OBJECTIVETo observe the clinical effects of essential hypertension treated with acupuncture at Siguan [Hegu (LI 4) and Taichong (LR 3)], Quchi (LI 11) and Xingjian (LR 2).

METHODSSixty cases of essential hypertension were randomly divided into an acupuncture group and a medication group, 30 cases in each group. Two groups of acupoint, which were (1) Siguan [Hegu (LI 4) and Taichong (LR 3)] and (2) Quchi (LI 11), Xingjian (LR 2), were selected alternatively in the acupuncture group, once everyday. In the medication group, captopril was prescribed for oral administration 25 mg per time, three times per day. Seven days made one session in both groups and totally three sessions were required.

RESULTS(1) After treatment, the blood pressure were decreased significantly in the two groups (all P < 0.01). Compared with the medication group, the diastolic pressure after 14 days, 21 days of treatment in the acupuncture group was decreased significantly (both P < 0.01). (2) In the terms of TCM syndrome score, the improvement of dizziness, soreness and weakness of waist and knees, palpitations was significant in the acupuncture group compared with that in the medication group(all P < 0.05). (3) The acupuncture group had less adverse reactions compared with the control group (P < 0.05).

CONCLUSIONAcupuncture at Hegu (LI4) and Taichong (LR 3), Quchi (LI 11) and Xingjian (LR 2) can effectively decrease blood pressure; the effect of controlling diastolic pressure is better than captopril. It can also improve the symptoms of dizziness, soreness and weakness of waist and knees, and palpitations.

Acupuncture Points ; Acupuncture Therapy ; Adult ; Aged ; Blood Pressure ; Essential Hypertension ; Female ; Humans ; Hypertension ; physiopathology ; therapy ; Male ; Middle Aged ; Treatment Outcome ; Yin Deficiency ; therapy ; Yin-Yang

Administration, Oral ; Anti-Bacterial Agents ; administration & dosage ; Cytomegalovirus Infections ; drug therapy ; immunology ; virology ; Erythromycin ; administration & dosage ; Female ; Humans ; Infant ; Male ; T-Lymphocyte Subsets ; immunology ; Virus Replication

In recent years a number of qualitative research methods have gained popularity within the health care arena. Despite this popularity, different qualitative analysis methods pose many challenges to most researchers. The present paper responds to the needs expressed by recent Chinese medicine researches. The present paper is mainly focused on the concepts, nature, application of framework analysis, especially on how to use it, in such a way to assist the newcomer of Chinese medicine researchers to engage with the methodology.
Humans ; Medicine, Chinese Traditional ; Qualitative Research ; Research ; Research Design

OBJECTIVE TNF- related apoptosis- inducing ligand(TRAIL)is a promising cancer therapeutic agent due to its minimal toxicity to normal tissues and remarkable apoptotic activity in tumors. However, most breast cancer cells are resistant to TRAIL- induced apoptosis. Our objectives are to investigate the underlying molecular mechanisms and to develop strategies to overcome such resistance. METHODS To identify modulators of TRAIL-induced apoptosis, we carried out a genome wide siRNA screen. To validate the screening result, we either silenced or overexpressed the identified genes in various breast cancer cells and changes in growth and TRAIL-induced cell apoptosis were determined in vitro and in an orthotopic xenograft mouse model. Finally, we investigated whether small molecules targeting the identified genes improve the effectiveness of TRAIL-therapy. RESULTS We unexpectedly identified androgen receptor (AR) to be responsible for TRAIL resistance. While AR is classically viewed as the key factor in prostate cancer progression, we found that AR expression levels were markedly elevated in human invasive breast cancer specimens including triple- negative breast cancers (TNBC) that are highly aggressive with poor prognosis. Importantly, breast cancer cell lines express different levels of AR that correlated with their TRAIL resistance. AR overexpression in MDA- MB- 231 and MDA- MB- 436 cells suppressed the TRAIL sensitivity whereas knockdown of AR rendered MCF-7 and MDA-MB-453 cells sensitive to TRAIL-induced apoptosis. AR overexpression also induced TRAIL resistance in breast tumors in vivo. Further, we observed an upregulation of the TRAIL receptor, death receptor 5 (DR5) in breast cancer cells, following the removal or inhibition of AR by its antagonists Casodex and MDV3100. Treatment with AR antagonists also enhanced TRAIL- induced breast cancer cell apoptosis. CONCLUSION AR signaling suppresses TRAIL-induced breast cancer cell apoptosis, in part, by suppressing DR5 expression, and a combination of AR antagonists together with TRAIL may be a novel and effective therapy for TNBC.

Animals ; Blood Glucose ; drug effects ; Body Weight ; drug effects ; Chronic Disease ; Female ; Hypoxia ; physiopathology ; KATP Channels ; drug effects ; Male ; Propylamines ; pharmacology ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley

A method for the determination of Fe, Co, Mn and Ni in synthetic diamonds by inductively coupled plasma atomic emission spectrometry ( ICP-AES) was proposed. The synthetic diamond sample was decomposed completely, while the sample was burned in air at 1000 ℃ for 10 h, and then a mixed acid of H2 SO4 , aqua regia and HClO4 was used for the dissolving the residue of the sample. In this method, the limits of detection of Fe, Co, Mn and Ni were 0. 0147, 0. 0018, 0. 0006 and 0. 0027 mg/L, respectively. Under the optimum condition, Fe, Co, Mn and Ni in synthetic diamond sample were determined. The values of RSDs (n=7) were less than 0. 5%. The recoveries of added standard were 94. 0%-105. 0%.

A method for the simultaneous determination of oxygen and nitrogen in synthetic diamonds by inert gas high temperature extraction-impulse heating method was proposed. The sample weight, the selection of analysis power and the calibration curves of oxygen and nitrogen were discussed. Oxygen and nitrogen in analytical samples are determined. Values of RSDs (n=7) for oxygen and nitrogen were less than 4. 5% and 4. 0% respectively. The analytical results of oxygen and nitrogen obtained by the proposed method were in good agreement with those by inert gas fusion-impulse heating method.

OBJECTIVE: To study the expression of interferon-λ1 (IFN-λ1) in respiratory epithelial cells in children with human rhinovirus (HRV) infection. METHODS: Sputum samples and nasopharyngeal swabs were collected from the children who were hospitalized due to acute respiratory infection from February to October, 2017. Bacterial culture was performed, and nucleic acid test was performed for 11 respiratory pathogens. A total of 90 children with positive HRV alone were enrolled as the HRV infection group, and 95 children with positive respiratory syncytial virus (RSV) alone were enrolled as the RSV infection group. A total of 50 healthy children who underwent outpatient physical examination during the same period of time and had negative results for all pathogen tests were enrolled as the healthy control group. Nasopharyngeal swabs were collected from all groups, and quantitative real-time PCR was used to measure viral load and the mRNA expression of IFN-λ1. RESULTS: In the HRV infection group, there was no significant difference in the mRNA expression of IFN-λ1 between boys and girls and across all age groups (P>0.05). In the HRV infection group, there was no correlation between the mRNA expression of IFN-λ1 and HRV load (P>0.05). The mRNA expression of IFN-λ1 in the HRV infection group was significantly higher than that in the healthy control group (P<0.05), but significantly lower than that in the RSV infection group (P<0.05). CONCLUSIONS HRV can induce the expression of IFN-λ1 in respiratory epithelial cells, suggesting that IFN-λ1 may play an important role in anti-HRV infection in children.
Antiviral Agents ; Child ; Epithelial Cells ; Female ; Humans ; Interferons ; Male ; Picornaviridae Infections ; Respiratory Tract Infections ; Rhinovirus

Adolescent ; Adult ; Dust ; analysis ; Female ; Health Status ; Humans ; Industry ; Male ; Middle Aged ; Occupational Exposure ; analysis ; Quartz ; Young Adult

OBJECTIVETo investigate the anti-fibrosis effects and mechanisms of fenofibrate on hepatic fibrosis using a mouse model of fibrosis induced by carbon tetrachloride (CCl4).

METHODSTwenty-six male C57BL mice were divided into the following three groups: CCL4-induced untreated model control (n = 10), CCl4-induced fenofibrate-treated model (n = 10), and uninduced/untreated normal control (n = 6). All animals were sacrificed after the 5 weeks of induction and treatment. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA) and procollagen III amino-terminal peptide (PIIINP) were determined by routine biochemistry assays. Liver content of hydroxyproline (HYP) was measured by spectrophotometry. Liver content of malonic aldehyde (MDA) and superoxide dismutase (SOD) was measured by enzymatic assays. mRNA expression levels of liver fibrosis-associated factors were determined by PCR, and included alpha-smooth muscle actin (a-SMA), transforming growth factor-beta1 (TGFbeta1), type I collagen-alpha (Collagen1a), peroxisome proliferator-activated receptor-alpha (PPARa), and the inflammatory cytokines tumor necrosis factor alpha (TNFa) and interleukin-6 (IL-6). Finally, the degree of inflammation and fibrosis were assessed by histological analysis using hematoxylin-eosin and Sirius red staining.

RESULTSCompared to the untreated model group, the fenofibrate-treated model group showed significantly lower levels of serum ALT (55.72+/-1.20 vs. 38.72+/-1.25 IU/L), HA (236.20+/-17.57 vs. 152.9+/-13.06 mug/L) and PIIINP (41.66+/-1.89 vs. 34.32+/-1.53 mug/L) (all P less than 0.05). The fenofibrate-treated group also showed a significantly higher level of hepatic SOD content (untreated model: 67.00+/-4.65 vs. 101.1+/-5.32) but significantly lower level of hepatic MDA content (14.67+/-0.93 vs. 10.17+/-0.60 nmol/mg) and lower level of hepatic HYP content (0.67+/-0.80 vs. 0.41+/-0.50 mg/g) (all, P less than 0.05). In addition, the fenofibrate-treated group showed significantly reduced mRNA expression levels of a-SMA (6.83+/-0.88 vs. untreated model: 11.57+/-1.31), TGFbeta1 (67.83+/-4.65 vs. 112.30+/-4.81), Collagen1a (67.83+/-4.65 vs. 112.30+/-4.81), TNFa (17.43+/-2.32 vs. 37.83+/-4.69), and IL-6 (4.00+/-0.49 vs. 5.62+/-0.54), but significantly increased PPARa (0.30+/-0.03 vs. 0.18+/-0.03) (all, P less than 0.05). Finally, the degree of CCL4-induced hepatic fibrosis was attenuated by the fenofibrate treatment.

CONCLUSIONFenofibrate can reduce the degree of liver fibrosis in mice induced by CCl4. The mechanism may involve up-regulation of PPARa, inhibition of the inflammatory response, and enhancement of SOD antioxidant activity.

Animals ; Fenofibrate ; therapeutic use ; Inflammation ; drug therapy ; Liver Cirrhosis, Experimental ; drug therapy ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; PPAR alpha ; metabolism ; Superoxide Dismutase ; metabolism