Aim:To characterize the immune response to YCP, a polysaccharide (PS) isolated from marine filamentous fungus Phoma herbarum YS4108. Methods:YCP was coupled to bovine serum albumin (BSA) to construct three neoglycoproteins which are different in their degrees of substitution (DSs; ≈ 3, ≈ 6, or ≈ 10 mol of BSA carrier/mol of YCP hapten, respectively), and their immunogenicities were evaluated in mice following subcutaneous immunization,respectively. IgG subclasses against the PS and the carrier protein were measured in addition to the total IgG and IgM antibodies for YCP induced by the neoglycoproteins. Results: While unconjugated PS was weakly immunogenic, theneoglycoprotein induced vigorous primary IgM and booster IgG responses to PS and the carrier protein. Interestingly,the IgG subclass distribution was different between PS and the carrier protein; for PS, the IgG response was predominant of IgG2a subclass with approximately low levels of IgG2b and IgG1, while the response to the carrier protein was mainly of the IgG1 subclass with relatively low levels of IgG2a and IgG2b, and the lowest of IgG3. Conclusion:YCP has the potential to elicit preferentially IgG2a as the dominant isotype antibody in mice.

Objective To establish the analysis criteria of nucleoplasmic bridges (NPB) and a dose-response curve of NPB frequencies in human peripheral blood lymphocytes irradiated by 60Co γ-rays.Methods Human peripheral blood samples were collected from three healthy males,and were irradiated with 0,1,2,3,4,5 and 6 Gy of 60Co γ-rays.A cytokinesis-block micronucleus assay was carried out to analyze NPBs and micronuclei (MN) in binucleated cells.Results NPBs in binucleated cells at each dose level of γ-ray was conformed to the Poisson distribution.The dose-response curve of the γ-ray-induced NPB frequencies in human peripheral lymphocytes followed the linear-quadratic model y =(1.39 × 10-3)x2 + (4.94 × 10-3)x (R2 =0.981,P ＜ 0.05).Conclusions The dose-response curve of NPB frequencies in human peripheral blood lymphocytes induced by 0-6 Gy 60Co γ-rays was established.

SUMMARY We described 1 case of autoimmune lymphoproliferative syndrome ( ALPS) , first diagnosed in our hospital, and reviewed the recent literature. The 11-month old male patient presented with a histo-ry of splenomegaly and hepatomegaly since 1 month after birth. He suffered recurrent infectious diseases including cytomegalovirus infection, parvovirus B19 infection and chronic diarrhea disease. Besides, his symptoms included hemolytic anemia and thrombocytopenia. The laboratory abnormality indicated an ex-panded population of alpha/beta double-negative T cells (DNTs) (27. 18% of lymphocytes, 35. 16% of CD3 + T lymphocytes) in peripheral blood, and autoantibodies including antinuclear antibody, double-stranded DNA and rheumatic factor were positive. Hyper gamma globulinemia and positive direct Coombs tests were seen in the patient. His parents were both healthy and denied autoimmune diseases. We iden-tified a heterozygous point mutation in exon 3 of the FAS gene carrying c. 309 A>C, resulting in a single base pair substitution in exon 3 of FAS gene which changed the codon of Arg103 to Ser103 . Unfortunate-ly, we were unable to obtain the gene results of the child' s parents. The patient was treated with glu-cocorticoids in our hospital and with mycophenolatemofetil in other hospital. And we were informed that his anemia condition relieved through the telephone follow-up, but he still suffered recurrent infections, hepatomegaly and splenomegaly still existed. As we all know ALPS is characterized by defective lympho-cyte apoptosis, and thus cause lymphoproliferative disease and autoimmune disease, and increase the risk of lymphoma. It is more likely to be misdiagnosed as other diseases. ALPS should be suspected in the case of chronic lymphadenopathy, splenomegaly and autoimmune features. Flow cytometry approach is helpful for the diagnosis. Immunosuppressive drugs are the necessary treatment.

1-Alkyl-2-acetylglycerophosphocholine Esterase ; blood ; genetics ; Adolescent ; Asthma ; blood ; enzymology ; genetics ; Child ; Child, Preschool ; Female ; Gene Expression Regulation, Enzymologic ; Genotype ; Humans ; Infant ; Male ; Mutation ; Polymerase Chain Reaction

Aged ; Alzheimer Disease ; drug therapy ; physiopathology ; Brain ; physiopathology ; Chitosan ; pharmacology ; therapeutic use ; Electroencephalography ; Female ; Humans ; Male ; Phospholipids ; pharmacology ; therapeutic use

OBJECTIVETo investigate the salvage therapy for a child with refractory and ( or) repeatedly-relapsed Langerhans cell histiocytosis.

METHODData of a patient with Langerhans cell histiocytosis whose disease relapsed repeatedly treated with cladribine was collected and analyzed and the related literature was reviewed.

RESULTThe initial symptoms developed 3 months after his birth, multiple systems (skin, skeleton, lung, liver) were involved; he was sequentially treated with LCH-III-Group I, JLSG-96, DAL-HX90 chemotherapeutic regimens. The patient got relapses for more than 3 times, but the disease got completely controlled after being treated with cladribine when the patient was 6 years old. The dosage was 10 mg/(m2 · d) for 4 days, and one course lasted for 28 days, the third to fifth courses of treatment used Arac in combination, the whole treating time lasted for 5 months. The patient remained in persistent remission for 8 months since discontinuation of treatment. "Langerhans cell histiocytosis" "refractory" "cladribine" were used as the key words to search in the data bases CNKI, Wanfangdata and Pubmed, 11 articles were picked. According to the literature, the effective rate of cladribine in treatment of repeatedly relapsing Langerhans cell histiocytosis was 44%-100%, with a good response of 22%-86%, the dose was 5-13 mg/(m2 · d). The main side effects were hematological system damages and infection.

CONCLUSIONThe effect of commonly used chemotherapeutic regimens is limited for children with refractory and (or) repeatedly-relapsed Langerhans cell histiocytosis and cladribine can be used as an alternative therapeutic option of the salvage therapy.

Child ; Cladribine ; therapeutic use ; Histiocytosis, Langerhans-Cell ; drug therapy ; Humans ; Immunosuppressive Agents ; therapeutic use ; Male ; Recurrence ; Skin

Castleman Disease ; genetics ; pathology ; surgery ; Diagnosis, Differential ; Female ; Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Humans ; Hyperplasia ; Lung ; pathology ; surgery ; Lung Diseases ; genetics ; pathology ; surgery ; Lymph Nodes ; pathology ; Middle Aged

Actins ; metabolism ; Adenocarcinoma ; pathology ; Adult ; Diagnosis, Differential ; Endometriosis ; pathology ; Epithelium ; pathology ; Female ; Gastrointestinal Stromal Tumors ; pathology ; Hamartoma ; metabolism ; pathology ; Humans ; Muscle, Smooth ; pathology ; Stomach Diseases ; metabolism ; pathology

Animals ; Carcinoma, Hepatocellular ; blood supply ; pathology ; therapy ; Cell Line, Tumor ; Cells, Cultured ; Cytotoxicity, Immunologic ; immunology ; Female ; Humans ; Interleukin-12 ; pharmacology ; Interleukin-2 ; pharmacology ; Killer Cells, Natural ; cytology ; drug effects ; immunology ; Liver Neoplasms, Experimental ; blood supply ; pathology ; therapy ; Lymphocyte Activation ; drug effects ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Microcirculation ; drug effects ; Random Allocation ; Xenograft Model Antitumor Assays

Objective To investigate the effect of physical training on plasma N-terminal pro-brain natri- uretic peptide(NT-proBNP)levels in patients with chronic heart failure(CHF).Methods Eighty NYHAⅡ-ⅢCHF patients were randomly divided into a training group(n=42)and a control group(n=38).A 6-minute walk- ing test was performed within 24 hours after the patients were admitted.The 6-minute walking distance and plasma NT-proBNP levels were determined before and after 8 weeks of programmed physical training.The patients of both groups were treated with routine drugs for heart failure.6-minute walk training was only performed in the training group twice a day for 8 weeks.Results Physical training could significantly reduce plasma NT-proBNP levels and improve performance on the 6-minute walking test.Conclusions Physical training could significantly reduce plas- ma NT-proBNP levels and improve the motor function of patients with CHF,and could be helpful in delaying the de- velopment of CHF.