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Biomedical subjects

M Haas

Publications and source records attributed to M Haas.

At least 271 records · Page 15Linked to original sources
PubMed1986

Autocrine growth and progression of murine X-ray-induced T cell lymphomas.

Primary tumors of X-ray-induced murine T cell lymphomas comprise autocrine, growth factor-dependent cells. We have grown cell lines from primary X-ray-induced thymic lymphomas (PXTLs) under conditions which minimize the progression of the cells from factor dependence to factor independence. All (22) PXTL lines grown secrete a growth factor which supports their own growth and which we will call lymphoma growth factor LGF. LGF-dependent cells are non-tumorigenic or poorly tumorigenic, do not clone in soft agar, have no detectable rearrangements in the c-myc or Pim-1 region and possess near diploid or pseudodiploid karyotypes without evidence for trisomy of chromosomes nos. 15 or 17. PXTL-secreted LGF has no interleukin 1, 2, or 3 activity nor do LGF-secreting cells synthesize detectable IL-1, -2, or -3 mRNA. LGF contains no detectable interferon or GM-CSF activity in specific bioassays. Purified EGF, TGF beta, and interleukin preparations are inactive on LGF-dependent PXTL cells. Thus LGF appears to be a new growth factor that is required for the proliferation of non-progressed T lymphoma cells. Upon progression PXTL cells become growth factor independent, are highly tumorigenic in vivo, clone in soft agar, and assume a near triploid karyotype containing numerous chromosomal aberrations. Thus in X-ray-induced lymphomagenesis an autocrine, LGF-dependent phase precedes the progressed phase characterized by rearrangements in the myc and/or Pim-1 regions as well as by many chromosomal aberrations visible in the karyotype.

Animals↗
PubMed1986

Psychological vulnerability to alcoholism: studies in internal scanning deficit.

Three studies considered the predispositional role of impaired internal scanning in alcoholism. Scanning represents the person's sensitivity to internal stimulation and the extent to which the person utilizes internally generated information. The first study found that more acute alcoholic patients displayed poorer scanning than more chronic alcoholics. This finding contra-indicates deficit scanning as an effect of alcoholism and suggests that this impairment antecedes the alcoholic disorder. Two further studies tested the possible antecedent status of deficit scanning. Adolescent wards of the juvenile court, judged to be more at risk for alcoholism, were poorer scanners than their counterparts with fewer drinking-related problems. Male college students with a greater number of alcohol-related problems also proved to be poorer scanners. It is proposed that limited scanning contributes to alcoholic vulnerability by depriving the person of information vital to the control of drinking behaviour.

Adolescent↗
PubMed1986

Coinfection with viruses carrying the v-Ha-ras and v-myc oncogenes leads to growth factor independence by an indirect mechanism.

The concomitant expression of certain oncogenes can transform normal diploid rodent cells into transplantable tumorigenic cells. The mechanism by which these oncogenes collaborate is unclear. Recent findings (M. Oshimura, T. M. Gilmer, and J. C. Barrett, Nature [London] 316:636-639, 1985) raise the possibility that karyotypic changes, including monosomy for chromosome 15, are required to induce tumorigenicity in Syrian hamster embryo cells transfected in vitro with v-Ha-ras and v-myc DNAs. We studied the effect of the oncogenes v-Ha-ras and v-myc, introduced by viral infection, on murine hematopoietic cells. The induction of growth factor independence by the two oncogenes was used as an in vitro correlate of tumorigenicity. After a period of reduced growth rate reminiscent of the growth rate of cells in crisis, the doubly infected cells became growth factor independent. These cells showed a great variability in their karyotypes.

Animals↗
PubMed1985

Oncogene expression in murine splenic T cells and in murine T-cell neoplasms.

The differential expression of a series of proto-oncogenes has been examined in a group of cultured murine T-cell lymphomas that were induced following virus inoculation into, or X irradiation of, C57BL/6 mice. Two classes of T lymphoma cell lines were studied: growth factor-dependent (autocrine) cells, and growth factor-independent T lymphoma cells. Cell lines that were established from X-irradiation-induced T lymphomas were growth factor dependent, whereas T lymphoma lines grown from virus-induced tumors were generally growth factor independent. Of 18 cellular proto-oncogenes studied, five (c-myc, c-myb, c-abl, c-rasHa, c-rasKi) were consistently expressed in all cell lines tested. Thirteen other proto-oncogenes (c-mos, c-sis, c-rel, c-yes, c-fes3, c-fes4, c-fos, c-fms, c-src, c-erbA, c-erbB, int-1, Pim-1) were not expressed in any of the T lymphoma cells tested. Concanavalin A-stimulated spleen cells, representative of replicating T cells, expressed c-myc, c-abl, and Pim-1, suggesting that the products of these proto-oncogenes are involved in T-cell proliferation. The results indicate no qualitative differences (albeit some quantitative differences) in proto-oncogene expression between the growth factor-dependent and growth factor-independent cells. This suggests that expression of the five proto-oncogenes is in itself not sufficient to induce the progression of the growth factor-dependent cells to their fully growth factor-independent counterparts. Changes in the regulation of one or more of the five active proto-oncogenes, i.e., from an inducible to a constitutive state, and/or additional changes in the expression of other cellular genes may be required to induce the transformation of neoplastic T cells from growth factor dependence to growth factor independence.

Animals↗
PubMed1985

p-Chloromercuribenzenesulfonic acid stimulation of chloride-dependent sodium and potassium transport in human red blood cells.

The organic mercurial p-chloromercuribenzensulfonic acid (PCMBS) reversibly increases fluxes of sodium and potassium across the human red blood cell membrane. We examined the effect of different monovalent anions on cation fluxes stimulated by PCMBS. A substantial portion of the fluxes of both cations was found to have a specific anion requirement for chloride or bromide, and was not observed when chloride was replaced by nitrate, acetate or methylsulfate. The chloride-dependent component of the cation fluxes was only observed when the cells were exposed to PCMBS concentrations of 0.5 mM or greater. Furosemide (1 mM) did not inhibit the PCMBS-stimulated cation fluxes. The observed anion specificity is directly associated with the transport process rather than PCMBS binding to the membrane. A portion of the potassium transport stimulated by PCMBS appears to involve K+-K+ exchange; however, Na+ + K+ cotransport is not stimulated by this sulfhydryl reagent.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1985

Effect of norepinephrine on swelling-induced potassium transport in duck red cells. Evidence against a volume-regulatory decrease under physiological conditions.

Duck red cells exhibit specific volume-sensitive ion transport processes that are inhibited by furosemide, but not by ouabain. Swelling cells in a hypotonic synthetic medium activates a chloride-dependent, but sodium-independent, potassium transport. Shrinking cells in a hypertonic synthetic medium stimulates an electrically neutral co-transport of [Na + K + 2 Cl] with an associated 1:1 K/K (or K/Rb) exchange. These shrinkage-induced modes can also be activated in both hypo- and hypertonic solutions by beta-adrenergic catecholamines (e.g., norepinephrine). Freshly drawn cells spontaneously shrink approximately 4-5% when removed from the influence of endogenous plasma catecholamines, either by incubation in a catecholamine-free, plasma-like synthetic medium, or in plasma to which a beta-receptor blocking dose of propranolol has been added. This spontaneous shrinkage resembles the response of hypotonically swollen cells in that it is due to a net loss of KCl with no change in cell sodium. Norepinephrine abolishes the net potassium transport seen in both fresh and hypotonically swollen cells. Moreover, cells swollen in diluted plasma, at physiological pH and extracellular potassium, show no net loss of KCl and water ("volume-regulatory decrease") unless propranolol is added. Examination of the individual cation fluxes in the presence of catecholamines demonstrates that activation of [Na + K + 2Cl] co-transport with its associated K/Rb exchange prevents, or overrides, swelling-induced [K + Cl] co-transport. These results, therefore, cast doubt on whether the swelling-induced [K + Cl] system can serve a volume-regulatory function under in vivo conditions.

Animals↗
PubMed1985

Envelope gene and long terminal repeat determine the different biological properties of Rauscher, Friend, and Moloney mink cell focus-inducing viruses.

The nucleotide sequence of the envelope (env) gene and the long terminal repeat (LTR) of an infectious clone of Rauscher mink cell focus-inducing (R-MCF) virus has been determined and compared with the published env gene and LTR sequences of Friend (F)- and Moloney (M)-MCF viruses. The sequence shows that R-MCF virus, like other MCF viruses, is a recombinant virus. Its env gene contains sequences which were acquired from an env gene in the mouse genome and which confer on the MCF virus its dualtropic host range. Unlike F-MCF and M-MCF viruses, R-MCF virus will not replicate in NIH 3T3 cells. The deduced amino acid sequence for the gp70 of R-MCF differs from that of F- and M-MCF viruses by 15 amino acids between residues 49 and 138 of gp70. These differences in amino acid sequences may be responsible for the inability of R-MCF virus to replicate in NIH 3T3 cells. The host range of two hybrid viruses constructed in vitro is consistent with this hypothesis. R-MCF virus and Friend murine leukemia virus (F-MLV) show 98% identity in their env gene 3' from the acquired env sequences. This contrasts with 82% identity between the env gene of R-MCF virus and M-MLV. The LTR of R-MCF shows 98% identity with the LTR of F-MCF as compared to 88% identity with the LTR of M-MCF. This striking similarity between the sequences of R-MCF, F-MCF, and F-MLV is surprising since the Rauscher virus and the Friend virus are thought to have originated independently. The high degree of similarity suggests that Rauscher and Friend viruses have a common origin. In contrast to M-MLV, which induces predominantly a lymphoid disease, R- and F-MCF viruses induce an erythroproliferative disease in NIH Swiss mice. A hybrid R-MCF virus with a genome derived primarily from R-MCF virus and a 3' end including the U3 region derived from M-MLV induces a lymphoid disease instead of an erythroid disease. This result indicates that it is the U3 region which determines the tissue specificity of the MCF virus-induced disease. It is suggested that the putative viral enhancers in the U3 region play two roles in the process of leukemogenesis: in the Friend and Rauscher disease, the viral enhancers act by increasing the transcription of the MCF env gene; in the thymic lymphoma, the enhancers activate mainly the expression of cellular genes.

Amino Acid Sequence↗
PubMed1985

Cytologic and histologic observations on the sex hormone dependence of the vulva.

The usefulness of vaginal cytology in the assessment of hormonal function is well accepted. Our study established that the epithelial horny cells exfoliated from the vulvar skin also exhibit morphologically visible signs of hormonal activity. Cytologic analysis of 429 vulvar smears from 174 women during 88 cycles and postmortem histologic examination of vulvar specimens from an additional 65 women showed parakeratotic keratinization to be significantly more frequent premenopausally than postmenopausally. A vulvar "parakeratotic index" was developed that fluctuates along with the well-known eosinophilic and karyopyknotic indices of the vagina and corresponds to the plasma estradiol concentrations during the cycle. Administration of estrogens in postmenopausal women initiates a striking increase in the index, which is otherwise quite low during that phase of life.

Adult↗
PubMed1984

Immunoreactive trypsin in the adult respiratory distress syndrome.

With the purpose of studying the role of proteinases in the development of ARDS, plasma levels of immunoreactive trypsin (IRT) and amylase were measured in 43 intensive care patients at risk of developing ARDS (22 polytrauma, seven abdominal surgery, four burns, two DIC and eight pancreatitis). Twenty four of these 43 patients developed ARDS and 31 presented abnormal IRT values (above 70 micrograms/L). Twenty-one of these 31 patients had ARDS; a significant correlation thus appeared between ARDS and abnormal IRT values. In nine patients, IRT values were higher than 800 micrograms/L and remained high for 3 to 4 days. A statistically significant correlation also appeared between abnormal IRT and septic phenomena: 20 patients with high IRT values presented septic problems. When IRT values were high, amylase values were often also abnormal: 12 of 23 patients with high IRT had abnormal amylase levels (the eight patients with documented pancreatitis were excluded); no other clinical signs or symptoms of pancreatitis were present in these patients. IRT could be one of the mediators of ARDS in septic patients. It is not clear that the pancreas is the origin of IRT in all cases.

Abdomen↗
PubMed1984

[Cytologic and histologic studies of hormone dependence of the skin of the external female genitalia].

The value of vaginal cytology for functional hormonal diagnosis is generally recognized. Largely unknown was that the cornified cells obtained from the skin of the vulva likewise show morphologically demonstrable signs of hormonal effects. The cytological analysis of 429 cytological smears of the vulva obtained from 174 women during 88 cycles and the histological analysis of excisions of the vulva obtained at 65 female autopsies showed that the parakeratotic type of cornification is significantly more frequent in the premenopause than in the postmenopause. During the menstrual cycle a parakeratosis index can be identified which is parallel to the well known eosinophilic and karyopyknotic indices of cytological smears from the vagina and corresponds as well to the cyclic levels of estradiol in the serum. Exogenous administration of estrogen during the menopause results in a drastic increase of the parakeratotic index which is normally low following the menopause. These observations show that not only the uncornified squamous epithelium of the vagina but also the cornified squamous epithelium of the vulva reacts to endogenous and exogenous hormonal stimulation although in a different pattern.

Age Factors↗
PubMed1984

Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells.

In a previous paper we described the induction by x-irradiation or radiation-induced leukemia virus-inoculation of two classes of lymphoid T-cell neoplasms: The first class, designated T-cell lymphoblastoma (TCLB), consists of growth-factor-dependent eudiploid cells that home to the spleen and give rise to splenic tumors on injection into syngeneic mice; the second class, designated T-cell lymphoma (TCL), consists of growth-factor-independent aneuploid or pseudodiploid cells that give rise to local tumors at the site of subcutaneous injection. This paper describes the generation of a family of growth-factor-independent aneuploid or pseudodiploid TCL cells after the injection into the thymus of growth-factor-dependent diploid TCLB cells. In contrast to the donor TCLB cells, the resulting TCL cells could be cloned in semisolid medium, produced local tumors at the site of subcutaneous injection, and proliferated in a growth-factor-independent fashion in vitro. The induced growth-factor-independent TCL cells were chromosomally and phenotypically unstable and continued to evolve both in vivo and in vitro. After propagation in the thymus, the cells often showed stable translocations in addition to the evolving aneuploidy. We propose that the chromosome abnormalities induced during the proliferation of growth-factor-dependent TCLB cells in the thymus constitute a general mechanism by which neoplastic cells progress from growth-factor dependency to independency.

Animals↗