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PubMed1986

Toxicity of anguidine in mice.

A characteristic of the trichothecene mycotoxin, anguidine, is its extreme toxicity to organs with populations of rapidly dividing cells. In preparation for evaluation of compounds that may protect against anguidine toxicity, we measured the LD50 of anguidine administered by gastric gavage (ig) or intraperitoneal injection (ip) and studied the dose- and time-dependent effects of anguidine on lymphohematopoietic organs, intestine, and testis, and measured hematocrit and peripheral blood leukocyte counts in male CD-1 mice. The ig LD50 at 96 hr was 15.5 mg/kg; after ip administration the LD50 at 96 hr was 20.0 mg/kg. Characteristic changes caused by sublethal doses of anguidine were cell depletion and necrosis in lymphohematopoietic organs, multifocal necrosis of intestinal epithelium, and diffuse necrosis of germinal epithelium followed by progressive tubule degeneration in the testes. There was leukocytosis due to both lymphocytosis and neutrophilia in the first few hours following anguidine exposure, followed by lymphopenia, neutropenia, and anemia by 3 days. After lethal doses, the intestinal necrosis was transmural, and there was extensive necrosis of lymphohematopoietic organs. There was rapid recovery after sublethal anguidine exposure of all anguidine-sensitive organs except for testis where decreased weights and abnormal spermatogenesis persisted for the 2-week observation period. Our results suggest that intestinal necrosis is an important cause of death following anguidine exposure. Atrophy of seminiferous tubules may have some value as an indicator of prior anguidine exposure, but the testicular changes are not unique to this compound.

Animals↗
PubMed1975

Quantitative assessment of the electroencephalogram in renal disease.

EEGs wre recorded from renal patients to determine if there are quantifiable characteristic changes in the EEG was quantified by calculating the percentage of spectral power in the bandwidth 3-7 c/sec referrred to a frequency range of 3-13 c/sec and by computing the mean frequency of the dominant rhythm in the EEG. Blood urea nitrogen and creatinine concentrations, as well as a self-assessment of the patient's clinical condition, were recorded. The general finding of this research is that EEG slowing, as evaluated by power spectral techniques, is correlated with uremia-associated variables. 1. In a non-dialyzed patient population with renal failure, slowing in the EEG was found to be directly corelated with increased creatinine concentrations. 2. Quantitative measures of slow wave activity computed using power spectral techniques were found to be highly corelated with an estimate of slowing made by an electroencephalographer. 3. Compared with undialyzed azotemic patients, malignant hypertensive patients with comparable serum creatinine concentrations typically displayed increased slow wave activity, while slowing was generally reduced in the dialyzed patient population. 4. A series of EEGs recorded from one patient during the first three dialyses of her life revealed that slow wave activity decreased during each successive dialysis. In another patient, all quantified EEG values recorded prior to renal transplantation significantly improved after transplantation...

Adolescent↗
PubMed1989

[Interpretation of mechanograms of the quadriceps femoris muscle twitch from technical, methodologic and physiologic aspects].

It is proved, that the physiological interpretation of the peaks in the quadriceps femoris muscle twitch mechanogramme is possible. The measuring chain (sensor-amplifier-magnetic data recorder-plotter) has a resonance frequency of 170 Hz and is suitable for the true representation of the tension-time-course. In order to compare the tensions with one another, it is necessary to standardize the tensions on the lower leg or body mass. Considering the fact that the twitch mechanogramme is a summation of the contractions of the fast twitch fiber (FTF) and slow twitch fiber population (STF), it has been assumed that both FTF and STF show contraction peaks. Essential methodological influences on the tension-time-course result from the relationship between tension sensor and biological system (lower leg mass). The measuring chain and lower leg mass represent a feather-mass system. The provoked oscillations of the lower leg mass may produce methodological peaks in the twitch mechanogramme. In general, the mechanogramme shows contractions superimposed by mechanical processes. The tonogramme shows that the tension-time-course of the twitch is characterized by several peaks too. In the tonogramme characteristic changes depending on the portion of the quadriceps femoris muscle (rectus femoris, vastus lateralis) can be seen. Following the muscle action potential (MAP) there are frequently reflex-MAP's variable in form and amplitude in the time range between 120-180 ms after the stimulus impulse. They allow to explain the peaks in the mechanogramme with contraction times (CT) of 140-160 ms, or they provoke an extension of the relaxation times. Some reflex-MAP may have a latency of only 80 ms. The analysis of the methodological components influencing the mechanogramme of the muscle twitch shows that the interpretation as FT- or ST-peaks has to be done from the point of view of physiology. The following results indirectly speak for the interpretation as FT- or ST-peaks (CT: 30-50 ms and 75 to 95 ms, respectively). There are the corresponding average CT for groups with clearly different lower leg mass, the relatively higher increase of the peaks with CT between 60-70 ms after a maximal voluntary contraction (MVC) of 10 seconds, the higher average tensions for the ST-peaks by long distance runners and the results for the CT when the lower leg mass is artificially elevated. Furthermore the mechanogrammes of the long distance runners show that the maximum may come to a CT of 100-130 ms.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

ABO, MN, Kell, Hp and Gm1 markers in elderly humans.

The prevalence of the markers of blood groups ABO, MN, Kell, Hp, Gm1 was determined in 723 persons belonging to three age groups: from 61 to 91 years, and was compared with a similar study in a population of adults aged 20 to 60 years. It was found that with respect to MN markers the proportion of NN homozygotes was significantly increased, mainly in females aged 71-80 years. In the haptoglobin system a considerable increase was noted in the prevalence of Hp 1-1 phenotype and the appearance of ahaptoglobinaemia. Increased prevalence of the Gm1 marker was observed only in females aged 71-80 years. On the other hand, no significant differences were noted in the frequency of the phenotypes of the ABO and Kell blood groups. These preliminary results confirm the stability of the serological polymorphism in the ABO and Kell blood groups, and in the remaining blood groups studied a natural selection may be supposed to exist. Characteristic changes in the distribution of the frequency of the determined genetic markers encourage the continuation of such studies.

ABO Blood-Group System↗
PubMed1976

Effects of progesterone, prostaglandin F2alpha and its analogue ICI 81008 on the excitability and threshold of the uterus.

Forty-eight uterine strips were excised from 24 New Zealand white rabbits and studied in vitro. Sixteen strips were examined when eight animals were 25 days pregnant, 24 strips when 12 animals were about 12 hours postpartum, and eight strips about 12 hours after four animals received a single dose of 5 mg. progesterone (P) at spontaneous delivery. When after repeated exposures to electric fields (60 cycles per second, alternating current, of optimum strength, four seconds' duration at intervals of 30 seconds) the approximately 0.5 Gm. strips developed approximately 40-50g wall tension (WT) in steady state, the field strength was reduced in graded steps from 12 v per 5 cm. to 10, 8, 6, 4 and 3 v per 5 cm. and WT recorded. By measuring the effect on WT of "decreasing electric field stimulation" (DEFS), myometrical excitably and threshold were characterized and quantitated. The technique is based on the relationship between the fraction of myometrial cells activated in the total cell population and WT. As the stimulus is decreased in graded steps from optimal to increasingly suboptimal, DEFS activates fewer and fewer cells reflected by the decrease in WT. Threshold is defined by the strength of the minimum electric field which provokes WT and subthreshold by the field strength which fails to excite. Thus fractional WT averages the excitability of cells in the tissue and thus DEFS characterizes this important parameter of uterine function and quantitates threshold under a variety of regulatory conditions. The comparative study of excised uteri in three different endocrine states showed that the regulatory conditions of normal pregnancy (P levels 9 ng. per milliliter) suppressed excitability and increased threshold (to 6 v per 5 cm.). Post partum (P levels 1 ng. per milliliter) excitability increased and threshold decreased (to 4 v per 5 cm.), unless P treatment prevented this characteristic change by suppressing excitability and increasing threshold (to 6 v per 5 cm.). Both regulatory agents, prostaglandin F2alpha (PGF2alpha) and its analogue ICI 81008, increased excitability and decreased threshold significantly in picogram per milliliter concentrations. However, this effect was observed only when the P levels were low. These compounds had little effect, even in manogram per milliliter concentrations, when the P levels were high. The studies also revealed a close relationship between threshold and spontaneous uterine activity. Low threshold promoted while high threshold suppressed spontaneous activity. In similar concentrations the oxytocic actions of PGF2alpha and ICI 81008 were similar but the effect of ICI 81008 was prolonged through strong binding at myometrical sites.

Animals↗
PubMed1991

Natural killer (NK) cells in HTLV-I-associated myelopathy/tropical spastic paraparesis-decrease in NK cell subset populations and activity in HTLV-I seropositive individuals.

We examined natural killer (NK) cell activity and NK cell subset populations in 18 patients with HTLV-I associated myelopathy (HAM)/tropical spastic paraparesis (TSP), ten HTLV-I seropositive asymptomatic carriers and 20 seronegative healthy controls. The NK cell activity was significantly decreased in HAM/TSP, compared with that in controls. The percentages of NK cell subsets, such as CD16+, CD11b+, CD56+, CD16+ CD56-, CD16-CD56+, CD16+CD8-, or CD16+CD3+ cells were significantly decreased in HAM/TSP patients. Of particular interest is that the percentage of CD16+CD3+ cells, which have a wide spectrum of cytotoxic properties commonly seen in NK, lymphokine activated killer (LAK) and antibody-dependent cellular-cytotoxic (ADCC) effector cells, was significantly decreased in HAM/TSP as compared to asymptomatic carriers as well as controls. The percentage of CD16+CD3+ cells correlated inversely with the value of spontaneous proliferation of peripheral blood lymphocytes (SPP), which is a characteristic change observed in HAM/TSP.

Adult↗
PubMed1988

Appearance and phenotypic characterization of circulating Leu 19+ cells in cancer patients receiving recombinant interleukin 2.

The effects of recombinant interleukin 2 (rIL-2) therapy on peripheral blood mononuclear cells expressing the Leu 19 surface marker were evaluated in 20 cancer patients. Leu 19 is a protein with a molecular weight of 220,000 expressed on 15% of normal peripheral blood mononuclear cells and is found on a majority of cells that mediate non-major histocompatibility complex-restricted cytotoxicity. Increased relative and absolute numbers of circulating Leu 19+ cells were observed in all patients receiving rIL-2. Increases in Leu 19+ cells were due in part to the development of a subpopulation of "bright" Leu 19+ cells (Leu 19b+) that possessed a higher density of membrane Leu 19 antigen than Leu 19+ cells assayed prior to therapy. Further characterization of rIL-2 induced Leu 19+ cells by dual immunofluorescence revealed considerable phenotypic heterogeneity within this population based on the coexpression of "dim" CD8 (CD8d+), CD16, and CD2 markers. The percentage of Leu 19+ CD8d+ cells was increased during rIL-2 therapy and comprised up to 60% of all circulating Leu 19+ cells. CD16+ and CD16- subsets of Leu 19+ cells were also increased by rIL-2. The density of CD16 antigen coexpression varied inversely with the density of Leu 19. Conversely, whereas the percentage of Leu 19 cells coexpressing CD2 was also increased by rIL-2 administration, the density of CD2 antigen expression was higher on the Leu 19b+ subset of cells. The development of circulating lymphokine-activated killer activity in three patients was temporally associated with the development of increased levels of circulating Leu 19+ cells. These studies demonstrate that rIL-2 administration induces preferential increases in cells expressing the natural killer and lymphokine-activated killer cell-associated marker Leu 19 and that these increases are associated with the development of circulating lymphokine-activated killer activity. Furthermore, Leu 19+ cells are comprised of phenotypically heterogeneous subsets which undergo characteristic changes during rIL-2 administration.

Antigens, Differentiation↗
PubMed1985

Intestinal microbial flora after feeding phytohemagglutinin lectins (Phaseolus vulgaris) to rats.

Incorporation of purified phytohemagglutinin (PHA) lectins derived from red kidney beans (Phaseolus vulgaris) in the diet of weanling rats will cause growth failure, malabsorption of nutrients, and bacterial overgrowth in the small intestine. These effects are not caused by feeding a similar quantity of PHA to germfree rats. To define the morphological and bacterial changes on the mucosal surfaces of the jejunum, ileum, and cecum in greater detail, we pair fed two groups of weanling rats isocaloric, isonitrogenous diets with or without 0.5% PHA protein. On the jejunal surfaces of control rats, the mucous layer was a confluent covering with sparsely scattered bacteria and protozoa. In PHA-treated rats, the mucous layer was thin and discontinuous, and the microvillous surface of the tissue was extensively populated by bacterial cells of two distinct morphotypes--a gram-negative rod and a gram-positive coccobacillus. In all PHA-treated animals, these bacteria formed adherent monospecific or mixed adherent microcolonies on the tissue surface. Tissue damage was observed in PHA-exposed jejunal tissue as evidenced by vesiculation of the microvillous plasma membrane and by damage to the brush border membrane. On the ileal surfaces of control rats, there was a thick mucous layer within which small numbers of bacteria and protozoa were seen. Segmented filamentous bacteria were anchored in the tissue surface. In PHA-treated rats, the ileal surface was only incompletely covered by a mucous layer, and the overlying mucosal surface was extensively covered by large numbers of protozoan cells (predominantly Hexamita muris). Most of the ileal surfaces not covered by the mucous layer were occupied and virtually occluded by an overgrowth of these protozoan cells with occasional cells of Giardia muris and the tissue-associated segmented bacillus. In the ceca of control rats, the mucosa was incompletely covered by a discontinuous mucous layer and colonized by an unnamed Spirillum sp., other bacteria, and occasional protozoa. The cecal surfaces of PHA-treated rats retained most of their incomplete overlying mucous layer, which was heavily colonized by the same type of Spirillum sp. seen in untreated animals; intestinal crypts were colonized. These descriptive morphological studies demonstrate that exposure to purified PHA in the diet caused characteristic changes in the microbial ecology of the small intestine. The changes in microbial flora contributed to the malabsorption of nutrients in the small intestines of PHA-fed animals.

Animals↗
PubMed1990

[The changes of population and distribution of S-phase cells in precancerous lesions of rat bladder revealed by the method of bromodeoxyuridine labeling].

We studied whether bromodeoxyuridine (BrdU)-labeling method showing the population and/or distribution of S-phase cells in tumor tissues is useful to detect the precancerous lesions of bladder. The bladder lesions were induced by 0.05% N-butyl-N (4-hydroxybutyl) nitrosamine (BBN) in drinking water for ten weeks in five male rats (Wistar-Imamichi). BrdU (50 mg/kg) was injected to intraperitoneal space two hours before the resection of the bladder. The detection of positive cells (S-phase cells taking BrdU) was performed by peroxidase-antiperoxidase method. From five bladder specimens 144 lesions (simple hyperplasia (S)-73, papillary or nodular hyperplasia (PN)-57, papilloma (Pa)-14) were analysed. The labeling index (the ratio of positive cells to all epithelial cells in one lesion) showed no significant difference among the lesions (S, PN, and Pa). For analyses of the distribution patterns of S-phase cells, we investigated whether positive cells aside from basal layers and/or the serial positive cells in basal layers were seen or not in each lesion. The ratios of lesions containing positive cells aside from basal layers were 11% (8/73), 60% (34/57) and 100% (14/14) in S, PN and Pa lesions. The serial positive cells in basal layers were observed in 6% (4/73), 25% (14/57) and 50% (7/14) of S, PN and Pa lesions. Those differences were statistically significant. Above mentioned results suggest that the appearance of S-phase cells aside from basal layers and/or the serial S-phase cells in basal layers is characteristic change in precancerous lesions, which is useful for sooner detection of bladder carcinogenesis.

Animals↗
PubMed1986

Proto-oncogene c-myc is expressed in cerebellar neurons at different developmental stages.

During post-natal cerebellar development the steady-state levels of c-myc transcripts exhibit characteristic changes. As determined by the S1 nuclease protection assay the level of c-myc transcript, which is very high in the late embryonic cerebellum, decreased to low levels shortly after birth. One week later there is a second period of c-myc mRNA accumulation followed by a marked decline to finally reach the low adult value. The second peak of high c-myc mRNA level correlates well with the proliferation of granule cell precursors, and it is characterized by a marked change in the ratio of the two types of transcripts started at the known c-myc promoters 1 and 2. This indicates a change in the cell population involved in the transcription of the c-myc gene. In situ hybridization shows transiently elevated c-myc mRNA levels in neurons of the cerebellar cortex. At post-natal days 3 and 10 (P3 and P10) c-myc transcripts are detectable in the superficial external granular layer composed primarily of mitotically active (neural precursor) cells. Purkinje cell somata show cytoplasmic label at P10. These large postmitotic neurons undergo rapid differentiation at this developmental stage. In the adult cerebellum the low c-myc mRNA level is apparently due to Purkinje cells with barely detectable amounts of c-myc transcripts. The vast majority of mature cerebellar neurons, the internal granule cells, have no specific hybridization signal for c-myc. We conclude that neurons in vivo can accumulate c-myc messenger during proliferation and/or differentiation, perhaps as a cellular response to an external signal.

Aging↗
PubMed1987

The leakage of serum proteins across the blood-nerve barrier in hereditary and inflammatory neuropathies. An immunohistochemical and morphometric study.

The leakage of eight different serum proteins and immunoglobulins across the blood-nerve barrier (BNB) was studied by means of the peroxidase-antiperoxidase method in hereditary and inflammatory neuropathies and graded semiquantitatively with respect to endoneurial staining intensity and distribution. These data were compared with the degree of alterations of the myelinated nerve fibre population evaluated by morphometric analysis. Our series of 18 human sural nerve biopsies included seven hereditary neuropathies (three HMSN I, two HMSN II, two tomaculous neuropathies), nine inflammatory neuropathies (seven polyneuritis, two hypertrophic neuritis) and two normal controls. In HMSN II and in tomaculous neuropathy there was no enhanced endoneurial staining for serum proteins despite of a severe nerve fibre loss, whereas in HMSN I a rise of serum proteins of small and moderate molecular size like albumin and IgG was demonstrated in the endoneurial space indicating an impaired BNB function. Qualitative changes of the BNB with leakage also of high molecular weight proteins were observed in polyneuritis and hypertrophic neuritis, irrespective of the degree of nerve fibre changes. Our results show that fibre loss and alteration of the BNB are not correlated. The unselective leakage of serum proteins through the BNB appears to be a characteristic change in inflammatory neuropathies leading to proteinous edema. With regard to the subperineurial accentuation of the endoneurial edema it will be discussed that the vascular diffusion barrier is more fragile than the perineurial diffusion barrier.

Adolescent↗
PubMed1990

Both alpha 1- and beta-adrenoceptor stimulation determine the time course of the inotropic effect of noradrenaline in rabbit heart.

It has been a matter of controversy whether alpha 1-adrenoceptor stimulation contributes to the final inotropic and lusitropic responses in mammalian myocardium to noradrenaline during concomitant and unopposed beta-adrenoceptor stimulation. In the present paper we report studies that compare time courses of the inotropic and lusitropic responses to separate and combined alpha 1- and beta-adrenoceptor stimulation, respectively, in electrically driven rabbit papillary muscles by a submaximal concentration of noradrenaline. Separate alpha 1- or beta-adrenoceptor stimulation (presence of appropriate receptor blocker) showed the characteristic slow and fast development, respectively, of the inotropic responses. Qualitatively, the respective characteristic changes were also observed: alpha 1-adrenoceptor stimulation caused a negative lusitropic effect giving a prolongation of the time to peak tension (TPT), while beta-adrenoceptor stimulation caused a pronounced positive lusitropic effect giving a shortening of TPT. The time course of the inotropic response to combined adrenoceptor stimulation had characteristics that deviated from the respective time courses to separate alpha 1- or beta-adrenoceptor stimulation thus indicating a contribution from both adrenoceptor populations to the final inotropic response. Combined alpha 1- and beta-adrenoceptor stimulation gave a pronounced positive lusitropic response as might be expected due to the obviously dominating role of the beta-adrenergic component. However, the maximal lusitropic effect and the shortening of TPT were both slightly less during combined adrenoceptor stimulation compared to separate beta-stimulation thus indicating an influence of the alpha 1-adrenoceptor mediated negative lusitropic effect. Quantitatively, the separate alpha 1- and the separate beta-adrenoceptor mediated inotropic effects were not additive. In accordance with other recent studies, this indicated an inhibitory interaction between the two adrenergic receptor populations in myocardium.

Animals↗
PubMed1989

Noninvasive determination of age-related changes in the human arterial pulse.

Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload.

Aging↗
PubMed1975

Cell electrophoretic studies on the cellular immune response to Candida albicans in rabbits.

Rabbits were sensitized intracutaneously with Candida albicans total antigen by a series of booster injections. The electrophoretic migration time of lymph node lymphocytes was related to the time after injection. Two lymphocyte sub-populations could be distinguished. The proportion of each, changed during the course of the immune response. Characteristic changes also took place after in vitro incubation with Candidin. The results have been compared with agglutination titers and are discussed in relation to bursa and thymus-derived cells. The electrophoretic method may be valuable for the diagnosis of candidiasis.

Animals↗
PubMed1986

An experimental analysis of the origins of somatostatin-like immunoreactivity in the dentate gyrus of the rat.

In previous studies, fibers demonstrating somatostatin-like immunoreactivity were observed in the outer half of the molecular layer of the dentate gyrus in the rat and monkey. They occupy the same region as those of the perforant pathway that originates in the entorhinal cortex. Numerous somatostatin immunoreactive neuronal cell bodies were also observed in the hilar region, though stained axonal profiles could not be followed from these cells into the molecular layer. In the present study, several experimental procedures were employed to determine the origin of the somatostatin-positive fibers in the molecular layer. Transection of the perforant path fibers resulted in such characteristic changes as shrinkage of the molecular layer and sprouting of AChE-positive fibers. There was no apparent decrease, however, in the density of somatostatin-positive fibers. In fact, since the stained fibers occupied a narrower band in the shrunken molecular layer, their density appeared greater. Injections of kainic acid into the hilar region produced a lesion of hilar neurons, including those positive for somatostatin. In the region of cell loss, there was a marked reduction of somatostatin-immunoreactive fibers in the ipsilateral molecular layer, with no detectable changes in the homotopic contralateral molecular layer. The distribution of AChE fibers, which presumably have an extrinsic origin, was not altered by the treatment. In a final series of experiments, the retrograde tracer wheat germ agglutinin-horseradish peroxidase (WGA-HRP) was injected into the hilar region and sections were prepared for the simultaneous demonstration of the tracer and of somatostatin-like immunoreactivity. Somatostatin-positive neurons demonstrating WGA-HRP reaction product were observed primarily in the ipsilateral hilar region, but a few double-labeled cells were also seen in the same area of the contralateral side. These studies indicate that a population of intrinsic neurons located in the polymorphic layer of the dentate gyrus projects to the outer half of the ipsilateral molecular layer. A similar, but very much smaller, projection also extends to the contralateral dentate gyrus. Taken together, these projections appear to account for much of the somatostatin-like immunoreactivity in the molecular layer of the dentate gyrus.

Animals↗
PubMed1988

Age related changes in the human plastron: a roentgenographic and morphologic study.

Characteristic changes that can be demonstrated on roentgenograms occur with increasing age in the plastron (chest plate) of humans. These alterations include progressive ossification in the costal cartilages (located characteristically in the sternal rib end, centrichondrally, and peristernally--often with sex and age distinctive patterns), maturation of the newly formed bone with trabeculation formation, loss of the smooth contour of the costo-manubrial junction, cupping of rib ends, osteoporotic changes, and arthritic changes in the sternal head of the clavicles. The sequence of development of these alterations has been examined by X-ray of 1965 cadavers of 15 years of age or over and correlated with the gross bone and cartilage morphology changes in many cases. This technique allows for age determination within 5 years of real age in 55% of cadavers and within 25% of real age in 95% of all cadavers. The greatest departures from real age are in the over-60-year groups. The same roentgenograms can allow for correct sex prediction in 99% of the population.

Adolescent↗
PubMed1985

Differential sensitivity of human breast cancer cell lines to the growth-inhibitory effects of tamoxifen.

In eight estrogen receptor (ER)-positive breast cancer cell lines (including three sublines of MCF-7) and five ER-negative breast lines, the action of the nonsteroidal antiestrogen, tamoxifen, was studied, and the concentrations of ER and antiestrogen binding site were measured. The concentration of antiestrogen binding site was significantly [P less than 0.005] greater in ER-positive cells [236,600 +/- 29,900 (SE) sites/cell] than in ER-negative cell lines [66,600 +/- 16,800 sites/cell]. In ER-positive cell lines, a cell cycle phase-specific growth-inhibitory effect, 20% inhibitory dose less than 0.1 to 1.0 microM, was seen which was shown for some representative cell lines to be estrogen reversible. Within this group of cell lines, the degree of tamoxifen-induced inhibition of growth correlated with control population doubling time, but not ER or antiestrogen binding site concentration. The changes in cell cycle kinetic parameters characteristic of all ER-positive lines were a decrease in percentage of S-phase cells and a corresponding increase in percentage of G0-G1 cells. In all cell lines, 5 to 12.5 microM tamoxifen caused cytotoxicity, and this was shown to be estrogen-irreversible in 3 representative cell lines; moreover, estradiol synergistically enhanced the cytotoxic effects of tamoxifen under some experimental conditions. The cell cycle effects of tamoxifen in three ER-negative cell lines (Hs0578T, MDA-MB-231, MDA-MB-330) were decreased proportions of G0-G1 cells with an increase in percentages of S and G2+M cells. These results implied that the mechanism of tamoxifen cytotoxicity may differ in ER-positive and ER-negative breast cancer cells. However, although the ER-negative BT-20 line was much less sensitive to tamoxifen than were the ER-positive cells, growth inhibition and cytotoxicity in this line were associated with a slight decrease in percentage of S-phase cells. These results confirm that ER-positive breast cancer cells are more sensitive (4- to greater than 75-fold) than ER-negative breast cells to the growth-inhibitory effects of tamoxifen and demonstrate that, in all ER-positive cells, growth inhibition and cytotoxicity are accompanied by characteristic changes in cell cycle kinetic parameters. In contrast, different mechanisms may be involved in the effects of tamoxifen on different ER-negative cell lines.

Breast Neoplasms↗