Bodily Secretions ; virology ; Humans ; Pharynx ; virology ; Pneumonia ; diagnosis ; virology ; Respiratory System ; virology

OBJECTIVE: To explore the relationship between the expression of EIIIA+ fibronectin in incised wound of rat's skin and injury time. METHODS: The wounding model was established by cutting the dorsal skin of 48 adult SD rats. The rats were sacrificed at the pre-set injury time as immediately, 0.5 h, 1 h, 2 h, 3 h, 4 h, 6 h, and 8 h. The skin samples were taken at the margin of wound. The expression of the EIIIA? fibronectin was detected by immunohistochemistry and Western blotting and the relationship be- tween its expression and injury time was observed. Results The expression of EIIIA+ fibronectin was not observed immediately. The basal cell of skin began to show positive expression 0.5 h after injury. With the extension of injury time, positive staining became stronger. The value of relative optical density was gradually increased with prolonged injury time by the Western blotting analysis. CONCLUSION The expression of EIIIA+ fibronectin could be used for estimation of injury time in the early stage of skin injury.
Animals ; Fibronectins/metabolism* ; Immunohistochemistry ; Proteins/metabolism* ; Rats ; Rats, Sprague-Dawley ; Skin/metabolism* ; Staining and Labeling ; Time Factors

Morphine is a widely used opioid analgesic, but great individual differences in response to morphine such as sensitivity to analgesia and susceptibility to tolerance, which due to chronic morphine treatment, are great challenges for clinicians to optimize treatment strategy. Genetic factors play an important role in individual variability to morphine treatment. Individual responses to morphine are influenced by various gene-encoded-proteins implied in pharmacokinetics and pharmacodynamics. Variants of P-glycoprotein encoding gene ABCB1 regulate transportation and distribution of morphine and affect analgesic effect. Diversity in UDP-glucuronosyl transferase encoding gene UGT2B7, whose encoding product catalyzing morphine to glycosylated metabolites contribute to different response to morphine in a pharmacokinetic way. Nevertheless, variants in μ-opioid receptor encoding gene OPRM1 and catechol-O-methyltransferase encoding gene COMT regulate morphine-induced downstream signaling and influence morphine analgesia in a pharmacodynamic way. It is necessary to employ individuals with more complex genetic diversity and screen in a larger scope through a more comprehensive system to find the key genes involved in individual differences of morphine analgesia in future research. Elucidating the association between genetic variability and individual differences will help to figure out the mechanism of pharmacogenetic regulation in morphine analgesia. It will provide basis for personalized and accurate utility of morphine or even combining with gene therapy to improve the analgesic effect.

Sirtuin1 (Sirt1) is a NAD-dependent class III histone deacetylase (HDAC), and regulates pulmonary immune/inflammatory system and the aging process mainly through post-translational modification. Sirt1 could become a potential target for treatment of lung diseases due to participating in the development of a variety of lung diseases. In this paper, physiological characteristics, biological activities, modification regulations and its relationship with chronic obstructive pulmonary emphysema, asthma and lung cancer are reviewed.
Animals ; Asthma ; metabolism ; Benzamides ; pharmacology ; Humans ; Lung Diseases ; metabolism ; Lung Neoplasms ; metabolism ; Naphthols ; pharmacology ; Protein Processing, Post-Translational ; Pulmonary Disease, Chronic Obstructive ; metabolism ; Sirtuin 1 ; antagonists & inhibitors ; metabolism ; physiology ; Stilbenes ; pharmacology

OBJECTIVETo study the role of NY-ESO-1 and LAGE-1 cancer-testis antigens as targets for immunotherapy and the relationship between corresponding gene expression and biologic behavior of hepatocellular carcinoma (HCC).

METHODSThe expression of NY-ESO-1 and LAGE-1 was studied in frozen tumor tissues from 30 cases of HCC by reverse transcriptase-polymerase chain reaction and immunohistochemistry. NY-ESO-1 expression and its distribution were further studied by immunohistochemistry in a tissue array contained 191 cases of HCC.

RESULTSNY-ESO-1 and LAGE-1 mRNAs were expressed in 33.3% (10/30) and 16.7% (5/30) of HCC respectively. Either NY-ESO-1 or LAGE-1 was expressed in 36.7% (11/30) cases. NY-ESO-1 was expressed mainly in the cytoplasm of tumor cells. It was positive in 13.8% (24/174) cases of HCC. There was an increased expression of NY-ESO-1 from 6.8%, 3/44 in small HCC, 16.2%, 21/130 in advanced HCC and 23.1%, 12/52 in metastatic HCC. The expression in the non-metastatic group was 9.8% (12/122). The differences between the metastatic group and non-metastatic group (< 0.05) and between normal liver tissue and HCC (< 0.01) were statistically significant. There was no relationship between NY-ESO-1 expression and tumor size. NY-ESO-1 and LAGE-1 were not detected in adjacent normal liver tissue.

CONCLUSIONSNY-ESO-1 and LAGE-1 are expressed in a high percentage of HCC, especially in cases with metastasis. It is thus possible that NY-ESO-1/LAGE-1 can serve as targets for antigen-specific immunotherapy in HCC and NY-ESO-1 peptide vaccination may be of use for patients with advanced HCC.

Adult ; Aged ; Antigens, Neoplasm ; biosynthesis ; genetics ; Antigens, Surface ; biosynthesis ; genetics ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Liver ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Male ; Membrane Proteins ; biosynthesis ; genetics ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Staging ; RNA, Messenger ; biosynthesis ; genetics

Currently, about 300 million people worldwide are affected by asthma. Most of these sufferers inhale immunosuppressants (ie corticosteroids) and beta-adrenergic receptor agonists for their asthma treatment. However, about 5%-10% of patients of asthma have poor response to such treatment. Investigation of kinase signaling pathway and nuclear transcription factor as a target molecule in the treatment of allergic asthma has been the concern of scholars home and abroad. This paper reviewed inhibitors of kinase signaling pathway and nuclear transcription factors for the treatment of asthma.
Animals ; Asthma ; drug therapy ; enzymology ; Humans ; Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; Phosphatidylinositol 3-Kinase ; antagonists & inhibitors ; Protein Kinase Inhibitors ; therapeutic use ; Protein-Tyrosine Kinases ; antagonists & inhibitors ; metabolism ; Signal Transduction ; Transcription Factors ; antagonists & inhibitors

OBJECTIVETo compare the efficacy between synchronized intermittent mandatory ventilation (SIMV) and pressure support ventilation with volume guarantee (PSV+VG) in the weaning phase of preterm infants with respiratory distress syndrome (RDS).

METHODSForty preterm infants with RDS who were admitted to the neonatal intensive care unit between March 2016 and May 2017 were enrolled as subjects. All infants were born at less than 32 weeks' gestation and received mechanical ventilation. These patients were randomly and equally divided into SIMV group and PSV+VG group in the weaning phase. Ventilator parameters, arterial blood gas, weaning duration (from onset of weaning to extubation), duration of nasal continuous positive airway pressure (NCPAP) after extubation, extubation failure rate, the incidence rates of pneumothorax, patent ductus arteriosus (PDA) and bronchopulmonary dysplasia (BPD), and the mortality rate were compared between the two groups.

RESULTSThe PSV+VG group had significantly decreased mean airway pressure, weaning duration, duration of NCPAP after extubation, and extubation failure rate compared with the SIMV group (P<0.05). There were no significant differences in arterial blood gas, mortality, or incidence rates of pneumothorax, PDA and BPD between the two groups (P>0.05).

CONCLUSIONSFor preterm infants with RDS, the PSV+VG mode may be a relatively safe and effective mode in the weaning phase. However, multi-center clinical trials with large sample sizes are needed to confirm the conclusion.

OBJECTIVETo establish a mouse model of iron overload by intraperitoneal injection of iron dextran and investigate the impact of iron overload on bone marrow hematopoiesis.

METHODSA total of 40 C57BL/6 mice were divided into control group, low-dose iron group (12.5 mg/ml), middle-dose iron group (25 mg/ml), and high-dose iron group (50 mg/ml). The control group received normal saline (0.2 ml), and the rest were injected with intraperitoneal iron dextran every three days for six weeks. Iron overload was confirmed by observing the bone marrow, hepatic, and splenic iron deposits and the bone marrow labile iron pool. In addition, peripheral blood and bone marrow mononuclear cells were counted and the hematopoietic function was assessed.

RESULTSIron deposits in bone marrow, liver, and spleen were markedly increased in the mouse models. Bone marrow iron was deposited mostly within the matrix with no significant difference in expression of labile iron pool.Compared with control group, the ability of hematopoietic colony-forming in three interventional groups were decreased significantly (P<0.05). Bone marrow mononuclear cells counts showed no significant difference. The amounts of peripheral blood cells (white blood cells, red blood cells, platelets, and hemoglobin) in different iron groups showed no significant difference among these groups;although the platelets were decreased slightly in low-dose iron group [(780.7±39.60)×10(9)/L], middle dose iron group [(676.2±21.43)×10(9)/L], and high-dose iron group [(587.3±19.67)×10(9)/L] when compared with the control group [(926.0±28.23)×10(9)/L], there was no significant difference(P>0.05).

CONCLUSIONSThe iron-overloaded mouse model was successfully established by intraperitoneal administration of iron dextran. Iron overload can damage the hepatic, splenic, and bone marrow hematopoietic function, although no significant difference was observed in peripheral blood count.

Animals ; Bone Marrow ; drug effects ; physiopathology ; Disease Models, Animal ; Hematopoiesis ; drug effects ; Iron Overload ; chemically induced ; physiopathology ; Iron-Dextran Complex ; administration & dosage ; toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Spleen ; drug effects

OBJECTIVETo study the prevalence of hypertension and glucose/lipid metabolism induced by chronic obstructive pulmonary disease (COPD) in hospitalized patients and their correlations to age and gender.

METHODSA retrospectively prevalence survey was conducted among the in-patients with COPD treated in General Hospital of PLA, Peking Union Medical College Hospital and Beijing Hospital between January 1st, 2000 and March 20th, 2010.

RESULTSA total of 4960 COPD patients were selected, including 3570 male and 1390 female patients with a mean age of 72.2∓10.4 years. Among these patients, hypertension had the highest prevalence (40.3%), followed by diabetes/impaired glucose tolerance (18.8%) and then by hyperlipidemia/fat protein metabolism (6.9%). The prevalence of hyperlipidemia/lipoprotein metabolism in the COPD patients over 80 years old decreased significantly with age. The prevalence of hypertension increased with age. In patients over 50 years old, the prevalence of hypertension was significantly higher in female than in male patients (P<0.05). The prevalence of diabetes/impaired glucose tolerance increased with age in male patients but decreased in female patients aged :80 years (P<0.05). Female patients in 60-69.9 and 70-79.9 years groups had significantly higher incidence of diabetes/impaired glucose tolerance than male patients (P<0.05), but not at older ages. The incidence of hyperlipidemia/lipoprotein metabolism disorder increased with age in both male and female patients aged below 80 years (P<0.05), but in 60-69.9 and 70-79.9 year groups, female patients had a significantly higher incidence than male patients (P<0.05); at the ages :80 years, the incidences was lowered in both women and men without a gender-specific differences (P>0.05).

CONCLUSIONSThe data we obtained concerning the prevalence of hypertension and glucose/lipid metabolism disorder, age distribution, and gender characteristics of the COPD patients provide a clear target for secondary prevention of COPD.

Aged ; Aged, 80 and over ; Female ; Glucose Metabolism Disorders ; complications ; Humans ; Hypertension ; complications ; Lipid Metabolism Disorders ; complications ; Male ; Middle Aged ; Pulmonary Disease, Chronic Obstructive ; complications ; Retrospective Studies

OBJECTIVEGenetic factors are thought to be involved in the development of vitiligo. The aim of this study is to explore the possible genetic model of vitiligo by analyzing the genetic characteristics of 815 patients from Zhejiang province.

METHODSData for 815 patients with vitiligo together with their first- and second-degree relatives were obtained using a standardized questionnaire. All these information was requested to confirm the answers about family history in order to reduce the possibility of 'recall' bias. The 815 probands would include 411 (50.43%) males and 404 (49.57%) females with a varied age from 2 months to 71 years old. Since the information on general prevalence of vitiligo in this area was absent, a control group was set up to facilitate the calculations of heritability degree. 468 persons of the control group were from non-vitiligo population with a sex ratio of 241(male): 227(female) with varied age of 4 months to 80 years old. Both gender and age were comparable between the vitiligo and the control population. The inheritance pattern estimation, heritability calculation and complex segregation analysis were performed with Penrose method, Falconer regression method and SAGE-REGTL program.

RESULTSIn 815 vitiligo probands, 128 had and 687 had not family histories, with a heritability rate of 15.7%. The vitiligo prevalence in proband's first degree relatives was 2.580%, higher than the prevalence of 0.618% in second degree relatives, and both of them were higher than general prevalence: 0.192%. By Penrose method, the rates on different catagories were as follows: sibling prevalence rates s = 0.080 18; population prevalence rate q = 0.001 92; s/q = 41.76. The ratio of s/q did not approach 1/2q (260.42) or 1/4q (130.21), but approached 1/square root of q(22.82), suggesting vitiligo was consistent with a mode of polygenic inheritance. Using Falconer's method, heritabilities of vitiligo in first-and second degree relatives of probands were 59.61% (95% confidence interval 65.37-53.84) and 55.20% (95% confidence interval 43.88-66.52), respectively. The weighted average of heritability in all relatives was 58.7% (95% confidence interval 53.56-63.83). The results of complex segregation analysis suggested that major gene model including the Mendelian dominant, recessive and additive hypotheses were not rejected (P > 0.05). Purely environmental model and no transmission model were rejected at a 0. 001 significance level. According to AIC, Mendelian dominant inheritance was the best-fitted hypothesis.

CONCLUSIONGenetic factors played an important role in the occurrence of vitiligo, and the genetic model of vitiligo could serve as the polygenetic or multifactorial inheritance with major gene trait.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Child, Preschool ; China ; epidemiology ; Female ; Humans ; Infant ; Male ; Middle Aged ; Models, Genetic ; Vitiligo ; epidemiology ; genetics ; Young Adult