Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Breast ; pathology ; Breast Neoplasms ; drug therapy ; pathology ; Cyclophosphamide ; therapeutic use ; Diagnosis, Differential ; Doxorubicin ; therapeutic use ; Female ; Follow-Up Studies ; Humans ; Lymphoma, B-Cell ; drug therapy ; pathology ; Lymphoma, Large B-Cell, Diffuse ; drug therapy ; pathology ; Male ; Middle Aged ; Prednisone ; therapeutic use ; Sarcoma ; pathology ; Spleen ; pathology ; Splenic Neoplasms ; drug therapy ; pathology ; Vincristine ; therapeutic use

Objective To investigate the criteria for assessing the clinical therapeutic effect of chronic urticaria in China.Methods The application of criteria for assessing the clinical therapeutic effect of chronic urticaria in China and their applicable scope were analyzed by frequency analysis and K-means clustering analysis, respectively.Results The criteria for assessing symptoms and therapeutic effect were different in the 857 papers included in this study. SSRI was used in 549 (64.17) out of the 857 papers included in this study.K-means clustering analysis showed that the applicable scope of SSRI with curative rate ( 100%≥SSRI>90%) , improvement rate ( 90%≥SSR<60%) , Significant effect rate (60%≥SSRI>20%) , and no response rate (20%≥SSR≥0%) as its criteria was wider than that of frequency analysis.Conclusion The criteria for the clinical assessment of chronic urticaria and its drug treatment effect should be unified and standardized.

Adult ; Antibodies, Monoclonal ; metabolism ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cyclophosphamide ; therapeutic use ; Diagnosis, Differential ; Doxorubicin ; therapeutic use ; Follow-Up Studies ; Humans ; Leukocyte Common Antigens ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; drug therapy ; metabolism ; pathology ; Male ; Mucin-1 ; metabolism ; Prednisone ; therapeutic use ; Receptor Protein-Tyrosine Kinases ; metabolism ; Vincristine ; therapeutic use

Objective To identify the important risk factors for type 2 Diabetes Mellitus (T2DM) and develop effective strategies to address the problem of T2DM.Our study aimed to evaluate the association between apolipoprotein E (ApoE) genetic polymorphism and type 2 diabetes,and to provide clues for the etiology of T2DM.Methods Based on the criteria of inclusion and exclusion,we extracted,pooled,analyzed and assessed the case-control studies of ApoE polymorphism and T2DM published in PubMed,Web of Science,Medline,WanFang,VIP,and CNKI databases by R soft-ware (version 3.4.3).We used Random-effect models when heterogeneity was present in between-study,and fixed-effect models otherwise.Results We had 59 studies covering 6,872 cases with T2DM and 8,250 controls,and compared the alleles and genotypes of ApoE between cases and controls.When we conducted a comparison between ApoE ε4 and ε3 alleles,we produced a pooled OR of 1.18 (95％ CI:1.09-1.28;P ＜ 0.001).ApoE ε2/ε2 genotype displayed a possible association with T2DM (OR =1.46;95％ CI:1.11-1.93;P =0.007),ε3/ε4 genotype showed a 1.11-fold risk (OR =1.11;95％ CI:1.01-1.22;P =0.039) and ε4/ε4 genotype had a 1.71-fold risk of developing T2DM (OR =1.71;95％ CI:1.33-2.19;P ＜ 0.001) when they were compared with ε3/ε3 genotype.Conclusions There is an association between ApoE polymorphism and T2DM:allele ε4 and genotypes (ε2/ε2,ε3/ε4,and ε4/ε4) are associated with the increased risk for the development of T2DM,and they may be risk factors for T2DM.

Severe acute pancreatitis (SAP) is a common acute abdomen clinical problem characterized by high mortality, multiple complications, complicated pathogenesis and difficult treatment. Recent studies found traditional Chinese medicine (TCM)monomers have markedly good effect for treating SAP. Many TCM monomers can inhibit pancreatin, resist inflammation, improve microcirculation and immunoloregulation, etc. to block the pathological progress of SAP in multiple ways, reduce complications and lower mortality with rapid effects. It is significant for enhancing SAP treatment to deeply understand the current situation in TCM monomers for treating SAP and take precious references therein. This article summarizes the treating effects and mechanisms of TCM monomers for SAP in recent years.

OBJECTIVETo explore roles of extracellular signal-regulated kinase (ERK) 1/2, p38 mitogen activated protein kinase (p38 MAPK) and nuclear factor (NF) -KB in expression of inducible nitric oxide synthase (iNOS) in rat alveolar macrophages induced by high mobility group box 1 (HMGB1 ).

METHODSPrimary rat alveolar macrophages (PRAMs) cultured in vitro were incubated with PD98059 ( inhibitor against ERK), SB203580 (inhibitor against p38 MAPK) , PDTC (inhibitor against NF-kappaB), or PD98059 plus SB203580 for 2 hours, respectively. HMGB1 was added into the cultures and incubated with cells for 6 hours. Total RNA of PRAMs was extracted and iNOS mRNA expression was semi-quantified with reverse transcription-polymerase chain reaction ( RT-PCR). Greiss reaction was applied to determine nitrite/nitrate (NO2-/NO3- ) concentration in PRAMs culture supernatants.

RESULTSExpression of iNOS mRNA and NO production in PRAMs culture supernatants were down-regulated by inhibition of ERK or p38 MAPK by PD98059 or SB203580, respectively (P <0. 05). Moreover, inhibition of iNOS expression and NO production was observed after simultaneous pretreatment with PD98059 and SB203580 (P < 0. 05). Expression of iNOS mRNA in PRAMs and NO production in PRAMs culture supernatants were down-regulated by inhibition of NF-kappaB by PDTC (P <0. 05).

CONCLUSIONCellular signal molecules of ERK, p38 MAPK, and NF-kappaB all participate in the expression of iNOS and NO production in PRAMs induced by HMGB1.

Animals ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; physiology ; Flavonoids ; pharmacology ; HMGB1 Protein ; pharmacology ; Imidazoles ; pharmacology ; Macrophages, Alveolar ; metabolism ; Male ; NF-kappa B ; antagonists & inhibitors ; physiology ; Nitric Oxide Synthase Type II ; biosynthesis ; Proline ; analogs & derivatives ; pharmacology ; Pyridines ; pharmacology ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Thiocarbamates ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; physiology

OBJECTIVETo describe the clinicopathologic features and immunophenotypes of carcinoid tumorlets in the lung with bronchiectasis, and to study the morphogenesis of these tiny tumors.

METHODSThe histopathologic characteristics of 3 bronchiectasis cases with carcinoid tumorlets, 11 bronchiectasis and 2 normal lungs were studied. Specific markers of the tiny tumors and the number of neuroendocrine cells (NECs) in the airway mucosa were immunohistochemically detected by EnVision method.

RESULTSThe tumorlets in the lungs presented as multi-focal nodules and most were displayed only under microscopy. These cells were arranged in clusters and foci of fascicles which were situated in the surrounding bronchial wall and bronchioles adjacent to bronchiectatic lesion, or in the scar tissues. The tiny tumors were consisted of short fusiform cells and small ovoid cells. Their nuclei were circular, oval or long fusiform and the cells were strongly argyrophilic on Grimelius staining. Intensive positive immunostaining for calcitonin, chromogranin A, NSE and gastrin were detected. Weak positive for CK, EMA, S-100 and focal positive for HC, ACTH, 5-HT were also observed. Proliferative NECs in airway mucosa adjacent to the tiny tumors increased significantly in number, compared with those in the airway mucosa of bronchiectasis without tumorlets and normal lungs (P < 0.001, respectively).

CONCLUSIONSThe clinicopathologic features and immunophenotypes of carcinoid tumorlets resemble carcinoid tumors. They are the early stage of carcinoid development. Their development may be related to the chronic pulmonary damage resulting in hypoxia and stimulating the proliferation of NECs. These pulmonary carcinoid tumorlets can be used as a model to study the tumorigenesis of carcinoid carcinoma of the lung.

Adult ; Aged ; Bronchiectasis ; pathology ; Carcinoid Tumor ; chemistry ; pathology ; Female ; Humans ; Immunohistochemistry ; Lung Neoplasms ; chemistry ; pathology ; Middle Aged ; Morphogenesis ; Neurosecretory Systems ; pathology

OBJECTIVETo study the mutations in exon 5 of IkappaBalpha gene and their significance in Hodgkin lymphoma.

METHODSCD30-positive Reed-Sternberg cells and surrounding reactive lymphocytes were selected by laser microdissection technology from 6 microm-thick histologic sections of 7 Hodgkin lymphoma cells studied. Genomic DNA of these cells was extracted according to Qiagen micro DNAkit guide. Semi-nested polymerase chain reaction (PCR) and direct DNA sequencing were used to analyze exon 5 of IkappaBalpha gene.

RESULTSA mutation in exon 5 was identified in 3 of the 7 Hodgkin lymphoma cases. No mutation found in the surrounding reactive lymphocytes. The mutation site was located at codon 2084 (T-A, NT_026437), resulting in formation of a stop codon.

CONCLUSIONThe mutation identified in exon 5 of the IkappaBalpha gene in Hodgkin lymphoma may play a role in the pathogenesis of Hodgkin lymphoma.

Adolescent ; Adult ; Base Sequence ; DNA Mutational Analysis ; DNA, Neoplasm ; genetics ; Exons ; genetics ; Female ; Gene Deletion ; Hodgkin Disease ; genetics ; Humans ; I-kappa B Proteins ; genetics ; Male ; Middle Aged ; Molecular Sequence Data ; NF-KappaB Inhibitor alpha ; Point Mutation

OBJECTIVETo investigate the clinicopathologic feature, immunophenotype and differential diagnosis of cutaneous Rosai-Dorfman disease (CRDD).

METHODSClinical manifestation, morphologic features and immunohistochemical staining were studied in 8 cases of CRDD.

RESULTSAll 8 patients presented with multiple papules, nodules and/or coalescent patches or plaques distributing over the extremities or trunk, without lymphadenopathy or other systemic abnormalities. Microscopically, the lesions were located intradermally and/or subcutaneously. CRDD was characterized by the presence of S-100 positive histiocytic cells exhibiting emperipolesis, accompanying with infiltration of mixed inflammatory cells. Fibrosis, somewhere in vague storiform pattern due to stromal responses, with distribution of individual neutrophil microabscess was seen in cases with a long course of illness. Dilated vascular spaces in dermis containing numerous large typical histiocytes were seen in 2 cases.

CONCLUSIONSCRDD is a benign, persistent proliferative disease of histiocytes. Systemic involvement is rare, outcome favorable. It should be differentiated from other types of histiocytosis, dermatofibrosarcoma protuberans, xanthoma and lymphoproliferative disorders. Immunohistochemical staining for S-100 protein and CD68 is helpful in making a correct diagnosis.

Aged ; Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Diagnosis, Differential ; Female ; Histiocytosis, Sinus ; metabolism ; pathology ; surgery ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Prognosis ; S100 Proteins ; metabolism ; Skin Diseases ; metabolism ; pathology ; surgery

OBJECTIVETo identify hereditary nonpolyposis colorectal cancer (HNPCC) families based on the germline mutations of MLH1 and MSH2 mRNA.

METHODSRNA was extracted from the peripheral blood of the 14 members from 12 different families fulfilling Amsterdam Criteria II. The germline mutations of MLH1 and MSH2 mRNA were detected by cDNA sequencing analysis following reverse transcription-PCR(RT-PCR) with special primers, heat-resistance reverse transcriptase, and expand long template PCR. DNA was extracted from the peripheral blood of the 14 members, the corresponding exons, in which mutations were found using the above method, were amplified with Taq enzyme, sequencing analysis was followed.

RESULTSSix germline mutations were detected and identified from the 6 different families based on mRNA, 4 of them to be in MLH1, the other 2 in MSH2. The MLH1 mutations distribute in the exon 8, 12, 16, and 19. The MSH2 mutations distribute in exons 1 and 2. The 6 mutations were identified from the corresponding exons respectively in genomic DNA sequencing analysis. The mutation types involve in 4 missense, 1 silent, and 1 non-coding area mutations. Five out of the 6 mutations have not been reported previously. Five out of the 6 mutations were pathological, involving in 5 different families. The five families were identified to HNPCC families.

CONCLUSIONHNPCC family can be identified with RNA-based sequencing of MLH1 and MSH2 from peripheral blood, which has the advantages of both cost, time saving and high sensitivity.

Adaptor Proteins, Signal Transducing ; Biomarkers, Tumor ; genetics ; Carrier Proteins ; genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis ; diagnosis ; genetics ; Female ; Germ-Line Mutation ; Humans ; Male ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; genetics ; Mutation ; Neoplasm Proteins ; genetics ; Nuclear Proteins ; genetics ; RNA, Messenger ; analysis