This cohort study assessed the structural relationships among social support, acculturation, and postpartum depressive symptoms experienced by marriage-based immigrant mothers in Taiwan. Data were collected at 1 and 6 months postpartum from 203 immigrant mothers married to Taiwanese men in Taipei, Taiwan. The structural equation modeling results showed that social support and postpartum depression were directly and negatively related. Higher social support and lower depression at 1 month postpartum were related to a positive social attitude (i.e., accepting attitude toward mainstream society). Social attitude was a moderator of the relationship between depression at 1 month and social support at 6 months postpartum, where a positive social attitude decreased the negative effect of depression at 1 month on social support at 6 months. Social support in the early postpartum period not only directly decreased postpartum depression, but also indirectly decreased postpartum depression through improving social attitude.

Chemotherapy is a major clinical treatment for managing patients with advanced and recurrent ovarian cancer. However, the clinical performance of chemotherapy is limited, and adverse effects have been observed. Integrating chemotherapy with current chemotherapeutic drugs and novel antitumor ingredients might improve the clinical performance of current chemotherapy for ovarian cancer. The aqueous extract of Solanum nigrum leaves (AE-SN), a key ingredient in many traditional Chinese medicine formulae, has exhibited tumor suppression efficacy in numerous human cancer cells but not in ovarian cancer cells. In this study, tumor suppression efficacy was determined using the ES-2, SKOV-3, and OVCAR-3 human ovarian cancer cell lines. The half-maximal inhibitory concentrations of the AE-SN in ES-2 and SKOV-3 cells were 1.052 and 1.779 mg/mL, respectively. AE-SN treatment increased the accumulation of mammalian microtubule-associated protein 1 light chain 3 A/B, an autophagic cell marker, in all the tested cell lines; however, it activated the cleavage of caspase-3, an apoptotic marker, only in SKOV-3 cells. Furthermore, the AE-SN also promoted tumor suppression efficiency of cisplatin, doxorubicin, and docetaxel in the tested ovarian cancer cells. In addition, AE-SN-enhanced cell death was associated with AE-SN-induced caspase-3 cleavage in SKOV-3 cells. In conclusion, the AE-SN exhibited tumor suppression efficacy and improved the tumor suppression efficiency of cisplatin, doxorubicin, and docetaxel in human ovarian cancer cells. Therefore, the AE-SN is a candidate antitumor ingredient that can be used in developing future integrated chemotherapy for managing ovarian cancer.

Abstract:Chemotherapy is the main approach for treating advanced and recurrent carcinoma, but the clinical performance of chemotherapy is limited by relatively low response rates, drug resistance, and adverse effects that severely affect the quality of life of patients. An association between epithelial-mesenchymal transition (EMT) and chemotherapy resistance has been investigated in recent studies. Our recent studies have found that the aqueous extract of Solanum nigrum (AESN) is a crucial ingredient in some traditional Chinese medicine formulas for treating various types of cancer patients and exhibits antitumor effects. We evaluated the suppression of EMT in MCF-7 breast cancer cells treated with AESN. The mitochondrial morphology was investigated using Mitotracker Deep-Red FM stain. Our results indicated that AESN markedly inhibited cell viability of MCF-7 breast cancer cells through apoptosis induction and cell cycle arrest mediated by activation of caspase-3 and production of reactive oxygen species. Furthermore, mitochondrial fission was observed in MCF-7 breast cancer cells treated with AESN. In addition to elevation of E-cadherin, downregulations of ZEB1, N-cadherin, and vimentin were found in AESN-treated MCF-7 breast cancer cells. These results suggested that AESN could inhibit EMT of MCF-7 breast cancer cells mediated by attenuation of mitochondrial function. AESN could be potentially beneficial in treating breast cancer cells, and may be of interest for future studies in developing integrative cancer therapy against proliferation, metastasis, and migration of breast cancer cells.

Replicating virus vectors are attractive tools for anticancer gene therapy, but the potential for adverse events due to uncontrolled spread of the vectors has been a major concern. To design a tumor-specific retroviral replicating vector (RRV), we replaced the U3 region of the RRV ACE-GFP with a regulatory sequence consisting of the hepatitis B virus enhancer II (EII) and human α-fetoprotein (AFP) core promoter to produce ACE-GFP-EIIAFP, a hepatocellular carcinoma (HCC)-targeting RRV. Similar to ACE-GFP, ACE-GFP-EIIAFP exhibited robust green fluorescent protein (GFP) expression in HCC cells and, most importantly, it exhibited HCC-specific replication and did not replicate in non-HCC tumor cells or normal liver cells. We sequenced the promoter region of ACE-GFP-EIIAFP collected from serial infection cycles to examine the genomic stability of the vector during its replicative spread, and found that the vector could retain the hybrid promoter in the genome for at least six infection cycles. In vitro studies revealed that ACE-CD-EIIAFP and ACE-PNP-EIIAFP, which express the yeast cytosine deaminase and Escherichia coli purine nucleoside phosphorylase, respectively, exert a highly potent cytotoxic effect on HCC cells in the presence of their respective prodrugs. In vivo, ACE-CD-EIIAFP-mediated suicide gene therapy efficiently suppressed HCC tumor growth and no detectable RRV signal was observed in extratumoral tissues. These results suggest that the tumor-specific, suicide-gene-encoding RRV may fulfill the promise of retroviral gene therapy for cancer.

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.

ATP has been shown to activate the phospholipase C/diacylglycerol/protein kinase C (PKC) pathway. However, little is known about the downstream signaling events. The present study was designed to examine the effect of ATP on activation of the mitogen-activated protein kinase (MAPK) signaling pathway and its physiological role in human granulosa-luteal cells. Western blot analysis, using a monoclonal antibody that detected the phosphorylated forms of extracellular signal-regulated kinase-1 and -2 (p42(mapk) and p44 (mapk), respectively), demonstrated that ATP activated MAPK in a dose- and time-dependent manner. Treatment of the cells with suramin (a P2 purinoceptor antagonist), neomycin (a phospholipase C inhibitor), staurosporin (a PKC inhibitor), or PD98059 (an MAPK/ERK kinase inhibitor) significantly attenuated the ATP-induced activation of MAPK. In contrast, ATP-induced MAPK activation was not significantly affected by pertussis toxin (a G(i) inhibitor). To examine the role of G(s) protein, the intracellular cAMP level was determined after treatment with ATP or hCG. No significant elevation of intracellular cAMP was noted after ATP treatment. To determine the role of MAPK in steroidogenesis, human granulosa-luteal cells were treated with ATP, hCG, or ATP plus hCG in the presence or absence of PD98059. RIA revealed that ATP alone did not significantly affect the basal progesterone concentration. However, hCG-induced progesterone production was reduced by ATP treatment. PD98059 reversed the inhibitory effect of ATP on hCG-induced progesterone production. To our knowledge, this is the first demonstration of ATP-induced activation of the MAPK signaling pathway in the human ovary. These results support the idea that the MAPK signaling pathway is involved in mediating ATP actions in the human ovary.

Due to SB-NP's enhanced bioavailability, effective anti-HCV activity and an overall hepatoprotective effect, we suggest that SB-NP may be a cost-effective anti-HCV agent that merits further evaluation for the treatment of hepatitis C.

According to the theories of Traditional Chinese Medicine (TCM), energy runs through 12 meridians longitudinally up and down the body. The study objectives were to compare the meridian energy between subjects with and without abnormal gastroscopy findings. We applied a cross-sectional and correlational research design. The study included 1,223 participants who had their health examinations at a university hospital in Taipei from 1st August 2005 through 31st August 2007. Meridian energy was examined using a meridian energy analysis device. The gastroscopy was operated by certified gastroenterologists. Participants with abnormal stomach and esophageal findings using gastroscopy had significantly lower mean meridian energy. There were no significant differences in meridian energy between participants with and without abnormal duodenum findings. When all of the meridians were examined individually, participants with abnormal findings in esophagus and stomach had significantly lower meridian energy in each of the meridians. The results of this study demonstrated that structural abnormality in the gastric area was related to lower meridian energy. Whether enhancing meridian energy could improve gastric and esophageal health merits further studies.