Volume 94  ·   Issue 10  ·  2014

tuberous sclerosis complex (TSC) is a relatively common neurocutaneous syndrome with a population prevalence of 1/ (6 000 to 10 000). First reported by von Recklinghausen in 1862, TSC is an autosomal dominant disorder, but about 2/3 have no positive family history. Involvement of multiple organs such as brain, skin, peripheral nerves and kidneys can occur, and the clinical features are facial angiofibroma, epileptic seizures and mental retardation. Common neuronal migration disorders in the brain are common, and the typical manifestations are multiple nodules, which can be seen in the subependymal and cerebral cortex^[1]。 TSC has been lacking specific treatment and has a poor prognosis. Its pathogenic gene mutations have been identified in recent years^[2,3,4], revealed the specific significance of mammalian rapamycin target protein (mTOR) pathway overactivation in the pathogenesis of TSC, thus discovering targets that may reverse or even cure this disease^[5], and promising therapeutic drugs have been marketed^[6]This disease has attracted much attention.

To compare the accuracy of computer tomography (CT) plus diagnostic laparoscopy in preoperative staging of potentially resectable gastric cancer.

A total of 194 gastric cancer patients underwent combined CT and laparoscopic staging. Then the results were compared with those of pathologic TNM staging.

Comparing with pathologic TNM stage, the T staging accuracy of CT was lower than that of laparoscopy (72.7% vs 89.6%, χ²=7.844, P=0.005), the N staging accuracies of CT and laparoscopy were 55.6% and 70.1% (χ²=4.329, P=0.037) and the M staging accuracies 90.7% and 97.9% respectively (χ²=4.722, P=0.030). The diagnostic laparoscopy uncovered 14 patients with peritoneal metastases.

The value of CT is limited in preoperative staging of gastric cancer. However its accuracy may be enhanced by laparoscopy through detecting more peritoneal metastasis.

To explore the platelet activation status before and after coronary artery stent implantation at different timepoints.

The contents of CD62P (soluble P-selectin) and PAC-1 (platelet glycoprotein GPⅡb/Ⅲa fibrinogen receptor) in patients after coronary stent implantation were detected by flow cytometry (FCM) before, immediately after surgery, postoperative 2, 4, 6 and 24 h in peripheral blood.

In 65 cases, the levels of CD62P[40.63(25.14-51.01)%] and PAC-1[36.59(20.37-48.41)%] immediately after surgery were significantly higher than their preoperative values [14.79(9.85-26.66)%, 13.99(11.42-30.133)%] (P<0.05). And the postoperative levels of 2 h [8.64(4.48-15.67)%, 12.64(6.45-18.83)%], 4 h [7.91(4.56-12.94)%, 12.81(6.89-18.66)%], 6 h [6.53(4.12-9.27)%, 9.43(5.27-15.65)%] and 24 h [6.28(4.36-9.63)%, 10.38(4.63-18.11)%] decreased significantly versus their preoperative values (P<0.05).

Stenting of coronary endothelial damage within 2h may enhance platelet activation and boost the risk of thrombosis.

To explore the association of narcolepsy with human leukocyte histocompatibility antigen (HLA)-DQB1*0602 allele in Chinese narcoleptic patients and examine its relationship with different phenotypes.

A total of 1 223 narcoleptic patients (NC, narcolepsy with typical cataplexy, n=1 132; NWC, narcolepsy without cataplexy, n=91) diagnosed at Sleep Center of Peking University People's Hospital from August 1998 to July 2011 were recruited into this retrospective study. According to the onset age, they were divided into early-onset group (onset age ≤15y,n=1 037) and late-onset group (onset age >15y, n=181). All of them underwent a polymerase chain reaction with specific sequence primer (PCR-SSP) HLA-DQB1*0602 typing. And the cerebrospinal fluid levels of hypocretin-1 (hcrt-1) were measured in 156 narcoleptic patients and they were divided into hcrt deficiency group (hcrt-1<138 ng/L,n=115) and hcrt normal group (hcrt-1≥138 ng/L, n=41). And 728 healthy volunteers were selected as control group. The expression positivity of HLA-DQB1*0602 gene was analyzed for each group.

There were 1 223 narcoleptic patients including 825 males (67.5%) and 398 females (32.5%) with an average age of (16.6±12.6) years on visiting. There were 728 normal controls including 443 males (60.9%) and 285 females (39.1%) with an average age of (26.6±11.4) years on blood sampling. The positive rate of HLA-DQB1*0602 in narcoleptic, NC and NWC groups was 94.7% (1 158/1 223), 97.0% (1 098/1 132) and 65.9% (60/91) respectively. NC group had a higher rate of HLA-DQB1*0602 positivity (χ²=155.4, P=0.000). Both groups were higher than that in control group of 19.5% (142/728). The positive rate of HLA-DQB1*0602 in early-onset group was 95.5% (990/1 037) versus 90.1% (163/181) in late-onset group (χ²=9.25, P=0.010). Among those with hcrt-1 measurement, 98.3% (113/115) were HLA-DQB1*0602 positive in hcrt deficiency narcolepsy group versus 25.6% (11/43) in hcrt non-deficiency group (χ²=94.6, P=0.001).

HLA-DQB1*0602 is an important marker in this large sample of Chinese patients with narcolepsy. Its frequency is much higher in patients with cataplexy, early-onset age and hcrt-1 deficiency.

To explore the clinical features and treatments of mucosa-associated lymphoid tissue (MALT) lymphoma.

The clinical data of 80 MALT lymphoma patients treated from September 2000 to November 2012 were retrospectively analyzed.

Among them, 32(40.0%)had gastric MALT lymphoma and 48(60.0%) non-gastric MALT lymphoma. Gastric lymphoma associated anemia accounted for 50.0% (16/32) (25.0% (12/48) in non-gastric group, P=0.022). In non-gastric group, stage Ⅲ-Ⅳ diseases accounted for 35.4% (17/48) (12.5%(4/32)in gastric group, P=0.022). During a median follow-up of 30 months, the 5-year overall survival (OS) rate was 90.0% and 5-year progression-free survival (PFS) rate 67.0%. For the non-gastric group, surgery plus chemotherapy group was superior in PFS to surgery alone group (the 3-year PFS rate 83.0% and 33.0%; median PFS 43.4 months and 20.3 months) (P=0.040). Five-year OS in patients on first-line rituximab and chemotherapy without rituximab were 100.0% and 86.0% respectively (P=0.106). Short-term response (OR=0.258, P=0.020) and low albumin(OR=3.967, P=0.009)were independent factor for PFS.

Non-gastric MALT lymphoma is easily disseminated. Systemic treatment may be considered for advanced non-gastric MALT lymphoma. Surgery often leaves residual lesions for gastric MALT lymphoma.

To explore the roles of various transcription factors in the occurrence and development of prostate cancer.

A total of 139 specimens with prostate cancer (PCa) and 83 specimens with benign prostatic hyperplasia (BPH) from hospitalized patients at our hospital from 2008 to 2011 were enrolled. The mRNA expressions of c-Myc, Klf4, Nanog, Oct4A and Sox2 were determined by quantitative real-time polymerase chain reaction (PCR) and the expressions of Klf4 isoforms by conventional PCR. Immunohistochemical method was used for the detection of Klf4 protein via tissue microarray in 404 prostate samples.

No significant difference existed in the expressions of Nanog, Oct4A and Sox2 genes between BPH and PCa samples. And the expressions of c-Myc and Klf4 genes were significantly higher in PCa than those in BPH specimens. Immunohistochemical results showed that Klf4 protein could be detected in a large majority of epithelial prostatic cells irrespective of malignant transformation. However, it was predominantly located cytoplasmically in PCa tissues and remained consistent with the expression of a differentially spliced Klf4α isoform.

Klf4 is highly expressed in both BPH and PCa tissues. But in malignant cells, a specific gene product Klf4α is predominantly detectable in cytoplasm. The positioning of Klf4 protein may have an important relationship with its role in the tumorigenic process.

To explore the association of perioperative homologous blood transfusion (packed red blood cell, PRBC) and postoperative complications after radical gastrectomy in patients with gastric cancer.

From October 2010 to July 2013, a total of 636 patients undergoing radical gastrectomy at Department of Gastric, Duodenal & Pancreatic Surgery at Hunan Provincial Tumor Hospital were divided into 2 groups according to perioperative blood transfusion ( n=170, 26.73%) or not (n=466, 73.27%). Their clinicopathological data, such as age, gender, co-morbidities, surgical duration, intraoperative blood loss volume and pathological stage were retrospectively analyzed by case-control study model. And the transfusion group was further divided into subgroup by transfusion volume (total PRBC<3.0, 3.0-7.5 or >7.5 U) and timing (pre-, intra- or post-operative) to examine the association of transfusion volume and timing with postoperative complications by Logistic regression.

Thirty-two patients suffered from complications in the transfusion group (18.82%). And it was significantly more common than that in the control group (10.09% (47/466), P<0.01). Moreover, the complication rate (33.33%(12/36)) was obviously higher in the large transfusion volume group (PRBC>7.5 U) than with those in the moderate (15.53%(16/103),P=0.02) and low groups (12.90%(4/31), P=0.04). Infection was more common along with the total amount of transfused blood (6.45% (2/31), 10.68% (11/103) and 19.44% (7/36) in the low, moderate and large transfusion group respectively). Yet the differences were insignificant (P=0.22). There was no significant difference of complication rates among the pre-, intra- and post-operative transfusion group classified by transfusion time (P=0.39). And the postoperative infection rates were also insignificantly different (P=0.88). Further Logistic analysis revealed that perioperative transfusion (OR=2.71, 95% CI: 1.40-5.27, P<0.01) was an independent risk factor for postoperative complications after radical gastectomy.

Perioperative blood transfusion is significantly associated with postoperative complications after radical gastrectomy in patients with gastric cancer. And a positive correlation exists between infection and the amount of transfused blood. But there was no association between transfusion time and complications. Thus decreasing perioperative transfusion may reduce the incidence of postoperative complications and shorten the length of hospital stays.

To compare the long-term survival of patients with Barcelona Clinic Liver Cancer (BCLC) stage B hepatocellular carcinoma (HCC) undergoing either liver resection or transarterial chemoembolization (TACE) after propensity score matching (PSM).

One hundred sixty-seven and 70 BCLC-B HCC patients undergoing liver resection and TACE were retrospectively collected. PSM function of SPSS software was conducted to reduce confounding bias between the groups. And then survival analysis was performed for the matched data.

Fifty-three pairs of patients were successfully matched. And then survival analysis showed that the median survival periods and their 95% confidence intervals were 35.0 (26.3-43.7)months in the liver resection group versus 20.0(15.0-25.0) months in the TACE group. The 1, 3, 5 and 7-year survival rates were 91.0%, 49.0%, 30.0% and 17.0% in the liver resection group versus 73.0%, 25.0%, 8.0% and 5.0% respectively in the TACE group (P=0.001). Cox regression analysis revealed that TACE, total bilirubin ≥34.2 μmol/L, alpha fetoprotein ≥400 ng/ml and tumor number≥3 were independent risk factors of survival (hazard ratio >1, P<0.05).

The balance of covariates may be achieved through PSM. And for patients with BCLC-B HCC, liver resection provides better long-term overall survival than TACE.

To explore the pathogenesis of a family with inherited dysfibrinogenemia.

Coagulation parameters of peripheral venous blood of a family with inherited dysfibrinogenemia from November 2012 were measured. And platelet and fibrinogen functions were examined by thromboelastogram. The antigen concentration of fibrinogen was detected by immune nephelometry. All exons and exon-intron boundaries of FGA, FGB and FGG were amplified and subjected to mutation screening by direct/reverse sequencing. And the influences of mutant fibrinogen structure and function were analyzed and predicated by a molecular structure model.

The values of activated partial thromboplastin time (APTT), D-dimer and fibrinogen antigen of the propositus and his mother(Ⅰ-2), younger brother (Ⅱ-3), younger sister (Ⅱ-2) and daughter (Ⅲ-1) were all in normal reference value ranges. However thrombin time (TT) was significantly prolonged and the activity of fibrinogen was much lower compared to its antigenicity. Thromboelastogram indicated normal function of platelet and impaired function of fibrinogen of Ⅰ-2, Ⅱ-2 and Ⅲ-1. However the fibrinogen functions of proband and Ⅱ-3 became much more impaired. Mutation screening demonstrated the homozygous mutation of proband and Ⅱ-3 while Ⅰ-2, Ⅱ-2 and Ⅲ-1 showed heterozygous mutation of FGG c. 1001 A>C (p. Asn308Thr). No mutation was detected among other family members and reducing SDS-PAGE immunoblot showed no variants. Asn308, located at the interface of fibrinogen dimmer, participated in the fibrous structure assembling from the structure model. And mutation at this position will affect the stability of fiber structure.

FGG c. 1001 A>C mutation may account for dominant genetic dysfibrinogenemia in these family members.

To analyze the percentage and functional changes of natural kill (NK) cell in peripheral blood of myelodysplastic syndrome (MDS) patients so as to evaluate the relationships between these changes and hematopoietic functions and explore the role of NK cell in the pathogenesis of MDS.

By flow cytometry, the percentage of NK cell (CD3^-CD56⁺CD16⁺) in peripheral blood lymphocytes was detected in 20 MDS patients, 15 acute myelogenous leukemics (AML) and 15 normal controls from March 2013 to November 2013 at our hospital. NK cell activation receptors (NKG2D, NKp44), inhibitory receptors (CD158a, CD158b), perforin and granzyme-β of patients and normal controls were also detected. The correlation between these changes and hematopoietic functions, including the percentages of neutrophil granulocyte (ANC%), lymphocyte(Lym%), reticulocyte (RET%) and hemoglobin, thrombocyte in peripheral blood and the hematopoietic function in bone marrow (CD34⁺%) were evaluated.

(1) The percentage of NK cell (3.87%±0.97%) in MDS patients was significantly lower than that of normal controls (6.08%±1.37%, P<0.05) and higher than that of AML patients(2.58%±0.78%,P<0.05). (2) The expression of NKG2D in MDS patients (52.83%) was significantly lower than that of normal controls (86.36%,P<0.05) and higher than that of AML patients(42.00%,P<0.05). The expression of NKp44 in MDS patients (2.41%) was significantly higher than that of normal controls (0.62%) and AML patients (0.92%) (bothP<0.05). (3) The expression of CD158a in MDS and AML patients (5.46%±2.40%, 4.05%±1.89%) were significantly both lower than those of normal controls (7.97%±2.85%, bothP<0.05). The expression of CD158b had no significant difference among the 3 groups. (4) The expression of perforin in MDS patients (17.83%) was significantly lower than that of normal controls (59.79%,P<0.05) and higher than that of AML patients(13.06%,P<0.05). The expressions of granzyme-β in MDS and AML patients (21.54%, 30.65%) were significantly both lower than those of normal controls (83.42%, bothP<0.05). (5)The percentage of NK cell and the expression of NKG2D and NKp44 in MDS patients with low-risk group were in turn higher than those of high-risk group(4.06%±0.56% vs 3.59%±1.37%, 53.42%±6.85% vs 47.29%±8.08%, 2.46% vs 2.07%, allP<0.05), the expression of CD158a and CD158b were in turn lower than those of high-risk group, but bothP>0.05.(6) The percentage of NK was positively correlated with ANC%(r=0.780, P<0.05), but negatively with Lym% and the CD34⁺% in bone marrow (r=-0.543, -0.610, both P<0.05). The expression of CD158a was positively correlated with CD34⁺% in bone marrow (r=0.612, P<0.05). The expressions of NKp44, CD158a, perforin and granzyme-β of NK cells had no correlation with hematopoiesis (allP>0.05).

The lowered percentage and function of NK may cause the immunological dysfunction and lead to underkilling of pathological hematopoietic cells in MDS.

To explore the correlation between smoking and obstructive sleep apnea and hyponea syndrome (OSAHS).

The data were collected from a chart review of patients with sleep or sleep-breathing disorders undergoing overnight polysomnograpghy (PSG) at Sleep-Disordered Breathing Center of Guangxi from July 1, 2009 to June 30, 2012. Smoking history was quantified by retrospective questionnaires. A definite diagnosis of OSAHS was defined by an apnea-hypopnea index (AHI) (events/h) of > 15 events per hour. And those with AHI (events/h) between 5 and 15 were eliminated. The non-OSAHS subjects were defined by an AHI (events/h) <5 events per hour. The association of smoking status and severity with OSAHS was analyzed.

A total of 903 patients were excluded from 2 243 patients. The recruited subjects were divided into OSAHS (n=929) and non-OSAHS (n=411) groups. Smoking prevalence in OSAHS group was 47.1% versus 25.5% in non-OSAHS group. Logistic regression analyses were performed to examine the effects of smoking habits while adjusting for age, gender, body mass index (BMI) and drinking history. Current smokers were 1.446 times more likely to have OSAHS than non-smokers (95% CI: 1.079-1.939, P=0.013). Current smokers with pack-years ≥30 were more 2.382 times more likely to have OSAHS than non-smokers to have OSAHS (95% CI: 1.127-4.375, P=0.012). Current smokers diagnosed as having OSAHS with pack-years ≥30 had a more percentage of total sleep time (TST) spent with saturation of oxyhemoglobin (SaO₂)<90% ((20.5±23.1)% vs (15.6±18.8)%,P=0.004) and lower average SaO₂ ((69.4±10.3)% vs (73.2±9.7)%, P=0.000) during sleep than non-smokers diagnosed as having OSAHS. Current smokers diagnosed as having OSAHS with pack-years≥30 were 1.893 times more likely to spend > 5% of TST at SaO ₂<90% than non-smokers diagnosed as having OSAHS (95%CI: 1.046-3.423, P=0.035).

Smoking is associated with a significantly increased risk of OSAHS and nocturnal hypoxia in current smokers, especially those with ≥30 pack-years. And it exacerbates nocturnal hypoxia in OSAHS patients.

To explore the effects of cyclooxygenase-2 (COX-2) and its inhibitor valdecoxib in liver fibrosis.

Hepatic fibrosis was induced by carbon tetrachloride for 8 weeks in wild-type and COX-2 knockout mice. And the levels of hyaluronic acid (HA), collagen Ⅳ(Ⅳ-C), procollagen Ⅲ(PCⅢ) and α-smooth muscle actin (α-SMA) were determined. Cyclin D and cyclin E were measured in hepatic satellite cell (HSC) after a treatment of valdecoxib for 24 h or not.

HA, Ⅳ-C, PCⅢand α-SMA all had significant difference in 3 groups (control group: (180±13)μg/L, (56±9)μg/L, (39±13)μg/L, 2.49%±0.24% in control, F=78.52, 61.30, 41.96, 28.15, all P<0.05). HA, Ⅳ-C and α-SMA in wild-type liver fibrosis mice were higher than those in knockout counterparts ((413±60) vs (308±42)μg/L, (96±13) vs (74±10)μg/L, 8.99%±0.81% vs 4.72%±0.50%, allP<0.01). But PCⅢ were similar between two groups ((82±12) vs (72±15)μg/L,P=0.06). Wild-type mice expressed higher levels of cyclin D and cyclin E than those of knockout mice (0.96±0.15 vs 0.76±0.10, 0.94±0.13 vs 0.82±0.09, P=0.02, 0.04). The rates of cyclin D and cyclin E were 0.40±0.06 and 0.38±0.05, 0.35±0.04 and 0.37±0.06 respectively after a treatment of valdecoxib. And both deceased in hepatic satellite cell of wild-type and knockout mice (both P<0.01) versus those without valdecoxib.

COX-2 increases the activation and proliferation of HSC leading to liver fibrosis. And its inhibitor may depress liver fibrosis by decreasing the expressions of cyclin D and cyclin E in COX-2 dependent and(or) independent way.

To explore the effect of vitamin D analogs regulated mice urinary output on depressed expression of renin-angiotensin in paraventricular nucleus.

A total of 51 C57BL/6 mice were randomly divided into control (n=36) and vitamin D receptor knockout (VDR, n=15) groups. Then the tests of water deprivation, vitamin D analogue injection and 0.25% captopril water drinking were performed. Renin levels in paraventricular nucleus and plasma and aquaporin in kidney were determined by immunofluorescence, real-time polymerase chain reaction (PCR) and Western blot.

The urinary output of VDR knockout mice decreased markedly after 48 h water deprivation [(129±45 vs 1 354±224)ml/24 h, P<0.05] while there was little change of urinary and plasma osmalarity. The expression levels of AQP-4 and rennin in VDR knockout mice were higher than those of wild type. Renin and angiotensinⅡin periventricular nucleus of VDR knockout mice were higher than those of wild type and was reduced by injecting vitamin D analogs into wild type. Rennin activity: (139±31vs 185±56)mcU/ml; angiotensinⅡ: (33±32 vs 72±27)pg/ml, (bothP<0.05). There was statistically significant differences. The expression of c-fos in periventricular nucleus in VDR knockout mice was higher and it could be inhibited after an injection of vitamin D analog.

Thirsty in central nervous system is inhibited by vitamin D analogs through reduced renin-angiotensin activity in paraventricular nucleus. Polydipsia and polyuria may be caused by a lack of vitamin D. Captopril lowers urinary output.

To explore the effects of different types of interferon (IFN) on the expression of hepatitis C virus(HCV) replication-related miRNAs in human hepatocytes.

The levels of miRNAs in Huh7 cells treated with types Ⅰ (IFN-α, IFN-β), Ⅱ (IFN-γ) and Ⅲ (IFN-λ1) interferons (IFNs) were determined by real-time quantitative polymerase chain reaction (PCR). The levels of various miRNAs were compared among different IFN treatment groups.

The expression of miRNA-196, miRNA-296, miRNA-351, miRNA-431 and miRNA-448 in IFN-α, IFN-β and IFN-λ1 treated groups was higher than that in control group (474.5±57.7, 436.0±37.8, 431.3±43.5 vs 99.5±2.4; 389.5±44.0, 416.3±36.7, 284.8±20.9 vs 99.0±0.8; 453.3±51.1, 473.8±24.0, 522.0±40.3 vs 99.5±2.1; 288.3±44.9, 294.3±29.9, 450.0±29.5 vs 100.5±2.4; 319.0±35.4, 357.0±27.5, 446.5±61.2 vs 99.8±1.0; allP<0.05). The expression of miRNA-196, miRNA-351 and miRNA-448 in IFN-γ-treated group (271.3±29.6, 140.5±27.5, 177.8±23.4) was higher than that in control group(allP<0.05). But the expression of miRNA-431 and miRNA-296 had no significant difference between IFN-γ treated group and control group (bothP>0.05). The expression of miRNA-122 at difference concentrations (10, 100, 1 000 U/ml) of IFN-α, IFN-β, IFN-γ and IFN-λ1 (10, 100, 1 000 ng/ml) was lower than that in control gourp (49.3±4.9, 32.0±3.7, 24.5±3.7 vs 99.5±2.1; 53.5±1.9, 35.5±2.7, 25.8±4.0 vs 98.8±1.3; 60.8±7.1, 43.8±4.0, 33.5±4.2 vs 99.3±2.6; 50.0±2.9, 35.5±3.3, 22.3±3.8 vs 100.3±1.5; allP<0.01).

Different types of IFN increase the expression of miRNAs that inhibit HCV replication and decrease the expression of miRNA-122 that supports HCV replication. Thus the regulation of HCV replication-related miRNA expression is a general anti-HCV mechanism by different types of IFN. However, the regulation pattern by type Ⅱ IFN is different from those by other types of IFNs, implying that type Ⅱ IFN has different anti-HCV mechanisms from other types of IFN at miRNA level.

To evaluate the molecular targeting capacity and gene transfection efficiency of magnetic nanocomposite coupling with folic acid (FA) of PEG-PEI(-FA)-Alg-Fe3O4 adsorbing plasmid to folate receptor (FR) positive nasopharyngeal carcinoma (NPC) cell.

The phagocytosis of magnetic nanocomposite was examined in FR positive NPC HNE-1 and FR negative NPC CNE-2 cells. Prussian blue staining, transmission electron microscope (TEM) and flow cytometry were employed to analyze its gene transfection efficiency by observing the plasmid expression of green fluorescent protein (GFP) in two cell types. Nude mice with implanted HNE-1 and CNE-2 tumor received a tail vein injection of magnetic nanocomposite. And the phagocytosis of magnetic nanocomposite was observed by magnetic resonance imaging (MRI), iron staining and TEM.

HNE-1 cell could effectively ingest magnetic nanocomposite, there was a strong intracellular expression of GFP and the gene transfection efficiency was approximately 40.0%±3.0%. However, CNE-2 cell had virtually no uptake of magnetic nanocomposite, there was a weak intracellular expression of GFP and the gene transfection efficiency was approximately 4.5%±1.5%. The implanted HNE-1 tumor cell could efficiently swallow magnetic nanocomposite, but there was little phagocytosis of magnetic nanocomposite in implanted CNE-2 tumor cell.

The magnetic nanocomposite coupling with FA of PEG-PEI(-FA)-Alg-Fe₃O₄ adsorbing plasmid has excellent molecular targeting capacity and higher gene transfection efficiency.

Behcet syndrome (BS) occurs in Japan and the Mediterranean region, and can also be seen in China; Male incidence is higher than female^[1]。 The disease often involves the lungs, and pulmonary aneurysm is its common complication; Due to the lack of clinical understanding of this disease, it is easy to lead to misdiagnosis and misdiagnosis. From 1999 to 2009, a total of 7 patients with BS complicated with pulmonary aneurysm were treated in our hospital, which are summarized as follows.

high mobility group (HMG) proteins are non-histone nuclear proteins present in almost all eukaryotic cells. Since it was first discovered that HMGB1 can be released to extracellular mediation of inflammatory response, HMGB1 as an important inflammatory mediator and pro-inflammatory cytokine has attracted widespread attention at home and abroad. Hepatic ischemia reperfusion injury (IRI) is a complex pathophysiological process involved by various inflammatory factors^[1]In recent years, a large number of studies have shown that HMGB1 is involved in multi-organ IRI and can provide a new target for the prevention and treatment of IRI. The relationship between HMGB1 and liver IRI in recent years is reviewed.

Schmidt – Wolf et al.^[1]Cytokine-induced killer cells (CIK cells) with high proliferative capacity and high cytotoxicity were first reported in 1991. CIK cells are promising effector cells for adoptive cellular immunotherapy (ACI). The main effector cells that play a killing role in CIK cells simultaneously express CD3 and CD56 membrane proteins, and have the strong antitumor activity of T lymphocytes and the unrestricted tumor killing characteristics of natural killer cells (NK cells) major histocompatibility complex (MHC), so they are also called NK-like T cells^[2]。 CIK cells derived from peripheral blood have been widely used in adoptive immunotherapy for tumors, but due to their short survival time and strong allogeneic immunogenicity, there are some limitations in clinical application. However, CIK cells derived from umbilical cord blood had weak immunogenicity, rapid proliferation, long survival time, and low incidence of graft versus host disease (GVHD) after reinfusion^[3]In addition, cord blood has a wide range of sources and is economical, and its clinical application as a novel source of CIK cells has received widespread attention. However, the cognition of the biological and functional characteristics of cord blood CIK is not perfect, and further exploration is needed. The in vitro culture, anti-tumor mechanism and clinical application of cord blood CIK are summarized as follows.

At present, comparative effect study (CER) has become the focus of researchers in many disciplines, including clinical and public health. The Journal of the American Medical Association identified "Comparative Effects Studies" as one of the topics of the 2012 journal^[1]And published a series of papers on comparative effect studies in April 2012. While there are multiple versions of the current definition of CER, it is central to "comparing the advantages and disadvantages of different existing interventions and intervention strategies in terms of prevention, diagnosis, treatment and disease rehabilitation, based on different database resources and measurements, in real-world clinical scenarios"^[2]Ultimately, "respond to the needs expressed by patients, clinicians and other decision-makers, thereby assisting patients, physicians and decision-makers in making informed decisions to improve health care for individuals and populations"^[3]。