• Journal of Hospice and Palliative Care
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• v.16 no.4
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• pp.205-215
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• 2013

Most terminally ill cancer patients experience various physical and psychological symptoms during their illness. In addition to pain, they commonly suffer from fatigue, anorexia-cachexia syndrome, nausea, vomiting and dyspnea. In this paper, I reviewed some of the common non-pain symptoms in terminally ill cancer patients, based on the National Comprehensive Cancer Network (NCCN) guidelines to better understand and treat cancer patients. Cancer-related fatigue (CRF) is a common symptom in terminally ill cancer patients. There are reversible causes of fatigue, which include anemia, sleep disturbance, malnutrition, pain, depression and anxiety, medical comorbidities, hyperthyroidism and hypogonadism. Energy conservation and education are recommended as central management for CRF. Corticosteroid and psychostimulants can be used as well. The anorexia and cachexia syndrome has reversible causes and should be managed. It includes stomatitis, constipation and uncontrolled severe symptoms such as pain or dyspnea, delirium, nausea/vomiting, depression and gastroparesis. To manage the syndrome, it is important to provide emotional support and inform the patient and family of the natural history of the disease. Megesteol acetate, dronabinol and corticosteroid can be helpful. Nausea and vomiting will occur by potentially reversible causes including drug consumption, uremia, infection, anxiety, constipation, gastric irritation and proximal gastrointestinal obstruction. Metoclopramide, haloperidol, olanzapine and ondansetron can be used to manage nausea and vomiting. Dyspnea is common even in terminally ill cancer patients without lung disease. Opioids are effective for symptomatic management of dyspnea. To improve the quality of life for terminally ill cancer patients, we should try to ameliorate these symptoms by paying more attention to patients and understanding of management principles.

• Journal of Life Science
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• v.25 no.5
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• pp.523-532
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• 2015

A variety of previous pharmacological studies have suggested Liriope platyphylla (L. platyphylla) may exert beneficial biological effects on inflammation, diabetes, neurodegenerative disorder, obesity, constipation, and atopic dermatitis. In addition, hydrocolloid membranes (HCMs) have attracted attention in dermatological care, including in the treatment of scleroderma skin ulcers, cutaneous ulcers, permanent tympanic membrane perforations, pressure sores, and decubitus ulcers in the elderly. To investigate the therapeutic effects of HCM containing an aqueous extract of L. platyphylla (HCM-LP) on second-degree burn wounds, their physico-chemical properties were analyzed and the therapeutic effects were observed in SD rats after treatment with HCM-LP for 14 days. Significant declines in tensile strength (38.4%) and absorptiveness (46.3%), as well as an increase in surface roughness (38.1%) were detected in HCM-LP compared with that of HCM. In SD rats with burned skin, the wound diameter was shorter in the HCM-LP treated group than in the GZ group on post-surgical day 14, while the significant improvements in scar tissue reduction, epithelium regeneration, angiogenesis, and extracellular matrix deposition were observed in the HCM-LP-treated group during all experimental periods. Overall, these results suggest HCM-LP may accelerate the process of healing the burn injury skin of SD rats through the regulation of angiogenesis and connective tissue formation.

• Journal of Life Science
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• v.23 no.1
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• pp.15-23
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• 2013

AprE51 from Bacillus amyloliquefaciens CH51 is a 27 kDa subtilisin-like protease with fibrinolytic activity. AprE51-6 showing increased catalytic activity was produced previously. To enhance the thermostability of AprE51-6, 2 residues, Gly-166 and Asn-218 based on B. subtilis subtilisin E were mutated by site-directed mutagenesis. The results of the mutational analysis showed that substitution of arginine for Gly-166 (AprE51-7) increased the fibrinolytic activity 1.8-fold. An N218S mutant (AprE51-8) also increased the fibrinolytic activity up to 4.5-fold in a fibrin plate assay. Purified AprE51-7 and AprE51-8 mutants had a 1.9- and a 2.5-fold higher $k_{cat}$, respectively, and a 2.1-1.9-fold lower $K_m$, respectively. This resulted in a 3.8- and a 4.7-fold increase in catalytic efficiency ($k_{cat}/K_m$), respectively, relative to that of wild-type AprE51. AprE51-8 had a broader pH range than AprE51-6 and nattokinase, especially at an alkaline pH value. In addition, AprE51-8 showed higher thermostability than AprE51-6 at $60^{\circ}C$. The half-lives of AprE51-7 and AprE51-8 at $50^{\circ}C$ were 21.5 and 27.3 min, respectively, which are 2.0 and 2.6 times longer, respectively, than that of the wild-type AprE51.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.516-524
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• 1997

Background : Cancer invasion and metastasis require the dissolution of the extracellular matrix in which several proteolytic enzymes are involved. One of these enzymes is the urokinase-type plasminogen activator(u-PA), and plasminogen activator inhibitors(PAI-1, PAI-2) also have a possible role in cancer invasion and metastasis by protection of cancer itself from proteolysis by u-PA. It has been reported that the levels of u-PA and plasminogen activator inhibitors in various cancer tissues are significantly higher than those in normal tissues and have significant correlations with tumor size and lymph node involvement. Here, we measured the concentration of plasma u-PA and PAI-1 antigens in the patients with lung cancer and compared the concentration of them with histologic types and staging parameters. Methods : We measured the concentration of plasma u-PA and PAI-1 antigens using commercial ELISA kit in 37 lung cancer patients, 21 benign lung disease patients and 24 age-matched healthy controls, and we compared the concentration of them with histologic types and staging parameters in lung cancer patients. Results : The concentration of u-PA was $1.0{\pm}0.3ng/mL$ in controls, $1.0{\pm}0.3ng/mL$ in benign lung disease patients and $0.9{\pm}0.3ng/mL$ in lung cancer patients. The concentration of PAI-1 was $14.2{\pm}6.7ng/mL$ in controls, $14.9{\pm}6.3ng/mL$ in benign lung disease patients, and $22.1{\pm}9.8ng/mL$ in lung cancer patients. The concentration of PAI-1 in lung cancer patients was higher than those of benign lung disease patients and controls. The concentration of u-PA was $0.7{\pm}0.4ng/mL$ in squamous cell carcinoma, $0.8{\pm}0.3ng/mL$ in adenocarcinoma, 0.9ng/mL in large cell carcinoma, and $1.1{\pm}0.7ng/mL$ in small cell carcinoma. The concentration of PAI-1 was $22.3{\pm}7.2ng/mL$ in squamous cell carcinoma, $22.6{\pm}9.9ng/mL$ in adenocarcinoma, 42 ng/mL in large cell carcinoma, and $16.0{\pm}14.2ng/mL$ in small cell carcinoma. The concentration of u-PA was 0.74ng/mL in stage I, $1.2{\pm}0.6ng/mL$ in stage II, $0.7{\pm}0.4ng/mL$ in stage IIIA, $0.7{\pm}0.4ng/mL$ in stage IIIB, and $0.7{\pm}0.3ng/mL$ in stage IV. The concentration of PAI-1 was 21.8ng/mL in stage I, $22.7{\pm}8.7ng/mL$ in stage II, $18.4{\pm}4.9ng/mL$ in stage IIIA, $25.3{\pm}9.0ng/mL$ in stage IIIB, and $21.5{\pm}10.8ng/mL$ in stage IV. When we divided T stage into T1-3 and T4, the concentration of u-PA was $0.8{\pm}0.4ng/mL$ in T1-3 and $0.7{\pm}0.4ng/mL$ in T4, and the concentration of PAI-1 was $17.9{\pm}5.6ng/mL$ in T1-3 and $26.1{\pm}9.1ng/mL$ in T4. The concentration of PAI-1 in T4 was significantly higher than that in T1-3. The concentration of u-PA was $0.8{\pm}0.4ng/mL$ in M0 and $0.7{\pm}0.3ng/mL$ in M1, and the concentration of PAI-1 was $23.6{\pm}8.3ng/mL$ in M0 and $21.5{\pm}10.8ng/mL$ in M1. Conclusions : The plasma levels of PAI-1 in lung cancer were higher than benign lung disease and controls, and the plasma levels of PAI-1 in T4 were significantly higher than T1-3. These findings suggest involvement of PAI-1 with local invasion of lung cancer, but it should be confirmed by the data on comparison with pathological staging and tissue level in lung cancer.