Research progress on Akkermansia muciniphila in human intestine / 中华临床感染病杂志

Recent studies heve demonstrated that Akkermansia muciniphila (A.muciniphila) plays an important role in human health and disease , including regulating the development of the immune system and the metabolic phenotype of the host.This article reviews the research progress on A.muciniphila in recent years, focusing on the basic characteristics , the influencing factors of colonization , and the underlying mechanism of maintaining intestinal homeostasis of A.muciniphila.Additionally, the article summarizes the potential association between A.muciniphila and the chronic metabolic diseases such as obesity , atherosclerosis,diabetes mellitus and infectious diseases.The perspect of A.muciniphila as a new generation of probiotics in clinical medicine and the challenge for its industrialization are also discussed in the article .

Antibiotics-mediated intestinal microbiome perturbation aggravates tacrolimus-induced glucose disorders in mice / 医学前沿

Both immunosuppressants and antibiotics (ABX) are indispensable for transplant patients. However, the former increases the risk of new-onset diabetes, whereas the latter impacts intestinal microbiota (IM). It is still unclear whether and how the interaction between immunosuppressants and ABX alters the IM and thus leads to glucose metabolism disorders. This study examined the alterations of glucose and lipid metabolism and IM in mice exposed to tacrolimus (TAC) with or without ABX. We found that ABX further aggravated TAC-induced glucose tolerance and increased insulin secretion. Combined treatment resulted in exacerbated lipid accumulation in the liver. TAC-altered microbial community was further amplified by ABX administration, as characterized by reductions in phylum Firmicutes, family Lachnospiraceae, and genus Coprococcus. Analyses based on the metagenomic profiles revealed that ABX augmented the effect of TAC on microbial metabolic function mostly related to lipid metabolism. The altered components of gut microbiome and predicted microbial functional profiles showed significant correlation with hepatic lipid accumulation and glucose disorders. In conclusion, ABX aggravated the effect of TAC on the microbiome and its metabolic capacities, which might contribute to hepatic lipid accumulation and glucose disorders. These findings suggest that the ABX-altered microbiome can amplify the diabetogenic effect of TAC and could be a novel therapeutic target for patients.

Effect of miR-27a on cell proliferation and apoptosis in human melanoma cell line WM239 / 国际肿瘤学杂志

Objective To investigate the effect of miR-27a mimic and inhibitor on proliferation and apoptosis in melanoma cell line WM239. Methods The miR-27a mimic,inhibitor and its negative control were transfected into WM239 cells. The transfection efficiency was evaluated by fluorescence microscope. The expres-sion of miR-27a was detected by real-time fluorescent quantitative PCR. The proliferation of cells was detected by MTT. The cell apoptosis and cell cycle were analyzed by flow cytometry. Results The transfection efficiency in WM239 cells was 80% to 90%. The expression of miR-27a was markedly up-regulated in miR-27a mimic group (2-△△CT value is 26. 98 ± 0. 01),with statistically significant difference(t= -1 123. 67,P=0. 00);and the miR-27a inhibitor group showed lower expression of miR-27a(2-△△CT value is 0. 96 ± 0. 02),there was no statisti-cally significant difference compared with normal control group(t=0. 04,P=0. 06). The proliferation of cells was obviously inhibited in miR-27a mimic group,and there was statistically significant difference compared with normal control group[absorbance of 72 h(0. 45 ± 0. 02)∶(0. 72 ± 0. 01),F=129. 56,P﹤0. 05]. The percent-age of WM239 cells in G0-G1 phase was increased[(74. 83 ± 1. 46)∶(63. 73 ± 1. 25),F=30. 33,P﹤0. 05], and the percentage of WM239 cells in S phase and G2-M phase were decreased[(21. 33 ± 1. 75)∶(27. 50 ± 1. 25),F=14. 98,P﹤0. 05;(3. 90 ± 1. 31)∶(8. 80 ± 2. 10),F=3. 66,P﹤0. 05]. The apoptosis rate of cells was significantly increased in miR-27a mimic group compared with normal group[(29. 67 ± 0. 91)%∶(1. 44 ± 0. 85)%,F=530. 90,P﹤0. 01],but the inhibitor group had no obvious effect on cell cycle and cell apoptosis. Conclusion MiR-27a can suppress melanoma cell proliferation and act as a tumor suppressor gene,which is rel-evant to induce cell apoptosis and block cell cycle in G0-G1 phase.

Risk Factors for Plagiocephaly and Brachycephaly / 中国康复理论与实践

Objective To investigate the factors related with plagiocephaly and brachycephaly. Methods 239 infants with plagiocephaly and brachycephaly were investigated, and analyzed with univariate analyses and multivariate Logistic regression analysis. Results The fac-tors, such as gestational age birth (OR=0.636, P<0.001), birth weight (OR=0.095, P<0.001), time of hospitalization (OR=1.307, P<0.001), preterm birth (OR=2.649, P<0.001), stay in newborn intensive care unit (OR=4.456, P<0.001), change the position (OR=0.046, P<0.001), accepted early intervention guidance (OR=0.054, P<0.001), were significantly related with plagiocephaly and brachycephaly. Conclusion Preterm birth, low birth weight, and newborn complications are the risk factors for plagiocephaly and brachycephaly, while change the posi-tion and early intervention may prevent it.

Risk Factors for Plagiocephaly and Brachycephaly / 中国康复理论与实践

@#Objective To investigate the factors related with plagiocephaly and brachycephaly. Methods 239 infants with plagiocephaly and brachycephaly were investigated, and analyzed with univariate analyses and multivariate Logistic regression analysis. Results The factors, such as gestational age birth (OR=0.636, P<0.001), birth weight (OR=0.095, P<0.001), time of hospitalization (OR=1.307, P<0.001), preterm birth (OR=2.649, P<0.001), stay in newborn intensive care unit (OR=4.456, P<0.001), change the position (OR=0.046, P<0.001), accepted early intervention guidance (OR=0.054, P<0.001), were significantly related with plagiocephaly and brachycephaly. Conclusion Preterm birth, low birth weight, and newborn complications are the risk factors for plagiocephaly and brachycephaly, while change the position and early intervention may prevent it.

Chemokine receptor 4 and tumors / 国际肿瘤学杂志

Chemokine receptor 4 (CXCR4) belongs to G protein-coupled receptor superfamily.It can induce immune cells-directed chemotaxis,thus keeping their homeostasis.CXCR4 expresses on a variety of tissues and cells.In different tumors and at different stages of tumors,CXCR4 expression is significantly higher than that in normal tissues.CXCR4 plays an important role in tumor progression since it is involved in tumor cell proliferation,adhesion,invasion and metasta.

Chemokine receptor 4 and tumors / 国际肿瘤学杂志

Chemokine receptor 4 (CXCR4) belongs to G protein-coupled receptor superfamily.It can induce immune cells directed chemotaxis and keep their homeostasis.CXCR4 expresses on a variety of tissues and cells.In different tumors and at different stages of tumor,CXCR4 expression is significantly higher than that in normal tissue.CXCR4 plays an important role in tumor progression since it is involved in tumor cell proliferation,adhesion,invasion and metastasis.

Effect of Early Intervention on General Movements in Preterm Infants during Fidgety Movement / 中国康复理论与实践

Objective To investigate the effect of early intervention on general movements (GM) in preterm infants during fidgety move-ment. Methods 315 preterm infants during fidgety movement period were divided into intervention group (n=160) and control group (n=155). The intervention group accepted very early intervention program consisted of hospital intervention and family intervention, and the control group accepted routine treatment and nursing. The incidences of different kinds of GMs were compared. Results There is no statisti-cal difference (χ2=0.641, P=0.726) in writhing movement before intervention, and the fidgety movement presented more in the intervention group than in the control group (χ2=8.710, P=0.003), while the absence of fidgety movement was significantly fewer (χ2=5.685, P=0.017) af-ter intervention. Conclusion Very early intervention can reduce the incidence of absence of fidgety movement and improve fidgety move-ment.

Changes of the peripheral Thelper cell cytokines of patients with chronic hepatitis B during antiviral treatment / 中华传染病杂志

Objective To determine the changes of peripheral levels of T helper cell cytokines of patients with chronic hepatitis B (CHB) during antiviral treatment,and to further explore its clinical significance.Methods The plasma levels of interleukin (IL)-2,IL-6,IL-10,interferon (IFN)-γ and tumor necrosis factor(TNF)-α of thirty-three CHB patients during antiviral treatment (entecavir) were measured using enzyme linked immunosorbont assay (ELISA).And their biochemical indicators of liver function were determined.The differences of cytokines levels before and after antiviral treatment were compared using ANOVA.The correlations between the changes of cytokines and alanine transaminase (ALT),hepatitis B virus (HBV) DNA levels were analyzed.Results Levels of IFNγ before and 12,24,48 weeks after treatment were (5.98±2.77),(5.95±3.37),(2.93±2.15) and (9.29±4.65) pg/mL,respectively (F=3.845,P＜0.05),which were positively correlated with ALT levels (r =0.396,P＜0.05).Both TNF-α and IL-10 levels declined after antiviral treatment,which were significantly different at different time points (F=20.156 and 16.695,respectively; both P＜0.05),and both levels of TNF-α and IL-10 were positively correlated with ALT levels (r=0.354and 0.316,respectively; both P＜0.05) and positively correlated with HBV DNA levels (r=0.382and 0.386,respectively; both P＜0.05).While both IL-2 and IL-6 levels were not significantly different between before and after antiviral treatment (F=0.010 and 0.932,respectively; both P＞0.05).The serum levels of ALT and HBV DNA before and after antiviral treatment were all significantly different (F=17.69 and 198.98,respectively; both P＜0.05),which declined gradually during treatment and were positively correlated (r =0.581,P＜0.05).Conclusions IL-10,IFNγand TNF-α may be involved in the pathologic process of CHB,and closely related to the deterioration of the disease.Monitoring plasma levels of these cytokines during antiviral treatment could be useful to understand the immune status and evaluate the efficacy of antiviral drugs.

Evaluating the combinative effects on human lymphocyte DNA damage induced by ultraviolet ray C plus 1.8 GHz microwaves using comet assay in vitro.

The objective of this study was to observe whether 1.8 GHz microwaves (MW) (SAR, 3 W/kg) exposure can influence human lymphocyte DNA damage induced by ultraviolet ray C (UVC). The lymphocytes, which were from three young healthy donors, were exposed to 254 nm UVC at the doses of 0.25, 0.5, 0.75, 1.0, 1.5 and 2.0 J m(-2), respectively. The lymphocytes were irradiated by 1.8 GHz MW (SAR, 3 W/kg) for 0, 1.5 and 4 h. The combinative exposure of UVC plus MW was conducted. The treated cells were incubated for 0, 1.5 and 4 h. Finally, comet assay was used to measure DNA damage of above treated lymphocytes. The results indicated that the difference of DNA damage induced between MW group and control group was not significant (P>0.05). The MTLs induced by UVC were 1.71+/-0.09, 2.02+/-0.08, 2.27+/-0.17, 2.27+/-0.06, 2.25+/-0.12, 2.24+/-0.11 microm, respectively, which were significantly higher than that (0.96+/-0.05 microm) of control (P<0.01). MTLs of some sub-groups in combinative exposure groups at 1.5-h incubation were significantly lower that those of corresponding UVC sub-groups (P<0.01 or P<0.05). However, MTLs of some sub-groups in combinative exposure groups at 4-h incubation were significantly higher that those of corresponding UVC sub-groups (P<0.01 or P<0.05). In this experiment it was found that 1.8 GHz (SAR, 3 W/kg) MW exposure for 1.5 and 4 h did not enhance significantly human lymphocyte DNA damage, but could reduce and increase DNA damage of human lymphocytes induced by UVC at 1.5-h and 4-h incubation, respectively.

Effects of 1.8 GHz radiofrequency field on DNA damage and expression of heat shock protein 70 in human lens epithelial cells.

To investigate the DNA damage, expression of heat shock protein 70 (Hsp70) and cell proliferation of human lens epithelial cells (hLEC) after exposure to the 1.8 GHz radiofrequency field (RF) of a global system for mobile communications (GSM). An Xc-1800 RF exposure system was used to employ a GSM signal at 1.8 GHz (217 Hz amplitude-modulated) with the output power in the specific absorption rate (SAR) of 1, 2 and 3 W/kg. After 2 h exposure to RF, the DNA damage of hLEC was accessed by comet assay at five different incubation times: 0, 30, 60, 120 and 240 min, respectively. Western blot and RT-PCR were used to determine the expression of Hsp70 in hLECs after RF exposure. The proliferation rate of cells was evaluated by bromodeoxyuridine incorporation on days 0, 1 and 4 after exposure. The results show that the difference of DNA-breaks between the exposed and sham-exposed (control) groups induced by 1 and 2 W/kg irradiation were not significant at any incubation time point (P > 0.05). The DNA damage caused by 3 W/kg irradiation was significantly increased at the times of 0 and 30 min after exposure (P < 0.05), a phenomenon that could not be seen at the time points of 60, 120 or 240 min (P > 0.05). Detectable mRNA as well as protein expression of Hsp70 was found in all groups. Exposure at SARs of 2 and 3 W/kg for 2 h exhibited significantly increased Hsp70 protein expression (P < 0.05), while no change in Hsp70 mRNA expression could be found in any of the groups (P > 0.05). No difference of the cell proliferation rate between the sham-exposed and exposed cells was found at any exposure dose tested (P > 0.05). The results indicate that exposure to non-thermal dosages of RF for wireless communications can induce no or repairable DNA damage and the increased Hsp70 protein expression in hLECs occurred without change in the cell proliferation rate. The non-thermal stress response of Hsp70 protein increase to RF exposure might be involved in protecting hLEC from DNA damage and maintaining the cellular capacity for proliferation.

Detecting the cytogenetic effects in workers occupationally exposed to vincristine with four genetic tests.

To study the human genetic damage induced by vincristine (VCR), the cytogenetic effects in workers occupationally exposed to vincristine were studied with micronucleus (MN) test, comet assay, hypoxantinepho-guanine phosphoribosyl-transferase (hprt) gene mutation assay and T-cells receptor (TCR) gene mutation assay. Fresh peripheral blood samples were collected from the workers and controls. Fifteen workers from a plant producing antineoplastic drug (vincristine) and 15 controls were matched according to age, gender and smoking. The results of MN test showed that the mean micronuclei rate (MNR) and mean micronucleated cells rate (MCR) in 15 workers were 17.80+/-1.88 per thousand and 13.67+/-1.56 per thousand, respectively, which were significantly higher than those (3.73+/-0.80 per thousand and 3.13+/-0.59 per thousand) in controls (P<0.01). It was found in the comet assay that the mean tail length (MTL) of 15 workers and 15 controls were 1.72+/-0.15 microm and 0.71+/-0.01 microm, respectively, there was significant difference between workers and controls for MTL (P<0.05), but the difference between the mean tail moment (MTM, 0.29+/-0.03) of 15 workers and MTM (0.17+/-0.05) of 15 controls was not significant (P>0.05). The results of hprt gene mutation assay showed that the average mutation frequency of hprt (Mf-hprt) in workers was 1.03+/-0.02 per thousand, which was significantly higher than that (0.87+/-0.01 per thousand) in controls (P<0.05). Meanwhile, the results of TCR gene mutation assay indicated that Mfs-TCR of workers and controls were 2.52+/-0.34 x 10(-4) and 1.51+/-0.11 x 10(-4), respectively, there was a significant difference between workers and controls (P<0.01). It is found in the results of our study that the genetic damage is detectable in 15 workers occupationally exposed to vincristine.

Studying the synergistic damage effects induced by 1.8 GHz radiofrequency field radiation (RFR) with four chemical mutagens on human lymphocyte DNA using comet assay in vitro.

The aim of this investigation was to study the synergistic DNA damage effects in human lymphocytes induced by 1.8 GHz radiofrequency field radiation (RFR, SAR of 3 W/kg) with four chemical mutagens, i.e. mitomycin C (MMC, DNA crosslinker), bleomycin (BLM, radiomimetic agent), methyl methanesulfonate (MMS, alkylating agent), and 4-nitroquinoline-1-oxide (4NQO, UV-mimetic agent). The DNA damage of lymphocytes exposed to RFR and/or with chemical mutagens was detected at two incubation time (0 or 21 h) after treatment with comet assay in vitro. Three combinative exposure ways were used. Cells were exposed to RFR and chemical mutagens for 2 and 3h, respectively. Tail length (TL) and tail moment (TM) were utilized as DNA damage indexes. The results showed no difference of DNA damage indexes between RFR group and control group at 0 and 21 h incubation after exposure (P>0.05). There were significant difference of DNA damage indexes between MMC group and RFR+MMC co-exposure group at 0 and 21 h incubation after treatment (P<0.01). Also the significant difference of DNA damage indexes between 4NQO group and RFR+4NQO co-exposure group at 0 and 21 h incubation after treatment was observed (P<0.05 or P<0.01). The DNA damage in RFR+BLM co-exposure groups and RFR+MMS co-exposure groups was not significantly increased, as compared with corresponding BLM and MMS groups (P>0.05). The experimental results indicated 1.8 GHz RFR (SAR, 3 W/kg) for 2h did not induce the human lymphocyte DNA damage effects in vitro, but could enhance the human lymphocyte DNA damage effects induced by MMC and 4NQO. The synergistic DNA damage effects of 1.8 GHz RFR with BLM or MMS were not obvious.

Detecting DNA repair capacity of peripheral lymphocytes from cancer patients with UVC challenge test and bleomycin challenge test.

The objective of this study was to evaluate DNA repair capacity of cancer patients with the bleomycin (BLM) challenge test and the UVC challenge test. The human peripheral lymphocytes were collected from 33 patients with different kinds of cancers and 33 controls in the same hospital. The lymphocytes of each subject were divided into two groups: (1) In the BLM challenge test, the lymphocytes were treated with BLM (20 microgml(-1)) for 30 min, and repaired for 15 min. The DNA damage before and after BLM exposure was detected with comet assay to assess DNA repair capacity. (2) In the UVC challenge test, the lymphocytes were exposed to UVC (254 nm) at the dose of 1.5 Jm(-2). DNA damage of lymphocytes was measured before UVC exposure and at 90 and 240 min after UVC exposure using comet assay, then DNA repair percentage (DRP) was calculated. The results of this study indicate that the average DRPs of cancer patients were 75.63 +/- 3.11 and 68.98 +/- 4.19% calculated with tail length (TL) and tail moment (TM), respectively, in the BLM challenge test, which were significantly lower than those (91.11 +/- 1.09 and 88.19 +/- 1.71%) of controls (P < 0.01). Also, the mean DRPs of cancer patients were 49.19 +/- 3.47 and 58.27 +/- 3.64% calculated with TL and TM, respectively, in the UVC test, which were significantly lower than those (77.52 +/- 2.06 and 83.12 +/- 2.36%) of controls (P < 0.01). The correlation between the DRPs (%) drawn with TL and TM in the BLM test or between the DRPs (%) drawn with mean TL and mean TM in the UVC challenge test were significant (P < 0.05). The DNA repair capacity measured with the BLM and UVC challenge tests in 33 cancer patients was significantly lower than that in controls.

Measuring the genetic damage in cancer patients during radiotherapy with three genetic end-points.

In this paper the genetic damage for three genetic end-points was studied in cancer patients during radiotherapy using the micronucleus test, comet assay and hprt gene mutation test. The subjects were from: (i) a group of 24 patients suffering from various types of cancers; (ii) a group of 23 controls matched according to age, sex and smoking. Blood samples were collected from the controls and from the cancer patients prior to radiotherapy and after cumulative radiation doses of 10, 30 and 50 Gy. The results of the micronucleus test indicated that the mean micronuclei rate (MNR) and mean micronucleated cells rate (MCR) in the cancer patients prior to radiotherapy were 12.46 and 11.29 per thousand, respectively, which were significantly higher than those (6.65 and 5.96 per thousand) in controls (P < 0.01). However, the results of the comet assay and hprt gene mutation test showed no significant difference between untreated cancer patients and controls (P > 0.05). The mean MNR/MCR at 0, 10, 30 and 50 Gy in cancer patients increased with the cumulative dose, being 12.46, 35.83, 64.63 and 85.00 per thousand for MNR and 11.29, 31.25, 53.63 and 67.28 per thousand for MCR, respectively. Similar results were obtained in the comet assay and hprt gene mutation test. Meanwhile, it was found that there was inter-individual variability in response to radiotherapy among patients.

The Interventional Sclerotherapy of Renal Cysts Guided by CT / 实用放射学杂志

Objective To compare the results of single and repeated percutaneous sclerotherapy in patients with simple renal cysts .Methods 96 patients with simple renal cysts underwent needle aspiration and sclerotherapy under CT guidance. 45 patients (group A) underwent one session of sclerotherapy with 99.7% ethanol immediately after aspiration and 51 patients (group B) underwent repeated sclerotherapy at least twice. The patients were followed up using ultrasonography or CT at 3～6 months intervals. The complete or almost disappearance of the renal cyst was considered a successful treatment.Results The efficacy of treatment was significantly different in two group . The overall effective rate were 91.1% and 98.8% in group A and group B , respectively. The rate of complete regression was significantly better in group B (80.4%) than in group A (62.2%,?

Imaging Diagnosis and Misdiagnosis of Multi-nodular Bronchioalveolar Carcinoma / 实用放射学杂志

Objective To study the imaging features and the reason of misdiagnosis of multi-nodular bronchioalveolar carcinoma(BAC).Methods 33 cases with the BAC proved by pathology,were reviewed,including 20 males and 13 females,the age ranged from 34～76 years with an average age of 54.2 years.X-ray there were over twice X-ray filmes in all cases,and CT scans with GE 9800 Quick were performed in 30 cases . The imaging features were analysed . Results Imaging findings : Miliary noduli were inhomogeneous in distribution,size and density.The large noduli generally located at the periphery of lung or under the pleura and noduli were focused together,“vacuole sign” was present in 72.7% cases and the noduli were around the vacuole,and lobulated.69.7% of nodule focuses were in company with consolidatory shade . The rate of X-ray misdiagnosis was 75.8%, in which 72.0% were misdiagnosed as TB . CT misdiagnostic rate was 36.4%.The misdiagnostic reasons were unsufficient in consideration of clinical symptom and imaging findings.Conclusion The BAC is the developmental stage of cancer.The accurate diagnosis can be improved if clinical-imaging features are analysed properly,and reexamination and comparison are taken carefully.