Lesion pathology predicts response to plasma exchange in secondary progressive MS.
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Progress over the past 30 years has revealed many strengths of the rainbow trout as an alternative model for environmental carcinogenesis research. These include low rearing costs, an early life-stage ultrasensitive bioassay, sensitivity to many classes of carcinogen, a well-described tumor pathology, responsiveness to tumor promoters and inhibitors, and a mechanistically informative nonmammalian comparative status. Low-cost husbandry, for example, has permitted statistically challenging tumor study designs with up to 10,000 trout to investigate the quantitative interrelationships among carcinogen dose, anticarcinogen dose, DNA adduct formation, and final tumor outcome. The basic elements of the trout carcinogen bioassay include multiple exposure routes, carcinogen response, husbandry requirements, and pathology. The principal known neoplasms occur in liver (mixed hepatocellular/cholangiocellular adenoma and carcinoma, hepatocellular carcinoma), kidney (nephroblastoma), swim bladder (adenopapilloma), and stomach (adenopapilloma). Trout possess a complex but incompletely characterized array of cytochromes P450, transferases, and other enzymic systems for phase I and phase II procarcinogen metabolism. In general, trout exhibit only limited capacity for DNA repair, especially for removal of bulky DNA adducts. This factor, together with a high capacity for P450 bioactivation and negligible glutathione transferase-mediated detoxication of the epoxide, accounts for the exceptional sensitivity of trout to aflatoxin B1 carcinogenesis. At the gene level, all trout tumors except nephroblastoma exhibit variable and often high incidences of oncogenic Ki-ras gene mutations. Mutations in the trout p53 tumor suppressor gene have yet to be described. There are many aspects of the trout model, especially the lack of complete organ homology, that limit its application as a surrogate for human cancer research. Within these limitations, however, it is apparent that trout and other fish models can serve as highly useful adjuncts to conventional rodent models in the study of environmental carcinogenesis and its modulation. For some problems, fish models can provide wholly unique approaches.
Many pathologies involve face. Among them, many have craniofacial growth consequences. The authors' aims are to analyze some of these pathologies, where clinical observations emphasize the role of the different craniofacial growth patterns. Despite a complex relation between the malformative part and the deformative one, untreated observations provide a better understanding of some craniofacial growth defects. Syndromes can be classified in 4 categories, involving the primitive causes of the clinical finding: 1. organic abnormalities of one or many functional matrix, 2. localized abnormalities of the anatomical structures, 3. general abnormalities of the conjunctive tissue, 4. mixed syndromes. Many observations will presented.
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OBJECTIVE: To study the clinicopathologic characteristics, prognostic factors, response to chemotherapy, chemotherapy-caused disease-free interval and overall survival of small cell carcinoma of uterine cervix (SCCUC). METHODS: Twelve patients with SCCUC were treated from 1995 to 1999, with their clinic ophathologic data retrospectively analyzed. Their stages were I b(1) 2, I b(2) 4, II a 3, II b 1, III b 1 and IV b1. All 12 samples were assessed through immunohistochemical methods including epithelial cell markers and neuroendocrine cell markers, showing positive results in all. Nine early stage patients underwent radical hysterectomy with pelvic lymphadenectomy. Five of these 9 patients had received neoadjuvant chemotherapy (NCH) once or twice before operation, three patients received adjuvant chemotherapy (ACH) once to six times after operation. Three patients with advanced lesions received concurrent chemotherapy twice to four times. RESULTS: 44.4% (4/9) of patients treated by pelvic lymphadenectomy showed positive lymph node metastasis. The average disease free intervals of patients who showed positive or negative pelvic lymph node were 16.1 and 25.7 months, overall survival of 19 and 32 months. The success rate of surgery in the NCH group was 100%, 60% of whom showed chemotherapy response pathologically. They showed overall response rates of 80% (4/5), 20% CR (1/5) and 60% PR (3/5). CONCLUSION: Poor prognosis of small cell carcinoma of uterine cervix, even the early lesions, is due to its high incidence of pelvic lymph metastasis. The risk factor of this lesion is high sensitivity to chemotherapy, but chemotherapeutic long-term survival should be studied further with more allotted material.
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Recombinant BCGs (rBCGs) containing extrachromosomal plasmids with different HIV-1 insert sequences: nef, env (V3J1 and E9Q), gag p17 or whole gag p55 were evaluated for their immunogenicity, safety and persistent infection in BALB/c mice. Animal injected with, rBCG-plJKV3J1, rBCG-pSO gag p17 or rBCG-pSO gag p55 could elicit lymphocyte proliferation as tested by specific HIV-1 peptides or protein antigen. Inoculation with various concentration of rBCG-pSO gag p55 generated satisfactory specific lymphocyte proliferation in dose escalation trials. The rBCG-pSO gag p55 recovered from spleen tissues at different time interval post-inoculation could express the HIV protein as determined by ELISA p24 antigen detection kit. This result indicated that the extrachromosomal plasmid was stable and capable to express Gag protein. It was also demonstrated that rBCGs did not cause serious pathological change in the inoculated animals. The present study suggested the role of BCG as a potential vehicle for using in HIV vaccine development.
T cell homeostasis is required for normal immune responses and prevention of pathological responses. Transforming growth factor beta (TGFbeta) plays an essential role in that regulation. Owing to its broad expression and inhibitory effects on multiple immune cell types, TGFbeta regulation is complex. Through recent advances in cell-specific targeting of TGFbeta signaling in vivo, the role of TGFbeta in T cell regulation is emerging. We demonstrated here a critical role for TGFbeta in regulating effector vs regulatory T cell homeostasis.
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