chemotherapy fatigue and immune status in breast cancer patients, suppressed the expression of Leptin/AMPK signaling pathway-related factor and leukocyte counts, and significantly reduced the rate of mitochondrial DNA mutations in peripheral blood leukocytes. CONCLUSION: The Leptin/AMPK signaling pathway may be the key molecular pathway affecting the occurrence of fatigue after chemotherapy in breast cancer patients. Leptin may improve post-chemotherapy fatigue in breast cancer patients by activating AMPK phosphorylation and alleviating mitochondrial functional impairment.

Effects of Mind-Regulation Acupuncture Therapy on Serum Ghrelin, Gastric Inhibitory Polypeptide, Leptin, and Insulin Levels in Breast Cancer Survivors with Cancer-Related Fatigue: A Randomized Controlled Trial.

Aim: The aim of this research is to analyze the effects of mind-regulation acupuncture on serum ghrelin, gastric inhibitory polypeptide, leptin, and insulin levels, fatigue, quality of sleep, depression, and quality of life in survivors of breast cancer with cancer-related fatigue. Methods: Total 136 breast cancer survivors with cancer-related fatigue were randomly allocated to the mind-regulation acupuncture group and the control group in a 1:1 ratio, with 68 cases in each group. Finally, 57 cases each in both groups completed the study. The serum ghrelin, gastric inhibitory polypeptide, leptin, and insulin levels were measured in pre-treatment and post-treatment. The 20-item Multidimensional Fatigue Symptom Inventory, Pittsburgh Sleep Quality Index, Hamilton Depression Scale, and Karnofsky Performance Status were used to evaluate patients' fatigue, quality of sleep, symptoms of depression, and quality of life, respectively. Results: In post-treatment, the serum ghrelin, gastric inhibitory polypeptide, leptin, and insulin levels significantly reduced, 20-item Multidimensional Fatigue Symptom Inventory, Pittsburgh Sleep Quality Index, and Hamilton Depression scores were remarkably decreased, whereas the Karnofsky Performance Status scores were significantly increased in mind-regulation acupuncture group and control group comparing to those pre-treatment, while those in mind-regulation acupuncture group changed more significantly. The 20-item Multidimensional Fatigue Symptom Inventory, Pittsburgh Sleep Quality Index, and Hamilton Depression scores were remarkably lower, and remarkably higher Karnofsky Performance Status scores in the mind-regulation acupuncture group were seen than those in the control group. Conclusion: Mind-regulation acupuncture could reduce serum ghrelin, gastric inhibitory polypeptide, leptin, and insulin levels of breast cancer survivors with cancer-related fatigue. In addition, it alleviates cancer-related fatigue, sleep disturbance, and depression in these survivors and improves their quality of life. Therefore, mind-regulation acupuncture may have potential as an alternative and complementary therapy for breast cancer survivors with cancer-related fatigue.

D2-Net: Dual Disentanglement Network for Brain Tumor Segmentation With Missing Modalities.

Multi-modal Magnetic Resonance Imaging (MRI) can provide complementary information for automatic brain tumor segmentation, which is crucial for diagnosis and prognosis. While missing modality data is common in clinical practice and it can result in the collapse of most previous methods relying on complete modality data. Current state-of-the-art approaches cope with the situations of missing modalities by fusing multi-modal images and features to learn shared representations of tumor regions, which often ignore explicitly capturing the correlations among modalities and tumor regions. Inspired by the fact that modality information plays distinct roles to segment different tumor regions, we aim to explicitly exploit the correlations among various modality-specific information and tumor-specific knowledge for segmentation. To this end, we propose a Dual Disentanglement Network (D2-Net) for brain tumor segmentation with missing modalities, which consists of a modality disentanglement stage (MD-Stage) and a tumor-region disentanglement stage (TD-Stage). In the MD-Stage, a spatial-frequency joint modality contrastive learning scheme is designed to directly decouple the modality-specific information from MRI data. To decompose tumor-specific representations and extract discriminative holistic features, we propose an affinity-guided dense tumor-region knowledge distillation mechanism in the TD-Stage through aligning the features of a disentangled binary teacher network with a holistic student network. By explicitly discovering relations among modalities and tumor regions, our model can learn sufficient information for segmentation even if some modalities are missing. Extensive experiments on the public BraTS-2018 database demonstrate the superiority of our framework over state-of-the-art methods in missing modalities situations. Codes are available at https://github.com/CityU-AIM-Group/D2Net.

Actein contributes to black cohosh extract-induced genotoxicity in human TK6 cells.

Black cohosh extract (BCE) is one of the most popular botanical products for relieving menopausal symptoms. However, recent studies indicate that BCE is not only ineffective for menopausal therapy but also induces genotoxicity through an aneugenic mode of action (MoA). In this study, the cytotoxicity of five constituents of BCE was evaluated in human lymphoblastoid TK6 cells. Among the five constituents, actein (up to 50 µM) showed the highest cytotoxicity and was thus selected for further genotoxicity evaluations. Actein caused DNA damage proportionally to concentration as evidenced by the phosphorylation of the histone protein H2A.X (γH2A.X) and resulted in chromosomal damage as measured by the increased percentage of micronuclei (%MN) in cells. In addition, actein activated DNA damage response (DDR) pathway through induction of p-ATM, p-Chk1, and p-Chk2, which subsequently induced cell cycle changes and apoptosis. Moreover, both BCE and actein increased intracellular reactive oxygen species (ROS) production, decreased glutathione levels, and activated the mitogen-activated protein kinases (MAPK) signaling pathway. N-acetylcysteine, a ROS scavenger, attenuated BCE- and actein-induced ROS production, apoptosis, and DNA damage. These findings indicate that BCE- and actein-induced genotoxicity is mediated, at least partially, through oxidative stress. Taken together, our data show that actein is likely one of the major contributors to BCE-induced genotoxicity.

Astaxanthin improved the storage stability of docosahexaenoic acid-enriched eggs by inhibiting oxidation of non-esterified poly-unsaturated fatty acids.

This study assessed the potential and mechanism of action of astaxanthin, to improve the stability of docosahexaenoic acid (22:6(n-3); DHA) enriched egg products, during storage at 4 °C. The reduction in DHA content after 42 days of storage in astaxanthin-DHA eggs (from hens fed supplemental astaxanthin and DHA) was <3%, whereas the reduction in regular-DHA eggs (hens fed DHA only) was over 17%. Astaxanthin also decreased production of oxidation products including 4-hydroxy-2-hexenal, 4-hydroxy-2-nonenal and malondialdehyde in eggs during storage, thus markedly improving the oxidative stability of DHA-enriched eggs. The yolk lipidomic profile showed higher intensities for most DHA-containing lipids, especially DHA-phosphatidylcholine, DHA-phosphatidylethanolamine and DHA-non-esterified fatty acid, compared with regular-DHA eggs. Astaxanthin acts primarily by suppressing oxidation of DHA-non-esterified fatty acid, which minimizes the degradation of DHA and appears to be the primary protection mode of yolk DHA during storage.

Selenium Deficiency Induces Pathological Cardiac Lipid Metabolic Remodeling and Inflammation.

SCOPE: Selenium (Se) disequilibrium is closely involved in many cardiac diseases, although its in vivo mechanism remains uncertain. Therefore, a pig model is created in order to generate a comprehensive picture of cardiac response to dietary Se deficiency. METHODS AND RESULTS: A total of 24 pigs are divided into two equal groups, which were fed a diet with either 0.007 mg kg-1 Se or 0.3 mg kg-1 Se for 16 weeks. Se deficiency causes cardiac oxidative stress by blocking glutathione and thioredoxin systems and increases thioredoxin domain-containing protein S-nitrosylation. Energy production is disordered, as free fatty acids are overloaded, the tricarboxylic acid cycle is strengthened, and three respiratory chain proteins enhance S-nitrosylation. Excess free fatty acids lead to increased synthesis of diacylglycerol, phosphatidylcholine, and phosphatidylethanolamine, where the latter two are vulnerable to oxidation and causes an increase in malondialdehyde. Moreover, increased palmitic acid enhances de novo ceramide synthesis and accumulation. Additionally, Se deficiency initiates inflammation via cytosolic DNA-sensing pathways, which activates downstream interferon regulatory factor 7 and nuclear factor kappa B. CONCLUSIONS: The present study identifies a lipid metabolic vulnerability and inflammation initiation pathway via Se deficiency, which may provide targets for human redox imbalance-induced cardiac disease treatment.

NIR/MRI-Guided Oxygen-Independent Carrier-Free Anti-Tumor Nano-Theranostics.

Imaging-guided photothermal therapy (PTT)/photodynamic therapy (PDT) for cancer treatment are beneficial for precise localization of the malignant lesions and combination of multiple cell killing mechanisms in eradicating stubborn thermal-resistant cancer cells. However, overcoming the adverse impact of tumor hypoxia on PDT efficacy remains a challenge. Here, carrier-free nano-theranostic agents are developed (AIBME@IR780-APM NPs) for magnetic resonance imaging (MRI)-guided synergistic PTT/thermodynamic therapy (TDT). Two IR780 derivatives are synthesized as the subject of nanomedicine to confer the advantages for the nanomedicine, which are by feat of amphiphilic IR780-PEG to enhance the sterical stability and reduce the risk from reticuloendothelial system uptake, and IR780-ATU to chelate Mn2+ for T1 -weighted MRI. Dimethyl 2,2'-azobis(2-methylpropionate) (AIBME), acting as thermally decomposable radical initiators, are further introduced into nanosystems with the purpose of generating highly cytotoxic alkyl radicals upon PTT launched by IR780 under 808 nm laser irradiation. Therefore, the sequentially generated heat and alkyl radicals synergistically induce cell death via synergistic PTT/TDT, ignoring tumor hypoxia. Moreover, these carrier-free nano-theranostic agents present satisfactory biocompatibility, which could be employed as a powerful weapon to hit hypoxic tumors via MRI-guided oxygen-independent PTT and photonic TDT.

Mechanistic Evaluation of Black Cohosh Extract-Induced Genotoxicity in Human Cells.

Black cohosh extract (BCE) is marketed to women as an alternative to hormone replacement therapy for alleviating menopausal symptoms. Previous studies by the National Toxicology Program revealed that BCE induced micronuclei (MN) and a nonregenerative macrocytic anemia in rats and mice, likely caused by disruption of the folate metabolism pathway. Additional work using TK6 cells showed that BCE induced aneugenicity by destabilizing microtubules. In the present study, BCE-induced MN were confirmed in TK6 and HepG2 cells. We then evaluated BCE-induced DNA damage using the comet assay at multiple time points (0.5-24 h). Following a 0.5-h exposure, BCE induced significant, concentration-dependent increases in %tail DNA in TK6 cells only. Although DNA damage decreased in TK6 cells over time, likely due to repair, small but statistically significant levels of DNA damage were observed after 2 and 4 h exposures to 250 µg/ml BCE. A G1/S arrest in TK6 cells exposed to 125 µg/ml BCE (24 h) was accompanied by apoptosis and increased expression of γH2A.X, p-Chk1, p-Chk2, p53, and p21. Conditioning TK6 cells to physiological levels of folic acid (120 nM) did not increase the sensitivity of cells to BCE-induced DNA damage. BCE did not alter global DNA methylation in TK6 and HepG2 cells cultured in standard medium. Our results suggest that BCE induces acute DNA strand breaks which are quickly repaired in TK6 cells, whereas DNA damage seen at 4 and 24 h may reflect apoptosis. The present study supports that BCE is genotoxic mainly by inducing MN with an aneugenic mode of action.

Combination of urine and faeces metabolomics to reveal the intervention mechanism of Polygala tenuifolia compatibility with Magnolia officinalis on gastrointestinal motility disorders.

OBJECTIVES: To explore the intervention mechanism of combining Polygala tenuifolia (PT) with Magnolia officinalis (MO) on gastrointestinal motility disorders caused by PT. METHODS: Urine and faeces of rats were collected; the effects of PT and MO on the gastric emptying and small intestine advancing rates in mice were analysed via ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UHPLC-Q-TOF-MS) to determine the potential metabolites. Changes in the metabolic profiles of the urine and faeces were revealed by untargeted metabolomics, followed by multivariate statistical analysis. The integration of urine and faeces was applied to reveal the intervention mechanism of PT-MO on PT-induced disorders. KEY FINDINGS: PT + MO (1:2) improved the gastrointestinal function in mice suffering from PT-induced gastrointestinal motility disorder. Metabolomics indicated that the PT-MO mechanism was mainly associated with the regulations of 17 and 12 metabolites and 11 and 10 pathways in urine and faeces, respectively. The common metabolic pathways were those of tyrosine, purine, tricarboxylic acid cycle, pyruvate and gluconeogenesis, which were responsible for the PT-MO intervention mechanism. CONCLUSIONS: The PT-MO (1:2) couple mechanism mitigated the PT-induced disorders, which were related to the energy, amino acid and fatty metabolisms.

l-Borneol Exerted the Neuroprotective Effect by Promoting Angiogenesis Coupled With Neurogenesis via Ang1-VEGF-BDNF Pathway.

At present, Stroke is still one of the leading causes of population death worldwide and leads to disability. Traditional Chinese medicine plays an important role in the prevention or treatment of stroke. l-borneol, a traditional Chinese medicine, has been used in China to treat stroke for thousands of years. However, its mechanism of action is unclear. After cerebral ischemia, promoting angiogenesis after cerebral ischemia and providing nutrition for the infarct area is an important strategy to improve the damage in the ischemic area, but it is also essential to promote neurogenesis and replenish new neurons. Here, our research shows that l-borneol can significantly improve the neurological deficits of pMCAO model rats, reduce cerebral infarction, and improve the pathological damage of cerebral ischemia. and significantly increase serum level of Ang-1 and VEGF, and significantly decrease level of ACE and Tie2 to promote angiogenesis. PCR and WB showed the same results. Immunohistochemistry also showed that l-borneol can increase the number of CD34 positive cells, further verifying that l-borneol can play a neuroprotective effect by promoting angiogenesis after cerebral ischemia injury. In addition, l-borneol can significantly promote the expression level of VEGF, BDNF and inhibit the expression levels of TGF-ß1 and MMP9 to promote neurogenesis. The above suggests that l-borneol can promote angiogenesis coupled neurogenesis by regulating Ang1-VEGF-BDNF to play a neuroprotective effect. Molecular docking also shows that l-borneol has a very high binding rate with the above target, which further confirmed the target of l-borneol to improve cerebral ischemic injury. These results provide strong evidence for the treatment of cerebral ischemia with l-borneol and provide reference for future research.

Benzoinum from Styrax tonkinensis (Pierre) Craib ex Hart exerts a NVU protective effect by inhibiting cell apoptosis in cerebral ischaemia rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Benzoinum (Styraceae) is a traditional Chinese medicine used to treat stroke and other cardio-cerebrovascular diseases for thousands of years. Benzoinum has also proven to have diverse pharmacological activity, but the neuroprotection mechanism of apoptosis in ischaemic stroke was not determined. AIM OF THIS STUDY: To investigate the protective effect of a neurovascular unit (NVU) and the mechanisms of benzoinum on cerebral ischaemic rats. MATERIALS AND METHODS: The neuroprotective activity of benzoinum against middle cerebral artery occlusion (MCAO)-induced cerebral ischaemic injury. Neurological scores, 2,3,5-Triphenyltetrazolium chloride (TTC) staining, and hematoxylin-eosin staining (HE) staining were conducted to evaluate the neurological damage. Infarction rate and denatured cell index (DCI) were also calculated. The ultrastructure of neuron and blood-brain-barrier (BBB) was observed by transmission electron microscopy (TEM). Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect Bax, Bcl-2 and Caspase 3 expression. Furthermore, Claudin 5 also was detected through immunohistochemistry. RESULTS: Benzoinum could significantly improve neurological function score and reduce cerebral infarction rate and DCI. In addition, benzoinum alleviated pathomorphological change and apoptosis in the brain tissue of MCAO rats. The results of TEM and claudin 5 expression of immunohistochemistry showed that benzoinum could play a neuroprotective effect in NVU. Also, benzoinum-enhanced Bcl2, and reduced Bax and Bax/Bcl-2 and Caspase 3, suggest that benzoinum provided a neuroprotective effect by inhibited cell apoptosis. CONCLUSION: Benzoinum could play a neuroprotective role and regulate apoptosis for repair and stabilisation of NVU. This anti-apoptosis activity might be associated with the downregulation of Bax and Caspase 3, and the upregulation of Bcl2. Our present findings provide a promising medication for the treatment of ischaemic stroke.

Selenium Deficiency-Induced Pancreatic Pathology Is Associated with Oxidative Stress and Energy Metabolism Disequilibrium.

Selenium (Se) is an essential micronutrient that plays a crucial role in development and physiological processes. The present study aimed to investigate the effects of Se deficiency on pancreatic pathology and the potential mechanism in pigs. Twenty-four castrated male Yorkshire pigs were divided into two groups and fed a Se-deficient diet (0.007 mg Se/kg) or a Se-adequate diet (0.3 mg Se/kg) for 16 weeks. The serum concentrations of insulin and glucagon, Se concentration, histologic characteristics, apoptotic status, antioxidant activity, free radical content, and major metabolite concentrations were analyzed. The results showed that Se deficiency reduced the concentrations of insulin and glucagon in the serum and of Se in pancreas, decreased the number of islets and cells in the local islets, and induced pancreatic apoptosis. Se deficiency caused a redox imbalance, which led to an increase in the content of free radicals and decreased the activity of antioxidant enzymes. Of 147 targeted metabolites judged to be present in pancreas, only hypotaurine and D-glucuronic acid had differential concentrations with the false discovery rate < 0.05. Pathway analysis using metabolites with differential expression (unadjusted P < 0.05, fold change > 1.4 or < 0.67) found that 8 glycolytic metabolites were significantly increased by Se-deficient, whereas most of the tricarboxylic acid cycle and pentose phosphate pathway metabolites were not significantly changed. Our studies indicated that Se deficiency-induced pancreatic pathology was associated with oxidative stress and enhanced activity of glycolysis, which may provide gaining insight into the actions of Se as a diabetogenic factor.

Neuroprotection of benzoinum in cerebral ischemia model rats via the ACE-AngI-VEGF pathway.

AIMS: Stroke is a devastating event with a limited choice of intervention. Benzoinum is frequently used to treat stroke in traditional Chinese medicine. Our team has found that the neuroprotection of benzoinum may related to angiogenesis, but the exact biological mechanism is unclear. The objective of this study was to explore its biological mechanism of angiogenesis in cerebral ischemia model rats. MAIN METHODS: First, network pharmacology and molecular docking were performed to predict the possible targets and mechanisms of benzoinum in treating ischemic stroke. The best dose was then selected according to pharmacodynamic indexes such as those for neurological deficit, cerebral infarction rate, and brain histopathology in middle cerebral artery occlusion (MCAO) model rats. Finally, RT-PCR, Western Blot and immunohistochemical analysis were applied to verify the prediction results from molecular docking. KEY FINDINGS: Network pharmacology and molecular docking demonstrated that the targets of treating cerebral ischemia were PDE4D, ACE and TTR, and the mechanism may be related to the ACE-AngI-VEGF signaling pathway. Experimental verification results suggested that 0.50 g/kg and 1.00 g/kg benzoinum could significantly protect against neurological deficit and reduce cerebral infarction rate in the cerebral cortex and hippocampus in MCAO model rats. At an optimal dose, benzoinum could significantly up-regulate VEGF, SHH and ANG-1, yet down-regulate ACE expression in MCAO model rats. SIGNIFICANCE: Balsamic acid is the active ingredient of benzoinum that protects against ischemic stroke and the possible mechanism is related to the promotion of angiogenesis via regulating ACE-AngI-VEGF pathway.

[Ginger-partitioned moxibustion in the prevention of nausea and vomiting induced by chemotherapy in lung cancer：a randomized controlled trial].

OBJECTIVE: To observe the effect of ginger-partitioned moxibustion intervention on gastrointestinal reaction, the quality of life, the counts of blood platelet (PLT) and white blood cells (WBC) after chemotherapy in lung cancer patients. METHODS: The lung cancer patients treated with chemotherapy were randomized into observation group (30 cases) and control group (30 cases). In the control group, the intravenous injection with Tropisetron(5 mg) was given 1 h before chemotherapy. In the observation group, in addition to the same treatment as the control group, 2 hours after chemotherapy, ginger-partitioned moxibustion was applied to bilateral Zusanli (ST36), bilateral Neiguan (PC6) and bilateral Tianshu (ST25) for 20 min each time. The treatments were conducted once daily for 3 days. Separately, 2 days before chemotherapy, 24 h and 7 days after chemotherapy, the gastrointestinal reaction score and the score of the quality of life, the PLT and WBC counts were observed in the two groups. RESULTS: The effective rate of the gastrointestinal reaction degree in the observation group were higher than those in the control group 24 h and 7 days after chemotherapy (P<0.05). Twenty-four hours after chemotherapy, the score of the quality of life, the PLT and WBC counts were lower as compared with those before the treatment in both groups respectively(P<0.05). Seven days after chemotherapy, the score of the quality of life, the PLT and WBC counts in the observation group were higher than those in the control group (P<0.05). CONCLUSION: The ginger-partitioned moxibustion achieves the definite clinical effect of the prevention of nausea and vomiting induced by chemotherapy in lung cancer. This therapy is simple in operation, high in safety, absent in obvious adverse reactions and high in patient's compliance.

Selenium deficiency-induced redox imbalance leads to metabolic reprogramming and inflammation in the liver.

Selenium (Se) intake disequilibrium is associated with many human diseases (e.g., Keshan disease and type 2 diabetes). To understand the mechanism of Se deficiency-induced hepatic pathogenesis, a pure line pig model was established by feeding a diet with either 0.07 mg/kg Se or 0.3 mg/kg Se for 16 weeks. The hepatic metabolome, lipidome, global proteome, and whole transcriptome were analyzed. Se deficiency causes a redox imbalance via regulation of selenoproteins at both the mRNA and protein level, and blocks the glutathione anti-oxidant system along with enhanced glutathione synthesis and catabolism. The Warburg effect was observed by enhanced activation of the glycolysis and phosphate pentose pathways. The tricarboxylic acid cycle was dysfunctional since the preliminary metabolites decreased and shifted from using glycolysis origin substrates to a glutamine catabolism-preferred metabolic mode. The reprogrammed central carbon metabolism induced widely restrained lipid synthesis. In addition, a Se deficiency initiated inflammation by activating the NF-κB pathway through multiple mechanisms. These results identified the potential metabolic vulnerability of the liver in response to a Se deficiency-induced redox imbalance and possible therapeutic or intervention targets.

Development and application of a HPLC-ICP-MS method to determine selenium speciation in muscle of pigs treated with different selenium supplements.

Dietary selenium deficiency is recognized as a global problem. Pork is the most widely consumed meat throughout the world and an important source of selenium for humans. In this study, a reliable approach was developed for analyzing selenium and its speciation in the muscles of pigs after different selenium treatments. The selenium source deposition efficiency was ranked as: selenomethionine > methylselenocysteine > selenite, and the muscle selenium content had a dose effect with selenomethionine supplementation. In total, four species of selenium were detected in the muscles of pigs and the distributions of these selenium species were greatly affected by the dietary selenium supplementation forms and levels. Selenomethionine (>70% of total selenium) and selenocystine (>11%) were the major selenium species, followed by methylselenocysteine and selenourea. Therefore, selenium-enriched pork produced from selenomethionine is a good source for improving human dietary selenium intake.

Lipidomics analysis for identifying the geographical origin and lactation stage of goat milk.

Goat milk samples of three lactation stages (colostrum, mature and late milk) were collected from three farms and analyzed with an untargeted method based on UPLC-Q-Exactive Orbitrap Mass Spectrometry and multivariate statistics. A total of 14 lipid subclasses and 756 lipid molecules were identified in samples. Five lipid subclasses and 51 lipid molecules in milk were significantly different among different geographical origins. Two lipid subclasses and 26 lipid molecules were significantly different among different lactation stages. Combined with the partial least squares discriminant analysis results of lipid molecules with a VIP value (Variable Importance in the projection) higher than 1, totally 38 and 19 lipid molecules could be used as potential indicators to identify geographical origins and lactation stages, respectively. Based on six and five selected molecules, the correct rates of discrimination models for geographical origin and lactation stage respectively reached 100% and 96%.

Arsenic-Containing Qinghuang Powder () is an Alternative Treatment for Elderly Acute Myeloid Leukemia Patients Refusing Low-Intensity Chemotherapy.

OBJECTIVE: To analyze the overall survival (OS) of elderly acute myeloid leukemia (AML) patients treated with oral arsenic-containing Qinghuang Powder (, QHP) or low-intensity chemotherapy (LIC). METHODS: Forty-two elderly AML patients treated with intravenous or subcutaneous LIC (1 month for each course, at least 3 courses) or oral QHP (3 months for each course, at least 2 courses) were retrospectively analyzed from January 2015 to December 2017. The main endpoints of analysis were OS and 1-, 2-, 3-year OS rates of patients, respectively. And the adverse reactions induding bone marrow suppression, digestive tract discomfort and myocardia injury were observed. RESULTS: Out of 42 elderly AML patients, 22 received LIC treatment and 20 received QHP treatment, according to patients' preference. There was no significant difference on OS between LIC and QHP patients (13.0 months vs. 13.5 months, >0.05). There was no significant difference on OS rates between LIC and QHP groups at 1 year (59.1% vs. 70.0%), 2 years (13.6% vs. 15%), and 3 years (4.6% vs. 5.0%, all >0.05). Furthermore, there was no significant difference of OS on prognosis stratification of performance status > 2 (12 months vs. 12 months), age> 75 year-old (12.0 months vs. 12.5 months), hematopoietic stem cell transplant comorbidity index >2 (12 months vs. 13 months), poor cytogenetics (12 months vs. 8 months), and diagnosis of secondary AML (10 months vs. 14 months) between LIC and QHP patients (>0.05). CONCLUSION: QHP may be an alternative treatment for elderly AML patients refusing LIC therapy.

[Effect of acupuncture in different time on nausea and vomiting induced by chemotherapy of lung cancer].

OBJECTIVE: To observe the effect of acupuncture in different time on nausea and vomiting induced by chemotherapy of lung cancer. METHODS: A total of 150 patients with chemotherapy for lung cancer were randomized into a No.1 observation group, a No.2 observation group and a control group, 50 cases in each one. Excluded the dropped-off cases, finally, there were 49 cases in the No.1 observation group, 44 cases in the No.2 observation group and 47 cases in the control group. In the control group, 30 min before chemotherapy, the slow intravenous injection with tropisetron hydrochloride was used, 5 mg each time, once a day for 3 days. In the No.1 observation group, 30 min before chemotherapy, the slow intravenous injection with tropisetron hydrochloride was given combined with acupuncture. The acupoints selected were Zusanli (ST 36), Zhongwan (CV 12) and Neiguan (PC 6). The needles were retained for 30 min. The treatment was given once a day for 3 days totally. In the No.2 observation group, 30 min before chemotherapy, the slow intravenous injection with tropisetron hydrochloride was used, and 30 min after chemotherapy, acupuncture treatment was exerted. The acupoints and needling method were same as those in the No.1 observation group. Before and after treatment, the digestive reaction score, Karnofsky performance status scale (KPS) score and white blood cell count were all observed in the three groups. Additionally, the therapeutic effect and adverse reaction were observed and the therapeutic effect was compared among the treatment with acupuncture in different time. RESULTS: On the 2nd day of chemotherapy, the effective rates were 85.7% (42/49) and 75.0% (33/44) in the No.1 observation group and the No.2 observation group respectively, both higher obviously than 68.1% (32/47) in the control group (P<0.05), and the effective rate in the No.1 observation group was higher obviously than the No.2 observation group (P<0.05). On the 3rd day of chemotherapy, the effective rates were 81.6% (40/49) and 61.4% (27/44) in the No.1 observation group and the No.2 observation group respectively, both higher obviously than 57.5% (27/47) in the control group (P<0.05), and the effective rate in the No.1 observation group was higher obviously than the No.2 observation group (P<0.05). Compared before treatment, the KPS scores after treatment were obviously lower in the three groups (P<0.05), and the decreased value of KPS score in the No.1 observation group was much lower than the control group and the No.2 observation group (P<0.05). After 3-day chemotherapy, the white blood cell count was all reduced in each group, but the decreased value was not different statistically among the groups (P>0.05). CONCLUSION: Acupuncture combined with the slow intravenous injection with tropisetron hydrochloride achieve the satisfactory effect of prevention and treatment for vomiting induced by chemotherapy of lung cancer. The acupuncture intervention before chemotherapy greatly improves the effect on the nausea and vomiting induced by chemotherapy of lung cancer.