An experiment was carried out to determine the importance of holding time after hatching on the performance of male broiler chickens. This was done by transferring the chicks from the hatchery to the poultry house at intervals of 24 h. The weight and composition of the yolk residue on time of transfer were also determined. At 21 and 40 days of age, feed intake and body weight were inversely related to the period of holding. The chicks did not compensate for their posthatching body weight loss. The growth retardation caused by 24-and 48-h holding was equivalent at market age to 1 or 2 days body weight gain, respectively. There were no differences among treatments for feed utilization or mortality. (

W E describe a patient with a unique mantle-cell lymphoma, with cycles of acute illness alternating with spontaneous remissions. During the acute phase the patient had fever, generalized lymphadenopathy, hepatosplenomegaly, increased liver-enzyme concentrations, leukocytosis, and thrombocytopenia. These bouts remitted after two to three weeks without treatment. Fifteen such cycles were documented over a period of 50 months.During the acute phase blast-like B lymphocytes in the blood expressed surface IgM, IgD, and CD5, whereas during clinical remission a small population of IgM and CD5 ϩ lymphocytes persisted. Two B-cell clones with differently rearranged heavy-chain genes consistently appeared in the blood during the recurrent acute phases. During the spontaneous remissions, one clone (termed the "acute clone") regressed while the second clone remained relatively stable. These findings suggest that proliferation and death of the acute-clone cells determined the cyclic nature of the disease. The lymphoma cells of the acute phase, but not those of remission, were shown to undergo spontaneous apoptosis in vitro. This process was enhanced by inhibitors of messenger RNA and protein synthesis, suggesting that it was regulated by preexisting factors with short halflives. No molecular alterations were demonstrated in bcl -2 and p53 genes, which are known to regulate apoptosis. C ASE R EPORTA 61-year-old man was hospitalized in March 1990 because of a high fever, perspiration, abdominal pain, and vomiting of one week's duration. Physical examination revealed generalized lymphadenopathy, splenomegaly (spleen palpable 3 cm below the costal margin), and hepatomegaly (liver tip palpable 5 cm below the costal margin). Laboratory tests revealed a hemoglobin level of 14 g per deciliter, leukocytosis (68,000 leukocytes per cubic millimeter), and a platelet count of 44,000 per cubic millimeter. The differential white-cell count showed 12 percent segmented and 88 percent mononuclear cells, 70 percent of which were blast-like, with large cleaved nuclei and prominent nucleoli. Examination of the bone marrow showed heavy infil-tration by the lymphoid cells with the same morphologic features. A lymph-node biopsy revealed intermediate-grade malignant lymphoma of the diffuse mixed, predominantly small-cleaved-cell type. Cellsurface markers of peripheral mononuclear cells showed that 80 to 90 percent were B cells expressing IgMk and CD5 but not CD10. The diagnosis of mantle-cell lymphoma was established. The t(11;14) translocation, common in mantle-cell lymphoma, 1 was not detected.The bilirubin concentration was 2.8 mg per deciliter (48 m mol per liter), the serum uric acid concentration was 9.6 mg per deciliter (571 m mol per liter), the blood urea nitrogen concentration was 56 mg per deciliter (20 mmol per liter), and liver-enzyme levels were substantially increased. Serologic tests for Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, human T-cell lymphotropic virus type I, herpesviruses 1 and 6, and hepatitis A, B, ...

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Summary. Factor VII was purified from a lyophilized powder of PTC complex (Hemoplex, Cutter Laboratories) and an antiserum was prepared in rabbits to the partially‐purified fraction. The antiserum was found to inhibit specifically factor VII of normal plasma and the activity of the purified factor‐VII preparation. Inactive factor‐VII‐like material was detected in the plasma of one out of nine patients with factor‐VII deficiency and the Dubin‐Johnson syndrome (DJS), as well as in the plasma of patients on short‐term Coumadin therapy. No inactive factor VII could be detected in the plasma of patients on prolonged Coumadin therapy or in the plasma of two patients with hereditary factor‐VII deficiency. The methodological problems are discussed.