Challenging anticoagulation therapy for multiple primary malignant tumors combined with thrombosis: A case report and review of literature.

BACKGROUND: Venous thromboembolism significantly contributes to patient deterioration and mortality. Management of its etiology and anticoagulation treatment is intricate, necessitating a comprehensive consideration of various factors, including the bleeding risk, dosage, specific anticoagulant medications, and duration of therapy. Herein, a case of lower extremity thrombosis with multiple primary malignant tumors and high risk of bleeding was reviewed to summarize the shortcomings of treatment and prudent anticoagulation experience. CASE SUMMARY: An 83-year-old female patient was admitted to the hospital due to a 2-wk history of left lower extremity edema that had worsened over 2 d. Considering her medical history and relevant post-admission investigations, it was determined that the development of left lower extremity venous thrombosis and pulmonary embolism in this case could be attributed to a combination of factors, including multiple primary malignant tumors, iliac venous compression syndrome, previous novel coronavirus infection, and inadequate treatment for prior thrombotic events. However, the selection of appropriate anticoagulant medications, determination of optimal drug dosages, and establishment of an appropriate duration of anticoagulation therapy were important because of concurrent thrombocytopenia, decreased quantitative fibrinogen levels, and renal insufficiency. CONCLUSION: Anticoagulant prophylaxis should be promptly initiated in cases of high-risk thrombosis. Individualized anticoagulation therapy is required for complex thrombosis.

Crohn's disease as the intestinal manifestation of pan-lymphatic dysfunction: An exploratory proposal based on basic and clinical data.

Crohn's disease (CD) is caused by immune, environmental, and genetic factors. It can involve the entire gastrointestinal tract, and although its prevalence is rapidly increasing its etiology remains unclear. Emerging biological and small-molecule drugs have advanced the treatment of CD; however, a considerable proportion of patients are non-responsive to all known drugs. To achieve a breakthrough in this field, innovations that could guide the further development of effective therapies are of utmost urgency. In this review, we first propose the innovative concept of pan-lymphatic dysfunction for the general distribution of lymphatic dysfunction in various diseases, and suggest that CD is the intestinal manifestation of pan-lymphatic dysfunction based on basic and clinical preliminary data. The supporting evidence is fully summarized, including the existence of lymphatic system dysfunction, recognition of the inside-out model, disorders of immune cells, changes in cell plasticity, partial overlap of the underlying mechanisms, and common gut-derived fatty and bile acid metabolism. Another benefit of this novel concept is that it proposes adopting the zebrafish model for studying intestinal diseases, especially CD, as this model is good at presenting and mimicking lymphatic dysfunction. More importantly, the ensuing focus on improving lymphatic function may lead to novel and promising therapeutic strategies for CD.

High-fat diet aggravates colitis via mesenteric adipose tissue derived exosome metastasis-associated lung adenocarcinoma transcript 1.

BACKGROUND: Obesity is associated with an increased risk of developing Crohn's disease (CD), higher disease activity, and comparatively worse clinical outcomes. AIM: To investigate the role of mesenteric adipose tissue-derived exosomes in the pathogenesis of CD aggravation in obese individuals. METHODS: First, we induced colitis in mice initiated on high-fat and normal diets and compared the severity of colitis. We then extracted and identified exosomes from mesenteric adipose tissue and determined the levels of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in mesenteric adipose tissue-derived exosomes and the colon. Next, we demonstrated an interaction between MALAT1 and the miR-15a-5p/activating transcription factor 6 (ATF6) axis. Finally, we explored the effects of mesenteric adipose tissue-derived exosomes extracted from mice fed a high-fat or normal diet on the severity of 2,4,6-trinitrobe-nzenesulfonic acid (TNBS)-induced colitis and ATF6-related endoplasmic reticulum stress pathways. RESULTS: High-fat diet was found to aggravate TNBS-induced colitis in mice. The expression of MALAT1 in mesenteric adipose tissue-derived exosomes of high-fat diet-fed mice increased. The increased expression of MALAT1 in colon tissue exacerbated TNBS-induced colitis and activated the ATF6 endoplasmic reticulum stress pathway. This effect was partially reversed by the reduced expression of MALAT1 and overexpression of miR-15a-5p. CONCLUSION: Mesenteric adipose tissue-derived exosome-encapsulated long noncoding RNAs MALAT1 targets the colon and aggravates TNBS-induced colitis in obese mice, which may potentially act on the miR-15a-5p/ATF6 axis and activate endoplasmic reticulum stress.

Aesculetin exhibited anti-inflammatory activities through inhibiting NF-кB and MAPKs pathway in vitro and in vivo.

ETHNOPHARMACOLOGICAL RELEVANCE: Aesculetin (6,7-dihydroxy-2H-1-benzopyran-2-one) has been reported to exhibit potent anti-inflammatory property both in vitro and in vivo. AIMS OF THIS STUDY: In this study, we evaluated the anti-inflammatory effect and investigated underlying molecular mechanisms of aesculetin in LPS-induced RAW264.7 macrophages and DSS-induced colitis. MATERIALS AND METHODS: In this study, the production of NO, TNF-α, and IL-6 were measured to identify the aesculetin with potent anti-inflammatory effect. Then, the underlying anti-inflammatory mechanisms were explored by western blotting in LPS-induced cells. Next, we verify the anti-inflammatory potential of aesculetin in DSS-induced colitis in vivo. The clinical symptoms of colitis, including weight loss, DAI, colon length and MPO activity, and the secretion of TNF-α and IL-6 were evaluated. Finally, Western blot analysis was applied to further investigate underlying mechanism in DSS-induced colitis model. RESULTS: Our studies showed that aesculetin exhibited anti-inflammatory potential by inhibiting NO, TNF-α, and IL-6 production and reducing iNOS and NLRP3 expression in LPS-induced RAW264.7 cells. Mechanically, we found that aesculetin significantly inhibited LPS-induced activation of NF-κB and MAPKs signaling pathways. In DSS-induced mouse model, the colitis-related symptoms were relieved by treatment with aesculetin. Besides, aesculetin also inhibited the secretion of TNF-α and IL-6, and the activation of NF-κB and MAPKs signaling pathways in DSS-induced colitis. CONCLUSIONS: The anti-inflammatory effect of aesculetin was connected with its inhibition on the activation of NF-κB and MAPKs signaling pathways both in vitro and in vivo. Therefore, aesculetin was expected to be developed as an anti-inflammatory drug.

Palmitoylation in Crohn's disease: Current status and future directions.

S-palmitoylation is one of the most common post-translational modifications in nature; however, its importance has been overlooked for decades. Crohn's disease (CD), a subtype of inflammatory bowel disease (IBD), is an autoimmune disease characterized by chronic inflammation involving the entire gastrointestinal tract. Bowel damage and subsequent disabilities caused by CD are a growing global health issue. Well-acknowledged risk factors for CD include genetic susceptibility, environmental factors, such as a westernized lifestyle, and altered gut microbiota. However, the pathophysiological mechanisms of this disorder are not yet comprehensively understood. With the rapidly increasing global prevalence of CD and the evident role of S-palmitoylation in CD, as recently reported, there is a need to investigate the relationship between CD and S-palmitoylation. In this review, we summarize the concept, detection, and function of S-palmitoylation as well as its potential effects on CD, and provide novel insights into the pathogenesis and treatment of CD.

M-Phase Phosphoprotein 9 upregulation associates with poor prognosis and activates mTOR signaling in gastric cancer.

The function of M-Phase Phosphoprotein 9 (MPHOSPH9) has not been investigated in gastric cancer yet. In the present study, the public cancer databases Oncomine and TCGA were analyzed, and MPHOSPH9 was found upregulated in gastric cancer tumor tissues. Immunohistochemistry (IHC) was also carried out to further confirm the results, and IHC analysis showed MPHOSPH9 was elevated in tumor tissues compared with the paracancerous tissues. QRT-PCR analysis also revealed that MPHOSPH9 mRNA was upregulated in gastric cancer cell lines. In addition, Kaplan-Meier estimates showed gastric cancer patients with high MPHOSPH9 level predicted a poor prognosis. Then, Western blot and CCK-8 assay showed overexpressed MPHOSPH9 enhanced gastric cancer cell proliferation, but MPHOSPH9 knockdown suppressed gastric cancer cell proliferation. Additionally, Western blot showed that MPHOSPH9 regulated the activation of mTOR, and overexpressed MPHOSPH9 reduced the inhibitory effects of mTOR inhibitors on cell survival in gastric cancer cells. Taken together, our results suggested that MPHOSPH9 .could be an oncogene in gastric cancer by regulating mTOR signaling.

[Comparative study on serum transitional components of Huatan Jiangqi Capsules in rats under pathological and physiological status].

The differences of transitional components and metabolic processes of Huatan Jiangqi Capsules(HTJQ) in rats under normal physiological and pathological conditions of COPD were analyzed by UPLC-Q-TOF-MS. The rat COPD model was established by passive smoking and intratracheal instillation of lipopolysaccharide. After the normal and COPD model rats were douched with HTJQ, the blood was collected from hepatic portal vein and the drug-containing serum samples were prepared by methanol precipitation of protein. Then, 10 batches of drug-containing serum samples of HTJQ were prepared and analyzed by UPLC serum fingerprint to evaluate the quality and stability of drug-containing serum samples. UPLC-Q-TOF-MS was used to collect the mass spectrometric information of the transitional components. Twenty-eight transitional components of HTJQ in normal rats and 25 transitional components of HTJQ in COPD model rats were identified by UPLC-Q-TOF-MS. Under pathological and physiological conditions, there were not only the same transitional components in rat serum, but also corresponding differences. Further studies showed that there were also differences in the metabolic process of transitional components between the two conditions. In normal rats, most of the metabolic types of transitional components were phase I reactions. In COPD model rats, phase Ⅰ reactions decreased and phase Ⅱ reactions increased correspondingly. With UPLC-Q-TOF-MS technology, the differences of transitional components and the metabolism process of HTJQ in rats under normal physiological and pathological conditions were analyzed. The results showed that types of transitional components and the activity of some metabolic enzymes would be changed in COPD pathological state, which would affect the metabolic process of bioactive components in vivo. It laid a foundation for further elucidating the metabolic process and pharmacodynamic substance basis of HTJQ.

Effect of the in vivo application of granulocyte colony-stimulating factor on NK cells in bone marrow and peripheral blood.

Granulocyte colony-stimulating factor (G-CSF) has been widely used in the field of allogeneic haematopoietic stem cell transplantation (allo-HSCT) for priming donor stem cells from the bone marrow (BM) to peripheral blood (PB) to collect stem cells more conveniently. Donor-derived natural killer (NK) cells have important antitumour functions and immune regulatory roles post-allo-HSCT. The aim of this study was to evaluate the effect of G-CSF on donors' NK cells in BM and PB. The percentage of NK cells among nuclear cells and lymphocyte was significantly decreased and led to increased ratio of T and NK cells in BM and PB post-G-CSF in vivo application. Relative expansion of CD56bri NK cells led to a decreased ratio of CD56dim and CD56bri NK subsets in BM and PB post-G-CSF in vivo application. The expression of CD62L, CD54, CD94, NKP30 and CXCR4 on NK cells was significantly increased in PB after G-CSF treatment. G-CSF treatment decreased the IFN-γ-secreting NK population (NK1) dramatically in BM and PB, but increased the IL-13-secreting NK (NK2), TGF-ß-secreting NK (NK3) and IL-10-secreting NK (NKr) populations significantly in BM. Clinical data demonstrated that higher doses of NK1 infused into the allograft correlated with an increased incidence of chronic graft-vs-host disease post-transplantation. Taken together, our results show that the in vivo application of G-CSF can modulate NK subpopulations, leading to an increased ratio of T and NK cells and decreased ratio of CD56dim and CD56bri NK cells as well as decreased NK1 populations in both PB and BM.

The mechanisms of IL-17A on promoting tumor metastasis.

In recent decades, extensive studies have indicated that IL-17A plays an important role in tumor progression and metastasis, but the underlying mechanisms are not immediately clear. In this review, we examined the literature from the recent years concerning the study of IL-17A in four kinds of tumor transfer paths, including hematogenous metastasis, lymphatic metastasis, local invasion and transcoelomic metastasis, to summarize the roles and underlying mechanisms of IL-17A on tumor metastasis.

Hsa_circ_0020397 regulates colorectal cancer cell viability, apoptosis and invasion by promoting the expression of the miR-138 targets TERT and PD-L1.

Colorectal cancer (CRC) is a common human gastrointestinal cancer, and recent studies indicate that circular RNA (circRNA) may regulate cancer development. In this study, we assess the role of circRNA specifically in colorectal cancer. Our quantitative PCR assays demonstrate an upregulation of the circRNA has_circ_0020397 and a downregulation of miR-138 in CRC cells, as well as a negative correlation between these two. Using a dual-luciferase reporter assay, we show evidence of miR-138-binding sites on hsa_circ_0020397, and that overexpression of hsa_circ_0020397 could inhibit the downregulation of luciferase activity by miR-138. Although hsa_circ_0020397 did not influence miR-138 expression per se, has_circ_0020397 did inhibit miR-138 activity, as examined via the expression of miR-138 targets telomerase reverse transcriptase (TERT) and programmed death-ligand 1 (PD-L1). Control treatments with plasmids overexpressing linear hsa_circ_0020397 did not have these effects. Hsa_circ_0020397 promoted cell viability and invasion of CRC cells and inhibited their apoptosis, whereas miR-138 had the opposite effect. Nevertheless, hsa_circ_0020397 antagonized miR-138 suppression of cell growth. When TERT or PD-L1 expression was suppressed with siRNAs, the above functions of hsa_circ_0020397 were attenuated, suggesting that hsa_circ_0020397 can regulate CRC cell viability, apoptosis and invasion by promoting the expression of miR-138 target genes. These findings support the role of circRNA in CRC pathogenesis.

[Pollution Characteristics of Heavy Metals in PM2.5 and Their Human Health Risks Among the Coastal City Group Along Western Taiwan Straits Region, China].

PM2.5 samples were collected from 11 sampling sites in the coastal city group along western Taiwan Straits region, China, and these heavy metal elements (Zn, Cu, Pb, Ni, Cr, As) were detected using particle-induced X-ray emission (PIXE) method. The pollution characteristics, enrichment factors and source apportionment of heavy metals in PM2.5 were analyzed, and furthermore, their human health risks were determined. The result showed concentration distribution was obviously different between PM2.5 and heavy metals in the city group, for the main sources (e.g. construction dust and ground dust) for PM2.5 were not the main contribution to these heavy metals. The enrichment factors of Zn, Cu, Pb, Mn, Ni, Cr, As exceeded 10, which suggested these metals were enriched and significantly impacted by anthropogenic pollution. Three main groups of heavy metals in PM2.5 were identified by principal component analysis (PCA-MLR), such as coal combustion and traffic emissions (70.59%), multiple sources (coal and oil combustion, pyrometallurgical process, 17.55%) and other industry (11.86%). The risk levels for carcinogenic heavy metals (Ni, Cr, As) and non-carcinogenic heavy metals (Zn, Cu, Pb, Mn) were lower than the average level of risk acceptance (10-6), which suggested these heavy metals did not cause harm to human health in these cities.

[Pollution Assessment and Source Analysis of Metals in PM2.5 in Haicang District, Xiamen City, China].

To determine the spatial-temporal distributions and potential sources of metals in PM2.5 and assess health risks from heavy metals, 348 PM2.5 samples were collected in the Haicang District of Xiamen, China from April 2015 to January 2016. Metals (K, Ca, Na, Mg, Al, Zn, Cu, Fe, Ti, As, V, Mn, Ba, Co) in PM2.5 were detected using an X-ray fluorescence analyzer (XRF). Pollution assessment was performed via enrichment factor calculation and health risk assessment. Potential sources were explored using Pearson's correlation coefficient, principal component analysis, and the HYSPLIT Trajectory Model. Results showed that the total concentration of 14 metal elements contributed to 5.4%-10.6% of PM2.5 during the sampling period. The total concentration of metals was higher in spring and winter than those in summer and autumn. The concentrations were higher in the port and the industrial areas than in residential areas and background locations, in agreement with the seasonal and spatial distribution of PM2.5. The frequency of PM2.5 daily concentrations exceeding the Chinese Ambient Air Quality Standards was higher in the port and residential areas in the summer due to operations at the port and the wind direction. Zn concentration was the highest in the industrial area followed by the background location. Meanwhile, the highest concentration of V was observed in the port area; V concentration in the residential area was high in the summer. These variations in Zn and V indicated that the elements emitted in the polluted areas migrated easily to residential and background areas. K concentrations were the highest in winter and As showed a higher rate of exceeding the standard in winter and spring, indicating that activities, such as biomass burning and coal combustion in the winter severely impacted air quality. The enrichment factors of Cu, Zn, As, Co, Na, and Mn varied considerably, from 67 to 8,449. The total risk level for non-carcinogenic heavy metals (Zn, Cu, Mn) was lower than the average level of risk acceptance (1×10-6 a-1) and Mn contributed 74%-88% of the total risk level of Zn, Cu, and Mn. The combined results of the correlation analysis and the principal component analysis revealed that metals in PM2.5 were mainly came from re-suspension of ground dust, motor vehicle emissions, coal combustion, industrial emissions, and heavy oil combustion, with contributions of 34.5%, 12.5%, 10.6%, and 7.8% respectively. The HYSPLIT Trajectory Model showed that Xiamen was affected by the local air mass in spring, autumn, and winter, but not in summer. Moreover, the rise of PM2.5 in spring and winter was attributed to air masses traveling through the Yangtze River Delta.

Controlled peritoneal drainage improves survival in children with abdominal compartment syndrome.

BACKGROUND: Children with massive ascites can develop abdominal compartment syndrome (ACS), which has been identified as an independent risk factor for mortality. OBJECTIVES: The objective of this study was to assess the effectiveness of volume-controlled percutaneous catheter drainage (PCD) for treating children with massive ascites and ACS. METHODS: A retrospective descriptive study was conducted; Comprising 12patients with ACS with massive ascites treated with volume-controlled PCD in a pediatric intensive care unitof a university hospital in southern China from April 2011 to June 2013. RESULTS: The etiology of ascites in these children included abdominal tumor (8/12), capillary leak after liver or kidney transplantation (2/12) and urine leakage (2/12). Intra-abdominal hypertension was closely associated with multiple organ dysfunction and high mortality. Digestive and pulmonary functions were the most frequently affected by ACS, while the cerebrum was the least involved. Treatment with ultrasound-guided PCD significantly decreased intra-abdominal pressure, abdominal circumference, and indices of organ dysfunction. PCD treatment also significantly improved glomerular filtration rate and PaO2/FiO2. Complications of PCD included abdominal infection (1/12) and electrolyte imbalance (4/12). The mortality rate of patients treated with PCD was 25%, which was lower than previous reports. CONCLUSIONS: Controlled peritoneal drainage is a minimally invasive and safe decompression method that is effective in patients with ACS, and should be considered in children with massive ascites.

Donor Th17 cells and IL-21 may contribute to the development of chronic graft-versus-host disease after allogeneic transplantation.

The roles of Th17 cells and IL-21 in the pathogenesis of chronic graft-versus-host disease (cGVHD) in patients who undergo allogeneic transplantation are still unknown. Here, we examined this question by monitoring eight patients with new-onset cGVHD for the presence of Th17 cells, Th1 cells, and IL-21. Allografts from an additional 41 patients were also analyzed for Th17 and Th1 cells. Out of these 41 patients, the last 32 enrolled patients were further analyzed for Th17 cells, Th1 cells, and plasma IL-21 levels at day 30 post-transplantation regarding cGVHD. Th17 cells and IL-21 plasma levels were significantly increased at cGVHD onset and drastically decreased after complete remission. Patients who received a higher number of Th17 cells in their allograft had a higher incidence of cGVHD compared with patients who received a lower number of Th17 cells. Meanwhile, positive plasma IL-21 levels at day 30 post-transplantation predicted cGVHD occurrence. These results suggest that Th17 cells and IL-21 may contribute to the development of cGVHD.

Salvianolic acid B reverses the epithelial-to-mesenchymal transition of HK-2 cells that is induced by transforming growth factor-ß.

Salvianolic acid B (Sal B) is the most abundant bioactive molecule from Radix Salviae Miltiorrhizae, and has recently been used for treating renal fibrosis in traditional Chinese medicine. Here we investigated the ability reversal of Sal B to reverse the transdifferentiation of human kidney proximal tubular epithelial cells that was induced by transforming growth factor-beta 1 (TGF-ß1). The effects of Sal B on HK-2 cell morphology were observed by phase contrast microscopy, while alpha smooth muscle actin and E-cadherin were studied by immunocytochemistry and real-time reverse transcription polymerase chain reaction, respectively. Exposure of HK-2 cells to TGF-ß1 for 72 h induced a complete conversion of the epithelial cells to myofibroblasts. When HK-2 cells were co-incubated with Sal B and TGF-ß1 for a further 72 h, the morphology of myofibroblasts returned to that of proximal tubular epithelial cells, whereas the myofibroblast phenotype was maintained after exposure of cells to TGF-ß1 for 144 h. Sal B reduced alpha smooth muscle actin levels and increased E-cadherin levels compared with their epithelial-to-mesenchymal transition controls. The reversal effect of Sal B was dose-dependent. That Sal B reverses the epithelial-to-mesenchymal transition in vitro suggests that it could possibly facilitate the repair of tubular epithelial structures and the regression of renal fibrosis in injured kidneys.

[A comparison of NK cell subsets between rhG-CSF mobilized peripheral blood grafts and bone marrow grafts from healthy donors].

OBJECTIVE: To analyze the difference in NK cell subsets between recombination human granulocyte colony-stimulating factor (rhG-CSF) mobilized peripheral blood grafts (G-PB) and bone marrow grafts (G-BM) from healthy donors. METHODS: From July 2009 to September 2009, G-PB and G-BM from 28 related donors were collected to analyze lymphocytes, NK cells and NK cell secretion of interferon-γ (IFN-γ, NK1), interleukin-13 (IL-13, NK2), transforming growth factor-ß (TGF-ß) and interleukin-10 (IL-10, NKr) by flow cytometry. RESULTS: The percentage of lymphocytes in G-PB was significantly higher than that in G-BM (P < 0.01). The proportions of NK cells and NK1, NK2, NKr subsets among lymphocytes were significantly higher in G-BM than in G-PB (P < 0.05), and so were the percentage of NK2, NKr cells among NK cells (P < 0.01), but no significant difference in the percentage of NK1 cells among NK cells between G-PB and G-BM. The ratios of IL-13 and IFN-γ, of TGF-ß and IFN-γ, or of IL-10 and IFN-γ in G-BM were significantly higher than those in G-PB (P = 0.010, 0.002, or 0.000, respectively). CONCLUSION: The increased proportion of NK2 and NKr in G-BM might be helpful to explain the lower immunoreactivity of G-BM than that of G-PB, although the proportion of NK1 in G-BM and G-PB is similar.

IL-17-producing T cells contribute to acute graft-versus-host disease in patients undergoing unmanipulated blood and marrow transplantation.

The aim of this study was to investigate the effects of IL-17-producing T cells, including Th17 and Tc17 cells, on acute graft-versus-host disease (aGVHD) in patients who had undergone granulocyte colony-stimulating factor (G-CSF)-mobilised peripheral blood progenitor cell (PBPC) and G-CSF-primed bone marrow (G-BM) transplantation. Allografts from forty-one patients were analysed for IL-17-producing T cells with respect to aGVHD. Furthermore, ten patients with aGVHD onset were monitored for the presence of Th17 cells in the peripheral blood by flow cytometry. Patients who received a higher dose of Th17 cells in the G-BM (>8.5 × 10(4) /kg, p=0.005) or a higher dose of Tc17 cells in PBPC (>16.8 × 10(4) /kg, p=0.001) exhibited a higher incidence of aGVHD. An increased Th17 population (up to 4.99% CD4(+) T lymphocytes) was observed in patients with aGVHD onset. In contrast, the percentage of Th17 population decreased drastically in aGVHD patients following treatment to achieve partial and complete remission (p=0.013 and p=0.008, respectively). All percentages of Th17 and Tc17 cells were significantly reduced after in vivo G-CSF application. Our results suggested that IL-17-producing T cells contributed to aGVHD. The application of G-CSF in vivo aided in reducing the occurrence of aGVHD through a decrease in IL-17 secretion by T cells.

[Effects of rhG-CSF mobilization on Th17 cells in donors' peripheral blood and bone marrow grafts].

The study was aimed to explore the effects of recombination human granulocyte colony-stimulating factor (rhG-CSF) on Th17 cells in donors' peripheral blood (GPB) and bone marrow grafts (GBM). 25 healthy donors were injected subcutaneously with rhG-CSF 5 µg/(kg·d) for 5 consecutive days. GBM and GPB were harvested after injection on day 4 and 5 respectively. Some of these donors' steady-state bone marrow (SSBM) and steady-state peripheral blood (SSPB) were harvested before rhG-CSF injection. The changes of IL-17 secreted by T cells in donor BM and PB before and after mobilization were detected by flow cytometry. The results showed that the ability to secrete IL-17 from CD4(+) T cells and CD8(+) T cells in GBM was significantly lower than those in SSBM (GBM vs SSBM Th17/CD4(+) T, 0.74% ± 0.27% vs 1.78% ± 1.19%, p < 0.05; Tc17/CD8(+)T, 0.19% ± 0.16% vs 0.36% ± 0.37%, p < 0.05), changes in peripheral blood and bone marrow were same (GPB vs SSPB Th17/CD4(+) T, 1.82% ± 0.91% vs 3.26% ± 1.89%, p < 0.01; Tc17/CD8(+) T, 0.21% ± 0.17% vs 0.44% ± 0.28%, p < 0.01). The ratios of Th17/CD4(+) T and Tc17/CD8(+) T in GPB were higher than in GBM (p < 0.05, p < 0.01). It is concluded that rhG-CSF in vivo can inhibit the generation of Th17 cells both in bone marrow and peripheral blood grafts, and it may be partial reason for GPB/GBM mixed transplantation without increasing the GVHD incidence.

[Adrenal lesions in patients of multiple endocrine neoplasia type 1].

OBJECTIVE: To investigate the prevalence and characteristics of adrenal lesions in Chinese multiple endocrine neoplasia type 1 (MEN-1) patients. METHODS: Adrenal CT scan and clinical manifestations were retrospectively reviewed in 32 consecutive MEN-1 patients who were evaluated at our hospital during January 1986 to December 2009. RESULTS: Adrenal lesions were identified in 16 of 32 (50%) MEN-1 patients. Five (31.3%) patents with adrenal involvement showed bilateral lesions, including bilateral adenoma (n=1), bilateral hyperplasia (n=2) and adenoma and hyperplasia on each side (n=2). Unilateral adrenal lesion was presented in 11 (68.7%) patients. Among which, 63.6% had adenomas with a mean diameter of 2.3 cm (0.8-4.0 cm) and the remainder was of hyperplasia or enlargement. In two patients, functioning adrenal abnormalities were detected including Cushing adenoma (n=1) and aldosterone-secreting adenoma (n=1). CONCLUSIONS: The prevalence of adrenal lesion in MEN-1 patient is similar between China and western countries. These tumors are mostly benign, small and nonfunctioning. Taking into account a high incidence of adrenal carcinoma in previous foreign studies, routine screening and close surveillance are still recommended for adrenal lesions in MEN-1 patients.

[Effects of PTEN over-expression on phosphatidyl inositol 3-kinase/protein kinase B signal pathway in ovarian epithelial cancer cells].

OBJECTIVE: To evaluate the effect of exogenous wild PTEN gene stable transfected into human ovarian cancer cell line HO-8910 on phosphatidyl inositol 3-kinase (PI3K)/protein kinase B (Akt) signal pathway and cells proliferation. METHODS: Wild-type PTEN recombinant eukaryotic expression plasmid was constructed and then was transfected into HO-8910 cells by lipofectamine 2000. The expression of PTEN, Akt1, Akt2, PI3K mRNA and protein of PTEN were tested by reverse transcription (RT)-PCR and Western blot. The proliferation of HO-8910 after wild PTEN gene transfected was measured by methyl thiazolyl tetrazolium (MTT). RESULTS: Wild-type PTEN gene was successfully transfected into HO-8910 cells. The results of RT-PCR and western bolt showed that there were the significant expression high level of PTEN mRNA and protein after infected by wild-PTEN plasmid than those in the control [(17,372 ± 23) vs. (39 ± 1) vs. (78 ± 4) copies/ml, P < 0.05]. While the expression of mRNA of Akt1, Akt2 and PI3K were decreased clearly than those in the control [(28 ± 2) vs. (115 ± 5), (7 ± 1) vs. (18 ± 2), (61 ± 2) vs. (84 ± 2) copies/ml, all P < 0.05]. The proliferation rate of HO-8910 cells was obviously slower than those in the control (90 158 ± 47 vs. 148,251 ± 65 vs. 250,115 ± 62, P < 0.05). CONCLUSION: Transfection of PTEN may increase the expression of PTEN and inhibit the proliferation of HO-8910 cells, in which PI3K/Akt signal pathway is inhibit significantly.