Porous carbon nanoparticles ( NPC) were prepared by ZnCl2 activation and carbonization using citrus waste as carbon source. A sample pretreatment method with NPC as dispersive solid phase extraction (d-SPE ) absorbent was established for the determination of organophosphorus pesticides in fruits and vegetables by gas chromatography. The NPC was characterized by scanning electron microscopy (SEM), X-ray diffraction ( XRD), FT-IR spectra, Raman spectroscopy, Brunauer, Emmett and Teller surface area(BET). Those results showed that the NPC was an amorphous porous carbon material with pore size in the range of 0-15 nm. Its specific surface area and pore volume were 1243 m2 / g and 1. 28 cm3 / g, respectively. The analysis conditions, including the amount and clean up time of adsorbent, were optimized by analysis of 14 kinds of oranophosphorus pesticides in fruits and vegetables with gas chromatography-flame photometric determination(GC-FPD). Moreover, the comparison for NPC with commercial materials of PSA, C18 and GCB was investigated in this study. The results indicated that the purification time was only 2 min using 0. 01 g NPC. The cost of NPC was about 25% of C18 , 21% of PSA and 16% of GCB. Because of the porous structure of NPC, the purification efficiency was significantly higher than the three commercial materials mentioned above. Under the optimum conditions, the calibration curves of the 14 organophosphorus pesticides were linear in the range of 0. 02-1. 00 mg / L with good correlation coefficients (R2>0. 99) and detection limits (S / N=3) of 0. 63-5. 30 μg / kg. The recoveries of the pesticides at three spiked levels ranged from 71. 3% to 114. 7%with the relative standard deviations (RSDs) of 0. 9% -12. 9% . The method is simple, rapid, sensitive, and low cost, and can satisfy the requirements of detection of organophosphorus pesticide residues in fruits and vegetables, displaying a good application prospect.

Objective To investigate clinical symptoms,pathophysiology and brain imaging features of Chinese familial cerebral cavernous angiomas.Methods Head MRI examination,clinical and pathophysiological examination were performed in a Chinese family with one proband of cerebral cavernous malformation.The disease atlas of the family was drawn.The patients indicative of a surgery underwent resection of hemangioma whose pathophysiology and microstructure were observed.Results Nine familial cerebral cavernous angiomas patients were found to have multiple intracranial lesion in the 18 family members,the penetrance being 50%,conforming to the feature of autosomal incomplete dominance inheritance.Four patients with skin cavernous hemangioma had familial cerebral cavernous angiomas.MRI was the most sensitive modality for the diagnosis of cavernous angioma.With T_2-Weighted sequences,the lesion was typically characterized by an area of mixed signal intensity,with a central reticulated core and a peripheral rim of decreased signal intensity related to deposition of hemosiderin.Gradient-echo(GRE)MRI could find microcavernous hemangiomas that would not be found in other sequences.Cavernous angiomas were typically discrete multilobulated berrylike lesions that contained hemorrhage in various stages of evolution.Histological homogeneity and overlap with other vascular malformations such as capillary telangictasia was common.Cavernous angiomas were composed of endothelial-linked sinusoidal spaces not separated by significant amounts of neural tissue.Hemorrhagic residua were common.Clots at different stages of evolution within the lesion were seen.The basic membranes of sinus became thick and soft.Parts of it were layered.Conclusions Familial cerebral cavernous angiomas is an autosomal incomplete dominance inheritance disease.Cavernous angiomas are composed of endothelial-linked sinusoidal spaces not separated by significant amounts of neural tissue.There are more than one focus in every patients and the skin cavernous angiomas is the foundation of diagnosing familial cerebral cavernous angiomas.Gradient-echo imagine sequence MRI(3.0 T)could be the"golden standard".

OBJECTIVETo study the promotion effect of stromal cell-derived factor 1 (SDF-1) on the migration of epidermal stem cells (ESC) in the healing process of frostbite-wound model ex vivo.

METHODSA three-dimensional model of full-thickness frostbite of skin was constructed (with slot-like wound) out of skin equivalent. The expression of SDF-1 in wound stroma was observed with immunohistochemistry staining on post injury days (PID) 3 and 7. The model frostbite wounds were divided into control group (treated with PBS 50 microL per wound), SDF-1 group (treated with 100 ng/mL SDF-1, 50 microL per wound), and AMD3100 group [treated with 100 ng/mL AMD3100 (50 microL per wound) for 30 minutes, and then SDF-1 50 microL was added per wound]. The redistribution of ESC around wound was observed.

RESULTSThe expression of SDF-1 in wound stroma increased gradually on PID 3 and 7. Compared with those in control and AMD3100 groups, there were more ESC and epithelial cell layers, and more integrin beta(1)-positive cells appeared at the basal layer of wound in SDF-1 group, and some of the positive cells migrated upward to epidermis.

CONCLUSIONSSDF-1 contributes to wound repair through promoting ESC to migrate toward and gather around wound edge. This may be one of the mechanisms of ESC participating in wound repair.

Cell Movement ; Chemokine CXCL12 ; metabolism ; Epidermis ; cytology ; Frostbite ; metabolism ; therapy ; Humans ; Stem Cells ; cytology ; Wound Healing

Adenomatous Polyps ; pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Endoscopy, Digestive System ; Female ; Gastric Fundus ; pathology ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Stomach Neoplasms ; pathology

OBJECTIVESTo observe the role of PPARgamma during the activation process of hepatic stellate cells (HSC).

METHODSBy morphology and RT-PCR, we study the changes of expression of PPARgamma in culture-activated HSC or in vivo activated HSC induced by dimethylnitrosamine (DMN).

RESULTSIn vitro, the expression level of PPARgamma in freshly isolated HSC (0.72+/-0.01) significantly reduced to 0.48+/-0.03 on the third day of culture (t = 19.8372, P<0.01), and reduced 70% on the seventh culture-day and could not be detected after the second passage. In vivo, HSC freshly isolated from normal control rats expressed PPARgamma (0.76+/-0.01). During the development of rat liver fibrosis induced by DMN, the expression level significantly reduced to 0.46+/-0.02 after the third injection of DMN (t = 29.5318, P<0.01), and reduced 66% on the end of first week and could not be detected on the end of second and third week.

CONCLUSIONThe expression of PPARgamma might play an important role on the maintenance of resting-form of HSC, and the reduction of expression of PPARgamma might be an early event during the activation process of HSC.

Animals ; Liver ; cytology ; Liver Cirrhosis ; etiology ; pathology ; Male ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; physiology ; Transcription Factors ; physiology

OBJECTIVETo explore the method for early diagnosis and pathogenesis of MYH9-related syndrome through analysis of the clinical manifestation and gene mutation of a Chinese family with MYH9-related syndrome.

METHODSPeripheral blood samples were collected from a three-generation Chinese family with MYH9-related syndrome (11 individuals, including 3 patients) and 100 healthy individuals. Polymerase chain reaction (PCR) amplification and direct sequencing of DNA were performed to analyze mutations of MYH9 gene.

RESULTSThrombocytopenia, increased volume of platelet, and granulocyte inclusion bodies were found in the patients with MYH9-related syndrome via a peripheral blood test. A missense mutation of a base pair (G-A) in exon 30 was revealed by PCR amplification and direct sequencing of MYH9 of the proband. That lead to Asp-Asn substitution at position 1424 (D1424N mutation). The mutation was the same as in other patients with MYH9-related syndrome. It was not found in healthy people from the Chinese family or in the other 100 healthy individuals.

CONCLUSIONSPatients with MYH9-related syndrome show diverse symptoms. Mutation of MYH9 gene may be the molecular mechanism of MYH9-related syndrome, and D1424N mutation of MYH9 has not been reported in Chinese people. Early diagnosis of MYH9-related syndrome can be carried out by investigating family history and making early examinations.

Adult ; Aged ; Asian Continental Ancestry Group ; genetics ; Child, Preschool ; Female ; Humans ; Molecular Motor Proteins ; genetics ; Mutation ; Myosin Heavy Chains ; genetics ; Thrombocytopenia ; genetics

OBJECTIVETo explore the methods for constructing the digital three-dimensional model of fetal heart.

METHODSOriginal two-dimensional CT image data sets were collected from 4 abortion fetuses with fetal malformations but not heart malformation or chromosomal abnormalities. The three-dimensional fetal heart model was reconstructed using Mimics14.0 software.

RESULTSIn the reconstructed three-dimensional fetal heart, the left atrium, left ventricle, right atrium, right ventricle, the ascending aorta, the main pulmonary and their branches, the superior cava and inferior vena cava were marked with different colors, and these structures could be displayed individually or with other structures. This model also allowed three-dimensional arbitrary scaling, shifting or rotation at any angle, and the diameter of the each vessel could be measured with the software.

CONCLUSIONThe fetal heart model can be successfully reconstructed from the CT datasets using three-dimensional reconstruction software to facilitate clinical and anatomical teaching.

Female ; Fetal Heart ; anatomy & histology ; Heart Atria ; anatomy & histology ; Heart Defects, Congenital ; Heart Ventricles ; anatomy & histology ; Humans ; Imaging, Three-Dimensional ; Models, Anatomic ; Pregnancy ; Software ; Tomography, X-Ray Computed ; Vena Cava, Inferior ; anatomy & histology

Objective: To investigate the efficacy of RCDOP (Rituximab, cyclophosphamide, liposome doxorubicin, vincristine and prednisone) regimen in patients with de novo diffuse large B-cell lymphoma (DLBCL), especially in those patients with multiple extra-nodal involvement or Bulky diseases. Methods: A total of 87 newly diagnosed DLBCL patients who received RCDOP regimen from October 2012 to October 2017 were enrolled into this study. Survival functions were estimated using the Kaplan-Meier method and compared by the log-rank test, and χ² tests were used for categorical data. Results: Among the 87 DLBCL patients treated with RCDOP regimen, 81 patients achieved complete remission (CR) or partial remission (PR), with ORR as 93.1%. Patients were further classified into groups, according to the risk factors, such as IPI scores, multiple extra-nodal involvement, bulky disease, age>60, tumor Ki-67>80%, elevated serum LDH level and advanced Ann Arbor stage. The progression-free survival (PFS, P=0.084) and overall survival (OS, P=0.515) had no statistical difference among the IPI low risk (0-1 score) group, intermediate risk (2-3 scores) group and high risk (4-5 scores) group. Similarly, no statistical difference were fou nd in PFS and OS of patients with extra-nodal involvements ≥2 (P=0.303 and P=0.624), with bulky disease (P=0.518 and P=0.466), with age>60 (P=0.600 and P=0.183), with elevated serum LDH level (P=0.054 and P=0.880), with advanced Ann Arbor stage (P=0.075 and P=0.286), and with tumor Ki-67 over 80% (P=0.190 and P=0.109), when compared with those of patients without these risk factors. Conclusion RCDOP can improve the therapeutic effect and prognosis of DLBCL patients with certain high risk factors, such as intermediate and high IPI risks, multiple extra-nodal involvements, bulky disease, age over 60, elevated LDH level, advanced Ann Arbor stage and tumor Ki-67 over 80%.

Objective: To investigate the efficacy of RCDOP (Rituximab, cyclophosphamide, liposome doxorubicin, vincristine and prednisone) regimen in patients with de novo diffuse large B-cell lymphoma (DLBCL), especially in those patients with multiple extra-nodal involvement or Bulky diseases. Methods: A total of 87 newly diagnosed DLBCL patients who received RCDOP regimen from October 2012 to October 2017 were enrolled into this study. Survival functions were estimated using the Kaplan-Meier method and compared by the log-rank test, and χ(2) tests were used for categorical data. Results: Among the 87 DLBCL patients treated with RCDOP regimen, 81 patients achieved complete remission (CR) or partial remission (PR), with ORR as 93.1%. Patients were further classified into groups, according to the risk factors, such as IPI scores, multiple extra-nodal involvement, bulky disease, age>60, tumor Ki-67>80%, elevated serum LDH level and advanced Ann Arbor stage. The progression-free survival (PFS, P=0.084) and overall survival (OS, P=0.515) had no statistical difference among the IPI low risk (0-1 score) group, intermediate risk (2-3 scores) group and high risk (4-5 scores) group. Similarly, no statistical difference were fou nd in PFS and OS of patients with extra-nodal involvements ≥2 (P=0.303 and P=0.624), with bulky disease (P=0.518 and P=0.466), with age>60 (P=0.600 and P=0.183), with elevated serum LDH level (P=0.054 and P=0.880), with advanced Ann Arbor stage (P=0.075 and P=0.286), and with tumor Ki-67 over 80% (P=0.190 and P=0.109), when compared with those of patients without these risk factors. Conclusion: RCDOP can improve the therapeutic effect and prognosis of DLBCL patients with certain high risk factors, such as intermediate and high IPI risks, multiple extra-nodal involvements, bulky disease, age over 60, elevated LDH level, advanced Ann Arbor stage and tumor Ki-67 over 80%.
Antineoplastic Combined Chemotherapy Protocols/therapeutic use* ; Cyclophosphamide ; Doxorubicin ; Humans ; Lymphoma, Large B-Cell, Diffuse/drug therapy* ; Prednisone ; Prognosis ; Treatment Outcome ; Vincristine

BACKGROUNDThe high mobility group A1 (HMGA1) proteins are architectural transcription factors found to be overexpressed in lung adenocarcinoma. Lentivirus-mediated RNA interference (RNAi) technology is a powerful tool for silencing endogenous or exogenous genes in human cancer cells. Our preliminary study shows that gemcitabine inhibits growth of the human lung cancer cell line SPCA-1 and induces apoptosis, and this effect might link with down-regulation of HMGA1 expression. This study aimed to investigate the chemosensitivity change of the lung adenocarcinoma cells SPCA-1 after HMGA1 inhibition by lentivirus-mediated RNAi.

METHODSWe studied a highly malignant lung adenocarcinoma cell line (SPCA-1 cells). Lentiviral short-hairpin RNA (shHMGA1) expression vectors targeting HMGA1 were used for generation of lentiviral particles. After being transfected into the lung adenocarcinoma cell line SPCA-1, the expression of HMGA1 was determined by retrotranscriptase polymerase chain reaction (RT-PCR) and Western blotting. The effect of gemcitabine on proliferation of positive and negative cells was observed by methyl thiazolyl tetrazolium (MTT) assay and clonogenic survival assay. Apoptosis was observed by flow cytometery. Chemosensitivity to gemcitabine was determined by IC50 analysis. Caspase activity was quantitated by a caspase colorimetric protease assay kit.

RESULTSHMGA1-siRNA silenced its target mRNA specifically and effectively in SPCA-1 cells. The apoptotic rates of the scramble control group were (7.43 ± 0.21)%, (11.00 ± 0.20)%, and (14.93 ± 0.31)%, and the apoptotic rates in the silenced group were (9.53 ± 0.42)%, (16.67 ± 0.45)%, and (25.40 ± 0.79)% under exposure to 0.05, 0.5 and 5.0 µg/ml of gemcitabine (P < 0.05). The IC(50) of the silenced group was (0.309 ± 0.003) µg/ml which was significantly lower than in the scramble control group, (0.653 ± 0.003) µg/ml (P < 0.05). It reduced cancer cell proliferation and increased apoptotic cell death after being treated with gemcitabine compared with the scramble control group. HMGA1 silencing resulted in reduction in the phosphorylation of Akt, and promoted the activation of caspases 3, 8 and 9 upon exposure to gemcitabine.

CONCLUSIONSLentivirus-mediated RNA interference of HMGA1 enhanced chemosensitivity to gemcitabine in lung adenocarcinoma cells. The mechanism may be associated with the PI-3K/Akt signal pathway. HMGA1 may represent a novel therapeutic target in lung cancer.

Antimetabolites, Antineoplastic ; pharmacology ; Blotting, Western ; Calcium-Transporting ATPases ; genetics ; metabolism ; Caspase 3 ; genetics ; metabolism ; Caspase 8 ; genetics ; metabolism ; Caspase 9 ; genetics ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Flow Cytometry ; Genetic Vectors ; genetics ; HMGA Proteins ; genetics ; metabolism ; Humans ; Lentivirus ; genetics ; RNA Interference ; physiology ; Reverse Transcriptase Polymerase Chain Reaction