Objective To study the imaging features and adequate interventional therapy of the diffuse type hepatic cellular carcinoma(HCC).Methods Fourteen patients with the diffuse type HCC underwent hepatic angiography and the adequate interventional therapy by TAI or TAE according to imaging appearances,blood supply and function of liver.Results ①Imaging appearances:the most common appearances of fourteen patients with the diffuse type HCC on DSA and CT included:tumor blood vessel was extensive and increased,tumor stain was extensive in left and right liver leaf(such as grain,small spot ,nodule shadows or low density area),liver enlarged obviously with liver cirrhosis,portal vein tumor thrombus,arteriopotal shunt and widespreadly scattered iodized oil,et al.②Therapeutic effect:the mean survival time of fourteen patients was 3 months,the longest survival period was 10 months and the shortest one was olny 15 days.Conclusion ①The specific appearances of the diffuse type HCC are diffuse small spot-like,frosted glass-like,double orbit-like and big liver-like.②The interventional therapeutic effect and prognosis of the diffuse type HCC are the worst than that of other type primary hepatic carcinoma.Selecting adequate interventional therapeutical plan can obviously prolong survival time of the patient.

ObjectiveTo evaluate CT characteristics of fungal ball in paranasal sinus caused by different fungi and to enhance differential diagnosis.MethodsCT results and clinical data of 74 patients with fungal ball arising from the paranasal sinuses proved by histopathology from 2007 to 2009 were analyzed retrospectively.The CT characteristics of fungal ball in paranasal sinus caused by different fungi were compared using x2 test with P ＜ 0.05 considered statistically significant.Results Among 74 mycotic pathogenic agents,aspergillus was found in 58 cases (including 36 cases with aspergilhs flavus,15 cases with aspergillus fumigatus and 7 with aspergillus versicolor),the others including 5 cases with penicillium,6 cases with schizophyllum commune,and 5 cases with scedosporium apiospermum.There were significant differences in the number of sinus involved ( single sinus involvement was seen in 29 cases caused by aspergillus group and 2 cases caused by non-aspergillus-group,respectively,with x2 =7.245,P =0.007 ),the incidence of fungus ball in ethmoid sinus [ 39.7％ ( 23/58 ) of cases caused by aspergillus group and 81.3 ％ ( 13/16 ) of cases caused by non-aspergillus-group,respectively,with x2 =8.685,P =0.003 ] and calcification (40 of 58 cases caused by aspergillus group and 5 of 16 cases caused by non-aspergillus-group,respectively,with x2 =7.485,P =0.006 ),the location of calcification ( 26 of 40 cases with central calcification and 14 of 40 cases with peripheral calcification in cases caused by aspergillus group,while all of 5 cases caused by non-aspergillus-group with peripheral calcification,x2 =7.697,P =0.006).However,there was no significant difference in the incidence of bilateral lesions ( x2 =1.002,P =0.317 ),maxillary sinus involvement ( x2 =0.020,P =0.888 ),sphenoidal sinus involvement ( x2 =0.704,P =0.401 ),frontal sinus involvement ( x2 =0.126,P =0.723 ),bony sclerosis ( x2 =2.024,P =0.155 ),lamellar calcification (x2 =2.045,P =0.153 ),complication of nasal polyps( x2 =0.018,P =0.893) and submucosal cyst( x2 =0.779,P =0.378 ).ConclusionsThe common CT characteristics of fungal ball in paranasal sinus are unilateral sinus involvement with inhomogeneous high-density soft tissue and lamellar calcification.The CT findings of fungal ball caused by non-aspergillus-group are ethmoid sinus involvement and calcification located on the periphery instead of the center of fungal ball.

Objective To investigate the effect of CTLA4-Ig chimera protein on mice mortality, histopathological changes, viral fiters, expression of CTLA4 protein on infiltrated T lymphocyte and the balance of Thl/Th2 in mice myocarditis caused by coxsackie virus B3 (CVB3). Methods A total of 106 four to six week-old male BALB/c mice were used in the experiments, which were divided into CTLA4-Ig group (n = 16), CVB3 group (n=40), IgG group (n =40) and normal control group(n = 10) randomly. The mice in CVB3 group, IgG group and CTLA4-Ig group were inoculated intraperitoneally with 0. 15 ml CVB3 and the mice in norreal control group with 0. 15 ml Eagle. The mice in IgG group and CTLA4-1g group were inoculated with IgG (0. I mg/kg) and CTLA4-Ig(0. 1 mg/kg) at 6 h and 72 h post inoculation(p, i. ), respectively, The surplus mice in each group were sacrificed at day 7 p.i. Light microscope was used to quantify the inflammation. The expression of CVB3 mRNA in mycardium were semi-quantified by real-time quantitative polymerase chain reaction (RQ-PCR). The expression of CTLA4 protein were analyzed by immunohistochemistry. The levels of IL-2, IL-4 and 1FN-γ in serum were measured by ELISA. Results The mice mortality, histopathological score and CVB3 mRNA in CTLA4-Ig group were lower than that in CVB3 group ( P < 0.05, P < 0.01, P < 0. 05, respectively). The expression of CTLA4 was significantly increased in CTLA4-Ig therapy group (P < 0.05 ). The serum level of IFN-γ of mice in CVB3 group were significantly higher than that in normal control group( P < 0.01 ). The serum level of IL-4 of mice in CVB3 group were much lower than that in normal control group( P < 0.01 ). The serum level of IL-2 in CVB3 group had no statistical significance with that in normal control group ( P > 0.05 ). The serum level of IFN-γ in mice of CTLA4-Ig group were much lower than that in CVB3 group ( P <0.01 ) and lgG group (P < 0. 01 ). The serum level of IL-4 of mice in CTLA4-Ig group were significantly higher than that in CVB3 group (P<0.01) and IgG group (P<0.01). The serum level of IL-2 in CTLA4-Ig group had no statistical significance with that in CVB 3 control group and lgG group ( P > 0. 0 5 ) . Conclusion CTLA4-Ig may relieve inflammation and reduce mice mortality by blocking the costimulation signals for T lymphocyte activation and reinforcing Th2 response.

Objective To analyze the etiological factor and genetic feature of a familial hemophagocytic lymphohistiocytosis patient with PRF1 mutation (FHL2) with human herpesvirus 7 (HHV7)infection and its family constellation. Methods Clinical characteristics, laboratory examinations of a FHL2 case with HHV7 infection were reported. HHV1-HHV8 virus DNA was screened by PCR; NK cell function was analyzed by flow cytometry; PRF1 gene mutations were analyzed by PCR and direct sequencing, structure of mutant PRF1 proteins were analyzed using ExPasy and I-TASSER server and genetics pedigree were analyzed. Results The patient's HHV7 viral was detected positive with DNA copy number of 350/106 peripheral nucleated cells. Flow cytometry analysis showed decrease both in proportion of perforin positive NK cells and perforin protein expression. Genetic testing showed PRF1 biallelic heterozygote mutations (c. 503G ＞ A/p. S168N and c. 1177T ＞ C/p. C393R) and pedigree analysis showed they were inherited. The patient was then treated with antivirus therapy, dexamethasone and VP16 therapy, but only achieved partial response. The patient was then followed by human leukocyte antigen 10/10 allele identical nonconsanguinity allogeneic hematopoietic stem cell transplantations (allo-HSCT) and soon the successful implantation of donor hematopoietic cells and persistent recovery was achieved. The patient was now surviving without recurrence for 9 months after allo-HSCT. Conclusions FHL is prone to be misdiagnosed as lymphoma. Genetic analysis of related gene mutation and herpes simplex virus detection will help in early and accurate diagnosis. Allo-HSCT is a fundamental treatment of FHL.

Objective To study the relationship between ischemic stroke and gene polymorphism of an-giotensin-converting enzyme (ACE), apolipoprotein E (APOE) and methylene tetrahydrofolate reductase (MTHFR) among the population of Zhuang nationality in western Gui. Methods We directly sequenced ACE, APOE and MTHFR genes in 149 cases of ischemic stroke and 109 cases of normal people in western Gui. χ2 test was used to measure the relationship between gene polymorphism and ischemic stroke. Hardy-Weinberg genetic equilibrium test was used to evaluate the reliability of these data. Results In the ischemic stroke group, 62 cases, 22 cases and 65 cases carried II genetype, DD genetype and ID genetype in ACE. χ2 test showed no relationship between ACE gene polymorphism and ischemic stroke. In analysis of the polymorpism of APOE in the ischemic stroke and control group, no relationship between APOE gene polymorphism and ischemic stroke was found by χ2 test. MTFHR gene polymorphism was significantly related with ischemic stroke by χ2 test (P = 0.019). Conclusion Polymorphism of gene MTFHR but neither ACE nor APOE is significantly associated with ischemic stroke.

Objective:To investigate the clinical characteristics of myelin oligodendrocyte glycoprotein antibody associated disorders (MOGAD) combined with anti- N-methyl- D-aspartate receptor (NMDAR) encephalitis. Methods:Sixty-five patients with MOGAD and 96 patients with anti-NMDAR encephalitis, admitted to our hospital from July 2018 to June 2021, were chosen in our study; 8 patients with MOGAD combined with anti-NMDAR encephalitis were selected as antibody double positive group; 21 patients with MOG antibody(+)/anti-NMDAR antibody(-) and 37 patients with anti-NMDAR antibody(+)/MOG antibody(-) were selected as controls. The differences of clinical characteristics of patients among these groups were compared.Results:(1) In these 8 patients from antibody double positive group, MOGAD and anti-NMDAR encephalitis occurred simultaneously in 6 patients, and anti-NMDAR encephalitis occurred prior to the episode of MOGAD in 2 patients. Autoimmune encephalitis was the dominant phenotype and demyelinating symptoms occurred in some patients. Both MOG antibody and anti-NMDAR antibody were detected in these 8 patients. MRI showed that lesions mostly involved in the cortex and subcortical white matter. Intravenous administration of high-dose methylprednisolone and immunoglobulin was given for patients at acute stage; two patients received mycophenolate mofetil treatment additionally during recurrence. After treatment, syndromes in these 8 patients got improvement. (2) There were no significant differences between patients from antibody double positive group and MOG antibody(+)/anti-NMDAR antibody(-) group in clinical manifestations, auxiliary examinations or treatments ( P>0.05). As compared with patients in antibody double positive group, patients in the anti-NMDAR antibody(+)/MOG antibody(-) group had significantly lower proportion of children and significantly higher modified Rankin scale (mRS) scores at the height of their illness ( P<0.05). As compared with patients in the MOG antibody(+)/anti-NMDAR antibody(-) group, patients in the anti-NMDAR antibody(+)/MOG antibody(-) group had significantly older onset age, significantly lower proportion of children, significantly higher proportion of patients with epilepsy and abnormal psychiatric behavior, significantly higher proportion of patients admitted to Intensive Care Unit, statistically higher mRS scores at the height of their illness, significantly lower proportion of patients with intracranial lesions, and significantly higher proportion of patients used immunoglobulin and plasma exchange ( P<0.05). Conclusion:MOG antibody and anti-NMDAR antibody can cause different clinical symptoms; when MOGAD patients have unusual symptoms, such as abnormal psychiatric behavior and epilepsy, or anti-NMDAR encephalitis patients develope demyelinating features, the possibility of MOGAD combined with anti-NMDAR encephalitis should be considered.

Objective:To study the transcriptional regulation of pilABCD by the master quorum sensing (QS) regulator OpaR in Vibrio parahaemolyticus. Methods:Total RNAs were extracted from the wild type (WT) and opaR mutant (Δ opaR) strain. Quantitative real-time PCR (qPCR) was employed to calculate the transcriptional variation of pilA (the first gene of pilABCD operon) between WT and Δ opaR. The regulatory DNA region of pilABCD was cloned into the corresponding restriction endonuclease sites of pHRP309 harboring a promoterless lacZ reporter gene. The recombinant pHRP309 plasmid was then transferred into WT and Δ opaR, respectively, to detect the β-galactosidase activity in cellular extracts using a β-Galactosidase Enzyme Assay System (Promega). The primer extension assay was applied to map the transcription start site of pilABCD using the total RNAs extracted from the WT strain as the template. The regulatory DNA region of pilABCD was amplified by PCR, and the over-expressed His-OpaR was purified under native conditions with nickel loaded HiTrap Chelating Sepharose columns (Amersham). Thereafter, the electrophoretic mobility shift assay (EMSA) was applied to analyze the DNA-binding activity of His-OpaR to the target DNA in vitro, and the DNase I footprinting assay was further employed to detect the DNA-binding sites of His-OpaR within the target DNA. Results:The results of qPCR and LacZ fusion assays showed that OpaR activated the transcription of pilABCD, leading to a gradual increase in the expression level of pilA with the extension of culture time. The primer extension assay detected only one transcription start site located at 155 bp upstream of pilA. The results of EMSA and DNase Ⅰ footprinting assays showed that His-OpaR protected two DNA regions located from -246 to -197 bp and -181 to -131 bp upstream of pilA. Conclusions:Vibrio parahaemolyticus OpaR activated the transcription of pilABCD in a direct manner.

Objective: To analyze the clinical characteristics and prognosis of 34 cases of acute myeloid leukemia (AML) with FLT3 internal tandem duplication (FLT3-ITD) and MLL gene rearrangement. Methods: The clinical data of 34 AML patients with FLT3-ITD and MLL gene rearrangement was compared and analyzed for the therapeutic efficacy, prognostic factors when treated with chemotherapy, chemotherapy combined with targeted therapy or allogenic hematopoietic stem cell transplantation (allo-HSCT). Results: Of the thirty-four cases with median age 41 (4-71) years old, 63.6% presented with white blood cells (WBC) greater than 30×10⁹/L, 39.4% greater than 50 × 10⁹/L respectively on admission. M₅ (35.3%) made up the highest proportion. The cytogenetic abnormality reached 61.8%, of which the complex cytogenetic abnormality accounted for 11.8%. Eleven patients (32.35%) had both FLT3-ITD and MLL gene abnormalities. In addition to FLT3 and MLL abnormalities, 23 patients (67.6%) had one or more other gene abnormalities (multiple gene abnormalities). Of the 34 cases, 29.4% patients went into complete remission (CR) after two courses of chemotherapy. 20.6% (7 patients) went into CR after 3 or more courses of chemotherapy. The rate of early relapse in the CR group was 52.9%. Patients with WBC>50×10⁹/L or multiple gene abnormalities had a lower remission rate (7.7%, 5.4%) after two courses of chemotherapy. CR rate for the patients with more than three gene abnormalities was 0. The total 2-year overall survival (OS) in the 34 patients was 28.8% (95% CI 13.5%-46.0%) and the disease-free survival (DFS) was 27.1% (95% CI 12.5%-44.0%). Of the 18 patients treated with chemotherapy alone or chemotherapy combined with targeted therapy, 17 cases died within 2 years and 1 lost follow-up after giving up treatment. For the 16 patients received allo-HSCT, the 3-year OS was 43.4% (95% CI 13.7%-70.4%) and DFS 42.7% (95% CI 13.4%-69.7%). Conclusion AML patients with FLT3-ITD and MLL gene rearrangement often presented with M₅, accompanied by hyperleukocytosis, cytogenetic or multiple gene abnormalities. Those patients were observed to have low response rate and high early relapse when treated with chemotherapy without allo-HSCT. Patients had multiple gene abnormalities may be an important poor prognostic factor. Allo-HSCT is an effective treatment which could significantly improve the prognosis and survival of AML patients with FLT3-ITD and MLL gene abnormalities.

Objective To study the type and corresponding clinical characteristics of primary hemophagocytic lymphohistocytosis (HLH) associated immune gene mutations in the refractory virus infection or HLH of unknown causes. Methods From December 2009 to July 2010, the patients with refractory virus infection or HLH of unknown causes were screened for the primary HLH associated immune genes mutations by DNA sequence analysis, including PRF1, UNC13D, STX11, STXBP2, SH2D1A and XIAP. The clinical characteristics and outcomes were followed up. Results Totally 25 patients with refractory virus infection or HLH of unknown causes were investigated for the 6 genes and 13 cases were found carrying gene mutations, composing of 6 of PRF1 mutation, 3 of UNC13D, and each one of STX11,XIAP, SH2D1A and STXBP2, respectively. Among the 13 cases with gene mutations, 5 suffered from Epstein-Barr virus associated HLH( EBV-HLH), 1 human herpes virus 7 associated HLH (HHV7-HLH),1 HLH without causes, 4 chronic activated EB virus infection (CAEBV) with 1 progressing to Hodgkin's lymphoma carrying abnormal chromosome of t ( 15; 17 ) (q22; q25 ) and hyperdiploid, 2 EBV associated lymphoma. Among the other 12 patients without gene mutation, 4 suffered from EBV-HLH with 1 progressing to peripheral T lymphoma, 8 suffered from CAEBV. Conclusions Primary HLH associated immune gene mutations are critical causes of refractory virus infection of unknown causes, most patients manifest as HLH,some cases appear in CAEBV and EBV associated lymphoma. DNA sequence analysis is helpful to early diagnosis and correct decision-making for treatment.

Coagulometer, known as blood coagulation analyzer, is a product that can provide accurate test results for medical diagnosis and treatment analysis by detecting a series of items closely related to thrombosis and hemostasis in coagulation reaction. On the basis of previous traditional methods, and with our deep understanding about the principles of hemagglutination detection, we propose a hemagglutination detection method by using the dual-magnetic circuit beads method. Then, the corresponding hemagglutination detection module is designed. The coagulation time of plasma can be measured by detecting the movement of the magnetic beads when the magnetic field intensity is appropriate. The activated partial thromboplastin time(APTT) of plasma is tested when the most suitable magnetic field intensity is found. The results preliminarily show that this blood coagulation test method is valid and the corresponding test module has a potential value in business.
Blood Coagulation ; Blood Coagulation Tests ; Magnetic Phenomena ; Magnetics ; Partial Thromboplastin Time