In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Hypoxia is associated with human non-small cell lung cancers (NSCLC), which are highly resistant to chemotherapy. The hypoxia inducible factor (HIF) as a transcription factor in response to hypoxia indicates that it could be a novel, tumor-specific target for anticancer therapy. We hypothesized that disruption of HIF pathway through lentiviral vector-mediated HIF-1alpha RNA interference (RNAi) could reverse the hypoxia-induced resistance to chemotherapy.', 'We transfected Human NSCLC cell lines, SPCA1 and A549 with HIF-1alpha specific RNAi lentiviral vectors as well as controls. HIF-1alpha silenced cells [SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-)] were screened by blasticidin. They were incubated in 19 or 0.5% O2 for 16 h followed by the assessment of chemosensitivity to cisplatin and doxorubicin with MTT and clonogenic assays. Quantitative RT-PCR and Western blot analysis were used to detect the expressions of HIF-1alpha mRNA and protein, respectively. Moreover, flow cytometry was used to monitor the expression of P-glycoprotein.', 'Exposure of SPCA1 and A549 cells to 0.5% O2 significantly increased resistance to cisplatin and doxorubicin, in contrast to cells incubated in normoxia. Transduction of SPCA1 with HIF-1alpha RNAi vector resulted in sequence specific silencing with 87.2 and 84.6% decreases of HIF-1alpha mRNA transcription and 97.3 and 94.8% of protein expressions in normoxia and hypoxia, respectively. Correspondingly, they are 89.2, 89.9% and 97.2, 88.4% decreases in A549 cells. Hypoxia-induced resistance to cisplatin and doxorubicin were reversed in SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-) cells. There was no significant P-glycoprotein increase induced by hypoxia in NSCLC cells.\Question: Is hypoxia-induced resistance to cisplatin and doxorubicin in non-small cell lung cancer inhibited by silencing of HIF-1alpha gene?
Our studies demonstrated that hypoxia-induced chemoresistance to cisplatin and doxorubicin in NSCLC cells is through the HIF pathway. MDR1 regulation may not be involved in hypoxia-induced chemoresistance. Combining delivery of HIF-1alpha RNAi lentiviral vector with cisplatin-related chemotherapy regimens may enable us to develop more effective strategy for NSCLC therapy.

Context: The aim of this study was to evaluate the effect of local injection of vasopressin on blood loss and secondary impact on complications during cesarean section in patients with placenta previa.', 'We retrospectively reviewed the medical records of all patients diagnosed with placenta previa admitted to our hospital. Two consecutive periods were compared. During period B, 59 patients underwent the local injection of a vasopressin solution (4 U in 20 mL of saline) into the placental implantation site after placental delivery. During period A, 50 patients underwent cesarean section without vasopressin injection, and were analyzed as a control group. The estimated blood loss was recorded, as were the complications during surgery. In addition, the expression of the vasopressin V1α receptor in uterine smooth muscle was evaluated by immunohistochemistry.', 'The mean estimated blood loss was significantly lower in the vasopressin group than in the control group. There were no statistically significant differences with surgical complications. The vasopressin V1α receptor was highly expressed in smooth muscle cells in the lower segment of the uterine body, whereas the immunoreactivity for the oxytocin receptor was faint in the lower segment.\Question: Does local injection of vasopressin reduce the blood loss during cesarean section in placenta previa?
The local injection of vasopressin into the placental implantation site significantly reduced the blood loss without increasing the morbidity.

Context: The apoptosis inhibitor-5 (API5), anti-apoptosis protein, is considered a key molecule in the tumor progression and malignant phenotype of tumor cells. Here, we investigated API5 expression in cervical cancer, its clinical significance, and its relationship with phosphorylated extracellular signal-regulated kinase 1 and 2 (pERK1/2) in development and progression of cervical cancer.', 'API5 effects on cell growth were assessed in cervical cancer cell lines. API5 and pERK1/2 immunohistochemical staining were performed on a cervical cancer tissue microarray consisting of 173 primary cervical cancers, 306 cervical intraepithelial neoplasias (CINs), and 429 matched normal tissues.', 'API5 overexpression promoted cell proliferation and colony formation in CaSki cells, whereas API5 knockdown inhibited the both properties in HeLa cells. Immunohistochemical staining showed that API5 expression increased during the normal to tumor transition of cervical carcinoma (P\u2009<\u20090.001), and this increased expression was significantly associated with tumor stage (P\u2009=\u20090.004), tumor grade (P\u2009<\u20090.001), and chemo-radiation response (P\u2009=\u20090.004). API5 expression levels were positively associated with pERK1/2 in cervical cancer (P\u2009<\u20090.001) and high grade CIN (P\u2009=\u20090.031). In multivariate analysis, API5+ (P\u2009=\u20090.039) and combined API5+/pERK1/2+ (P\u2009=\u20090.032) were independent prognostic factors for overall survival.\Question: Is apoptosis inhibitor-5 overexpression associated with tumor progression and poor prognosis in patients with cervical cancer?

API5 expression is associated with pERK1/2 in a subset of cervical cancer patients and its expression predicts poor overall survival, supporting that API5 may be a promising novel target for therapeutic interventions.