Biomedical subjects
Publications and source records attributed to K Nelson.
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The plasma level of free fatty acids (FFA) in adrenalectomized rats increases by 50% after treatment with aldosterone (2 microng/100 g rat). Lipolytic activity in peripheral fat tissue is lowered after adrenalectomy and doubles after in vivo administration of aldosterone to adrenalectomized rats (measured as free fatty acid release in vitro from epididymal fat tissue). Lypolysis of adipose tissue stimulated by the in vitro presence of ACTH also increases after in vivo administration of aldosterone. Incorporation of intravenously administered label from U-14C-palmitate into total extractable lipid of renal tissue is augmented 3 h after aldosterone administration to adrenalectomized rats, while no increase of the radioactivity is observed in total lipid from liver tissue. Treatment with aldosterone does not affect the total lipid content of kidney or liver in adrenalectomized rats. The oxygen consumption rate of kidney cortex slices with lactate, beta-hydroxybuterate or acetoacetate as substrates is lowered after in vivo administration of aldosterone to adrenalectomized rats. With slccinate, however, the respiratory rate of kidney slices increases after aldosterone treatment of adrenalectomized rats, the ouabain-sensitive respiration being more affected than the ouabain-insensitive respiration. An interpretation of the O2 consumption data implicating competition of lipid metabolism for CoA-SH is discussed.
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Antisera taken 1 or 2 days after inoculation of BALB/c mice with transplantable sarcoma cells or Moloney sarcoma virus (MSV) induce tumor-specific cell-dependent cytotoxicity in vitro. In the present experiments, lethally irradiated ("immunosuppressed") mice were tested for the early appearance of the serum factor responsible for this anti-serum-dependent cell-mediated cytotoxicity (E-ADC). BALB/c mice were infected with MSV, syngeneic sarcoma cells or sheep red blood cells 24 h following irradiation with 900 R. Sera were obtained from MSV and tumor cell recipients 48 or 72 h later and tested for E-ADC activity. Spleen cells from SRBC recipients were tested at day 4 or 5 for ability to form direct plaques in a modified Jerne plague assay. Although the anti-SRBC response was obliterated in the irradiated mice, the E-ADC response appeared to be unimpaired. These studies indicate that newly synthesized immunoglobulin is not required for the formation of the E-ADC factor.
Mitochondria of rat kidney red medulla form a single band (rho = 1.163) on a sucrose gradient, while mitochondria of the cortex form bands in 2 density regions, namely ca. 66% (M1) at rho = 1.173 and ca. 33% (M2) at rho = 1.163. The mitochondria of the red medulla contain more cytochrome a, more cytochrome b, and less cytochrome c, compared to the M1 population which predominates in cortex. Mitochondria from the red medulla show higher rates of Pi incorporation into total organically bound phosphorus in the presence of ADP, Pi, and oxidizable substrate than do mitochondria from cortex. However, in absence of added oxidizable substrate the reverse is observed, indicating that isolated cortex mitochondria contain more endogenous substrate. The superiority of the red medulla organelles in phosphorylation in the presence of substrate persists in preparations made according to LOWENSTEINS [3] procedure (shortened isolation time, removal of lysosomal enzymes by digitonin treatment). This shows that the observed differences are not artifacts due to different degrees of damage to the organelles by lysosomal attack.
Murine spleen cells mediate antibody-dependent cellular cytotoxicity (ADC) both to erythrocyte targets in a 51Cr release assay and to syngeneic tumor targets in a microcytotoxicity assay. The effector cells active in the two ADC assays can be separated by passage of the spleen cells through columns of Sephadex G-10 at 37 degrees C. Cells mediating ADC to sarcoma cells did not adhere to the G-10 and were recovered in the column effluent. These nonadherent cells were not cytotoxic to antibody-coated chicken red blood cells. Spleen cells which mediated ADC in a 51Cr release assay to the red cell targets adhered to G-10. Adherent effector cells could subsequently be recovered from the columns by elution with 5 X 10(-4) M EDTA.
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Spleen cells from BALB/c mice bearing syngeneic sarcomas and from BALB/c mice whose sarcomas had been excised were cultivated in vitro. The culture supernatants were tested for two activities: their ability (1) to supress ("block") specific lymph-node cell-mediated cytotoxic reactions directed against the respective neoplasms; and (2) to induce antibody-dependent cellular cytotoxicity (ADC) specific for the antigens of the respective tumors. Both specific activities, blocking and induction of ADC, were detected in culture supernatants from spleens of tumor-bearing mice, even when repeatedly harvested at intervals over a 7-day period. Supernatants of cultured spleen cells from mice whose sarcomas had been excised 3-4 weeks previously also had ADC but no blocking activity. Supernatnats of cultures treated with inhibitors of protein synthesis lacked both blocking and ADC activities; the inhibitory effect of cycloheximide on these activities, as well as on protein synthesis, was reversible. Factors in the culture supernatants responsible for blocking and for ADC were labelled when the culture were incubated with 14C-leucine. The labelled material was retained by, and could be eluted from, immunoadsorbents for mouse immunoglobulins. In addition, the labelled material bound preferentially to those tumor cells for which specific blocking or ADC activities were observed. The findings indicate that factors responsible for the blocking and ADC phenomena were indeed synthesized by the spleen cells in vitro.
The obstetric events leading to the birth of infants who developed respiratory distress syndrome (RDS) were evaluated. In a retrospective study of 100 consecutive cases it was determined that untimely or unwarranted physician intervention in the pregnancy was responsible for 15 per cent of cases and possibly responsible for another 18 per cent. Recommendations for prevention of "iatrogenic" RDS are made.
Spleen cells from BALB/c mice bearing syngeneic, methylcholanthrene-induced sarcomas were cultured in vitro. In agreement with previous observations, two tumor-specific activities could be demonstrated in the culture supernatants: the supernatants suppressed (blocked) specific lymph-node cell-mediated cytotoxicity directed against the respective neoplasm and they induced specific antibody-dependent-cellular cytotoxicity (ADC) mediated by lymph-node cells from non-immune mice. In the present study, the effects of specific depletion or enrichment of different celltypes on the ability to synthesize the blocking and ADC activities was explored. Spleen cells passed through columns of Sephadex G-10, which removed plasma cells and macrophages, no longer synthesized factors with ADC activity though synthesis of blocking factors continued. However, lysis of Thy-1-positive cells with antiserum and complement did abolish the synthesis of blocking factors. Spleen cells from tumor-bearing mice were then enriched for Thy-1-positive cells by selective removal of macrophages and plasma cells on G-10 columns and of immunoglobulin-bearing cells on anti-mouse immunoglobulin affinity columns. This T-cell-enriched population synthesized blocking factors and restored blocking factor synthesis in cultures depleted of Thy-1-positive cells. Simiarly enriched spleen cells from normal control mice did not synthesize tumor-specific blocking factors but partially restored synthesis of blocking factor in tumor-bearer spleen cultures depleted of Thy-1-positive cells.
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Sera from tumor-bearing mice induce specific cytotoxicity to tumor cells by non-immune lymphoid cells (antiserum-dependent cytotoxicity or ADC). When spleen cells from BALB/c mice bearing autochthonous or syngeneic sarcomas were cultured in vitro, culture supernatants were obtained which specifically sensitized sarcoma cells to injury in vitro by normal lymph-node cells (LNC). Culture supernatants of spleen cells from mice whose transplanted sarcomas had been excised also induced ADC. The ADC activity resided in the mouse immunoglobulin fraction of the culture supernatants and its synthesis did not depend on the presence of theta-positive cells. Following a brief in vivo exposure to culture supernatant with known ADC activity, LNC from non-immune mice specifically destroyed tumor cells in an in vitro assay.
As previously shown, sera from tumor-bearing mice can induce specific antiserum-dependent lymphoid cell-mediated cytotoxicity (ADC) to syngeneic tumor cells in vitro. The ADC activity in such sera is now shown to be removed by adsorption of the sera to Sepharose-linked rabbit anti-mouse immunoglobulin or to goat anti-mouse IgG2. Immunoglobulins recovered by elution from the affinity columns mediated ADC to the specific tumor cells. In addition, the eluted immunoglobulin passively "armed" normal lymph-node cells in vivo so they were specifically cytotoxic when tested in vitro. Sera taken 48 h after inoculation of tumor or syngeneic tumor cells (before the appearance of palpable tumor) were also shown previously to induce lymphoid cell-mediated cytotoxicity in vitro. This cytotoxic activity was not removed by adsorption of the sera to either anti-IgG or anti-IgM-linked Sepharose. Thus both IgG and an early-appearing serum component which is apparently neither IgG nor IgM can induce specific cell-mediated cytotoxicity by non-immune lymphoid cells in vitro.
Spleen cells from BALB/c mice which either bore syngeneic sarcomas or were normal controls were cultured in vitro. The culture supernatants of spleen cells from tumor-bearing mice inhibited (blocked) specific cell-mediated cytotoxicity to the tumor borne by the spleen donor. They also mediated specific antiserum-dependent cytotoxicity with control lymphoid cells. The appearance of blocking activity in culture supernatants was prevented by lysis of theta-positive spleen cells with antiserum and complement. The blocking activity was removed by passing culture supernatants through an anti-mouse immunoglobulin affinity column and was recovered in a 3 M NaSCN eluate of the column.
Between Jan 15 and March 15, 1971, forty-eight grade-school patients living in western Chicago were hospitalized with an encephalopathic illness. Fourteen of these children had illnesses compatible with Reye syndrome (encephalpathy with liver impairment). Most of the children showed evidence of central nervous system (CNS) dysfunction within ten days after onset of a febrile upper respiratory tract illness. Seizures developed in 11 of the 48 patients (including 4 of the 14 with Reye syndrome). Eight of the encephalopathic patients, including 6 of the 14 with Reye syndrome, died. Two children without Reye syndrome had abnormalities of liver enzymes coincident with cerebrospinal fluid pleocytosis. Sixteen of the 24 patients tested had titer rises in serum against influenza type B only; influenza type B was isolated from throat cultures of 2 patients. This, the seventh report of CNS complications (Reye syndrome) associated with influenza type B, suggests that surveillance for neurologic sequelae should become part of the epidemiologic evaluation of influenza epidemics.
A case of contact dermatitis from neutral red dye applied for treatment of herpes genitalis is presented. A review of the literature revealed 5 other patients with a similar reaction. We suggest that neutral red dye treatment for herpes should be used with caution in patients with an allergic history.