Cognitive behavioral therapy on personality characteristics of cancer patients.

BACKGROUND: The main treatment methods for cancer include surgery, radiotherapy, chemotherapy, targeted drug therapy and so on. Patients often feel anger, anxiety, depression, and other negative psychological reactions in the process of treatment. AIM: To explore the effects of cognitive behavioral therapy on the personality characteristics of cancer patients. METHODS: According to the matching design requirements, 150 cancer patients were divided into 3 groups based on sex, age, condition, and cultural background. Patients in the control group received conventional treatment. Patients in experimental group 1 received an intervention based on conventional treatment combined with cognitive behavioral therapy. Patients in experimental group 2 received family members' participation in addition to the treatment given in experimental group 1. An Eysenck personality questionnaire was used to investigate all the patients before and after the intervention, and the scores for psychosis, introversion, neuroticism, and concealment degree were analyzed. RESULTS: Compared with the control group, for experimental group 1 and experimental group 2 before and after the intervention, the four dimensions of mental quality, neuroticism, introversion and concealment degree all decreased, and the difference was statistically significant (P < 0.05). After the intervention, there were no obvious or statistically significant differences (P > 0.05) among the control group, experimental group 1, and experimental group 2 for two personality traits, psychoticism and neuroticism, both inside and outside degree and all four dimensions. CONCLUSION: Simple cognitive behavioral therapy could not change the personality characteristics of cancer patients quickly, but the patients' personality characteristics were significantly improved after treatment.

Neonatal Intrahepatic Cholestasis Caused by Citrin Deficiency with SLC25A13 Mutation Presenting Hepatic Steatosis and Prolonged Jaundice. A Rare Case Report.

Background: Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a rare autosomal recessive disease. The incidence of citrin deficiency is estimated between 1/10,000 and 1/20,000 in Taiwan. Case report: This report describes a case of a 42 day old female infant who suffered from prolonged jaundice, poor weight gain, and anemia. The initial total/direct bilirubin levels were 8.1/3.11 mg/dL. Liver biopsy was performed at 47 days old. The pathology revealed lobules marked with macrovesicular and microvesicular fatty metamorphosis. The serum amino acid profile showed elevated levels of threonine, methionine, citrulline, and arginine. Newborn screening disclosed normal results, but the genetic study revealed SLC25A13 mutation 851-854 del and 615 + 5G > A. The genetic study of her parents showed that the father carried the SLC25A13 mutation 851-854 del and the mother carried the SLC25A13 mutation 615 + 5G > A. Treatment with ursodeoxycholic acid decreased the bilirubin levels to a normal range at the age of 5 months. Conclusion: This report illustrates that hepatic steatosis is a feature of NICCD. For every young infant patient who develops cholestasis, the pediatrician must consider NICCD as a differential diagnosis even if newborn screening shows normal findings.

ERα determines the chemo-resistant function of mutant p53 involving the switch between lincRNA-p21 and DDB2 expressions.

Mutant p53 (mutp53) commonly loses its DNA binding affinity to p53 response elements (p53REs) and fails to induce apoptosis fully. However, the p53 mutation does not predict chemoresistance in all subtypes of breast cancers, and the critical determinants remain to be identified. In this study, mutp53 was found to mediate chemotherapy-induced long intergenic noncoding RNA-p21 (lincRNA-p21) expression by targeting the G-quadruplex structure rather than the p53RE on its promoter to promote chemosensitivity. However, estrogen receptor alpha (ERα) suppressed mutp53-mediated lincRNA-p21 expression by hijacking mutp53 to upregulate damaged DNA binding protein 2 (DDB2) transcription for subsequent DNA repair and chemoresistance. Levels of lincRNA-p21 positively correlated with the clinical responses of breast cancer patients to neoadjuvant chemotherapy and had an inverse correlation with the ER status and DDB2 level. In contrast, the carboplatin-induced DDB2 expression was higher in ER-positive breast tumor tissues. These results demonstrated that ER status determines the oncogenic function of mutp53 in chemoresistance by switching its target gene preference from lincRNA-p21 to DDB2 and suggest that induction of lincRNA-p21 and targeting DDB2 would be effective strategies to increase the chemosensitivity of mutp53 breast cancer patients.