13.56 MHz Triple Mode Rectifier Circuit With Extended Coupling Range for Wirelessly Powered Implantable Medical Devices.

In this work, a wide input/output range triple mode rectifier circuit operating at 13.56 MHz is implemented to power up medical implants. The proposed novel multi-mode rectifier circuit charges the load for an extended coupling range and eliminates the requirement of alignment magnets. The charging process is achieved in three different modes based on the voltage level of the received signal affected by the distance and the alignment of the inductively coupled coils. Current mode (CM) circuit is activated for loosely coupled coils whereas voltage mode (VM) rectification is proposed for high coupling ratios. Extended coupling range is covered with the activation of half wave rectification mode (HWM) in between CM and VM. The rectifier circuit utilizes these three modes in a single circuit operating at 13.56 MHz according to the receiver signal voltage. The circuit is implemented in TSMC 180 nm BCD technology with 0.9 mm2 active area and tested with printed coils. According to the measurements, the circuit operates in the received power range of 4 to 57.7 mW, which corresponds to 0.10-0.42 coupling range. The maximum power conversion efficiency (PCE) of each operation mode is 51.78%, 82.49%, and 89.34% for CM, HWM, and VM, respectively, while charging a 3.3 V load.

Which morphological abnormalities better define the elongation of transverse aortic arch: a magnetic resonance angiography study.

BACKGROUND: The aim of the study is to investigate the relation between morphological abnormalities that might indicate elongation of transverse aortic arch (ETA) and various aortic and thoracic measurements, and to determine which morphological criteria define the elongated transverse arch better. MATERIALS AND METHODS: Patients under 40 years of age who underwent contrast enhanced thoracic magnetic resonance angiography were included in the study. Images were evaluated for the presence of morphological arch abnormalities such as late take off (LTO) of left subclavian artery (LSA), flattening of the arch, and kinking at the posterior or anterior contour of the lesser curvature. Various aortic and thoracic measurements, including the distance between the orifices of the left common carotid artery (LCCA) and LSA, were made. Statistical relation between morphological abnormalities and these measurements was analysed. The effect of morphological abnormalities and their combinations on the distance between LCCA and LSA orifices was evaluated by linear regression analysis. RESULTS: Ninety three cases were included in the study. All morphological abnormalities and most of their combinations show statistically significant relation with longer LCCA to LSA distance. The parameters that most affected this distance were combination of flattening with LTO of LSA, anterior kinking and combination of anterior kinking with both flattening and LTO, respectively. CONCLUSIONS: Our study showed that the finding which best defines ETA is the combination of LTO and arch flattening. Therefore, we recommend using this combination in the diagnosis of ETA instead of the classical diagnostic criteria including combination of LTO and posterior kinking.

Elongated transverse aortic arch in subjects without turner syndrome: A preliminary computed tomography study.

The purpose of the present study was to investigate the presence of an elongated transverse aortic arch (ETA), which has been reported to be specific for Turner syndrome, in a population without Turner syndrome. A set of 1,012 patients (713 men, 299 women) under 40 years old, who underwent thoracic CT examination in our radiology department between July 2016 and December 2016, were included in the study. CT scans were performed by 16-slice scanners. CT images were retrieved from the picture archiving and communication system and retrospectively re-assessed by two radiologists. Diagnostic criteria for ETA, which are late take-off of the left subclavian artery (LSA), convex kinking of the inferior aortic arch along the lesser curvature and flattening of the transverse aortic arch, were searched in each case. The mean age of the study population was 25.5 ± 10.0 years. Late take-off of the LSA was detected in 17 (1.7%) subjects (10 men, 7 women). In six of these, the other criteria for ETA were not met. However, in the other 11 (1.1% of the study population) cases, in addition to late take-off of the LSA, aortic morphology was compatible with ETA. The dimensions of the aortic root and the ascending and descending aorta were within normal limits in all 17 cases. Our results supported the presence of ETA in subjects without Turner syndrome with ∼1.1% frequency. This is the first preliminary report regarding the frequency of ETA in non-Turner subjects. Clin. Anat. 31:887-890, 2018. © 2018 Wiley Periodicals, Inc.

Low back pain as the initial symptom of inferior vena cava agenesis.

Inferior vena cava (IVC) agenesis is a rare anomaly that is usually an incidental finding in radiologic work-up or it can rarely be symptomatic due to deep venous thrombosis of iliac veins. In this report, we present a case of IVC agenesis detected on lumbar spinal MR imaging scans by extensive epidural-paravertebral collateral vessels compressing the thecal sac and causing low back pain in a child.

Radiographic, CT, and MRI findings in primary pulmonary angiosarcoma.

We report a rare instance of primary pulmonary angiosarcoma presenting as a large solitary mass in the left upper lobe with mediastinal invasion. In particular, we emphasize the magnetic resonance (MR) imaging features, which included a markedly heterogeneous pattern consisting of hyperintense areas scattered throughout a background of intermediate signal intensity, rendering the lesion a cauliflower-like appearance especially on T2-weighted images. Being unreported so far in primary pulmonary angiosarcomas, these distinct MR imaging findings may be helpful in the differentiation of these neoplasms from lung cancers.

Novel carbapenem-hydrolyzing beta-lactamase, KPC-1, from a carbapenem-resistant strain of Klebsiella pneumoniae.

A Klebsiella pneumoniae isolate showing moderate to high-level imipenem and meropenem resistance was investigated. The MICs of both drugs were 16 microg/ml. The beta-lactamase activity against imipenem and meropenem was inhibited in the presence of clavulanic acid. The strain was also resistant to extended-spectrum cephalosporins and aztreonam. Isoelectric focusing studies demonstrated three beta-lactamases, with pIs of 7.2 (SHV-29), 6.7 (KPC-1), and 5.4 (TEM-1). The presence of bla(SHV) and bla(TEM) genes was confirmed by specific PCRs and DNA sequence analysis. Transformation and conjugation studies with Escherichia coli showed that the beta-lactamase with a pI of 6.7, KPC-1 (K. pneumoniae carbapenemase-1), was encoded on an approximately 50-kb nonconjugative plasmid. The gene, bla(KPC-1), was cloned in E. coli and shown to confer resistance to imipenem, meropenem, extended-spectrum cephalosporins, and aztreonam. The amino acid sequence of the novel carbapenem-hydrolyzing beta-lactamase, KPC-1, showed 45% identity to the pI 9.7 carbapenem-hydrolyzing beta-lactamase, Sme-1, from Serratia marcescens S6. Hydrolysis studies showed that purified KPC-1 hydrolyzed not only carbapenems but also penicillins, cephalosporins, and monobactams. KPC-1 had the highest affinity for meropenem. The kinetic studies also revealed that clavulanic acid and tazobactam inhibited KPC-1. An examination of the outer membrane proteins of the parent K. pneumoniae strain demonstrated that the strain does not express detectable levels of OmpK35 and OmpK37, although OmpK36 is present. We concluded that carbapenem resistance in K. pneumoniae strain 1534 is mainly due to production of a novel Bush group 2f, class A, carbapenem-hydrolyzing beta-lactamase, KPC-1, although alterations in porin expression may also play a role.

American Society of Microbiology 101st General Meeting. 20-24 May 2001, Orlando, FL, USA.

The application of sophisticated molecular biology, genetics and genomics has made possible the advanced analyses of microbial genes, the topology of DNA and chromosomes, and insight into the regulation of gene expression during all stages of the life cycle of microbes, both in vitro and in vivo. The struggle to control contagious pathogens continues world wide amidst resistance emergence to many classes of antimicrobial agents. Many hospital, research and community labs are applying themselves to a more thorough understanding of the molecular basis of this resistance. New drugs which improve on predecessor agents were presented. The following classes of antimicrobial agents were represented: quinolones, cephems, macrolides and natural products. New target opportunities against both lethal (essential) gene targets and virulence targets were presented throughout the conference. In addition, increasing attention to the involvement of microbial life forms in immune function and dysfunction were described in numerous presentations.

Characterization of the extended-spectrum beta-lactamase reference strain, Klebsiella pneumoniae K6 (ATCC 700603), which produces the novel enzyme SHV-18.

Klebsiella pneumoniae K6 (ATCC 700603), a clinical isolate, is resistant to ceftazidime and other oxyimino-beta-lactams. A consistent reduction in the MICs of oxyimino-beta-lactams by at least 3 twofold dilutions in the presence of clavulanic acid confirmed the utility of K. pneumoniae K6 as a quality control strain for extended-spectrum beta-lactamase (ESBL) detection. Isoelectric-focusing analysis of crude lysates of K6 demonstrated a single beta-lactamase with a pI of 7.8 and a substrate profile showing preferential hydrolysis of cefotaxime compared to ceftazidime. PCR analysis of total bacterial DNA from K6 identified the presence of a bla(SHV) gene. K6 contained two large plasmids with molecular sizes of approximately 160 and 80 kb. Hybridization of plasmid DNA with a bla(SHV)-specific probe indicated that a bla(SHV) gene was encoded on the 80-kb plasmid, which was shown to transfer resistance to ceftazidime in conjugal mating experiments with Escherichia coli HB101. DNA sequencing of this bla(SHV)-related gene revealed that it differs from bla(SHV-1) at nine nucleotides, five of which resulted in amino acid substitutions: Ile to Phe at position 8, Arg to Ser at position 43, Gly to Ala at position 238, and Glu to Lys at position 240. In addition to the production of this novel ESBL, designated SHV-18, analysis of the outer membrane proteins of K6 revealed the loss of the OmpK35 and OmpK37 porins.

Role of superoxide dismutase in in vivo and in vitro nitrate tolerance.

We assessed whether pharmacological inhibition of CuZn-superoxide dismutase (SOD) mimics the molecular mechanism of either in vitro or in vivo nitrovasodilator tolerance. In endothelium-intact aortic rings from in vivo tolerant rabbits the GTN- and acetylcholine (ACh)-induced maximal relaxation was attenuated by 36 and 23%, respectively. In vitro treatment of control rings with GTN (1 h 10 microM) similarly attenuated the vasorelaxant response to GTN, but not to ACh. Formation of superoxide radicals (*O2-) in endothelium-intact rings (lucigenin-chemiluminescence) increased 2.5 fold in in vivo tolerance, but significantly decreased in in vitro tolerance. The membrane associated NADH oxidase activity was increased 2.5 fold in homogenates of in vivo tolerant aortae, but was not changed in in vitro tolerant aorta. Conversely, SOD activity and protein expression was halved in in vivo tolerance, but SOD activity was not altered by in vitro tolerance. The *O2- scavenger tiron (10 mM) effectively restored the vasorelaxant response to GTN in in vivo tolerant aortic rings, but not the reduced response to GTN in in vitro tolerant rings. Pretreatment (1 h) of vessels with diethyldithiocarbamate (DETC; 10 mM) attenuated vasorelaxant responses to GTN and ACh, increased vascular *O2- production, and inhibited SOD activity in vessel homogenates to a similar degree as observed in in vivo tolerance. DETC-treatment of in vivo-tolerant vessels induced an additional increase in *O2- production. Increased *O2- production in in vivo nitrate tolerant aorta is associated with activation of vascular NADH oxidase and inactivation of CuZnSOD. Therefore, in vivo tolerance can be mimicked by in vitro inhibition of CuZnSOD, but not by in vitro exposure to GTN, which does not affect vascular *O2- production, NADH oxidase and CuZnSOD.

Escherichia coli DNA topoisomerase I copurifies with Tn5 transposase, and Tn5 transposase inhibits topoisomerase I.

Tn5 transposase (Tnp) overproduction is lethal to Escherichia coli. Genetic evidence suggested that this killing involves titration of E. coli topoisomerase I (Topo I). Here, we present biochemical evidence that supports this model. Tn5 Tnp copurifies with Topo I while nonkilling derivatives of Tnp, Delta37Tnp and Delta55Tnp (Inhibitor [Inh]), show reduced affinity or no affinity, respectively, for Topo I. In agreement with these results, the presence of Tnp, but not Delta37 or Inh derivatives of Tnp, inhibits the DNA relaxation activity of Topo I in vivo as well as in vitro. Other proteins, including RNA polymerase, are also found to copurify with Tnp. For RNA polymerase, reduced copurification with Tnp is observed in extracts from a topA mutant strain, suggesting that RNA polymerase interacts with Topo I and not Tnp.

Escherichia coli DNA topoisomerase I and suppression of killing by Tn5 transposase overproduction: topoisomerase I modulates Tn5 transposition.

Tn5 transposase (Tnp) overproduction is lethal to Escherichia coli. The overproduction causes cell filamentation and abnormal chromosome segregation. Here we present three lines of evidence strongly suggesting that Tnp overproduction killing is due to titration of topoisomerase I. First, a suppressor mutation of transposase overproduction killing, stkD10, is localized in topA (the gene for topoisomerase I). The stkD10 mutant has the following characteristics: first, it has an increased abundance of topoisomerase I protein, the topoisomerase I is defective for the DNA relaxation activity, and DNA gyrase activity is reduced; second, the suppressor phenotype of a second mutation localized in rpoH, stkA14 (H. Yigit and W. S. Reznikoff, J. Bacteriol. 179:1704-1713, 1997), can be explained by an increase in topA expression; and third, overexpression of wild-type topA partially suppresses the killing. Finally, topoisomerase I was found to enhance Tn5 transposition up to 30-fold in vivo.

Examination of the Tn5 transposase overproduction phenotype in Escherichia coli and localization of a suppressor of transposase overproduction killing that is an allele of rpoH.

Tn5 transposase (Tnp) overproduction is lethal to Escherichia coli. Tnp overproduction causes cell filamentation, abnormal chromosome segregation, and an increase in anucleated cell formation. There are two simple explanations for the observed phenotype: induction of the SOS response or of the heat shock response. The data presented here show that overproduction of Tnp neither induces an SOS response nor a strong heat shock response. However, our experiments do indicate that induction of some sigma32-programmed function(s) (either due to an rpoH mutation, a deletion of dnaK, or overproduction of sigma32) suppresses Tnp overproduction killing. This effect is not due to overproduction of DnaK, DnaJ, or GroELS. In addition, Tnp but not deltall Tnp (whose overproduction does not kill the host cells) associates with the inner cell membrane, suggesting a possible correlation between cell killing and Tnp membrane association. These observations will be discussed in the context of a model proposing that Tnp overproduction titrates an essential host factor(s) involved in an early cell division step and/or chromosome segregation.

Overexpression of the Tn5 transposase in Escherichia coli results in filamentation, aberrant nucleoid segregation, and cell death: analysis of E. coli and transposase suppressor mutations.

Overexpression of the Tn5 transposase (Tnp) was found to be lethal to Escherichia coli. This killing was not caused by transposition or dependent on the transpositional or DNA binding competence of Tnp. Instead, it was strictly correlated with the presence of a wild-type N terminus. Deletions removing just two N-terminal amino acids of Tnp resulted in partial suppression of this effect, and deletions of Tnp removing 3 or 11 N-terminal amino acids abolished the killing effect. This cytotoxic effect of Tnp overexpression is accompanied by extensive filament formation (i.e., a defect in cell division) and aberrant nucleoid segregation. Four E. coli mutants were isolated which allow survival upon Tnp overexpression, and the mutations are located at four discrete loci. These suppressor mutations map near essential genes involved in cell division and DNA segregation. One of these mutations maps to a 4.5-kb HindIII region containing the ftsYEX (cell division) locus at 76 min. A simple proposition which accounts for all of these observations is that Tnp interacts with an essential E. coli factor affecting cell division and/or chromosome segregation and that overexpression of Tnp titrates this factor below a level required for viability of the cell. Furthermore, the N terminus of Tnp is necessary for this interaction. The possible significance of this phenomenon for the transposition process is discussed.