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PubMed1998

Efficient coexpression and secretion of anti-atherogenic human apolipoprotein AI and lecithin-cholesterol acyltransferase by cultured muscle cells using adeno-associated virus plasmid vectors.

Plasma apolipoprotein AI (apoAI) and lecithin-cholesterol acyltransferase (LCAT) play important roles in reverse cholesterol transport, promoting the removal of excess cholesterol from peripheral cells and reducing formation of atherosclerotic lesions. Gene augmentation of either apoAI or LCAT, or both, are thus attractive targets for prevention or treatment of atherosclerosis. With the eventual aim of safe and efficient gene delivery to skeletal muscle, our chosen secretory platform for systemic delivery of anti-atherogenic proteins, we have constructed conventional and AAV-based plasmid vectors containing human apoAI or LCAT cDNAs; their efficacy was tested by lipoplex transfection of mouse C2C12 muscle cells or human 293 cells. The secretion of apoAI or LCAT by transduced cultures was two- to five-fold higher using AAV-based plasmid vectors than conventional plasmid vectors. Additionally, cells transfected with a bicistronic AAV-based vector containing an internal ribosome entry site (IRES) efficiently expressed both apoAI and LCAT simultaneously. Furthermore, AAV-based vector sequences were retained by host cells, whereas those of conventional plasmid vectors were lost. These studies indicate that ectopic overexpression of apoAI and LCAT in muscle tissue using AAV-based plasmid vectors might provide a feasible anti-atherogenic strategy in vivo.

Animals↗

PubMed1999

Changes in plasma apolipoprotein AI and AII concentrations in murine reactive amyloidosis.

Based on the recent findings that patients with systemic amyloidosis have reduced plasma apolipoprotein AII (apoAII) concentrations, this study assessed the behaviour of apolipoprotein AI (apoAI) and apoAII in a murine model of reactive amyloidosis. ICR mice were subjected to a single inflammatory stimulus and then sacrificed at the end of week 1 (group I), week 2 (group II) or week 8 (group III). Amyloid deposits were found in approximately one-half of the animals. Plasma apoAI and apoAII concentrations were reduced in all stimulated animals compared with control animals. In groups II and III, apoAII and apoAII/apoAI ratios were lower in the amyloidotic animals than in nonamyloidotic animals, similar to findings in the human amyloidosis patients. Both apoAI and apoAII mRNA in the liver were reduced in group I, but not in group II or III. Both apoAI and apoAII were detected immunohistochemically in the amyloid deposits in groups I and II, but not in group III. Thus, the reduction of plasma apoAs in the amyloid-forming phase may be due, in part, to the involvement of high-density lipoproteins in the deposits. However, that in the chronic phase may be affected by other mechanisms.

Amyloidosis↗

PubMed2002

Serum apolipoprotein AI levels in atherosclerotic and diabetic patients.

OBJECTIVE: To evaluate the association between Apolipoprotein AI (ApoAI), Apolipoprotein B100 (ApoB) and the presence of lower limb atherosclerotic occlusive disease. MATERIALS AND METHODS: Serum lipids, lipoprotein fractions, ApoAI, ApoB and Lp(a) were measured in 52 patients (28 diabetics and 24 non-diabetics) with lower limb occlusive disease. They were evaluated according to patients' glucose and compared with those in 75 healthy controls. RESULTS: There was a significant decrease in HDL-cholesterol and ApoAI serum levels (p = 0.000001) and an increase in Lp(a) (p = 0.000001) in patients as compared to controls. No difference was observed in total cholesterol, non HDL-cholesterol or triglycerides. Multiple regression analysis revealed a significant association between low ApoAI (or HDL) levels and the disease as well as between high Lp(a) levels and the disease. ApoAI (p = 0.0003), HDL-cholesterol (p = 0.00005) and total cholesterol (p = 0.01) levels were significantly lower in diabetic patients compared to non-diabetic patients. Lp(a) levels did not correlate with fasting glucose concentration. Multiple regression analysis revealed a significant association between low ApoAI (or HDL) levels and diabetes. CONCLUSION: Decreased ApoAI appears to be a main component of the dyslipidaemic serum profile observed in patients with atherosclerotic occlusive disease of the lower extremities. Increased Lp(a) levels is an independent risk factor. Decreased HDL-cholesterol is also involved in the dyslipidaemic profile.

Adult↗

PubMed2000

Induction of the apolipoprotein AI gene by fasting: a relationship with ketosis but not with ketone bodies.

Apolipoprotein AI (apoAI) expression is inversely related to the incidence of atherosclerosis. ApoAI expression is also influenced by the nutritional state and diabetes. We used both cell culture and animal models to examine the effect of fasting and ketoacidosis on apoAI gene expression. Two days of food deprivation in rats increased hepatic and intestinal apoAI mRNA by 2.6- and 2.3-fold, respectively (P < .05). The absolute concentration of plasma apoAI did not change. However, the plasma apoAI concentration relative to the plasma concentration of serum proteins was increased 23% (P < .05). In fasting rats, there was a significant positive correlation between the serum beta-hydroxybutyrate concentration and hepatic or intestinal apoAI mRNA level. Despite this correlation, changes in apoAI mRNA are probably not mediated by ketone bodies, since neither hepatic nor intestinal apoAI mRNA levels were altered in rats maintained on a ketogenic diet for 10 days or treated with isobutyramide, an orally active ketone analog. In addition, the activity of the rat apoAI promoter was not altered in Hep G2 cells treated with isobutyramide or fatty acids or exposed to hypoglycemic conditions, while dexamethasone increased promoter activity 1.9-fold (P < .05). These data indicate that metabolic changes other than ketone bodies, such as an increase in plasma glucocorticoids, may account for starvation-induced expression of apoAI.

3-Hydroxybutyric Acid↗

PubMed2002

Effects of dehydroepiandrosterone on rat apolipoprotein AI gene expression in the human hepatoma cell line, HepG2.

Serum apolipoprotein AI (apoAI) levels correlate with the risk of developing atherosclerosis. Previous studies have suggested that dehydroepiandrosterone (DHEA) lowers high-density lipoprotein (HDL)-cholesterol levels. We investigated whether or not DHEA may lower HDL-cholesterol levels by suppressing apoAI gene transcription in hepatocytes. ApoAI mRNA levels, assessed by Northern blotting, were suppressed in HepG2 cells treated with DHEA (34%) (10 microg/mL) or testosterone (36%) (T, 1 microg/mL). Estradiol alone (E2, 1 microg/mL) had relatively little effect on apoAI mRNA levels, while E2 in combination with DHEA prevented a decrease in apoAI mRNA levels compared to DHEA alone. To determine whether these effects were due to changes in apoAI gene transcription, HepG2 cells were transfected with a plasmid carrying the full-length promoter of the rat apoAI gene ligated into a chloramphenicol acetyltransferase (CAT) reporter construct. The plasmid pCMV.SPORT-beta-gal was included in each transfection to normalize the data to transfection efficiency. Cells were then cultured in the presence or absence of DHEA (10 microg/mL), T (1 microg/mL), 17alpha-methyltestosterone (MTT, 1 microg/mL), 5alpha-dihydrotestosterone (DHT, 1 microg/mL), E2 (1 microg/mL), or a combination of DHEA plus E2, T plus E2, MTT plus E2, and DHT plus E2, for 24 hours. CAT activity, relative to beta-galactosidase activity, was reduced by 19.6%, 57.6%, 38.6%, and 54.6% with DHEA, T, DHT, and MTT addition, respectively. E2 increased CAT activity by 43.8%. When the androgens (ie, DHEA, T, DHT, or MTT) were combined with E2, apoAI promoter activity was suppressed. We conclude, therefore, that androgens downregulate apoAI promoter activity in the presence or absence of E2. However, the changes in mRNA levels do not always reflect changes in promoter activity, suggesting that these steroids may have additional post-transcriptional effects on steady-state apoAI mRNA levels. It remains to be established if the transcriptional effects we observed are mediated through an androgen response element.

Animals↗

PubMed2004

High-density lipoprotein and apolipoprotein AI increase endothelial NO synthase activity by protein association and multisite phosphorylation.

NO propagates a number of antiatherogenic effects in the endothelium, and diminished availability has been associated with vascular disease. Recently it has been reported that phosphorylation of endothelial NO synthase (eNOS) at Ser-1179 is required to increase activity in response to stimuli, including high-density lipoprotein (HDL). The current study was undertaken to further examine the mechanism by which HDL activates eNOS and to specifically determine the role of the major apolipoprotein of HDL, apolipoprotein AI (ApoAI). Phosphorylation of eNOS residues Ser-116, Ser-617, Ser-635, Ser-1179, and Thr-497 after incubation with ApoAI and HDL was examined. There were significant increases in phosphorylation at Ser-116 in response to both HDL and ApoAI and similar magnitudes of dephosphorylation at Thr-497. Ser-1179 phosphorylation increased transiently but returned to basal level after 2.5 min. Data demonstrating activation of AMP activated protein kinase (AMPK) during HDL and ApoAI incubation suggests that AMPK may play a role in activation of eNOS. NO release in response to HDL and ApoAI stimulation in endothelial cells paralleled the time frames of phosphorylation, suggesting a causal relationship. Furthermore, ApoAI was found to associate with eNOS in endothelial cells and bind transfected eNOS in Chinese hamster ovary cells, whereas confocal data demonstrates colocalization of ApoAI and eNOS in the perinuclear region, suggesting a protein-protein interaction. Collectively, the results indicate that HDL and ApoAI increase eNOS activity by multisite phosphorylation changes, involving AMPK activation after protein association between ApoAI and eNOS.

AMP-Activated Protein Kinases↗

PubMed1985

Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV genes.

The genes for two of the proteins of the plasma lipid transport system, apolipoprotein AI (apoAI) and CIII (apoCIII) are closely linked in the human genome. An approximately equal to 30-kilobase (kb) DNA segment containing these genes and their flanking sequences has been cloned and extensively characterized. Hybridization studies revealed that a DNA fragment located 12 kb 3' to the apoAI gene contains sequences homologous to a 1.8-kb mRNA transcript in human fetal intestine and adult liver but not in fetal liver, kidney, heart, brain, or muscle. This DNA fragment was used as a probe to isolate a clone from an adult human liver cDNA library. The nucleotide sequence of this clone is 74.8% homologous to the cDNA sequence of rat apolipoprotein AIV (apoAIV), another protein of the lipid transport system, and codes for a protein that is 58.6% identical to rat apoAIV. These results indicate that apoAI, apoCIII, and apoAIV genes are closely linked in the human genome and suggest that all three of them are derived from a common ancestral precursor.

Amino Acid Sequence↗

PubMed1992

Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis.

A mutation in the gene for apolipoprotein AI (apoAI) was identified in an English family with autosomal dominant non-neuropathic systemic amyloidosis. The plasma of all affected individuals contained a variant apoAI with one additional charge, as well as normal apoAI. The propositus was heterozygous; the coding region of his apoAI gene contained both the normal sequence and a single-base substitution changing the codon for residue 60 of the mature protein from CTG (leucine) to CGG (arginine). Allele-specific oligonucleotide hybridization showed that the other affected individuals were also heterozygotes and that there was concordance of the mutant allele with the presence of variant plasma apoAI. Amyloid fibrils isolated from the spleen of the propositus consisted of proteins that ran as a doublet with an apparent mass of approximately 10 kDa in SDS/PAGE and a trace band at 28 kDa. Electrospray mass spectrometry of the purified 10-kDa material revealed components with mass corresponding to the N-terminal 88, 92, 93, and 94 residues of apoAI each with substitution of arginine for leucine. These observations were confirmed by direct protein sequencing and laser desorption time-of-flight mass analysis. No material with the normal apoAI sequence was detected. The trace band at 28 kDa yielded the N-terminal sequence of mature apoAI, indicating that intact or minimally degraded apoAI was also present in the fibril preparation. Discovery of this mutation and the detailed characterization of the apoAI fragments that form the amyloid fibrils open additional avenues for investigation of amyloidogenesis.

Amino Acid Sequence↗

PubMed1999

Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway.

We previously have described the cAMP-mediated induction of cholesterol and phospholipid efflux from the murine macrophage RAW264 cell line to lipid-free apolipoprotein acceptors. This induction of cholesterol efflux is associated with increased binding and association of apolipoprotein to the cells. In the present study, using primarily apolipoprotein AI (apoAI) as the acceptor, cAMP-dependent cholesterol efflux to apolipoprotein acceptors was associated with apoAI binding to coated pits, cellular uptake, and resecretion. After cell association and washing, 58% of the apoAI was resecreted during a 90-min chase period. In addition, after apoAI uptake and washing, cholesterol efflux was observed during a chase period without additional acceptors. Cholesterol efflux was partially blocked by chlorpromazine and hypertonic media, two inhibitors of coated pit endocytosis. Cholesterol efflux to apoAI was found to depend on extracellular calcium. By temporally separating the cAMP induction phase from the apoAI chase phase, calcium was found to be required during the apoAI chase phase rather than during the cAMP induction period. In the absence of calcium the 8-Br-cAMP-mediated induction of apoAI binding was maintained, but the specific apoAI cellular association was inhibited. The data are consistent with a model for cholesterol efflux to apolipoproteins that involves a calcium-dependent endocytic pathway, followed by recycling and the subsequent release of the nascent lipoprotein particle from the cell.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1995

Involvement of early growth response factor Egr-1 in apolipoprotein AI gene transcription.

Liver-specific expression of the apolipoprotein AI (apoAI) gene is mediated by transcription factors bound to three sites (A, B, and C) in the apoAI enhancer. Sites A and C bind various members of the nuclear receptor superfamily, including the orphan nuclear receptor apolipoprotein regulatory protein-1 (ARP-1); site B binds the liver-enriched factor hepatic nuclear factor-3. The immediate early growth response factor (Egr-1), which is transiently expressed in various pathophysiologic states of the liver, activates the apoAI enhancer and overcomes ARP-1-mediated repression of the enhancer in hepatoblastoma HepG2 cells. Deletion mapping analysis revealed two Egr-1 binding sites, E1 and E2, flanking site A. Erg-1 bound efficiently to both E1 and E2. Sp1 in HepG2 nuclear extracts bound to E2 but not E1. In HepG2 cells, E1 functioned as an Egr-1 response element, whereas E2 had high basal activity and was not further induced by Egr-1. Mutations that prevent Egr-1 binding to the apoAI enhancer abolished its responsiveness to Erg-1, while they had only minor effects on its constitutive activity. These mutations also diminished the ability of Egr-1 to overcome ARP-1-mediated repression. Elimination of transcription factor binding to sites A, B, or C reduced enhancer activity without affecting Egr-1-dependent activation. We argue that Egr-1 is recruited to the apoAI enhancer complex under unusual circumstances, such as those prevailing during liver regeneration, to maintain apoAI transcription levels by overriding prior transcriptional controls.

Apolipoprotein A-I↗

PubMed1995

Properties of an N-terminal proteolytic fragment of apolipoprotein AI in solution and in reconstituted high density lipoproteins.

Limited proteolysis was used to study the domain structure and to produce a large N-terminal fragment of human apolipoprotein AI (apoAI). Digestion of reconstituted high density lipoprotein (rHDL) prepared with apoAI and dipalmitoyl phosphatidylcholine or palmitoyloleoyl phosphatidylcholine by chymotrypsin, trypsin, elastase, and subtilisin generated a major fragment of 22 kDa. Under milder conditions proteolysis of lipid-free apoAI produced a fragment of similar size. The fragments shared the same N terminus as intact apoAI, and the chymotryptic fragment had a molecular weight of 22,384 as determined by electrospray ionization mass spectrometry. Thus the fragment consists of the N-terminal 192 amino acid residues of apoAI, and the region around Tyr192 seems to be especially accessible to proteases. In aqueous solution the fragment, apoAI-(1-192), had an alpha-helix content similar to that of apoAI (approximately 52%) but existed only as monomers and dimers. ApoAI-(1-192) lysed dimyristoyl phosphatidylcholine liposomes slowly compared with apoAI but did form rHDL complexes with palmitoyloleoyl phosphatidylcholine or dipalmitoyl phosphatidylcholine when prepared by the sodium cholate dialysis method. ApoAI-(1-192) rHDL exhibited sizes and size distributions distinct from apoAI rHDL but displayed similar stability against denaturation. The isolated apoAI-(1-192) rHDLs retained a high ability to activate lecithin-cholesterol acyltransferase, comparable with the most effective apoAI rHDL. The results suggest that the C-terminal domain of apoAI is crucial for self-association and initial lipid binding but is not involved in specific lecithin-cholesterol acyltransferase activation.

Amino Acid Sequence↗

PubMed1996

Control of apolipoprotein AI gene expression through synergistic interactions between hepatocyte nuclear factors 3 and 4.

Apolipoprotein AI (apoAI) gene expression in liver depends on synergistic interactions between transcription factors bound to three distinct sites (A, B, and C) within a hepatocyte-specific enhancer in the 5'-flanking region of the gene. In this study, we showed that a segment spanning sites A and B retains substantial levels of enhancer activity in hepatoblastoma HepG2 cells and that sites A and B are occupied by the liver-enriched hepatocyte nuclear factors (HNFs) 4 and 3, respectively, in these cells. In non-hepatic CV-1 cells, HNF-4 and HNF-3beta activated this minimal enhancer synergistically. This synergy was dependent upon simultaneous binding of these factors to their cognate sites, but it was not due to cooperativity in DNA binding. Separation of these sites by varying helical turns of DNA did not affect simultaneous binding of HNF-3beta and HNF-4 nor did it influence their functional synergy. The synergy was, however, dependent upon the cell type used for functional analysis. In addition, this synergy was further potentiated by estrogen treatment of cells cotransfected with the estrogen receptor. These data indicate that a cell type-restricted intermediary factor jointly recruited by HNF-4 and HNF-3 participates in activation of the apoAI enhancer in liver cells and suggest that the activity of this factor is regulated by estrogen.

Animals↗

PubMed1998

Estrogen regulation of the apolipoprotein AI gene promoter through transcription cofactor sharing.

Estrogen replacement therapy increases plasma concentrations of high density lipoprotein and its major protein constituent, apolipoprotein AI (apoAI). Studies with animal model systems, however, suggest opposite effects. In HepG2 cells stably expressing estrogen receptor alpha (ERalpha), 17beta-estradiol (E2) potently inhibited apoAI mRNA steady state levels. ApoAI promoter deletion mapping experiments indicated that ERalpha plus E2 inhibited apoAI activity through the liver-specific enhancer. Although the ERalpha DNA binding domain was essential but not sufficient for apoAI enhancer inhibition, ERalpha binding to the apoAI enhancer could not be detected by electrophoretic mobility shift assays. Western blotting and cotransfection assays showed that ERalpha plus E2 did not influence the abundance or the activity of the hepatocyte-enriched factors HNF-3beta and HNF-4, two transcription factors essential for apoAI enhancer function. Expression of the ERalpha coactivator RIP140 dramatically repressed apoAI enhancer function in cotransfection experiments, suggesting that RIP140 may also function as a coactivator on the apoAI enhancer. Moreover, estrogen regulation of apoAI enhancer activity was dependent upon the balance between ERalpha and RIP140 levels. At low ratios of RIP140 to ERalpha, E2 repressed apoAI enhancer activity, whereas at high ratios this repression was reversed. Regulation of the apoAI gene by estrogen may thus vary in direction and magnitude depending not only on the presence of ERalpha and E2 but also upon the intracellular balance of ERalpha and coactivators utilized by ERalpha and the apoAI enhancer.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Activation of apolipoprotein AI gene expression by protein kinase A and kinase C through transcription factor, Sp1.

Our previous finding that insulin induces apolipoprotein AI (apoAI) transcription points to the participation of intracellular signaling. This finding prompted us to ask whether two classical G-protein-coupled signaling pathways requiring activated protein kinase A (PKA) or kinase C (PKC) may also regulate apoAI. Therefore, human hepatoma, Hep G2 cells stably transfected with pAI.474-CAT, a reporter construct spanning -474 to -7 of apoAI DNA fused to chloramphenicol acetyltransferase (CAT) were treated with 10 microm forskolin (FSK) or 50 nm phorbol dibutyrate (PDBu) to activate PKA and PKC, respectively. Results showed that the apoAI promoter activity increased 4-5-fold following 24 h of treatment with either FSK or PDBu. Induction by either agent was blocked with actinomycin D but not the protein synthesis inhibitor, cycloheximide. The PKA inhibitor, PKI 14-22 amide, abrogated induction by FSK, 100 microm 8-bromo-cAMP, or 100 ng/ml cholera toxin, but it had no effect on activation via PKC. Similarly, PDBu induction was attenuated by 2 microm of the PKC inhibitor, GF109203X, but it did not affect FSK activity. Next we used deletional constructs to show that the actions of FSK and PDBu required the insulin-responsive core element (IRCE). This motif matched the consensus binding site for the transcription factor, Sp1. The binding of Sp1 to the IRCE was confirmed by gel-retardation and supershift analysis. Site-directed mutagenesis of the IRCE eliminated Sp1 action and induction by FSK or PDBu. Whereas overexpression of Sp1 enhanced basal and FSK or PDBu induced promoter activity, transfection of an antisense oligomer against Sp1 mRNA attenuated both parameters. In summary, activation of PKA or PKC increases apoAI promoter activity. The activity of both signaling pathways is mediated by the IRCE, a motif that binds the transcription factor, Sp1.

Apolipoprotein A-I↗

PubMed2004

Two homologous apolipoprotein AI mimetic peptides. Relationship between membrane interactions and biological activity.

Two related 18-amino acid, class A, amphipathic helical peptides termed 3F-2 and 3F14 were chosen for this study. Although they have identical amino acid compositions and many similar biophysical properties, 3F-2 is more potent than 3F14 as an apolipoprotein AI mimetic peptide. The two peptides exhibit similar gross conformational properties, forming structures of high helical content on a membrane surface. However, the thermal denaturation transition of 3F-2 is more cooperative, suggesting a higher degree of oligomerization on the membrane. Both 3F-2 and 3F14 promote the segregation of cholesterol in membranes containing phosphatidylcholine and cholesterol, but 3F-2 exhibits a greater selectivity for partitioning into cholesterol-depleted regions of the membrane. Magic angle spinning/NMR studies indicate that the aromatic residues of 3F-2 are stacked in the presence of lipid. The aromatic side chains of this peptide also penetrate more deeply into membranes of phosphatidylcholine with cholesterol compared with 3F14. Using the fluorescent probe, 1,3-dipyrenylpropane, we monitored the properties of the lipid hydrocarbon environment. 3F-2 had a greater effect in altering the properties of the hydrocarbon region of the membrane. The results are consistent with our proposed model of the effect of peptide shape on the nature of the difference in peptide insertion into the bilayer.

Amino Acid Sequence↗

PubMed1989

Cardiovascular and ventilatory responses during formalized T'ai Chi Chuan exercise.

T'ai Chi Chuan (TCC) is a widely practiced Chinese martial art said to physically develop balance and coordination as well as enhance emotional and mental health. TCC consists of a series of postures combined into a sequential movement providing a smooth, continuous, low-intensity activity. The purpose of this study was to examine the ventilatory and cardiovascular responses to the Long Form of Yang's style TCC. In addition, the subjects' TCC responses were compared to their ventilatory and cardiovascular responses during cycle ergometry at an oxygen consumption (VO2) equivalent to the mean TCC VO2. Six experienced (M = 8.3 yrs) male TCC practitioners served as subjects with data collected during the Cloud H and movement of the TCC exercise. Significantly (p less than .05) lower responses for ventilatory frequency (Vf) (11.3 and 15.7 breaths.min-1), ventilatory equivalent (VE/VO2) (23.47 and 27.41), and the ratio of dead space ventilation to tidal volume (VD/VT) (20 and 27%) were found in TCC in comparison to cycle ergometry. The percentage of minute ventilation used for alveolar ventilation was significantly higher during TCC (p less than .03) than cycle ergometry, with mean values of 81.1% and 73.1%, respectively. Cardiac output, stroke volume, and heart rate were not significantly different between TCC exercise and cycle ergometry at the same oxygen consumption. We concluded that, during TCC, expert practitioners show significantly different ventilatory responses leading to more efficient use of the ventilatory volume than would be expected from comparable levels of exertion on a cycle ergometer.

Adult↗

PubMed2000

Effectiveness and biomechanics of spinal orthoses in the treatment of adolescent idiopathic scoliosis (AIS).

In this prospective study, the effectiveness and biomechanical factors of spinal orthoses in the treatment of moderate adolescent idiopathic scoliosis (AIS) patients were investigated. In the first 20 months of orthotic treatment, the values of standing AP Cobb's angle, apical vertebral rotation, lumbar lordosis as well as thoracic kyphosis showed significant reduction (P<0.05), however, the angle of trunk inclination and trunk listing did not. The values of those reducible parameters reached their lowest values within the first 12 months of orthotic treatment and then the values gradually increased but they were still below the pre-brace values. The mean pressure of The pressure pads was found to be 7.09 +/- 1.77 kPa (53.2 +/- 13.3 mmHg) while the mean tension of the straps was 26.8 +/- 5.2N. The standing AP Cobb's angle strongly correlated with the pad pressure (correlation coefficient=0.931, p<(.05) and strap tension (correlation coefficient=0.914, p<0.05). The strap tension and pad pressure strongly correlated and the correlation coefficient was 0.873 (p<0.05). This suggests that in the consideration of biomechanical function of spinal orthoses, the focus may be upon how tightly the orthosis was fastened and if the location and direction of the pressure pads are the correct. Therefore, for enhancing independent standard tension should be set in each strap, and regular and close monitoring is needed.

Adolescent↗

PubMed1997

Structure of poly d(AI).poly d(CT) in two different packing arrangements.

X-ray diffraction analysis of poly d(AI).poly d(CT) in oriented and polycrystalline fibers has revealed the DNA structure to be a 10-fold, right-handed, antiparallel, Watson-Crick base paired double helix in two distinct packing arrangements corresponding to one and two helices, respectively, in the unit cell. The helix pitch is 32.1 A and 32.4 A in the two cases, almost 1.5 A shorter than in classical B-DNA. The resulting B'-DNA geometry, described in terms of a tetranucleotide repeat which is conformationally similar to B-DNA, has its minor groove closely shut and major groove correspondingly widened, thus striking a sharp morphological contrast to B-DNA. According to difference electron density maps, a spine of hydration along the minor groove connects both strands and provides structural stability; ordered sodium ions and water molecules are actively involved in bridging the phosphate groups of neighboring helices. The crystallographic R-values for these two allomorphs are 0.26 and 0.20, respectively, for data up to 3.0 A resolution.

Crystallography, X-Ray↗