Hope-based intervention for individuals susceptible to colorectal cancer: a pilot study

Individuals undergoing genetic testing for hereditary colorectal cancer (HCRC) are prone to develop psychological problems. This study investigated the short-term efficacy of a hope-based intervention program in increasing hope levels and decreasing psychopathology among HCRC genetic testing recipients. A longitudinal study was carried out on HCRC genetic testing recipients recruited by the Hereditary Gastrointestinal Cancer Registry. Participants joined a hope-based intervention program consisting of six sessions of weekly closed group therapy. Psychological questionnaires were administered immediately before the first and after the last sessions of the program measuring hope, anxiety and depression levels of the participants. There were 22 participants (7 men and 15 women) at a mean age of 49.4 ± 9.6 years. Women tended to have higher level of anxiety than men at pre-intervention. Paired sample t tests were conducted. Hope levels increased significantly from pre- to post-intervention (pre-total hope score = 5.56; post-total hope score = 6.07; t(1) = -0.281, p < 0.05). Anxiety level also decreased significantly from pre- to post-intervention (pre-anxiety score = 7.38; post-anxiety score = 5.90; t (1) = 2.35, p < 0.05). Our findings imply that hope-based intervention program would be effective in enhancing hope in HCRC genetic testing recipients. The program may also be more effective in alleviating anxiety than depression in these individuals. © 2012 The Author(s).published_or_final_versio

The use of right lobe liver grafts from living donors in high-urgency patients

Abstrac

A prospective longitudinal study of quality of life after resection of hepatocellular carcinoma

Hypothesis: Hepatic resection improves quality of life (QOL) in patients with resectable hepatocellular carcinoma (HCC). Design: A prospective longitudinal study. Setting: A university teaching hospital. Patients: Sixty-six consecutive patients undergoing resection of HCC, and 10 patients with unresectable HCC found after surgical exploration who were subsequently treated with transarterial chemoembolization (control group). Main Outcome Measure: Serial measurements of preoperative and postoperative QOL using the Functional Assessment of Cancer Therapy-General (FACT-G) Questionnaire for up to 2 years after surgery (at 3, 6, 9, 12, 18, and 24 months). Results: Among the 66 patients with resectable HCC, the mean postoperative QOL scores at 3 months after surgery were significantly higher than the mean preoperative QOL scores in domains related to physical, social, and emotional well-being and relationship with physicians. The mean total QOL score increased from 83.5 (SD, 9.4) before surgery to 94.1 (SD, 7.7) at 3 months after surgery (P<.001). No significant change of QOL scores at 3 months after surgery was observed in the control group. Twenty patients in the resected group died of early recurrence within 2 years after surgery, but their mean postoperative QOL scores remained higher than the preoperative QOL scores for most assessment times. In contrast, in the control group, the mean total QOL scores became significantly lower than the preoperative scores, starting 9 months after surgery. Forty-six patients in the resected group completed all QOL assessments. At all postoperative assessments, their mean QOL scores were higher than preoperative scores. Recurrence developed in 13 of the 46 patients within the 2-year study, and there was significant deterioration of QOL over time among these 13 (P<.001), whereas no significant change in QOL over time was observed among the 33 recurrence-free patients. Of various clinicopathologic factors, only advanced pTNM stage was significantly predictive of deterioration of QOL over time after resection of HCC. Conclusions: Hepatic resection results in significant enhancement of QOL in patients with HCC. Development of recurrence is the main factor leading to deterioration in QOL over time after resection of HCC.link_to_subscribed_fulltex

Guest-Anion-induced rotation-restricted emission in UiO-66-NH2and advanced structure elucidation

202209_bcwwAccepted ManuscriptRGCOthersNSFCPublishe

Controlled synthesis of Bi- And tri-nuclear Cu-oxo nanoclusters on metal-organic frameworks and the structure-reactivity correlations

202209 bchyVersion of RecordRGCPublishe

Increased inflammatory markers identified in the dorsolateral prefrontal cortex of individuals with schizophrenia

Upregulation of the immune response may be involved in the pathogenesis of schizophrenia with changes occurring in both peripheral blood and brain tissue. To date, microarray technology has provided a limited view of specific inflammatory transcripts in brain perhaps due to sensitivity issues. Here we used SOLiD Next Generation Sequencing to quantify neuroimmune mRNA expression levels in the dorsolateral prefrontal cortex of 20 individuals with schizophrenia and their matched controls. We detected 798 differentially regulated transcripts present in people with schizophrenia compared with controls. Ingenuity pathway analysis identified the inflammatory response as a key change. Using quantitative real-time PCR we confirmed the changes in candidate cytokines and immune modulators, including interleukin (IL)-6, IL-8, IL-1b and SERPINA3. The density of major histocompatibility complex-II-positive cells morphologically resembling microglia was significantly increased in schizophrenia and correlated with IL-1b expression. A group of individuals, most of whom had schizophrenia, were found to have increased inflammatory mRNA expression. In summary, we have demonstrated changes in an inflammatory response pathway that are present in 40% of people diagnosed with schizophrenia. This suggests that therapies aimed at immune system attenuation in schizophrenia may be of direct benefit in the brain

Constitutive ablation of caspase-6 reduces the inflammatory response and behavioural changes caused by peripheral pro-inflammatory stimuli

Abstract Traditionally, the family of caspases has been subcategorised according to their respective main roles in mediating apoptosis or inflammation. However, recent studies have revealed that caspases participate in diverse cellular functions beyond their canonical roles. Caspase-6 (C6) is one such protease known for its role as a pro-apoptotic executioner caspase and its aberrant activity in several neurodegenerative diseases. In addition to apoptosis, C6 has been shown to regulate B-cell activation and differentiation in plasma cells as well as macrophage activation. Furthermore, C6 has recently been postulated to play a role in mediating the inflammatory response through the production of TNF-α. In this study we further examine the role of C6 in mediating the inflammatory response and its contribution to the manifestation of behavioural abnormalities in mice. We find that C6 is a positive regulator of TNF-α transcription in macrophages and that ablation of C6 reduces lipopolysaccharide (LPS)-induced TNF-α levels in plasma. Furthermore, loss of C6 attenuates LPS-induced behavioural changes in mice and protects neurons from cytokine-mediated toxicity. These data further support the involvement of C6 in the inflammatory response and point to a previously unknown role for C6 in the pathophysiology of depression