Integrated detrital rutile and detrital zircon ages: a new perspective on the tectonic evolution of South China.

Paleogeographic reconstructions are of key importance for understanding the history of continental breakups and amalgamations during Earth's history. A special case is the history of the Asian continent, which, compared to other continents, consists of several large cratons and numerous smaller continental blocks. The history of the assembly of South China remains controversial in terms of the timing, Late Neoproterozoic or Early Paleozoic, and the participating continental blocks, e.

Survived and disappeared intra-oceanic arcs of the Paleo-Asian Ocean: evidence from Kazakhstan.

This paper reviews published and presents new data on U-Pb detrital zircon ages, and petrographic, geochemical and isotope (Sm-Nd, Lu-Hf) compositions obtained from greywacke sandstones of Kazakhstan in order to reconstruct fossil intra-oceanic arcs that once existed at Pacific-type convergent margins of the Paleo-Asian Ocean (PAO) in Paleozoic time. We focus on orogenic belts of central Kazakhstan (Itmurundy and Tekturmas) and eastern Kazakhstan (Zharma and Char) in the western Central Asian Orogenic belt. These orogenic belts host accretionary complexes with greywacke sandstones of early Paleozoic (central Kazakhstan) and middle-late Paleozoic (eastern Kazakhstan) ages.

Whole-mantle convection with tectonic plates preserves long-term global patterns of upper mantle geochemistry.

The evolution of the planetary interior during plate tectonics is controlled by slow convection within the mantle. Global-scale geochemical differences across the upper mantle are known, but how they are preserved during convection has not been adequately explained. We demonstrate that the geographic patterns of chemical variations around the Earth's mantle endure as a direct result of whole-mantle convection within largely isolated cells defined by subducting plates.

Fetus in the Bladder: Rare Complication of Vesicouterine Fistula.

The work presents a rare case of spontaneous migration of an 11-week fetus from the uterine cavity into the urinary bladder cavity through the long-standing vesicouterine fistula.

[Certain indices of blood and leukocyte index of intoxication caused by tumor].

While tumors stage III-IV of hollow organs involved lowered lymphocyte count matched by relatively high leukocyte index of intoxication, those parameters remained unchanged in parenchymatous cancer. Changes in lymphocyte count were both rarer and more irregular in all tumor sites. Similar changes occurred in post-operative pyo-destructive complications of hollow organs.

Low-density lipoprotein receptor and apolipoprotein A-I and B expression in human enterocytes.

Low-density lipoprotein receptor (LDL-R) was found to be expressed in human small intestine epithelial cells, enterocytes. The relative abundance of LDL-R mRNA and protein was compared with that of apolipoproteins A-I (apoA-I) and B (apoB) in enterocytes and two other cell types: CaCo-2 and HepG2. The LDL-R mRNA content was comparable in three cell types.

Epidermal anti-Inflammatory properties of 5,11,14 20:3: effects on mouse ear edema, PGE2 levels in cultured keratinocytes, and PPAR activation.

Background: 5,11,14 20:3 is similar to 20:4n-6 but lacks the internal Delta8 double bond essential for prostaglandin and eicosanoid synthesis. When previously fed to laboratory animals as a gymnosperm seed oil component it has shown anti-inflammatory properties.

Results: Herein, topically applied Podocarpus nagi methyl esters (containing 26% 5,11,14 20:3) were incorporated into mouse ear phospholipids, reduced 20:4n-6, and reduced 20:4n-6- and TPA-induced mouse ear edema.

Peroxisome proliferator-activated receptor-alpha enhances lipid metabolism in a skin equivalent model.

Peroxisome proliferator-activated receptors are involved in certain cell types such as adipocytes and hepatocytes, in the control of several pathways of lipid synthesis or catabolism by regulating the gene expression level of key lipid metabolizing enzymes. As the epidermis exhibits an extensive lipid metabolism necessary for the establishment of the barrier function, we have examined the role of peroxisome proliferator-activated receptor-alpha activation in this process. Living skin equivalents were treated with Wy 14,643, a selective peroxisome proliferator- activated receptor-alpha ligand, which enhanced greatly the synthesis of membrane coating granules, the organelles specialized in the processing of stratum corneum lipids.

Differential expression of peroxisome proliferator-activated receptor subtypes during the differentiation of human keratinocytes.

The expression of mRNA encoding peroxisome proliferator-activated receptor (PPAR) subtypes in human keratinocytes was determined by semiquantitative reverse transcriptase-polymerase chain reaction. When normal human keratinocytes were induced to differentiate by shifting the culture medium to high Ca2+ concentration, the expression of PPAR-alpha and -gamma mRNA was increased, whereas that of PPAR-delta remained unchanged. At the protein level, the expression of PPAR in cultured human keratinocytes was demonstrated by a DNA mobility shift assay and the functionality of the receptor subtypes was assessed by transactivation experiments.

Insulin down-regulates angiotensinogen gene expression and angiotensinogen secretion in cultured adipose cells.

Adipose tissue is an important source of angiotensinogen (AT) after liver. Since an association exists between body mass index, hypertension, and insulin-resistance, the role of insulin on the regulation of AT gene expression and AT secretion was examined in cultured Ob1771 and 3T3-F442A adipose cells. Within a physiological range of concentrations (1-17 nM), insulin exerted a negative effect on the abundance of AT mRNA and the secretion of AT.

Regulation by glucocorticoids of angiotensinogen gene expression and secretion in adipose cells.

Adipose cells are an important source of angiotensinogen (AT). Its activation product, angiotensin II, stimulates in vitro and in vivo the production and release of prostacyclin which acts as a potent adipogenic signal in promoting the terminal differentiation of preadipocytes to adipocytes. Since glucocorticoids are known to promote adipose cell differentiation in vitro as well as in vivo, their role in the regulation of AT gene expression and secretion has been investigated in cultured Ob1771 mouse adipose cells.

Regulation by fatty acids of angiotensinogen gene expression in preadipose cells.

Adipocytes represent an important source of angiotensiongen (AT). Angiotensin II (A-II) stimulates in vitro and in vivo the formation and release of prostacyclin which acts as a potent adipogenic signal in triggering the terminal differentiation of preadipocytes into adipocytes [Darimont, Vassaux, Gaillard. Ailhaud and Négrel (1994) Int.

Fatty acids and retinoids act synergistically on adipose cell differentiation.

Fatty acids and retinoids have been recently reported to act as positive effectors of adipose cell differentiation. Treatment of Ob1771 preadipose cells with selective agonists of retinoic acid receptors (RARs) in the presence of alpha-bromopalmitate, a non-metabolized fatty acid, led to a potent synergy in regard to the differentiation process, as assayed by the activity of glycerol-3-phosphate dehydrogenase. The most potent synergy was observed with compound CD 367, a potent agonist of RARs as well as with compound Am 580, a specific agonist of RAR alpha.

Retinoids are positive effectors of adipose cell differentiation.

Retinoids, especially all-trans retinoic acid (t-RA), have been reported in the last decade to inhibit the differentiation of preadipose cells. In those studies, however, the concentrations of t-RA were supraphysiological (0.1-10 microM range).

Regulation of cholesterol uptake in the rat intestinal cell line.

A new model to study cholesterol absorption in the rat intestinal cells is described. Rat intestine epithelial cells IRD98 were incubated with mixed micelles containing bile acid, phospholipid, cholesterol or its nonabsorbable analogue, sitosterol, and trace amounts of [3H]cholesterol or [14C]sitosterol. Cholesterol and sitosterol uptake was then determined following lipid extraction; specific cholesterol uptake was determined as the difference between cholesterol and sitosterol uptake.

Cholesterol uptake in the human intestine. Hypo- and hyperresponsiveness.

Cholesterol uptake was studied at the small intestine biopsies taken from patients without intestinal malfunction. Three distinct groups of patients were described: those with low (146 +/- 19) nmol/mm2 per 2 h), medium (455 +/- 18 nmol/mm2 per 2 h) and high (833 +/- 24 nmol/mm2 per 2 h) rates of cholesterol uptake. Positive correlation between cholesterol uptake and intestinal cholesterol synthesis was observed in the last two groups.

[Regulation of cholesterol absorption in human and rat small intestine epithelial cells].

Cholesterol absorption in human small intestine organ culture and rat small intestine epithelial cell culture IRD-98 has been studied using [14C] cholesterol, [3H] cholesterol and [14C] sitosterol. It has been found that cholesterol absorption is a dose- and time-dependent process, while sitosterol absorption is not and makes up to about 25% of the total cholesterol absorption. Cholesterol absorption appeared to be a specific process.

New model to study cholesterol uptake in the human intestine in vitro.

A new model to study cholesterol uptake in the human intestine in vitro is described. Human small intestine organ cultures were incubated with mixed micelles containing bile acid, phospholipid, and cholesterol or its nonabsorbable analogue, sitosterol; trace amounts of labeled cholesterol or sitosterol were added to the micelles. After incubation, the lipids were extracted from the cells and cholesterol and sitosterol uptake was evaluated.

Studies on the proteins involved in the interaction of high-density lipoprotein with isolated human small intestine epithelial cells.

Treatment of 125I-labelled high-density lipoprotein ([125I]HDL3) with monospecific polyclonal antibodies against apolipoproteins A-I and A-II resulted in a dose-dependent inhibition of the [125I]HDL3 binding to isolated human small intestine epithelial cells by 25% and 50%, respectively. Both antibodies also inhibited intracellular degradation of [125I]HDL3 by 80%. Treatment of enterocytes with polyclonal antibody against apolipoprotein A-I binding protein, a putative HDL receptor, inhibited both binding and degradation of [125I]HDL3 by these cells by 50%.

[Assessment of patients' condition by noninvasive methods of examination in the follow-up after Fontan's operation in atresia of the right atrioventricular ostium].

The article discusses the results of using noninvasive methods to study the condition of patients (20) in late-term periods after Fonten's operation in atresia of the right atrioventricular orifice. All patients were subjected to physical examination, electro-, phono- and echocardiography, radiological examination, radioisotope scintigraphy, and left ventriculography. Most patients change to functional class I in the late-term periods after the operation.

Inhibition of cholesterol synthesis and esterification regulates high density lipoprotein interaction with isolated epithelial cells of human small intestine.

The effect of two inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, lovastatin and monacolin L, and an inhibitor of acyl coenzyme A:cholesterol acyltransferase (ACAT), Sandoz compound 58-035, on the interaction of 125I-labeled high density lipoprotein-3 (HDL3) with isolated human enterocytes was studied. Both HMG-CoA reductase inhibitors inhibited cholesterol synthesis and 125I-labeled HDL3 binding and degradation by enterocytes; a strong correlation between changes in cholesterol synthesis and interaction of 125I-labeled HDL3 with cells was observed. Lovastatin caused reduction of the apparent number of 125I-labeled HDL3 binding sites without affecting the binding affinity.

Both apolipoproteins B-48 and B-100 are synthesized and secreted by the human intestine.

Apolipoprotein B (apoB), an apolipoprotein associated with very low density lipoproteins and the atherogenic low density lipoproteins (LDL), directs the metabolism of lipoprotein particles in plasma by interacting with the LDL receptor. Utilizing human intestinal biopsy organ cultures, we have studied the synthesis of intestinal apoB in man. Intestinal organ cultures from normal adults (n = 6) were incubated in the presence of protease inhibitors in media supplemented with [35S]methionine.

Inhibition of cholesterol synthesis by lovastatin tested on six human cell types in vitro.

Lovastatin (mevinolin) caused a strong and dose-dependent inhibition of cholesterol synthesis in six types of cultured human cells. Fifty percent inhibition of cholesterol synthesis in human enterocytes was observed at a lovastatin concentration of about 0.004 ng/ml and in other cells at a lovastatin concentration of about 0.