95 research outputs found
Management of Breathlessness in Patients With Advanced Cancer: A Narrative Review.
No full textBreathlessness is defined as “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.” It is a common and distressing symptom reported by patients with advanced malignancy. It occurs in up to 70% of patients with advanced cancer, and the symptom is aggravated with disease progression. This article reviews the etiology, assessment, and measurement of dyspnea in patients with advanced cancer. Because of its complex biopsychological etiology and manifestations, multidisciplinary approach with combination of both pharmacological and nonpharmacological interventions provides the best treatment plan for patients with dyspnea. © 2014, © The Author(s) 2014.link_to_subscribed_fulltex
The 'do-not-resuscitate' order in palliative surgery: Ethical issues and a review on policy in Hong Kong
No full textCopyright © Cambridge University Press 2015. A do-not-resuscitate (DNR) order, or advance directive, is commonly seen in the cases of palliative patients who express a wish to withhold specific resuscitative therapies in the event of a cardiac arrest. With recent technological advances, there are increasing numbers of palliative patients who undergo surgical interventions to treat their symptoms and discomfort. The decision to suspend DNR orders for palliative surgery is always a matter for debate. The present article describes a case and the ethical issues involved and gives some practical suggestions for those facing similar problems. We also review the latest DNR policy in Hong Kong.link_to_subscribed_fulltex
Durability and debond evaluation of high-rise concrete buildings using infrared thermography
No full textAuthor name used in this publication: W. L. LaiRefereed conference paper2012-2013 > Academic research: refereed > Refereed conference paperNot applicablePublishedCopyright retained by autho
Transcriptional regulation of the promoter of the rat frizzled related protein gene by CREB
No full textFrizzled related proteins (Frps) are secreted proteins structurally similar to frizzled receptors; they bind Wnt via the cysteine-rich domain and antagonize the Wnt signaling pathway. In this study, we have investigated the mechanisms regulating the transcriptional regulation of rat Frp (rFrp) promoter. From previous findings, we know that the transcriptional activation domain of rFrp resides in the region -202 to -144 relative to the transcription start site, and that it is essential for efficient promoter activity. The study presented here was designed to identify trans-acting factors that bind to this critical domain of the rFrp promoter and to elucidate the pathway involved in the regulation of rFrp expression. Electrophoretic mobility shift assay (EMSA) demonstrated that specific DNA-protein binding activities fall into two adjacent core sequences with (CTTTGGGGG) at -197 to -189 and (AGATGATGTAA) at -151 to -141 of the rFrp promoter. Reporter assay showed that these core sequences are both required for the activation of rFrp promoter. Mutation within either one or both core sequence drastically reduced the promoter activity. Southwestern blotting showed that the estimated molecular mass of the distinct binding protein to the (AGATGATGTAA) domain is about 43 kDa. Further EMSA suggested CREB as the trans-acting factor in the DNA-protein complex, which was out competed by CREB consensus oligonucleotides and supershifted by anti-CREB antibody. Overexpression of PKA and CREB also transactivated rFrp promoter, and dominant-negative CREB inhibited the promoter activity in transient reporter assays. More importantly, CREB, phosphorylated CREB and the adaptor protein CBP were found binding to the endogenous rFrp promoter using chromatin immunoprecipitation assay. Collectively, our results demonstrate the induction of rFrp promoter activity by PKA and CREB in vitro, and the binding of CREB and CBP to the rFrp promoter core motif in vivo.link_to_subscribed_fulltex
Suppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-B
No full textIn our previous study, a rat homolog of human nonmuscle myosin heavy chain-B (nmMHC-B) was identified by mRNA differential display comparing of transformed against nontransformed Rat 6 cells over-expressing mutant p53vaI135 gene. The nmMHC-B was found to be expressed in normal Rat 6 embryo fibroblast cell line, but markedly suppressed in the mutant p53vaI135-transformed Rat 6 cells. To examine the possible involvement of nmMHC-B in cell transformation, we first cloned and sequenced the full length cDNA of rat nmMHC-B, which was then cloned into an ecdysone-expression vector. The resulting construct was introduced into the T2 cell line, a mutant p53vaI135-transformed Rat 6 cells lacking the expression of the endogenous nmMHC-B. The clonal transfectants, expressing muristerone A-induced nmMHC-B, displayed a slightly flatter morphology and reached to a lower saturation density compared to the parental transformed cells. Reconstitution of actin filamental bundles was also clearly seen in cells over-expressing the nmMHC-B. In soft agar assays, nmMHC-B transfectants formed fewer and substantially smaller colonies than the parental cells in response to muristerone A induction. Moreover, it was strikingly effective in suppressing the tumorigenicity of the T2 cells when tested in nude mice. Thus, the nmMHC-B, known as a component of the cytoskeletal network, may act as a tumor suppressor gene. Our current finding may reveal a novel role of nmMHC-B in regulating cell growth and cell signaling in nonmuscle cells.postprin
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