Effectiveness of Traditional Chinese Medicine for Liver Protection and Chemotherapy Completion among Cancer Patients

While traditional Chinese medicine (TCM) is widely used among Chinese patients with cancer, studies evaluating the effectiveness of TCM using objective indicators are rare. We examined the effectiveness of TCM for liver protection and completion of chemotherapy among patients with cancer receiving chemotherapy. We used a case-control design to examine the medical records of patients with cancer who received chemotherapy in a teaching hospital in Taipei in 2004. A total of 184 courses of chemotherapy among 89 patients were studied. Of the 184 courses, 42 used TCM jointly with chemotherapy served as cases, while the remaining 142 courses served as controls. Outcome variables included counts of cancelled or delayed chemotherapies and liver function (aspartate aminotransferase, AST and alanine aminotransferase, ALT) 1 week before, during and 2 weeks after chemotherapy. Generalized estimating equations were used to analyze the data. Patients who had concomitant TCM with chemotherapy had lower serum ALT and AST during chemotherapy than the controls given that the age, sex, cancer stage, radiotherapy sites, cancer diagnosis and potential hepatotoxicity of the chemotherapeutic drugs were controlled for in the model [β  = −3.48, 95% confidence interval (CI) −10.08 to 3.11 for AST; β  = −5.95, 95% CI: −11.47 to −0.44 for ALT]. There was no significant difference between the case and control groups for odds of completing one course of chemotherapy. Use of TCM with chemotherapy resulted in protection of the liver during chemotherapy, as manifested by lower serum AST and ALT levels

The Impact of Individual Characteristics, Personality Traits, Perceived Risk on Young People's Intention to Participate in Overseas Working Holiday

AbstractThis paper analyzes whether individual characteristics, personality traits, and perceived risk will affect young people's intention to participate in overseas working holiday, and taking the three countries of Australia, the United States, and the United Kingdom as examples. The sample consists of young people and students at numerous universities and colleges, with ages ranging from 18 to 31. A total of 350 questionnaires were issued, and 204 valid questionnaires were recovered, with a return rate of 58.2%. Multiple regression was used to test hypotheses. The research results indicate that the factors influencing young people's intention to take working holiday in different countries were not entirely the same. It is found that age, work experience, neuroticism, extroversion, openness to experience, agreeableness, environmental and social risk, and agent and workplace risk may influence intention to participate in overseas working holiday. The research implications and recommendations are also presented

Exploring the value co-destruction model for on-line deviant behaviors of hotel customers

© 2019 Elsevier Ltd This study aims to build a value co-destruction model by exploring the online deviant behavior of hotel customers. Desire for revenge and desire for recovery are considered mediators. Hotel guests in notable Taiwan locations were surveyed via the Internet (no. = 601 valid responses). This study finds that negative emotion indirectly impacts negative electronic word of mouth (eWOM) with desire for revenge as a mediator. Furthermore, desire for recovery has the potential to mitigate the impact of negative emotion on negative eWOM. However, the desire for recovery is less intense than the desire for revenge. Based on these findings, this study concludes that emotion, by itself, does not result in action. Respondents only commit negative eWOM because they want to hurt the firm that wronged them. Respondents are also willing to entertain the idea of service recovery. However, desire for revenge is a stronger mediating factor

Plasma lipoprotein subfraction concentrations are associated with lipid metabolism and age-related macular degeneration

10.1194/jlr.M073684Journal of Lipid Research5891785-179

Recombinant VP1, an Akt Inhibitor, Suppresses Progression of Hepatocellular Carcinoma by Inducing Apoptosis and Modulation of CCL2 Production

BACKGROUND: The application of viral elements in tumor therapy is one facet of cancer research. Recombinant capsid protein VP1 (rVP1) of foot-and-mouth disease virus has previously been demonstrated to induce apoptosis in cancer cell lines. Here, we aim to further investigate its apoptotic mechanism and possible anti-metastatic effect in murine models of hepatocellular carcinoma (HCC), one of the most common human cancers worldwide. METHODOLOGY/PRINCIPAL FINDINGS: Treatment with rVP1 inhibited cell proliferation in two murine HCC cell lines, BNL and Hepa1-6, with IC₅₀ values in the range of 0.1-0.2 µM. rVP1 also induced apoptosis in these cells, which was mediated by Akt deactivation and dissociation of Ku70-Bax, and resulted in conformational changes and mitochondrial translocation of Bax, leading to the activation of caspases-9, -3 and -7. Treatment with 0.025 µM rVP1, which did not affect the viability of normal hepatocytes, suppressed cell migration and invasion via attenuating CCL2 production. The production of CCL2 was modulated by Akt-dependent NF-κB activation that was decreased after rVP1 treatment. The in vivo antitumor effects of rVP1 were assessed in both subcutaneous and orthotopic mouse models of HCC in immune-competent BALB/c mice. Intratumoral delivery of rVP1 inhibited subcutaneous tumor growth as a result of increased apoptosis. Intravenous administration of rVP1 in an orthotopic HCC model suppressed tumor growth, inhibited intra-hepatic metastasis, and prolonged survival. Furthermore, a decrease in the serum level of CCL2 was observed in rVP1-treated mice. CONCLUSIONS/SIGNIFICANCE: The data presented herein suggest that, via inhibiting Akt phosphorylation, rVP1 suppresses the growth, migration, and invasion of murine HCC cells by inducing apoptosis and attenuating CCL2 production both in vitro and in vivo. Recombinant protein VP1 thus has the potential to be developed as a new therapeutic agent for HCC

Seizure After Local Anesthesia for Nasopharyngeal Angiofibroma

We report a young male patient who experienced seizure after local injection of 3 mL 2% lidocaine with epinephrine 1:200,000 around a recurrent nasal angiofibroma. After receiving 100% oxygen via mask and thiamylal sodium, the patient had no residual neurologic sequelae. Seizure immediately following the injection of local anesthetics in the nasal cavity is probably due to injection into venous or arterial circulation with retrograde flow to the brain circulation. Further imaging study or angiography should be done before head and neck surgeries, especially in such highly vascular neoplasm

Insulin regulates glucose consumption and lactate production through reactive oxygen species and pyruvate kinase M2.

Although insulin is known to regulate glucose metabolism and closely associate with liver cancer, the molecular mechanisms still remain to be elucidated. In this study, we attempt to understand the mechanism of insulin in promotion of liver cancer metabolism. We found that insulin increased pyruvate kinase M2 (PKM2) expression through reactive oxygen species (ROS) for regulating glucose consumption and lactate production, key process of glycolysis in hepatocellular carcinoma HepG2 and Bel7402 cells. Interestingly, insulin-induced ROS was found responsible for the suppression of miR-145 and miR-128, and forced expression of either miR-145 or miR-128 was sufficient to abolish insulin-induced PKM2 expression. Furthermore, the knockdown of PKM2 expression also inhibited cancer cell growth and insulin-induced glucose consumption and lactate production, suggesting that PKM2 is a functional downstream effecter of insulin. Taken together, this study would provide a new insight into the mechanism of insulin-induced glycolysis

Deficiency of Mkrn2 causes abnormal spermiogenesis and spermiation, and impairs male fertility.

Although recent studies have shed insights on some of the potential causes of male infertility, new underlining molecular mechanisms still remain to be elucidated. Makorin-2 (Mkrn2) is an evolutionarily conserved gene whose biological functions are not fully known. We developed an Mrkn2 knockout mouse model to study the role of this gene, and found that deletion of Mkrn2 in mice led to male infertility. Mkrn2 knockout mice produced abnormal sperms characterized by low number, poor motility, and aberrant morphology. Disruption of Mkrn2 also caused failure of sperm release (spermiation failure) and misarrangement of ectoplasmic specialization (ES) in testes, thus impairing spermiogenesis and spermiation. To understand the molecular mechanism, we found that expression of Odf2, a vital protein in spermatogenesis, was significantly decreased. In addition, we found that expression levels of Odf2 were decreased in Mkrn2 knockout mice. We also found that MKRN2 was prominently expressed in the sperm of normal men, but was significantly reduced in infertile men. This result indicates that our finding is clinically relevant. The results of our study provided insights into a new mechanism of male infertility caused by the MKRN2 downregulation