Susceptibility of Chaotic Systems to Perturbations.
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Journal Article↗
Biomedical subjects
J Shan
Publications and source records attributed to J Shan.
Factors associated with bone mineral density in middle-aged men.
This cross-sectional population-based study examined the association of anthropometric and lifestyle risk factors with bone mineral density (BMD) in 218 white ambulatory men aged 50-64 from the Rancho Bernardo, California cohort. BMD was measured at the lumbar spine and hip using dual-energy X-ray absorptiometry and at the ultradistal wrist and midshaft radius of the forearm using single-photon absorptiometry. Body mass index (BMI) was significantly correlated with BMD at all four skeletal sites. Overall, 17.0% of men aged 55-64 were osteopenic (BMD > or = 2 SD below the distribution for ages 50-54) at one skeletal site, 16.5% were osteopenic at two sites, and 13.6% were osteopenic at three or more sites. Men who reported regular exercise had significantly higher BMD levels at the spine and hip. Men meeting the recommended daily allowance (RDA) for calcium intake (> or = 800 g/day) had significantly higher BMD levels at the spine and wrist. Alcohol intake and smoking were associated with differences of borderline significance in BMD at the spine. In analyses adjusted for BMI, weight change, exercise, smoking, drinking, and calcium intake, there was a significant independent age-related decline in BMD at the hip (0.008 g/cm2/year; p = 0.001), at the wrist (0.004 g/cm2; p < 0.01), at the forearm (0.006 g/cm2; p < 0.01), but not at the spine (0.005 g/cm2). These data, although cross-sectional, strongly suggest that age-related bone loss occurs in middle-aged men and that both physical activity and an adequate calcium intake are associated with better bone density.
Ambulatory Care↗
Primordial germ cell-derived mouse embryonic germ (EG) cells in vitro resemble undifferentiated stem cells with respect to differentiation capacity and cell cycle distribution.
Embryonic germ (EG) cells of line EG-1 derived from mouse primordial germ cells were investigated for their in vitro differentiation capacity. By cultivation as embryo-like aggregates EG-1 cells differentiated into cardiac, skeletal muscle and neuronal cells accompanied by the expression of tissue-specific genes and proteins as shown by RT-PCR analysis and indirect immunofluorescence. In comparison to embryonic stem (ES) cells of line D3 the efficiency of differentiation into cardiac and muscle cells was comparatively low, whereas spontaneous neuronal differentiation was more efficient than in D3 cells. Furthermore, the distribution of cell cycle phases as a parameter for the differentiation state was analysed in undifferentiated EG cells and ES cells and compared to data obtained for embryonic carcinoma (EC) cells of line P19 and differentiated, epithelioid EPI-7 cells. Flow cytometric analysis revealed similar cell cycle phase distributions in EG, EC and ES cells. In contrast, the somatic differentiated EPI-7 cells showed a longer G1-phase and shorter S- and G2/M-phases. Together, our results demonstrate that the differentiation state and capacity of EG cells in vitro resemble that of totipotent ES cells.
Animals↗
GHb is a better predictor of cardiovascular disease than fasting or postchallenge plasma glucose in women without diabetes. The Rancho Bernardo Study.
OBJECTIVE: To examine the relation between GHb, fasting plasma glucose (FPG), postchallenge plasma glucose (PCPG), and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) in older adults. RESEARCH DESIGN AND METHODS: A community-based study of 1,239 nondiabetic older adults followed for an average of 8 years, from baseline (1984-1987) to 1993. RESULTS: GHb, but not FPG or PCPG, was significantly related to CVD and IHD mortality in women but not men. The age-adjusted relative hazard for those in the highest quintile of GHb (> or = 6.7%) compared with women with lower levels was 2.37 for fatal CVD (95% CI = 1.30-4.31, P = 0.005) and 2.43 for IHD (95% CI = 1.12-5.25, P = 0.024). This association persisted after adjustment for all covariates (age, systolic blood pressure, BMI, LDL, HDL, triglycerides, cigarette smoking, antihypertensive medication use, and estrogen use). GHb was significantly associated with LDL and HDL levels in women, but the association between GHb and CVD or IHD persisted after adjustment for these lipoproteins. CONCLUSIONS: We concluded that GHb is a better predictor of CVD and IHD mortality than FPG or PCPG in women without diabetes; no single measure of glycemia was predictive in men. The reason for the sex difference is unexplained.
Adult↗
The vasorelaxing action of rutaecarpine: direct paradoxical effects on intracellular calcium concentration of vascular smooth muscle and endothelial cells.
We have examined both the hypotensive effect and the mechanism of intracellular Ca++ regulation, underlying rutaecarpine (Rut)-induced vasodilatation. An i.v. bolus injection of Rut in anesthetized Sprague-Dawley rats produced a dose-dependent hypotensive effect. In isolated rat aorta rings, Rut (0.1-3 mu M) inhibited the phasic and tonic responses of norepinephrine- and phyenylephrine-induced contractions, respectively, mainly through an endothelium-dependent mechanism. However, the vasorelaxing effect of Rut (3 microM) persisted in denuded aorta, although to a much less extent than in intact tissue. As determined by the fura-2/AM (1-[2-(5-carboxyoxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2'- amino-5'-methylphenoxy)-ethane-N,N,N,N-tetraacetic acid pentaacetoxymethyl ester) method, Rut (10 microM), in the presence of extracellular Ca++, suppressed the KCI-induced increment in the intracellular Ca++ concentration ([Ca++]i) of cultured vascular smooth muscle cells (VSMC). Rut (10 microM) also attenuated the norepinephrine-induced peak rise of [Ca++]i in VSMC placed in Ca++-free solution. On the other hand, Rut (1 and 10 microM) increased the level of [Ca++]i of cultured endothelial cells (EC) in the presence of extracellular Ca++. In conclusion, Rut acts on both VSMC and EC directly. In VSMC, it reduces [Ca++]i through the inhibition of Ca++ influx and Ca++ release from intracellular stores. In EC, Rut augments EC [Ca++]i by increasing Ca++ influx, possibly leading to nitric oxide release. The paradoxical regulation of Ca++ in both VSMC and EC acts simultaneously to cause vasorelaxation which could account, at least in part, for the hypotensive action. This is a most significant and a unique feature of this study.
Alkaloids↗
[Recurrence of early gastric cancer].
OBJECTIVE: To evaluate the features of recurrence of early gastric cancer. METHODS: 109 cases of early gastric cancer were subjected to surgical resection from 1972 to 1988. Apart from two died, all cases were followed up for more than 5 years. RESULTS: Eight cases (7.5%) died of other diseases. Ten cases (10.3%) died because of the recurrence of gastric cancer. Five cases (45.5%) had hematogenic metastasis to the liver or lung. Two cases had the recurrence of the cancer in lymph node. The recurrence in the residual stomach was found in 3 cases, in addition to a patient who was detected to have metastasis in Virchow's lymph node survival for 12 years after operation. The recurrence rate was higher in submucosal tumors (12.8%) than in mucosal tumors (8.0%), in lymphatic and vascular vessel invasion-positive cases (43%) than in negative cases (7.8%), in synchronous multiple gastric cancer (33.3%) than in solitary tumors (7.2%), in tumors of 1.5 cm or more in diameter (11.5%) than in tumors of less than 1.5 cm. The rate of hematogenic metastasis to the liver or lung was 45.5% (5/11), and the recurrence in the residual stomach was 27.3% (3/11) and in lymph node was 27.3% (3/11). CONCLUSION: Hematogenic metastasis is frequent.
Adenocarcinoma↗
Differentiation of pluripotent embryonic stem cells into the neuronal lineage in vitro gives rise to mature inhibitory and excitatory neurons.
Embryonic stem (ES) cells represent a suitable model to analyze cell differentiation processes in vitro. Here, we report that pluripotent ES cells of the line BLC 6 differentiate in vitro into neuronal cells possessing the complex electrophysiological and immunocytochemical properties of postmitotic nerve cells. In the course of differentiation BLC 6-derived neurons differentially express voltage-dependent (K+, Na+, Ca2+) and receptor-operated (GABAA, glycine, AMPA, NMDA receptors) ionic channels. They generate fast Na(+)-driven action potentials and are functionally coupled by inhibitory (GABAergic) and excitatory (glutamatergic) synapses as revealed by measurements of postsynaptic currents. Moreover, BLC 6-derived neurons express neuron-specific cytoskeletal, cell adhesion and synaptic vesicle proteins and exhibit a Ca(2+)-dependent GABA secretion. Thus, the ES cell model enables the investigation of cell lineage determination and signaling mechanisms in the developing nervous system from a pluripotential stem cell to a differentiated postmitotic neuron. The in vitro differentiation of neurons from ES cells may be an excellent approach to study by targeted gene disruption a variety of neuronal functions.
Action Potentials↗
Effects of dehydroepiandrosterone sulfate on cellular calcium responsiveness and vascular contractility.
Dehydroepiandrosterone sulfate (DHEAS) is an endogenous steroid having a wide variety of biological effects, but its physiological role remains undefined. Since an age-related decline of DHEAS corresponds to the progressive onset of atherosclerosis, cardiovascular diseases, and overall mortality, we investigated a possible protective role of DHEAS in vascular disease by studying the effects of this hormone (10(-7) to 10(-5) mol/L) on cytosolic free calcium and contractility in different in vitro vascular tissue preparations. DHEAS produced a significant, dose-dependent relaxation of isolated helical strips of rat tail artery precontracted with KCl (60 mmol/L) (89.7 +/- 18.7%, P < .01), arginine vasopressin (3 nmol/L) (27.3 +/- 7.1%, P < .01), and norepinephrine (0.1 mumol/L) (49.2 +/- 18.2%, P < .01). In isolated vascular smooth muscle cells DHEAS reversibly inhibited KCl (30 mmol/L)-induced elevations of cytosolic free calcium to 69.8 +/- 8.4% and 43.8 +/- 7.4% of the control response at 5 x 10(-7) and 5 x 10(-6) mol/L, respectively (P < .05 at both doses). These results provide evidence of a direct vascular action of DHEAS, in doses reflecting circulating levels in vivo, and suggest the possibility that these effects are mediated by modulation of intracellular calcium metabolism. We hypothesize that physiologically, DHEAS may serve to buffer vascular responsiveness to a wide variety of depolarizing and constrictor hormonal stimuli.
Analysis of Variance↗
Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells.
We have previously suggested that hyperglycemia per se may contribute to diabetic hypertensive and vascular disease by altering cellular ion content. To more directly investigate the potential role of glucose in this process, we measured cytosolic free calcium in primary cultures of vascular smooth muscle cells isolated from Sprague-Dawley rat tail artery before and after incubation with 5 (basal), 10, 15, and 20 mM glucose. Glucose significantly elevated cytosolic free calcium in a dose- and time-dependent manner, from 110.0 +/- 5.4 to 124.5 +/- 9.0, 192.7 +/- 20.4, and 228.4 +/- 21.9 nM at 5, 10, 15, and 20 mM glucose concentrations, respectively. This glucose-induced cytosolic free calcium elevation was also specific, no change being observed after incubation with equivalent concentrations of L-glucose or mannitol. This glucose effect was also dependent on extracellular calcium and pH, since these calcium changes were inhibited in an acidotic or a calcium-free medium, or by the competitive calcium antagonist lanthanum. We conclude that ambient glucose concentrations within clinically observed limits may alter cellular calcium ion homeostasis in vascular smooth muscle cells. We suggest that these cellular ionic effects of hyperglycemia may underlie the predisposition to hypertension and vascular diseases among diabetic subjects and/or those with impaired glucose tolerance.
Animals↗
[Relationship between the fetal axis and dystocia in cephalic presenting deliveries].
OBJECTIVE: To study the relationship between the fetal axis and dystocia in cephalic presenting deliveries. METHODS: The fetal axis of the observed cases in their late pregnancy were measured by the method which was designed by anatomical projection. During labor the cases with abnormal fetal axis were divided randomly into control group and study group. The abnormal fetal axis in the study group was corrected by hand. RESULTS: The abnormal fetal axis existed in 108 of 512 (21.1%) cases in late pregnancy and were divided into different degrees. The rate of severe degree was 51.8%. During labor 88 of 483 (18.2%) cases were severe degree. They were sub-divided into control group (30 cases) and study group (58 cases). The results showed: in the study group the descent of fetal-presentation was accelerated, the stage of labor became shorter, the incidence of persistent occipito-posterior or occipito-transverse position and operative delivery were decreased, and the postpartum hemorrhage out down also. CONCLUSIONS: The abnormality of fetal axis exists and it can affect the progress of labor. The abnormal fetal axis should be diagnosed and corrected in time. To some extent, it can reduce the mother's physical consumption in labor and decrease the incidence of dystocia.
Delivery, Obstetric↗
Molecular cloning and characterization of murine cyclin E.
Using a monoclonal antibody developed to a mouse trophectodermal carcinoma stem cell line E6496D lysate, we have identified the gene that encodes murine cyclin E. The cDNA contains a consensus cyclin box and a long 3' untranslated region and shares over 75% homology with human cyclin E cDNA. We show that the gene is expressed in fetal tissues, embryonal carcinoma F9 cells and yolk sac carcinoma PYS-2 cells, but is not expressed in preimplantation stages of development. In adult tissues, cycE mRNA is detectable in the spleen and to a lesser extent in the testis and brain. These data show that cycE is developmentally regulated and unevenly expressed in fetal and adult mouse tissues.
3T3 Cells↗
Vascular effects of 17 beta-estradiol in male Sprague-Dawley rats.
Bolus intravenous injections of 100 micrograms/kg 17 beta-estradiol significantly decreased the pressor responses to norepinephrine (NE; 0.3 microgram/kg) at the fourth, fifth, and sixth hour in anesthetized male Sprague-Dawley rats. At doses of 10(-6) to 3 x 10(-5) M, 17 beta-estradiol relaxed the sustained phase of contraction in male Sprague-Dawley rat tail artery helical strips precontracted in vitro by [Arg8]vasopressin (AVP), KCl, or NE. The effect was dose dependent. At doses of 3 x 10(-6) to 3 x 10(-5) M, it also decreased the initial phase of tension generation and extracellular Ca(2+)-dependent vasoconstriction induced by NE, AVP, or KCl in a dose-dependent manner in male Sprague-Dawley rat tail artery helical strips. 17 beta-Estradiol (2 x 10(-8) to 2 x 10(-6) M) decreased the voltage-dependent inward Ca2+ current and the intracellular free Ca2+ concentration ([Ca2+]i) increment induced by 15 mM KCl in a dose-dependent manner (3.6 x 10(-8) to 3.6 x 10(-6) M) in vascular smooth muscle cells (VSMC) isolated from male Sprague-Dawley rat tail arteries. We suggest that, at pharmacological doses, estrogen has a direct vasodilating effect on the rat tail artery that is mediated by its inhibitory effect on Ca2+ influx through voltage-dependent Ca2+ channels. The inhibitory effect of estrogen on the pressor responses to NE or AVP may be correlated with its modulation of VSMC [Ca2+]i through its actions on membrane Ca2+ channels.
Animals↗
PHF: the new parathyroid hypertensive factor.
Parathyroid Hypertensive Factor (PHF) was discovered in SHR rats as a circulating substance with a unique delayed (60-90 min) hypertensive effect when injected into a normotensive assay rat. Subsequently, this correlation with hypertension was established in humans, especially in low-renin, salt-sensitive patients. Animal model studies also confirmed this correlation. Endocrinectomy and glandular replacement studies suggested that the parathyroid gland was the source of PHF. Subsequently, glands and cells in culture were also shown to secrete the substance. Other studies verified the parathyroid origin of PHF. The mechanism of action of PHF was shown to rely mainly on the opening of L-type calcium channels in vascular smooth muscle cells with an increase in [Ca2++]i. It is known that diseases other than hypertension often show increased [Ca2++]i and clinical features similar to hypertension, among them Type II diabetes. A recent study shows a correlation between circulating PHF level and Type II diabetes irrespective of the blood pressure status of the patient. It is suggested that PHF may be a [Ca++]i modulator, an excessive amount of which in the circulation may act on various target tissues, resulting in various disease symptoms with hypertension as an example. There may be many other such PHF-related diseases yet to be identified.
Animals↗
Mechanism of the vascular action of parathyroid hypertensive factor.
The present studies investigated the effect of parathyroid hypertensive factor (PHF) on intracellular calcium regulation in VSMC. Nifedipine inhibited the hypertensive effect of PHF in Sprague-Dawley (SD) rats in vivo. PHF amplified the L-type calcium current in vascular smooth-muscle cells (VSMCs) isolated from SD rat tail artery. PHF potentiated the tension induced by norepinephrine (NE) in the presence of normal added CaCl2 and inhibited the tension dependent on Ca2+ release from intracellular calcium store(s) induced by NE in SD rat tail artery helical strips. PHF potentiated the intracellular free calcium concentration ([Ca2+]i) increment induced by KCl in cultured VSMCs from SD rat tail artery. All of the in vitro cellular calcium effects of PHF temporally correlated with its delayed hypertensive effect in vivo. PHF did not affect the accumulation of inositol phosphates in SD rat tail artery. Infusion of theophylline blunted the hypertensive effect of PHF in SD rats, suggesting that PHF may stimulate phosphodiesterase (PDE) activity. We suggest that PHF may potentiate the effects of other vasoconstrictors on calcium channels and increase [Ca2+]i, which would then lead to an increase in the responsiveness of the VSMC to other vasoconstrictors, and therefore an increase in blood pressure. The action of PHF may involve stimulation of PDE activity.
Animals↗
Clinical aspects of parathyroid hypertensive factor.
To determine the clinical significance of parathyroid hypertensive factor (PHF), physiological studies previously performed in animal models of hypertension were parallelled by human studies. These studies revealed that PHF-like activity is present in human hypertension, where it correlates with the salt-sensitive, low-renin state. As in spontaneously hypertensive rats, both supplemental calcium and calcium-channel blockers appear to be useful in the treatment of PHF-related hypertension. In primary hyperparathyroid patients, PHF presence is linked with the presence of hypertension. Postparathyroidectomy blood pressure falls in parallel with PHF levels. These preliminary human studies suggest that PHF may be a useful marker in the treatment of hypertension.
Animals↗
Cardiovascular effects of human parathyroid hormone and parathyroid hormone-related peptide.
Parathyroid hormone (PTH) is hypotensive in mammals and is a potent coronary vasodilator. Parathyroid hormone-related peptide (PTHrp) has been reported to have similar vascular activity. In the present study, the effects of human PTH (hPTH) and human PTHrp (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive rats. Isolated rat tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, PTHrp was several times more potent than PTH. PTHrp was also significantly more potent than PTH in relaxing tail artery precontracted with arginine vasopressin (AVP). PTHrp and PTH both inhibited the spontaneously contracting portal vein, but again PTHrp was significantly more potent. PTHrp (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of PTH. These data suggest that PTHrp is more potent than PTH in its cardiovascular actions. It is possible that PTHrp is the endogenous vasodilating ligand, and the structural similarity between PTH and PTHrp may explain the pharmacological action of PTH. It is therefore unlikely that PTH or PTHrp may be involved in the genesis or maintenance of hypertension. Because the parathyroid gland seems to be involved in some forms of essential hypertension, factor(s) other than PTH or PTHrp may be responsible.
Animals↗
Purification and structural characterization of parathyroid hypertensive factor.
Parathyroid hypertensive factor (PHF) has been purified from two sources of material: plasma of spontaneously hypertensive rats (SHRs) and culture medium from organ culture of SHR parathyroid glands. Chromatographic characteristics of PHF from these two sources are identical. Biological activity of PHF (assayed as the characteristic delayed hypertensive response in normotensive rats) is sensitive to degradation by treatment in base, and the enzymes trypsin, chymotrypsin, phospholipase C, and phospholipase D. PHF activity may also be extracted from source material with chloroform: methanol (4:1). A hypothetical structure for the active component of PHF is suggested. This is comprised of a peptide liked to a lysophospholipid.
Animals↗
[Synaptonemal complex analysis of 13/17 Robertsonian translocation in the domestic pig].
G and C-banding study of the chromosomes of several male pigs, indicate that all of these pigs carry rob(13;17). The karyotype is 2n = 37, XY, rob (13;17). In this paper, silverstained Synaptonemal Complexes (SCs) in surface-spread pachytene nuclei from these pigs are analysed by electron microscope. The result is as follows: Robertsonian translocation metacentrics rob (13;17) paired with homologous acrocentrics (13,17), forming a trivalent. All trivalents are in a cis configuration and there is delayed pairing in the trivalent. We measured every part of trivalent in the different stage of prophase (based on the morphology of XY-bivalent). It is shown that accompanying with rob(13;17) formation there has been a deletion in the proximal part of 13, 17 translocation chromosome. In the process of synapsis, the length adjustment phenomenon in the trivalent occurred: a. There is nonhomologous synapsis between the two short arms of the acrocentrics (13;17). The length of short SC varied. b. The position of the short SC, which is on the long SC(homologous synapsis of rob(13; 17) and 13, 17) moved, from one-fourth of long SC to one-tenth of it, near the end of 17 arm. These phenomenon is the result of a gradual length adjustment of lateral elements of 13,17 to the lateral element of the rob (13;17). We has discussed the mechanism of the trivalent synaptic adjustment, and it's important use to control the chiasmata and disjunction of the chromosomes.
Animals↗