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J L Cook

Publications and source records attributed to J L Cook.

At least 163 records · Page 9Linked to original sources
PubMed1982

DNA virus-transformed hamster cell--host effector cell interactions: level of resistance to cytolysis correlated with tumorigenicity.

Spontaneously cytolytic hamster spleen cells and BCG-activated hamster macrophages were used to examine susceptibilities to nonspecific effector cell-induced lysis among 13 DNA virus-transformed hamster cell lines exhibiting four different tumorigenic phenotypes. Hamster cells transformed by adenovirus type 12 (an oncogenic adenovirus serotype) or simian virus 40 (an oncogenic papovavirus) readily induced tumors in immunocompetent syngeneic hamsters and were relatively resistant to spleen-cell-induced lysis compared to cells transformed by adenovirus type 2 (a non-oncogenic adenovirus serotype) which induced tumors only in immunoincompetent hosts. Simian virus 40-transformed cells, which possess the unusual property of efficient tumor induction in allogeneic hosts, were uniquely resistant to lysis by activated macrophages. These differential patterns of susceptibility to cytolysis suggest an association between the level of transformed cell resistance to lysis by nonspecific host effector cells and the oncogenicity of the transforming virus. Furthermore, these data suggest that tumor-cell properties, other than those commonly associated with neoplastic transformation, determine the level of susceptibility or resistance to host effector cell mechanisms.

Adenoviridae↗
PubMed1982

Spectrum of tumorigenic phenotypes among adenovirus 2-, adenovirus 12-, and simian virus 40-transformed Syrian hamster cells defined by host cellular immune-tumor cell interactions.

The tumor-inducing capacities of adenovirus type 2-, adenovirus type 12-, and SV40-transformed LSH hamster embryo cell define a spectrum of four distinct tumorigenic phenotypes: type I, nononcogenic for newborn hamsters but oncogenic for nude mice; type II, oncogenic for newborn hamsters but nononcogenic in syngeneic adults; type III, oncogenic for both newborns and syngeneic adults; and type IV, almost equally oncogenic for syngeneic and allogeneic adult hamsters. Modulation of the cellular immune response of the recipient hamster by immunosuppression or by alloimmunization alters tumor susceptibility, suggesting that dynamic transformed cell-host cellular immune interactions determine the tumorigenic phenotype of a transformed cell line. There is no correlation between the immunogenicities of the transformed cell lines tested and their tumor-inducing capacities. However, a strong correlation exists between the ability of transformed hamster embryo cells expressing phenotype IV to produce tumors in allogeneic CB hamsters and their resistance to cytolysis in vitro by activated macrophages. These data suggest that, in addition to transformation, DNA viruses may convey specific tumorigenic phenotypes to the cells that they infect by inducing cellular traits that determine the inherent susceptibility or resistance of a cell to host cell-mediated immune destruction.

Adenoviridae↗
PubMed1981

Media-dependent subculture of nutritionally variant streptococci.

A case of infective endocarditis due to a strain of Streptococcus that demonstrated unusual nutritional requirements is reported. This strain was recognized as a nutritional variant because it could not be subcultured on certain routine primary plating and subculture media. The media-dependent recovery of this nutritionally variant Streptococcus is stressed, since media used routinely in some laboratories would result in this organism's being missed. Variability of routine media in supporting the growth of this isolate is also demonstrated.

Culture Media↗
PubMed1980

Resistance of simian virus 40-transformed hamster cells to the cytolytic effect of activated macrophages: a possible factor in species-specific viral oncogenicity.

Simian virus 40 (SV40)-transformed hamster cells were relatively resistant to the lytic effect of activated macrophages from animals with chronic intracellular infections. Conversely, SV40-transformed mouse and rat cells and adenovirus 2-transformed hamster cells were highly susceptible to destruction by tumoricidal activated macrophages. The pattern of resistance or susceptibility of SV40-transformed rodent cells was the same whether activated macrophage effectors were obtained from mice, random-bred hamsters, or the inbred LSH hamsters from which some of the SV40-transformed hamster lines were derived. The results suggest that resistance of transformed cells to macrophage-mediated cytolysis may explain in part the species-specific oncogenicity of this DNA virus.

Animals↗
PubMed1980

Presence of allograft-rejection resistance in simian virus 40-transformed hamster cells and its possible role in tumor development.

LSH Syrian hamster cells transformed in vitro by simian virus 40, which is oncogenic for hamsters, are resistant to rejection by adult allogeneic CB hamsters. In contrast, simian virus 40-transformed cells from other species are usually not oncogenic in immunocompetent autologous or isologous hosts. The ability of simian virus 40 to convey resistance to an allograft-type host response to transformed hamster cells may be important in determining the tumor-inducing capacity of these cells and could, in part, explain the species-specific oncogenicity of this virus.

Animals↗
PubMed1980

Injury of neoplastic cells by murine macrophages leads to inhibition of mitochondrial respiration.

Cytotoxic activated macrophages (CM) inhibited the growth of neoplastic L1210 cells in vitro but L1210 cell death was minimal to nonexistent. L1210 cells injured by CM were separated from macrophages and studied in an isolated system. CM-injured L1210 cells had an absolute requirement for glucose or another glycolyzable hexose (mannose or fructose) for at least 40 h after removal from macrophages. If the culture medium lacked sufficient concentration of one of these sugars, CM-injured L1210 cells died within 4 h. Uninjured L1210 cells cultured alone or with peptone-stimulated macrophages had no such requirement and maintained complete viability in hexoseless medium. The hexose requirement of CM-injured L1210 cells could not be fulfilled by other naturally occurring monosaccharides, glucose or mannose derivatives, or substrates that can be oxidized by mitochondria. The concentration requirements for glucose, mannose, and fructose by CM-injured L1210 cells correlated with the concentrations required to support maximal glycolysis of these sugars by other murine ascites cells. A concentration of 2-deoxy-D-glucose which completely inhibited L1210 cell glycolysis also complete prevented the ability of glucose or mannose to maintain viability of CM-injured L1210 cells. Interaction with CM led to inhibition of L1210 cell mitochondrial oxidative phosphorylation. This was supported by the findings that: (a) CM-injured L1210 cells had no Pasteur effect; their rate of aerobic glycolysis was the same as the rate of anaerobic glycolysis of uninjured L1210 cells, (b) Endogenous respiration of CM-injured L1210 cells was 15% of normal. Maximal inhibition of uninjured L1210 cell respiration by a specific mitochondrial poison (oligomycin) was nearly the same (13% of normal). It followed that CM-injured L1210 cells required hexose for chemical energy production via the glycolytic pathway. CM-induced mitochondrial injury occurred in five other neoplastic cell lines tested.

Animals↗
PubMed1979

Time-dependent kinetics. V: Time course of drug levels during enzyme induction (one-compartment model).

Equations were derived to describe the time course of drug levels during auto- and heteroinduction under a variety of input conditions. These equations were based on a pharmacokinetic theory of induction which assumes that metabolic clearance increases exponentially to a maximum value and that the rate of this increase is governed by the degradation rate constant of the induced enzyme (k'). Closed form solutions could be obtained only for intravenous single-dose (case I) and multiple-dose (case IV) administration. For each of the other cases, constant-rate intravenous infusion (case III), oral single-dose administration (case II), and multiple-dose administration (case V), an exact solution (not closed form) and an approximation (closed form) were derived. Two sets of equations were derived for each of the five cases to take into consideration the possibility of a latency term (lambda). Plots of drug amount X (or concentration C) vs. time (t) were constructed. In case I, a log X vs. t plot was convex, the slope increasing with time. In case II, X increased, reached a peak, and decayed as in case I. In case III (lambda greater than 5 ln 2V/Q) C reached a preinduction steady state before decreasing to a lower (induced) steady state. The behavior of C vs. t for cases IV and V was similar to that for case III. Determination of parameters was attempted in case III. Nonlinear least-square fitting of generated data with 3-9% error yielded reasonable estimates of k'.

Enzyme Induction↗
PubMed1979

Association of tumor induction by ultraviolet light-inactivated adenovirus 2-simian virus 40 recombinants with a specific segment of simian virus 40 DNA.

The nondefective (ND) adenovirus 2 (Ad2)-simian virus 40 (SV40) hybrid Ad2+ND4, which contains the segment of the SV40 genome between map positions 0.11 and 0.59, induced tumors in Syrian golden hamsters after inactivation by UV light. Ad2 and the Ad2+ND2 hybrid, which contains the segment of the SV40 genome between map positions 0.11 and 0.43, were not oncogenic after inactivation by UV light. These results showed that the incorporation of a specific segment of SV40 DNA into the Ad2 genome can alter the pathogenesis of the Ad2+ND4 virus by rendering it oncogenic for hamsters.

Adenoviridae↗
PubMed1979

Age-related and thymus-dependent rejection of adenovirus 2-transformed cell tumors in the Syrian hamster.

Adenovirus type 2-transformed hamster cell-induced newborn tumor lines were usually rejected when transplanted s.c. into 21-day-old syngeneic, weanling hamsters. The tumor-inducing capacity of two of these lines (Ad2HTL3 and Ad2HTL6) was tested in intact and neonatally thymectomized hosts. After s.c. injection of suspensions prepared from these lines, none of the weaning hamsters developed tumors while 100% of the newborns and 35.2% of neonatally thymectomized, weanling hamsters developed progressively enlarging neoplasms. The susceptibility of neonatally thymectomized hamsters to tumor challenge was directly related to the degree of immunosuppression observed following thymectomy as indicated by the amplitude of the in vitro response of blood leukocytes to concanavalin A. Pretreatment of thymectomized weanlings with syngeneic adult lymphoid cells (i.p.) resulted in a significant reduction in tumor susceptibility (p = 0.03). These findings suggest that acquisition of resistance to adenovirus type 2-transformed cells during the first 21 days of life may be a thymus-dependent cellular immune process.

Adenoviridae↗
PubMed1979

Rejection of adenovirus 2-transformed cell tumors and immune responsiveness in Syrian hamsters.

Transplantation of adenovirus type 2-transformed cell-induced newborn tumor lines to different aged hamsters revealed that the cell-mediated host defenses responsible for tumor graft rejection matured early in the second week of life. When light microscopic examinations were performed during the course of tumor development, the primary histopathological difference between progressing tumors removed from newborn or thymectomized weanling hamsters and regressing lesions from normal weanlings was the lack of an early, mononuclear cell infiltrate in neoplasms from newborn and thymectomized hosts. These results suggest that the maturation of cellular immunity determines resistance to tumor transplantation in this system. This conclusion was supported by the in vitro detection of concanavalin A-responsive lymphocytes in spleens from tumor-resistant suckling but not tumor-susceptible neonatal hamsters. Although the incomplete seeding of thymus-dependent lymphocytes to the peripheral lymphoid tissues of newborn hamsters may partially explain the deficient concanavalin A responses of neonatal spleen cells, there appears to be an additional requirement for a radioresistant, adherent accessory cell population. These findings suggest that the development of a cell-mediated immune response is necessary for the rejection of adenovirus type 2-transformed cells and transformed cell-induced tumors and that this response requires the interaction of T-cells and accessory cell populations.

Adenoviridae↗
PubMed1977

Staphylococcus aureus and the microbial ecology of atopic dermatitis.

Two surveys were conducted to ascertain the effect which Staphylococcus aureus has on resident flora and on skin of patients with eczema. Forty paired sites, normal and lesions, were sampled from 32 patients with chronic lichenified atopic dermatitis, and 162 sites covering the entire body of a patient with an acute flare of chronic atopic dermatitis were examined. In the first study, 34 lesions (85%) carried S. aureus, and 85% of these positive samples supported greater than 10(4) colony-forming units (CFU) of total aerobic bacteria/cm2. About 55% of normal sites carried S. aureus with 18% of such samples supporting greater than 10(4) CFU/cm2 total aerobic bacteria. Normal sites carried fewer but more diverse flora than lesions. The composition of flora on lesion sites was mainly S. aureus or S. epidermidis biotype 1, or both. At densities greater than 10(7) CFU/cm2, S. aureus constituted almost 100% of the total aerobic bacterial flora. The total body survey of the single eczema patient yielded similar results. Evidence supports the hypotheses that (1) S. aureus is able to exploit the environment of eczematous lesions and to influence the composition of cohabiting aerobic skin bacteria, and (2) its inhabitation of normal appearing sites is transitory.

Adolescent↗
PubMed1975

The 5'-termini of bacterial RNA. I. The monophosphorylated termini.

A two-dimensional fingerprint technique is described which separated oligonucleotides by length and number of phosphates present at the termini. The diversity of terminal nucleotide sequences was found to be quite restricted in bacterial 4-5 S RNA: in the strain used here the predominant dinucleotide species was pG-C, and the only trinucleotides produced were pG-G-Up and pG-G-Cp. Examination of total pulse-labeled RNA revealed the same restricted set of terminal trinucleotides.

Animals↗