[3 opinions on psychiatric treatment methods].
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Adolescent↗
Biomedical subjects
W Ryd
Publications and source records attributed to W Ryd.
MCG101-AA, a new ascites tumour in C57 mice. 4. Influence of enzyme treatment on transplantability and some in vitro characteristics.
The transplantabilities of trypsin and neuraminidase-treated 101-AA cells were compared with untreated cells. The cell doses required for growth were similar for enzyme-treated and control cells. Yet, trypsinized cells injected i.v. gave rise to less lung tumours and, in one experiment, they produced more extrapulmonary tumours than control cells or neuraminidase-treated cells. These findings were collated with some data on the effect of enzyme treatment on the tumour cell membranes, obtained by particle size analysis, cell electrophoresis, lectin agglutinability and sialic acid determinations. The importance of cell surface characteristics for specific metastasis patterns, in this case a peculiar "myotrophism", is discussed.
Animals↗
Alteration of metastases distribution by vaso-dilating drugs.
The effects of the two vasodilating substances, dihydralazine and the adrenergic alpha-receptor blocker phenoxybenzamine, were studied on the distribution and growth of MCG-L-SS metastases from intravenously injected tumour cells. Dihydralazine increased the total number of metastases in the body and both drugs increased the number in the lungs and the liver. Both drugs also increased the total metastasis volume in the liver. The effects might be secondary to the haemodynamic effects of the drugs, e.g. a changed distribution of the blood flow, more open capillaries and/or a changed hydrostatic capillary pressure.
Animals↗
Effects of EACA, AMCHA and guanethidine on metastases induced by intravenously injected tumour cells.
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Aminocaproates↗
Purity and transplantation properties of tumor cell suspensions.
Cell debris is inevitably produced by the mechanical and enzymatic procedures used to dissociate solid tumors. We investigated the influence of such debris on the i.v. and s.c. transplantability of B16 melanoma cells. Cell suspensions were centrifuged on a Percoll cushion to remove the debris, and the purified preparations were compared to untreated control suspensions. The i.v. injection of a massive dose (10(6) cells) of unpurified cells killed the animals within a few minutes, while the same amount of purified cells left the animals unaffected. When 5 X 10(5) cells were given, animals receiving purified cell suspensions had more extrapulmonary tumors at their time of death than those given unpurified cells. However, with a lower cell dose, 2 X 10(4) cells, there were no such differences in tumor incidence or distribution.
Animals↗
Radio-and chemotoxicity in mice during hypothermia.
BACKGROUND: The influence of hypothermia induced by chlorpromazine (10-15 mg/kg given intra-peritoneally) on the survival from radiation and chemotherapy exposure in C57B1-mice, with or without tumour inoculation, was studied. MATERIALS AND METHODS: The mice were exposed to either whole body irradiation (8 Gy), or doxorubicin (15 or 17.5 mg/kg i.p.), or cisplatin (20 mg/kg i. p.) and followed to ensuing death. The control mice maintained a rectal temperature of 38 degres C while those receiving chlorpromazine developed moderate hypothermia of 28 degrees C or 36 degrees C, dependent on the ambient temperature. RESULTS: Hypothermia of 28 degrees C protected the mice from radiation-induced death and acute doxorubicin toxicity, with males gaining more protection than females. The effects appeared dependent on temperature, not on chlorpromazine. Hypothermia protected the mice from acute cisplatin toxicity and increased the anti-tumour effects in both genders. Chlorpromazine itself did not cause toxicity, neither did it change the natural course of tumour progression. CONCLUSION: Hypothermia of 28 degrees C induced by chlorpromazine profoundly reduces radiation, doxorubicin-and cisplatin-induced toxicity in mice with males benefiting more than females. The hypothermia itself, not the chlorpromazine, was responsible for these effects. The anti-neoplastic activity was not compromised; rather, it was enhanced, particularly for cisplatin.
Animals↗
Cytologic diagnosis of bancroftian filariasis in a nonendemic area.
Parasitic infections are common in the developing countries, but the cytologic diagnosis of such infections is infrequent or rare. This paper presents four cases of filariasis caused by Wuchereria bancrofti diagnosed by cytologic examination and discusses some unusual observations. The finding of microfilariae in pleural fluid in the absence of the classic symptoms and signs of tropical pulmonary eosinophilia is highlighted. In two patients, nocturnal microfilaremia could not be demonstrated despite Nuclepore filtration, thus suggesting the possible merits of cytology in the primary diagnosis of a filarial infection. Even the diethylcarbamazine provocative test failed to elicit a peripheral microfilaremia in one patient, further emphasizing the importance of cytology as a diagnostic method in amicrofilaremic infections. Attention is drawn to the need for a high index of suspicion on the part of the cytologist in the identification of parasitic organisms in material from high-risk groups to achieve an early diagnosis of such infections and the prompt institution of appropriate chemotherapy. This may obviate the more serious pathologic changes of advanced disease, especially the disfigurement of chronic and late filariasis.
Adult↗
Chlorpromazine-induced hypothermia: effect on tumour progression and survival in mice.
The effect of chlorpromazine on tumour progression and survival, when used as a modifier of chemotherapy response and toxicity, was studied in mice. The dosage was 15 mg/kg i.p., tested to produce rectal hypothermia within 1 hour, lasting for at least 8 hours, at an ambient temperature of 28 degrees C. The drug or saline was given to inbred C57Bl/6J mice four days previously inoculated i.v. with MCG101-AA sarcoma cells. Little acute toxicity, except for the intended hypothermia, was observed. No influence on survival could be discerned, nor any influence upon distribution of tumour deposits. In this tumour model system, chlorpromazine can be used as a chemotherapy response modifier without significant effects per se.
Animals↗
Characterisation of a human endometrial adenocarcinoma established in vivo and in vitro.
A moderately differentiated human endometrial adenocarcinoma was heterotransplanted into nude mice and later established as a continuous in vitro cell line. Western blot analysis showed an accumulation of p53 protein in the cell line compared to the original tumour and heterotransplants. Sequential analysis of the p53 gene revealed point mutations in codons 175 and 248 in the cell line while no mutations were found prior to in vitro establishment. Immunohistochemistry confirmed the epithelial origin of the heterotransplants and of retransplants of the cell line. The intraperitoneal retransplants remained moderately differentiated, whereas subcutaneous retransplants became less differentiated. Heterotransplants were estrogen receptor (ER) positive and progesterone receptor (PgR) negative, indicating preservation of normal steroid receptor status. The ER could not be detected in the in vitro cell line using an enzyme immunoassay, but was detected with Western blot using a polyclonal antibody toward the carboxy terminus. After estradiol treatment, the in vitro cell line became weakly positive for the PgR, suggesting the ER mechanism was at least partly intact. Tumour growth in vivo was independent of endogenous estrogen but was inhibited when the tumour-bearing animals were treated with estradiol. Analysis of cell growth kinetics by flow cytometry (FCM) after bromodeoxyuridine (BrdU)-labelling revealed no difference in S-phase fraction (SPF) or labelling index (LI) between the treated and control groups. Cell loss (CL) was significantly increased from 42% to 89%, resulting in increased tumour volume doubling time (TVDT). Under in vitro conditions estradiol treatment resulted in an increase in cell doubling time and this growth retardation was accompanied by a significant decrease in SPF and LI. The estrogen responsive (inhibited) phenotype was thus preserved in the in vitro cell line but was probably mediated through another mechanism. This cell line thus appears to represent the development of a more malignant clone with divergent receptor function and growth behaviour, and provides us with an interesting new tool for the study of tumorigenesis in the human endometrium.
Adenocarcinoma↗
Estradiol induces DNA fragmentation in a human endometrial adenocarcinoma with estradiol-inhibited growth phenotype.
A moderately differentiated human endometrial adenocarcinoma heterotransplanted into nude mice was investigated for morphological and molecular changes in the tumours after treating the animals with estradiol. The tumour growth was previously characterised as estradiol-independent but responsive (inhibited) without any changes in cell proliferation. In response to hormonal treatment rather the cell loss factor increased. In this experiment tumours influenced by estradiol were investigated at different time-points after treatment by an in situ labelling technique to detect cells undergoing DNA fragmentation as a sign of apoptosis. Expression of the apoptosis related protein bcl-2 was evaluated by Western blotting. Tumours from animals treated with estradiol showed an increase in tumour volume doubling time from 5.4 days to 16 days compared to control tumours. Histologically, tumours influenced by estradiol were better differentiated than control tumours and showed a significant increase in cells staining positively with the in situ apoptosis detection technique. A parallel time dependent decreased expression of bcl-2 protein was observed. These results confirm our previous findings where estradiol influenced the cell loss factor without changes in the growth fraction, indicating increased apoptotic activity in response to hormonal treatment.
Adenocarcinoma↗