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On the whole, the Yi Xue Cong Zheng Lun written by Jing Xian, a famous doctor in modern Liaoning, outlines the unique vision of the narrative medicine focusing on "benevolence". To be specific, the writing is good at constructing narrative projection, and makes full use of the essence of relevant traditional culture such as the body-country integration idea, the military strategy and tactics and the calligraphy aesthetics concept to create narrative schema. It focus on the concrete example narration of the cultural ideology of Traditional Chinese Medicine(TCM), such as the concept of interlinked viscera, the ideology that the characteristics of the treatment remain the same as the external properties of the disease, the compatibility of opposite and complementary and the idea of making prescriptions and selecting optimal Chinese herbal medicines. In addition, Jing Xian has constructed his professional identity as a doctor of TCM through in-depth narrative reflection. From the perspective of narrative medicine, the study of Yi Xue Cong Zheng Lun has certain instruction and reference significance in the inheritance of TCM culture, and can help to promote the in-depth exploration and multi-dimensiona reflection of "modern Liaoning TCM culture".
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Triggering receptors expressed on myeloid cells-2 (TREM-2) is a newly discovered immunoglobulin receptor, which plays an important role in inflammation and immunoreaction. Several recent studies have shown that TREM-2 is aberrantly expressed in various types of cancers such as lung cancer, gastric cancer, liver cancer, colorectal cancer, renal carcinoma and glioma, and it is widely participated in regulating malignant tumor initiation, progression, invasion and metastasis through different signal pathways. TREM-2 is expected to provide evidence for the diagnosis and treatment of malignant tumors.
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Objective@#In order to investigate the clinical features and influence factors for incidence in patients with radiation-induced external auditory canal carcinoma (RIEACC).@*Methods@#The nasopharyngeal carcinoma (NPC) 16 patients who were diagnosised RIEACC after radiotherapy in the Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University from January 1990 to December 2017 were retrospectively analysis. The influence factors analysis were used Logistic regression analysis.@*Results@#Univariate analysis showed that age, somking history, family history of cancer and NPC stage were the influencing factors. Multi-factor logistic regression analysis showed that age, family history of cancer and NPC stage were independent risk factors.@*Conclusions@#RIEACC is rare complication of NPC patients received radiotherapy, which is also a multifactorial outcome. Age, family history of cancer and NPC stage is preliminary the main influencing factor. Although RIEACC has a low incidence, its malignancy should be highly vigilant.
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Objective In order to investigate the clinical features and influence factors for incidence in patients with radiation-induced external auditory canal carcinoma (RIEACC).Methods The nasopharyngeal carcinoma (NPC) 16 patients who were diagnosised RIEACC after radiotherapy in the Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University from January 1990 to December 2017 were retrospectively analysis.The influence factors analysis were used Logistic regression analysis.Results Univariate analysis showed that age,somking history,family history of cancer and NPC stage were the influencing factors.Multi-factor logistic regression analysis showed that age,family history of cancer and NPC stage were independent risk factors.Conclusions RIEACC is rare complication of NPC patients received radiotherapy,which is also a multifactorial outcome.Age,family history of cancer and NPC stage is preliminary the main influencing factor.Although RIEACC has a low incidence,its malignancy should be highly vigilant.
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Objective@#To explore the relationship between genotype and phenotype of ABCB11 deficiency.@*Methods@#Clinical data of two siblings with ABCB11 deficiency were retrospectively analyzed. Related literature from PubMed, CNKI and Wangfang databases was reviewed to date (up to August 2017) with 'ABCB11 gene’ or 'bile salt export pump’, 'cholestasis’ and 'child’ as key words.@*Results@#The patients were siblings. Both of them presented as jaundice, pruritus and hepatosplenomegaly since 3 days after birth. Significant laboratory findings on admission of the older sister included high total bilirubin, 170 µmol/L;conjugated bilirubin, 115.8 µmol/L;alanine aminotransferase, 168 U/L;total bile acid 186.3 µmol/L and normal gamma-glutamyl transpeptidase. While routine laboratory data of the younger brother were as follows: total bilirubin, 148.8 µmol/L;conjugated bilirubin, 96.3 µmol/L;alanine aminotransferase, 232.8 U/L;total bile acid 226 µmol/L, and normal gamma-glutamyl transpeptidase.Both received ursodeoxycholic acid and fat-soluble vitamins. Liver pathology of the younger brother showed giant hepatocytes with ballooning degeneration, focal necrosis and intrahepatic cholestasis. Both the patients harbor the same compound heterozygous mutations in ABCB11 gene, c.145C>T (p.Q49X) and c.1510G>A (p.E504K). The sister is 9 years old now, with normal liver function. Jaundice faded around 3 months after birth, pruritus relieved at age 5, and medications was stopped since then. The brother progressed to liver failure after an operation on perianal abscess when he was 8-month-old, and received living-related liver transplantation when he was 9 month and 20 days old (from his mother). Now he is 1 year and 5 months old, with normal liver function. Both are under our follow-up. Literature review revealed 18 ABCB11 deficiency patients from 7 families who had apparent different prognoses, within each family the siblings had the same ABCB11 gene mutation. Seven cases relieved after ursodeoxycholic acid therapy and/or partial external biliary diversion, 5 received orthotopic liver transplantation, 2 developed hepatocellular carcinoma and 4 cases died in childhood.@*Conclusions@#The clinical manifestations of ABCB11 deficiency may vary greatly in patients carrying the same genotype, even in siblings. Patients should be managed in individualized maner.
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Hereditary intrahepatic cholestasis is an important cause of death or disability in childhood. With the development of molecular medicine,a series of familial intrahepatic cholestasis caused by gene mutations (ATP8B1 deficiency,ABCB11 deficiency,ABCB4 deficiency,TJP2 deficiency,NR1H4 deficiency and MYO5B deficiency)have been discovered successively. If these patients do not receive early intervention,they often develop liver cirrhosis and liver failure in childhood. Therefore,early diagnosis and intervention are very important for improving prognosis.
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Objective To observe the effect of oxidized low-density lipoproteins (Ox-LDL),15-Deoxy-△ 12,14-prostaglandin J2 ( 15d-PGJ2 ),leukotrienes B4 ( LTB4 ) on mRNA expressions of peroxisome proliferator activated receptor γ2 ( PPARγ2 ),receptor activator of NF-κB ligand (RANKL),alkaline phosphatase ( ALP),and osteoprotegerin(OPG) in osteoblastic cells of rats; and to investigate the influence of these PPARγ2 endogenous ligands on bone metabolism.Methods Rat osteoblastic cells were cultured in vitro for 24 h in medium with different PPARγ2 endogenous ligands at various concentrations ( the final concentrations of Ox-LDL were 0,12.5,25,50μg/ml; the final concentrations of 15 d-PGJ2 were 0,10,20,30 μmol/L; the final concentrations of LTB4 were 0,0.1,1.0,10 μ mol/L).RT-PCR was performed to determine the mRNA expressions of PPARγ2,RANKL,ALP,and OPG in osteoblastic cells.Results RT-PCR analysis showed that Ox-LDL,15d-PGJ2,and LTB4 all down-regulated the mRNA expressions of RANKL,ALP,and OPG,while up-regulated the mRNA expressions of PPARγ2 in osteoblastic cells in a dose-dependent manner.Significant differences were found in interclass comparisons( P＜0.05 or P＜ 0.01 ).Conclusions These findings suggest that Ox-LDL,15d-PGJ2,and LTB4 suppress the expressions of osteogenic genes through activating the transcription activity of PPARγ2,and this may be a plausible mechanism of senile osteoporosis.