Changes in sexual life experienced by women in Taiwan after receiving treatment for breast cancer.

As the number of breast cancer survivors increases, these patients with sexual problems also increase. For breast cancer survivors, sexual problems are a common and painful experience. Although breast cancer survivors often encounter sexual problems, Taiwanese women are culturally conservative and patients rarely discuss sex problems with clinicians. In this study, we used qualitative methods to better understand the changes in sexual life and related care strategies for breast cancer survivors. Twenty interviews were conducted on clinical patients enrolled in hospitals that received breast cancer treatment. The data were analysed by performing a constant comparative analysis. Three themes emerged: the causes of changes in sexual life, internal response strategies and external response strategies. Ten subthemes were identified. Changes in sexual life in patients with breast cancer in this study included changes related to body image, influence of friends and family, age, genital problems, and illegal love of a partner. Breast cancer survivors can tolerate and regulate sexual life changes by adopting internal and external response strategies. Medical staff must be sensitive and must understand strategies for dealing with sexual life changes that may occur during cancer adjustment and how these strategies can help women's well-being in the rest of their lives.

Sexual Problems of Patients With Breast Cancer After Treatment: A Systematic Review.

BACKGROUND: Sexual health is a crucial part of quality of life in breast cancer survivors, regardless of their relationship status. However, previous studies have rarely used qualitative methods to explore the postoperative experiences and feelings of patients with breast cancer. OBJECTIVE: The aim of this study was to examine the causes of changes in sexual relationships of breast cancer survivors, methods for adaptation to these changes, and healthcare interventions to facilitate the patients' return to a normal life. INTERVENTIONS/STUDY METHODS: A survey was performed by using five electronic databases and electronic journals accessed through the Internet. The following keywords were used: "breast cancer," "sexual problem," "sexual dysfunction," and "qualitative." RESULTS: Seven articles were included in the literature review. Three main domains were explored, namely, reasons for sexual relationship changes; the way patients used to adapt to sexual life after the diagnosis of breast cancer; and intervention by healthcare workers. CONCLUSIONS: The results of this study can facilitate and encourage health professionals to identify, examine, and solve most of the patient's sexual problems by using the functional and medical framework of the healthcare system. IMPLICATIONS FOR PRACTICE: One practical recommendation of this study is the incorporation of sexual counseling units into the national healthcare system. Counselors in these units can help breast cancer survivors solve problems and improve sexual satisfaction between couples.

Low-dose ionizing radiation induces mitochondrial fusion and increases expression of mitochondrial complexes I and III in hippocampal neurons.

High energy ionizing radiation can cause DNA damage and cell death. During clinical radiation therapy, the radiation dose could range from 15 to 60 Gy depending on targets. While 2 Gy radiation has been shown to cause cancer cell death, studies also suggest a protective potential by low dose radiation. In this study, we examined the effect of 0.2-2 Gy radiation on hippocampal neurons. Low dose 0.2 Gy radiation treatment increased the levels of MTT. Since hippocampal neurons are post-mitotic, this result reveals a possibility that 0.2 Gy irradiation may increase mitochondrial activity to cope with stimuli. Maintaining neural plasticity is an energy-demanding process that requires high efficient mitochondrial function. We thus hypothesized that low dose radiation may regulate mitochondrial dynamics and function to ensure survival of neurons. Our results showed that five days after 0.2 Gy irradiation, no obvious changes on neuronal survival, neuronal synapses, membrane potential of mitochondria, reactive oxygen species levels, and mitochondrial DNA copy numbers. Interestingly, 0.2 Gy irradiation promoted the mitochondria fusion, resulting in part from the increased level of a mitochondrial fusion protein, Mfn2, and inhibition of Drp1 fission protein trafficking to the mitochondria. Accompanying with the increased mitochondrial fusion, the expressions of complexes I and III of the electron transport chain were also increased. These findings suggest that, hippocampal neurons undergo increased mitochondrial fusion to modulate cellular activity as an adaptive mechanism in response to low dose radiation.

Induction of survivin inhibition, G2/M cell cycle arrest and autophagic on cell death in human malignant glioblastoma cells.

Chemotherapy efficacy is limited by intrinsic and acquired resistance in glioblastoma (GBM); hence, novel tactics are crucial. Survivin has been demonstrated as a key resistant factor in GBM because of its function in inhibiting apoptosis, regulating autophagy, and in promoting G2/M cell cycle transition. Parthenolide has been reported to be an effective antitumor agent in a variety of tumor cells and decreases survivin level in leukemia cells. But the effect of parthenolide on survivin and the cell death process in GBM is still unknown. The aim of this study was to examine whether parthenolide had the potential to inhibit cell proliferation in the GBM cell line U373. The parthenolide-induced effects in relation to survivin suppression and cell death were further investigated. Our results showed that parthenolide substantially inhibited cell viability with IC50 values of approximate 16 µM. Treatment with parthenolide at the dose of 16 µM led to considerable downregulation of survivin, G2/M cell cycle arrest and Chk2 upregulation in cells. Parthenolide induced apoptosis in only a few cells and a slight increase in activated caspases 3 levels. By contrast, parthenolide induced a significant increase of intracellular autophagosomes and the expression of autophagy related proteins, including ULK1 and LC3 I/LC3 II, in the treated cells. These results suggested that parthenolide induced survivin inhibition, G2/M cell cycle arrest, and triggered cell death through autophagic cell death in the GBM cell line.

The therapeutic effect of modified Yu Ping Feng San on idiopathic sweating in end-stage cancer patients during hospice care.

End-stage cancer patients frequently suffer from idiopathic sweating of unknown cause. This study was to evaluate the effect (primary endpoint) of modified Yu Ping Feng San on idiopathic sweating and adverse reactions (secondary endpoint). Thirty two end-stage cancer patients receiving hospice care, with exclusion criteria including sweating due to known causes and taking drugs which may affect the sweating threshold were enrolled. Patients received modified Yu Ping Feng San for 10 consecutive days. The quantitative measurement of sweating showed 26 patients (81.3%) had complete remission of sweating, and the average time required to reach 50% reduction was 4.6 days. The visual analog scale (VAS) sweating score estimated by patients and care-givers showed that the mean reductions were 8.4 and 9.1 points, respectively. An increase in appetite was experienced by 65.6% of patients, after administration of modified Yu Ping Feng San. The most prevalent treatment-related complications were nausea (15.6%), diarrhea (9.3%) and allergy (3.1%) without severity greater than grade 2, and these were reversible after cessation of treatment. These results suggest that modified Yu Ping Feng San is a safe and effective treatment for idiopathic sweating of unknown cause in end-stage cancer patients.