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A case of brachial artery pseudoaneurysm in a premature infant is reported. The lesion was surgically resected, and arterial continuity restored by end to end anastomosis, The postoperative period and [...]

We present results of intense auroral kilometric radiation (AKR) sources direction finding based on single‐spacecraft k→vector source location performed in the frame of Interball‐2 mission (POLRAD experiment on board Auroral Probe). With our swept frequency analyzer we are not able to work with single AKR bursts generated in small, elementary sources, but we improve our signal‐to‐noise (s/n) ratio and determine direction to the AKR source region averaging data over 10 consecutive 4 kHz frequency steps. Measurements of directions to the AKR sources confirm recent Mutel et al. ([Mutel, R. L., 2008]) findings based on Cluster Very Long Baseline Interferometry (VLBI) data—AKR rays are mostly confined to the direction tangent to the auroral oval as measured in Mutel's tangent plane (TP) coordinates. In this paper we use additional coordinate system rotated with respect to TP coordinates in order to determine azimuths of AKR rays with respect to the auroral oval. We see cases of AKR propagation significantly deflected from the tangent plane. Additional information concerning geometry of auroral arc at the AKR source can help to distinguish between propagation along and propagation across the auroral cavity. Examples of instantaneous AKR visibility maps defined in this paper for both coordinate systems are shown and discussed. Using such map (valid for our spacecraft for relatively short observational periods of the order of 10 min), it is possible for known positions of the AKR sources in invariant latitude‐magnetic local time coordinates to visualize direction angles of AKR beams reaching the observer. Single s/c observations of intense AKR beaming confirm Mutel et al.'s findings based on Cluster/VLBI dataAKR visibility maps generated for single s/c visualize direction angles of observed AKR beamsCases of AKR propagation significantly deflected from the tangent plane have been observed

Background/Objective:: Subjects suffering from lipoprotein lipase (LPL) deficiency show very severe hypertriglyceridemia, often accompanied by recurrent bouts of pancreatitis. Dietary intervention is currently considered first-line treatment of this condition in paediatric age. The aim of our study was to compare the effects of dietary treatment with a low-fat diet alone and a low-fat diet enriched with omega-3-fatty acids. Subjects/Methods:: The data of 11 patients with LPL deficiency who were diagnosed in our lipid clinic between October 1997 and October 2007 were summarised. All patients had been treated with a low-fat diet, and in addition a group of five patients received supplements of omega-3-fatty acids over a period of at least 5 months. Results:: After adjustment for pre-intervention TG concentration, there was a statistically significant difference in post-intervention TG concentrations between the interventions, F(1,8)=13.529, P=0.006, partial ?2=0.628. Post-intervention-adjusted TG concentrations were statistically significantly greater in the low-fat diet group vs the w3 diet group (P<0.05). Conclusions:: We provide first evidence that a low-fat diet supplemented with omega-3-fatty acids results in a pronounced decrease in TG in paediatric patients affected with LPL deficiency. However, further studies are necessary to evaluate the long-term effects and safety of omega-3-fatty acids.

Recent evidence has implicated microRNAs (miRNAs) as potentially significant players in the acquisition of cancer-drug resistance in pancreatic and other cancers. To evaluate the potential contribution of miRNAs in acquired resistance to cisplatin in pancreatic cancer, we compared levels of more than 2000 human miRNAs in a cisplatin-resistant cell line (BxPC3-R) derived from parental (BxPC3) cells by step-wise exposure to increasing concentrations of the drug over more than 20 passages. The acquired drug resistance was accompanied by significant changes in the expression of 57 miRNAs, of which 23 were downregulated and 34 were upregulated. Employing a hidden Markov model (HMM) algorithm, we identified downregulation of miR-374b as likely being directly involved in acquisition of the drug-resistant phenotype. Consistent with this prediction, ectopic overexpression of miR-374b in the resistant BxPC3-R cells restored cisplatin sensitivity to levels approaching those displayed by the BxPC3 parental cells. The results are consistent with a growing body of evidence implicating miRNAs in acquired cancer-drug resistance and with the potential therapeutic value of these small regulatory RNAs in blocking and/or reversing the process.

Aim: This report investigated the relationship between anthropometric measurements of body fat distribution and lipid response to statins in hypercholesterolemic hypertensive patients. Methods: We prospectively examined 129 subjects who used either simvastatin 20 mg/day (no.=83) or atorvastatin 10 mg/day (no.=46) for 3 months. Anthropometry included evaluation of body mass index, waist and hip circumferences, and waist-to-hip-ratio. Results: Significant decreases in LDL (p<0.001), total cholesterol (p<0.001), and triglycerides (p=0.04) levels were detected after 3 months of therapy in the whole sample. At baseline, only an inverse correlation between waist circumference and HDL-cholesterol levels was detected (r=−0.18; p=0.04). Conversely, a direct relationship between hip circumference and HDL-cholesterol response to statins was found in the whole sample (r=0.24; p=0.006), while no other anthropometric measurement displayed significant correlation with lipid changes. The association between HDL-cholesterol response and hip circumference was further confirmed by stepwise regression analysis adjusted for baseline HDL-cholesterol levels, metabolic syndrome, body mass index, and waist circumference. Conclusions: Hip circumference, a surrogate marker of peripheral adiposity, is associated with HDL-cholesterol changes following statin therapy in hypertensive patients.

Ziel:Die Messung des aktuellen intravasalen Volumens mit Hilfe der Indikator-Verdünnungsmethode ist sowohl von klini-schem als auch von wissenschaftlichem Interesse. Bei der Ver-wendung des rasch eliminierten Farbstoffes Indocyanin-Grün (ICG) sind wiederholte Messungen und damit Verlaufskontrollen möglich. In der vorliegenden Studie sollten folgende Fragen geprüft werden: 1. Stimmen die von uns mit der ICG-Methode bei gesunden Probanden bestimmten Werte mit den in der Literatur angegebenen Kontrollwerten überein, und ist somit die Grundlage für die Durchführung weiterer klinischer Studien gegeben, und 2. Stimmen die Differenzen der vor und nach Eigenblutentnahme bzw. Retransfusion bestimmten Werte für das Plasmavolumen mit den tatsächlich entnommenen bzw. retransfundierten Volumina überein? Design:Prospektive Studie (an je 20 gesunden weiblichen bzw. männlichen Probanden). Rahmen:Forschungslabor einer anästhesiologischen Universitätsklinik. Teilnehmer:Je 20 gesunde weibliche bzw. männliche Probanden. Interventionen:Plasmavolumenbestimmung mit ICG vor und nach Entnahme von 10% des ge-schätzten Blutvolumens und nach Retransfusion. Ergebnisse:In der Gruppe der Frauen betrug das Plasmavolumen pro Körperoberfläche (PV/KO) 1639 ± 198 und bei den Männern 1687 ± 224 ml/m2 (Mittelwert ± SD). Durch die Eigenblutspende wurde den Frauen 188 ± 23 und den Männern 149 ± 26 ml/m2 PV entzogen. Die PV-Messung mit ICG ergab für diesen Ent-zug einen Wert von 198 ± 174 bzw. 171 ± 158 ml/m2 und für die Retransfusion 190 ± 169 bzw. 142 ± 154 ml/m2. Schluβfolgerungen:Die Kontrollwerte liegen in dem in der Literatur be-schriebenen Normbereich. Die gemessenen Differenzen der Plasmavolumina vor und nach Eigenblutspende bzw. nach Retransfusion stimmen mit den tatsächlich entnommenen Plasmavolumina im Mittel gut überein. Bei der klinischen Beurteilung im Einzelfall ist die methodisch bedingte hohe Standardabweichung zu berücksichtigen.

During the last decennia, our understanding of the neurobiological processes underlying learning and memory has continuously improved, leading to the identification of targets for the development of memory-enhancing drugs. Here we review a class of drugs which has more recently been identified: the phosphodiesterase (PDE) inhibitors. An overview is given of the different PDEs that are known and we focus on three PDEs which have been identified as possible relevant targets for memory improvement: PDE2, PDE4 and PDE5. PDEs differ in the substrate, i.e. cyclic adenosine monophosphate (cAMP) and/or cyclic guanosine monophosphate (cGMP), being hydrolyzed. Since these cyclic nucleotides have been suggested to play distinct roles in processes of memory, selective PDE inhibitors preventing the breakdown of cAMP and/or cGMP could improve memory. The present data suggest that PDE4 (cAMP) is involved in acquisition processes, although a possible role in late consolidation processes cannot be excluded. PDE5 (cGMP) is involved in early consolidation processes. Since PDE2 inhibition affects both cAMP and cGMP, PDE2 inhibitors may improve both memory processes. The field of PDEs is highly dynamic and new isoforms of PDEs are still being described. This may lead to the discovery and development of new memory enhancing drugs that selectively inhibit such isoforms. Such drugs may exert their effects only in specific brain areas and hence possess an improved side effect profile.

No abstracts.

Following a multiple-casualty construction disaster in Israel, members of The Center of Integrated Complementary Medicine joined in the emergency activity of the Shaare Zedek Medical Center. They administered homeopathic treatment to injured patients to supplement conventional orthopaedic treatment. This was to our knowledge the first time that complementary medicine had been used officially in conjunction with conventional medicine in an emergency situation. Our objective is to report and summarize the rationale, procedures and outcome of the complementary medicine intervention.

Recent experiments on `giant magnetoresistance' (GMR) and interlayer exchange coupling are reviewed. For a quantitative analysis of the coupling the frequency spectrum of coupled spinwave modes as observable by means of Brillouin light scattering can be evaluated. In the microscopic mechanism leading to GMR the contribution of spin-dependent scattering originating from interface roughness of the ferromagnetic/non-ferromagnetic interfaces is unambiguously identified in the case of Fe/Cr structures. We focus furthermore on the question of coupling mediated by semiconducting interlayers, which we investigated in the case of Fe_1−xSi_x and Si interlayers. Coupling across well ordered Si interlayers turns out to be surprisingly strong, in particular considering the fact that electrical CPP resistivity is found to be large.

Both purinergic stimulation and activation of cystic fibrosis transmembrane conductance regulator (CFTR) increases Cl secretion and inhibit amiloride-sensitive Na transport. CFTR has been suggested to conduct adenosine 5′-triphosphate (ATP) or to control ATP release to the luminal side of epithelial tissues. Therefore, a possible mechanism on how CFTR controls the activity of epithelial Na channels (ENaC) could be by release of ATP or uridine 5′-triphosphate (UTP), which would then bind to P2Y receptors and inhibit ENaC. We examined this question in native tissues from airways and colon and in Xenopus oocytes. Inhibition of amiloride-sensitive transport by both CFTR and extracellular nucleotides was observed in colon and trachea. However, nucleotides did not inhibit ENaC in Xenopus oocytes, even after coexpression of P2Y 2 receptors. Using different tools such as hexokinase, the P2Y inhibitor suramin or the Cl channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS), we did not detect any role of a putative ATP secretion in activation of Cl transport or inhibition of amiloride sensitive short circuit currents by CFTR. In addition, N ,2′- O -dibutyrylguanosine 3′,5′-cyclic monophosphate (cGMP) and protein kinase G (PKG)-dependent phosphorylation or the nucleoside diphosphate kinase (NDPK) do not seem to play a role for the inhibition of ENaC by CFTR, which, however, requires the presence of extracellular Cl.

A new manifestation of the Auroral Kilometric Radiation is put in evidence through the observations of the POLRAD wave experiment of the INTERBALL mission, the Wide Band Bursts of the AKR, or WBB AKR. It consists in bursts of radiation with a very broad bandwidth, typically 100 – 800 kHz. The whole frequency range is excited at once or in less than few minutes. This corresponds to the excitation of long segments of auroral field lines in a time often less that one minute. The sources of the emission are stretched along the field lines between altitudes ranging from 2000 to 20000 km. The relationship of these bursts to the development of auroral bulges, in the UV spectral range, is shown by the comparison of the POLRAD wave observations and those of the UV imager of the POLAR mission. It is shown that these bursts are generated during fast expansion of the auroral bulge. An accurate timing of the burst events is made with the time evolution of the frequency integrated wave energy flux. It shows that the bursts have a rise time of few minutes which is followed by an exponential relaxation with a characteristic time of few tens of minutes. The source of the bursts first expands along the field lines then it shrinks during the relaxation phase. The bursts are triggered few minutes before the maximum intensity of the UV auroral bulge. It is also shown that the bursts actually consist of a large number of individual broad bandwidth elements, each, lasting less than few seconds.

Regulator of G protein signaling (RGS) proteins function as GTPase-activating proteins (GAPs) that stimulate the inactivation of heterotrimeric G proteins. We have recently shown that RGS proteins may be regulated on a post-translational level (Benzing, T., Brandes, R., Sellin, L., Schermer, B., Lecker, S., Walz, G., and Kim, E. (1999) Nat. Med. 5, 913-918). However, mechanisms controlling the GAP activity of RGS proteins are poorly understood. Here we show that 14-3-3 proteins associate with RGS7 and RGS3. Binding of 14-3-3 is mediated by a conserved phosphoserine located in the Galpha-interacting portion of the RGS domain; interaction with 14-3-3 inhibits the GAP activity of RGS7, depends upon phosphorylation of a conserved residue within the RGS domain, and results in inhibition of GAP function. Collectively, these data indicate that phosphorylation-dependent binding of 14-3-3 may act as molecular switch that controls the GAP activity keeping a substantial fraction of RGS proteins in a dormant state.

Serotonin (5-HT) receptor agonists with high affinity for the different subtypes (i.e. 5-HT1A–1F, 5-HT2A–2C) of the 5-HT1- and 5-HT2receptor families have been shown to affect ingestive behavior. It has been assumed that: (1) stimulation of hypothalamic 5-HT2Cor 5-HT1Breceptors leads to a behaviorally specific hypophagic effect by accelerating satiety processes; (2) stimulation of 5-HT2Areceptors leads to a disruption of the feeding cascade; and (3) stimulation of 5-HT1Aand 5-HT2Breceptors leads to a hyperphagic effect. The present paper reviews studies performed with the relatively selective receptor agonists ipsapirone (5-HT1A), CP-94,253 (5-HT1B), BW 723C86 (5-HT2B) and ORG 37684 (5-HT2C), as well as the nonselective receptor agonists TFMPP (5-HT1B/2C), m-CPP (5-HT2C/1B) and DOI (5-HT2A/2C) in a variety of feeding paradigms in rats, both after systemic and local injection. These studies support a role for other neuroanatomical regions (i.e. brain stem) and behavioral mechanisms (i.e. appetitive processes) in the hypophagic effects of these compounds, possibly as a function of the administered dose. Studies with 5-HT receptor antagonists indicate that the proposed role of particular 5-HT1/2receptor subtypes in the hypophagic effects of these 5-HT receptor agonists may be more complicated than originally thought. Further characterization of the role of 5-HT1/2receptor subtypes in the control of ingestive behavior will require extensive pharmacological and behavioral studies, using more selective receptor agonists and antagonists and different behavioral procedures, as well as verification in transgenic animals.

Interleukin-10 (IL-10) is a cytokine that has pleiotropic effects on a variety of different cell types. Although many of the biologic responses induced by IL-10 are also induced by other cytokines, such as IL-6, IL-10 is relatively unique in its ability to potently inhibit production of pro-inflammatory cytokines in macrophages. In this study, we have used gain-of-function and loss-of-function genetic approaches to define the intracellular components involved in the different biologic actions of IL-10. Herein, we demonstrate that the ability of IL-10 to inhibit tumor necrosis factor alpha (TNFalpha) production in lipopolysaccharide-stimulated macrophages requires the presence of Stat3, Jak1, and two distinct regions of the IL-10 receptor intracellular domain. Macrophages deficient in Stat3 or Jak1 were unable to inhibit lipopolysaccharide-induced TNFalpha production following treatment with murine IL-10. Structure-function analysis of the intracellular domain of the IL-10 receptor alpha chain showed that whereas two redundant Stat3 recruitment sites (427YQKQ430 and 477YLKQ480) were required for all IL-10-dependent effects on either B cells or macrophages, expression of IL-10-dependent anti-inflammatory function required the presence on the intracellular domain of the IL-10 receptor of a carboxyl-terminal sequence containing at least one functionally critical serine. These results thus demonstrate that IL-10-induced inhibition of TNFalpha production requires two distinct regions of the IL-10 receptor intracellular domain and thereby establish a distinctive molecular basis for the developmental versus the anti-inflammatory actions of IL-10.

Epithelial Na+ channels (ENaC) are inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) upon activation by protein kinase A. It is, however, still unclear how CFTR regulates the activity of ENaC. In the present study we examined whether CFTR interacts with ENaC by interfering with the Nedd4- and ubiquitin-mediated endocytosis of ENaC. Various C-terminal mutations were introduced into the three alpha-, beta-, and gamma-subunits of the rat epithelial Na+ channel, thereby eliminating PY motifs, which are important binding domains for the ubiquitin ligase Nedd4. When expressed in Xenopus oocytes, most of the ENaC stop (alpha-H647X, beta-P565X, gamma-S608X) or point (alpha-P671A, beta-Y618A, gamma-P(624-626)A) mutations induced enhanced Na+ currents when compared with wild type alpha,beta,gamma-rENaC. However, ENaC currents formed by either of the mutant alpha-, beta-, or gamma-subunits were inhibited during activation of CFTR by forskolin (10 micromol/l) and 3-isobutyl-1-methylxanthine (1 mmol/l). Antibodies to dynamin or ubiquitin enhanced alpha,beta,gamma-rENaC whole cell Na+ conductance but did not interfere with inhibition of ENaC by CFTR. Another mutant, beta-T592M,T593A-ENaC, also showed enhanced Na+ currents, which were down-regulated by CFTR. Moreover, activation of ENaC by extracellular proteases and xCAP1 does not disturb CFTR-dependent inhibition of ENaC. We conclude that regulation of ENaC by CFTR is distal to other regulatory limbs and does not involve Nedd4-dependent ubiquitination.

Regulation of amiloride‐sensitive epithelial Na+channels (ENaC) is a prerequisite for coordination of electrolyte transport in epithelia. Downregulation of Na+conductance occurs when the intracellular Na+concentration is increased during reabsorption of electrolytes, known as feedback inhibition. Recent studies have demonstrated the involvement of αG0and αGi2proteins in the feedback control of ENaC in mouse salivary duct cells. In this report, we demonstrate that Na+feedback inhibition is also present in Xenopusoocytes after expression of rat α,β,γ‐ENaC. Interfering with intracellular αG0or αGi2signaling by coexpression of either constitutively active αG0/αGi2or dominant negative αG0/αGi2and by coinjecting sense or antisense oligonucleotides for αG0had no impact on Na+feedback. Moreover, no evidence for involvement of the intracellular G protein cascade was found in experiments in which a regulator of G protein signaling (RGS3) or β‐adrenergic receptor kinase (βARK) was coexpressed together with α,β,γ‐ENaC. Although some experiments suggest the presence of an intracellular Na+receptor, we may conclude that Na+feedback in Xenopusoocytes is different from that described for salivary duct cells in that it does not require G protein signaling.

Colonic crypt cells possess basolateral Ca²⁺-regulated K⁺ channels which support Cl^- secretion by providing the necessary driving force. The pharmacological characteristics of these channels were examined in Ussing chamber experiments of rat and rabbit colon mucosa by the use of blockers. The chromanol 293B, a blocker of K_VLQT1 channels, and clotrimazole (CTZ), a blocker of small Ca²⁺-activated K⁺ channels, blocked stimulated Cl^- secretion completely. Small-conductance Ca²⁺-activated K⁺ channels (SK) in excised basolateral patches of rat colonic crypts were inhibited concentration dependently by the imidazoles CTZ, NS004 and NS1619 and activated by 1-EBIO. These properties are similar to those of the known human SK channel (hSK4). hSK4-expressing Xenopus laevis oocytes showed ionomycin-activated and CTZ-inhibited K⁺ currents. When P2Y₂ receptors were coexpressed these currents were also activated by ATP. The concentration/response curve was identical to that of rat SK channels. In human colonocytes (T84) exposed to hSK4 antisense probes, but not to sense probes, carbachol-induced K⁺ currents were attenuated. With RT-PCR an hSK4 could be demonstrated in human colon and in T84 colonocytes. By homology cloning the SK of the rat colon (rSK4) was identified. This protein has a high homology to hSK4 and mouse IK1. These data indicate that the Ca²⁺-activated and imidazole-inhibited basolateral K⁺ current in the colon is caused by SK4 channels.

Enhanced osmotic water permeability has been observed in Xenopus oocytes expressing cystic fibrosis transmembrane conductance regulator (CFTR) protein. Subsequent studies have shown that CFTR activates an endogenous water permeability in oocytes, but that CFTR itself is not the water channel. Here, we show CFTR-dependent activation of endogenous water permeability in normal but not in cystic fibrosis human airway epithelial cells. Cell volume was measured by novel confocal x-z laser scanning microscopy. Glycerol uptake and antisense studies suggest CFTR-dependent regulation of aquaporin 3 (AQP3) water channels in airway epithelial cells. Regulatory interaction was confirmed by coexpression of CFTR and AQP3 cloned from human airways in Xenopus oocytes and of CFTR and rat AQP3 in Chinese hamster ovary cells. These findings indicate that CFTR is a regulator of AQP3 in airway epithelial cells.

Regulation of amiloride-sensitive epithelial Na channels (ENaC) is a prerequisite for coordination of electrolyte transport in epithelia. Downregulation of Na conductance occurs when the intracellular Na concentration is increased during reabsorption of electrolytes, known as feedback inhibition. Recent studies have demonstrated the involvement of αG 0 and αG i2 proteins in the feedback control of ENaC in mouse salivary duct cells. In this report, we demonstrate that Na feedback inhibition is also present in Xenopus oocytes after expression of rat α,β,γ-ENaC. Interfering with intracellular αG 0 or αG i2 signaling by coexpression of either constitutively active αG 0 /αG i2 or dominant negative αG 0 /αG i2 and by coinjecting sense or antisense oligonucleotides for αG 0 had no impact on Na feedback. Moreover, no evidence for involvement of the intracellular G protein cascade was found in experiments in which a regulator of G protein signaling (RGS3) or β-adrenergic receptor kinase (βARK) was coexpressed together with α,β,γ-ENaC. Although some experiments suggest the presence of an intracellular Na receptor, we may conclude that Na feedback in Xenopus oocytes is different from that described for salivary duct cells in that it does not require G protein signaling.

Secretion of Cl^- requires the presence of a K⁺ conductance to hyperpolarize the cell, and to provide the driving force for Cl^- exit via luminal Cl^- channels. In the exocrine pancreas Cl^- secretion is mediated by an increase in cytosolic Ca²⁺ ([Ca²⁺]_i). Two types of Ca²⁺-activated K⁺ channels could be shown in pancreatic acinar cells of different species. However, there are no data on Ca²⁺-activated K⁺ channels in rat pancreatic acini. Here we examine the basolateral K⁺ conductance of freshly isolated rat pancreatic acinar cells in cell-attached and cell-excised patch-clamp experiments. Addition of carbachol (CCH, 1 µmol/l) to the bath led to the activation of very small conductance K⁺ channels in cell-attached patches (n=27), producing a noisy macroscopic outward current. The respective outward conductance increased significantly by a factor of 2.10.1 (n=27). Noise analysis revealed a Lorentzian noise component with a corner frequency (f_c) of 30.33.5 Hz (n=19), consistent with channel activity in these patches. The estimated single-channel conductance was 1.50.4 pS (n=19). In cell-excised patches (inside out) from cells previously stimulated with CCH, channel activity was only observed in the presence of K⁺ in the bath solution. Under these conditions f_c was 47.611.9 Hz (estimated single-channel conductance 1.10.2 pS, n=20). The current/voltage relationship of the noise showed weak inward rectification and the reversal potential shifted towards E_K⁺ when Na⁺ in the bath was replaced by K⁺. Channel activity in cell-excised patches was slightly reduced by 10 mmol/l Ba²⁺ (23.62.1% of the total outward current) and was completely absent when K⁺ in the bath was replaced by Na⁺. Reduction of the [Ca²⁺]_i from 1 mmol/l to 1 µmol/l in cell-excised experiments decreased the current by 52.312.3% (n=5). Expression of K_VLQT1, one of the possible candidates for a small-conductance K⁺ channel in rat pancreatic acinar cells, was shown by reverse transcriptase polymerase chain reaction (RT-PCR). In fact, a K_VLQT-blocker (chromanol 293B) reduced channel activity in seven excised patches. These data suggest that CCH activates very small conductance K⁺ channels in rat pancreatic acinar cells, most likely via an increase in [Ca²⁺]_i.

The effect of drawing on the structure and molecular orientation of polyamide-6 fibers has been investigated by ¹³C solid-state NMR. The molecular orientation in the fibers is determined using a two-dimensional rotor synchronized magic-angle spinning (MAS) experiment. For the highly oriented fibers order parameters up to 〈P6〉 are determined. By using a ¹³C T1ρ filter, the orientation in the rigid (crystalline + rigid amorphous) and mobile (amorphous) regions are separately determined. The orientation in the rigid phase increases rapidly at low draw ratios up to λ = 3.5 and levels off at higher draw ratios (〈P2〉 ≈ 0.75). The mobile amorphous phase remains disordered for low draw ratios but orients rapidly for draw ratios above λ = 3.5. By using a ¹³C T1 filter, ¹³C MAS spectra of the crystalline phase are obtained, from which the relative amounts of the α- and γ-phase can be quantitatively determined using spectral deconvolution. It appears that upon drawing the ^α/γ ratio changes from ⁶⁰/40 for an undrawn fiber to almost completely α for a fully drawn fiber. The NMR results are qualitatively supported by wide-angle X-ray spectroscopy (WAXS) photos.