BACKGROUND:Placental mesenchymal stem cel s with rich sources are similar to bone marrow mesenchymal stem cel s in terms of morphology, surface markers and differentiation potential, which are one of ideal mesenchymal stem cel s in human body. However, there are few studies addressing the ultrastructure and phagocytotic function of human placental mesenchymal stem cel s and its physiological role in the the placenta has been little explored. OBJECTIVE:To investigate the ultrastrcture and phagocytotic function of placental mesenchymal stem cel s. METHODS:Placental mesenchymal stem cel s obtained from five placentae of normal pregnancy were cultured in vitro and observed for ultrastructure under transmission electron microscope. The fluorescent beads were added in the supernatant for 3 hours, and then the phagocytosis of placental mesenchymal stem cel s was evaluated by flow cytometry. RESULTS AND CONCLUSION:Under the transmission electron microscope, placental mesenchymal stem cel s had large nuclei with prominent nucleoli. In the cytoplasm, a plenty of rough endoplasmic reticula was seen, dilated or stacked. The cytoplasm was also rich in Golgi apparatus and lysosomes. The cel surfaces were covered by microvil i. The intercel ular junctions could be seen occasional y. A part of cel s from these five samples could phagocytose fluorescence beads, which ranged from 49.6%to 18.4%. The ultrastructural characteristics of placental mesenchymal stem cel s suggested these cel s were active to synthesize and secrete proteins and had phagocytotic function, indicating placental mesenchymal stem cel s may play a role in keeping the balance of micro-environments and clean the foreign substances in the placenta.

Objective To assess the clinical significance of endoscopic ultrasonography (EUS) in the diagnosis and preoperative staging of gastric cancer. Methods EUS was carried out in 22 patients inclu-ding 17 gastric cancer patients and 5 patients in suspicion. Helical CT scanning was performed in all of the patients and fine needle aspiration biopsies ( FNAB) were administrated to 5 suspicious patients. Compared the results of operation and pathology with those of tumor staging by estimating the depth of tumor invasion ( T) , local lymph node metastasis ( N) and metastasis to neighboring or remote organs ( M) in order to esti-mate the accuracy of diagnosis and TNM staging. The sensitivity and specificity of tumor-node-metastasis staging of gastric cancer by EUS were compared with those of the spiral CT according to the final histopatho-logical results. Results In 5 suspicious patients specimens were successfully obtained by FNAB under the guide of EUS with the pathological diagnosis of adenocarcinoma in 4 cases and signet ring cell carcinoma, 1 case. All patients underwent radical gastrectomy except one in T1N0M0, staging was treated by endoscopic mucosal resection (EMR). The sensitivity and specificity of EUS in T, N, and M stage were 84.9% and 74. 2% , 92. 1% and 77. 1% , 63. 4% and 87. 5% respectively; whereas those of CT in T, N, and M stage were 27. 3% and 75% , 31.5% and 100% , 50% and 100% respectively. The sensitivity of EUS in T and N staging were higher than those of CT with significant statistical difference (P

BACKGROUND: Long-term complications of cesarean section include placenta praevia, placenta accreta, cesarean scar pregnancy and uterine rupture. These life-threatening complications in pregnant women maybe result from the defects of endometrium and uterine smooth muscle as well as poorly formed decidua in the scar of cesarean section. Mesenchymal stem cells have the function of repairing tissue injuries, and the amount of cells homing to the site of injury may affect the effect of tissue repair. OBJECTIVE: To explore the distribution and homing of bone marrow mesenchymal stem cells from male rats into rat models of cesarean section. METHODS: Bone marrow mesenchymal stem cells isolated from male rats in vitro were cultured and identified. Female Wistar rats were randomized into two groups: cesarean section group and control group. Rats in the cesarean section group were given intravenous administration of bone marrow mesenchymal stem cells from male rats via the tail vein on day 21 after cesarean section, and non-operative rats in the control groups were given the same amount of bone marrow mesenchymal stem cells from male rats after natural delivery. Rats in the two groups were sacrificed on days 7 and 28 after cell injection. The distribution of bone marrow mesenchymal stem cells from male rats in tissues (including heart, lungs, livers, kidneys, and uterine scar) was detected by measurement of the SRY mRNA level using SPY-PCR. RESULTS AND CONCLUSION: In the cesarean section group, the SRY gene was most abundant in the lung, followed by the liver and the kidney on day 7 after injection, although the distribution of SRY gene in the heart and uterine scar was low; on day 28 after injection, the levels of SRY gene in the lung, liver and kidney decreased (P < 0.05), but had no significant changes in the heart and uterine scar (P > 0.05). In the control group, the distribution of SRY gene was similar to that in the cesarean section group on both days 7 and 28 after injection, and the levels of SRY gene in the heart and uterus were low. These findings reveal that allogeneic bone marrow mesenchymal stem cells implanted mainly distribute in tissues with abundant blood flow, including lungs, livers and kidneys. And the cell number decreases gradually over time. Since the amount of implanted cells in the heart and uterus is very low, the change with time is not obvious. Cesarean section injury has no impact on the distribution of bone marrow mesenchymal stem cells in pregnant rats and there is of course no increase in the homing and colonization of bone marrow mesenchymal stem cells in a cesarean scar.

BACKGROUNDChromosome 13q14 deletion (del13q14), chromosome 1q21 gain (amp1q21) and chromosome 17p13 deletion (del17p13) are the most frequent chromosomal aberrations in multiple myeloma (MM). They play an important role in prognosis. The aim of this study was to investigate the clinical significance of the chromosomal changes in Chinese MM patients.

METHODSInterphase fluorescence in situ hybridization (FISH) on bone marrow (BM) cells was performed in 72 enrolled MM patients. Relationships between chromosomal abnormalities and clinical features, response to therapies and prognosis were analyzed.

RESULTSAs a result of interphase FISH, 77.8% (56/72) patients had chromosome changes. The incidences of each probe were RB1 51.4% (37/72), D13S319 47.2% (34/72), 1q21 45.8% (33/72) and p53 22.2% (12/72). Osteolytic lesion, BM plasma cells index, serum calcium and serum M component were significantly correlated to del13q14. BM plasma cells and hemoglobin were correlated to amp1q21. Serum lactate dehydrogenase (LDH) was correlated with del17p13. Patients with del13q14 treated with bortezomib had a notably higher overall response rate than the patients treated with traditional chemotherapies (93% vs. 65%, P = 0.048). Patients carrying amp1q21 or/and del17p13 did not achieve satisfactory response to bortezomib. The median progression-free survival (PFS) for patients with amp1q21 was 5 months and patients without amp1q21 got 9-month PFS (P = 0.001). The median PFS for patients with del13q14 was 5 months (vs. 8 months, P = 0.026). The median PFS for patients with del17p13 was 3 months (vs. 8 months, P = 0.002). Patients with β(2)-microglobulin > 5.5 mg/L also had a worse outcome, whose median PFS was 5 months (vs. 8 months, P = 0.016).

CONCLUSIONSThe prevalence of chromosomal abnormalities of MM patients was similar in Chinese and Caucasian people. Genetic changes were associated with patients' responses to therapies and prognosis.

Adult ; Aged ; Asian Continental Ancestry Group ; Chromosome Aberrations ; Chromosome Deletion ; Humans ; In Situ Hybridization, Fluorescence ; Interphase ; Male ; Middle Aged ; Multiple Myeloma ; drug therapy ; genetics ; Prognosis

Objective: Hepatocellular carcinoma (HCC) is one of the most common malignant tumor worldwide. Metastasis is a marker of cancer deterioration in patients with liver cancer and a major cause of death. In order to develop effective therapeutic strategies, it is urgent to study the molecular basis of liver cancer metastasis. Methods: Immunohistochemistry was used to detect the expression of fatty acid synthase (FASN) in HCC. Wound healing and transwell cell invasion assays was used to confirm the role of FASN in liver cancer migration and invasion. Proteins that interacted with FASN were identified using iTRAQ (isobaric tag for relative and absolute quantification). Co-immunoprecipitation (Co-IP) and cellular immunofluorescence analysis were used to assess the interaction between FASN and signal transduction and transcription activator 3 (STAT3). The expression of STAT3, p-STAT3, matrix metalloproteinase (MMP)-2 and MMP-9 was detected after FASN knockdown using Western blot method. Statistical analysis was performed using the t-test. Results: Immunohistochemistry showed that the expression of FASN in HCC tissue was higher than that in adjacent tissues. iTRAQ, Co-IP and immunofluorescence analysis revealed that FASN interacted with STAT3. Western blot analysis showed that the expression of p-STAT3, MMP-2 and MMP-9 decreased after FASN knockdown. Conclusion FASN may promote the metastasis of liver cancer by interacting with STAT3 and affecting the expression of MMP-2/MMP-9.

Background Chromosome 13q14 deletion (del13q14), chromosome 1q21 gain (amp1q21) and chromosome 17p13 deletion (del17p13) are the most frequent chromosomal aberrations in multiple myeloma (MM). They play an important role in prognosis. The aim of this study was to investigate the clinical significance of the chromosomal changes in Chinese MM patients.Methods Interphase fluorescence in situ hybridization (FISH) on bone marrow (BM) cells was performed in 72 enrolled MM patients. Relationships between chromosomal abnormalities and clinical features, response to therapies and prognosis were analyzed.Results As a result of interphase FISH, 77.8％ (56/72) patients had chromosome changes. The incidences of each probe were RB1 51.4％ (37/72), D13S319 47.2％ (34/72), 1q21 45.8％ (33/72) and p53 22.2％ (12/72). Osteolytic lesion,BM plasma cells index, serum calcium and serum M component were significantly correlated to del13q14. BM plasma cells and hemoglobin were correlated to amp1q21. Serum lactate dehydrogenase (LDH) was correlated with del17p13.Patients with del13q14 treated with bortezomib had a notably higher overall response rate than the patients treated with traditional chemotherapies (93％ vs. 65％, P=0.048). Patients carrying amp1q21 or/and del17p13 did not achieve satisfactory response to bortezomib. The median progression-free survival (PFS) for patients with amp1q21 was 5 months and patients without amp1q21 got 9-month PFS (P=0.001). The median PFS for patients with del13q14 was 5 months (vs. 8 months, P=0.026). The median PFS for patients with del17p13 was 3 months (vs. 8 months, P=0.002).Patients with β2-microglobulin ＞5.5 mg/L also had a worse outcome, whose median PFS was 5 months (vs. 8 months,P=0.016).Conclusions The prevalence of chromosomal abnormalities of MM patients was similar in Chinese and Caucasian people. Genetic changes were associated with patients' responses to therapies and prognosis.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

To explore the biofilm inhibitory efficacy of perifosine against Pseudomonas aeruginosa (P. aeruginos) and its mechanisms. Twenty-fourwell plate was used to form biofilms at the bottom and crystal violet staining was used to determine the biofilm inhibitory effects of perifosine against P. aeruginosa, the wells without perifosine was set as control group. Glass tubes combined with crystal violet staining was used to detect the gas-liqud interface related bioiflm inhibitory effects of perifosine, the wells without perifosine was set as control group. Time-growth curved was used to detect the effects of perifosine on the bacteial planktonic cells growth of P. aeruginosa, the wells without perifosine was set as control group. The interaction model between perifosine and PqsE was assessed by molecular docking assay. The inhibitory effects of perifosine on the catalytic activity of PqsE was determined by detection the production of thiols, the wells without perifosine was set as control group. Binding affinity between perifosine and PqsE was detected by plasma surface resonance. The biofims at the bottom of the microplates and air-liquid interface were effectively inhibited by perifosine at the concentration of 4-8 μg/ml. There was no influence of perifosine on the cells growth of P. aeruginosa. The resuts of molecular docking assay indicates that perifosine could interacted with PqsE with the docking score of -10.67 kcal/mol. Perifosine could inhibit the catalytic activity of PqsE in a dose-dependent manner. The binding affinity between perifosine and PqsE was comfirmed by plasma surface resonance with KD of 6.65×10^-5mol/L. Perifosine could inhibited the biofilm formation of P. aeruginosa by interacting with PqsE.
Anti-Bacterial Agents/pharmacology* ; Bacterial Proteins/metabolism* ; Biofilms ; Molecular Docking Simulation ; Phosphorylcholine/analogs & derivatives* ; Pseudomonas aeruginosa/metabolism* ; Quorum Sensing