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We conducted two feedlot trials and one metabolism trial to evaluate the effect of barley level, barley bulk density, and physical form of roughage on lamb growth performance and digesta kinetics. Level of whole barley (50, 70, 90%) and type of roughage (chopped or pelleted alfalfa) were evaluated in Trial 1 (50 d period). Trial 2 (50 d) evaluated barley bulk density (heavy = 671 and light = 607 kg/m3), form of roughage (pelleted or chopped alfalfa), and level of barley (80 or 40%). The influence of treatments used in Trial 2 on digesta kinetics was evaluated in Trial 3. Gain:feed increased and DMI decreased (P < .10) linearly with increasing level of barley, and ADG and DMI were greater (P < . 10) for lambs fed pelleted vs chopped alfalfa in Trial 1. The 70% barley diet produced the highest yield grade and kidney-pelvic fat and the lowest leg score among barley levels (P < .10). Lambs fed pelleted alfalfa had heavier carcasses and a thicker body wall than lambs fed chopped alfalfa (P < .02). In Trial 2, DMI was less and gain:feed greater (P < .01) for lambs fed the heavy barley than for lambs fed the light barley and for the 80% barley diet compared to the 40% barley diet. Lambs fed pelleted alfalfa had greater dressing percentages than lambs fed chopped alfalfa. Backfat and body wall thickness were greater (P < .10) for lambs fed the 80% barley diet than for those fed the 40% barley diet. In Trial 3, retention time of barley was greater (P < .10) for lambs fed light rather than heavy barley, and retention time of alfalfa was greater (P < .10) for lambs fed chopped compared with pelleted alfalfa. Acetate:propionate ratio was greater (P < .10) for lambs fed light vs heavy barley and lambs fed the 40 vs 80% barley diets. Ruminal pH was lower (P = .05) and in situ barley digestion greater (P = .03) over time in lambs fed the 80% barley diet than in lambs fed the 40% barley diet. Feedlot lamb ADG was not always greatest with high levels of barley; however, gain:feed improved at the higher barley levels. The higher barley levels seemed to result in fatter lambs. 相似文献
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JT Sandlund T Fonseca T Leimig L Verissimo R Ribeiro V Lira CW Berard J Sixbey WM Crist L Mao G Chen CH Pui M Heim F Pedrosa 《Canadian Metallurgical Quarterly》1997,11(5):743-746
The purpose of this paper was to define the histologic distribution, clinical features, and treatment response of childhood non-Hodgkin lymphoma (NHL) in northeastern Brazil. We reviewed medical records and histopathologic studies of 98 children treated for NHL from 1980 to 1987 at a major pediatric cancer center in Recife, Brazil. Treatment outcome was evaluated in relation to tumor burden (stage and serum LDH) and type of therapy (LSA2L2 vs other multiagent chemotherapy). There was a striking predominance of the small noncleaved cell (Burkitt) subtype, which occurred in 92 of the 98 children and adolescents diagnosed with NHL. Subsequent analyses focused on these patients. The majority (n = 84) had advanced (stage III/IV) disease at diagnosis. The abdomen was the most common site of disease (84 cases); jaw involvement was rare (three cases). Five-year event-free survival (excluding treatment refusals) was significantly better for patients with limited vs advanced stage disease (75 +/- 14% vs 42 +/- 6%; P < 0.04). Elevated serum LDH (>500 U/l) was associated with a poorer outcome (P = 0.008). The type of chemotherapy did not affect EFS (P = 0.95). Only 39% of patients are long-term survivors, reflecting the high rate of septic deaths (25% of patients) and parental refusal/abandonment of therapy (10%). Epstein-Barr virus (EBV) was detected in tumor cells from eight of the 11 cases studied. In clinical presentation, these cases resemble sporadic Burkitt lymphoma, yet in their apparent responsiveness to LSA2L2 therapy and association with EBV, they do not. Childhood NHL in northeastern Brazil is predominantly of the Burkitt subtype, and is associated with clinical features that appear to distinguish it from the endemic and sporadic forms of this tumor. These cases may represent a third or intermediate subtype of Burkitt lymphoma. 相似文献
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CW Critchlow CM Surawicz KK Holmes J Kuypers JR Daling SE Hawes GM Goldbaum J Sayer C Hurt C Dunphy 《Canadian Metallurgical Quarterly》1995,9(11):1255-1262
OBJECTIVE: To determine the risk of developing high grade anal squamous intraepithelial neoplasia (HG-AIN) in relation to HIV infection and immunosuppression, after controlling for the effects of human papillomavirus (HPV) infection. DESIGN: Prospective cohort study of 158 HIV-seropositive and 147 HIV-seronegative homosexual men presenting to a community-based clinic with initially negative anal cytologic and colposcopic findings. METHODS: Subjects completed self-administered questionnaires, underwent cytologic screening, and standardized unaided and colposcopic examination of the proximal anal canal for presence of abnormalities suggestive of AIN. Anal specimens were screened for HPV DNA. RESULTS: HG-AIN developed in eight (5.4%) and 24 (15.2%) HIV-seronegative and -seropositive men, respectively. Risk of HG-AIN among HIV-seronegative men was associated with detection of anal HPV types 16 or 18 by Southern transfer hybridization (STH), detection of HPV 16 or 18 at the lower levels by polymerase chain reaction but not by STH, and with number of positive HPV tests; HG-AIN risk among HIV-seropositive men was associated with detection of HPV 16 or 18 only by STH, detection of HPV types other than 16 or 18, CD4 count < or = 500 x 10(6)/l, and number of positive HPV tests. HIV-induced immunosuppression remained an independent predictor of HG-AIN after adjusting for type and level of detection of HPV; HIV infection predicted HG-AIN risk after adjustment for number of positive HPV tests. CONCLUSIONS: The association of HG-AIN with HIV, independent of HPV type, level of HPV detection and number of positive HPV tests, suggests that this increased risk cannot be entirely explained by an effect of HIV on HPV detection. Future studies focusing on factors more specific to the local microenvironment in the anal canal should help clarify these issues. 相似文献
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Human papillomavirus (HPVs) adenovirus and simian virus 40 (SV40) are small DNA viruses which can show oncogenic activity. Although not otherwise related, all three have adopted very similar strategies to deregulate cell growth; each virus encoding oncoproteins which interact with the same cellular targets. Of particular interest are the interactions with the cell encoded pRB and p53 proteins, products of tumour suppressor genes. Somatic mutation results in the loss of the pRB and p53 function in many cancers and the contribution of the viruses to tumour development appears to reflect their ability to inactivate these cellular proteins. Both pRB and p53 negatively regulate progress through the cell cycle and the action of the viral proteins has highlighted the central importance of these tumour suppressor proteins in maintaining normal cell growth. 相似文献
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