bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selectivity for
d
-Lactate Incorporation into the Peptidoglycan Precursors of
Lactobacillus plantarum
: Role of Aad, a VanX-Like
d
-Alanyl-
d
-Alanine Dipeptidase
Authors: Deghorain Marie , Goffin Philippe , Fontaine Laetitia , Mainardi Jean-Luc , Daniel Richard , Errington Jeff , Hallet Bernard , Hols Pascal 
Published: March 2007

ABSTRACT

Lactobacillus plantarum
produces peptidoglycan precursors ending in
d
-lactate instead of
d
-alanine, making the bacterium intrinsically resistant to vancomycin. The ligase Ddl of
L. plantarum
plays a central role in this specificity by synthesizing
d
-alanyl-
d
-lactate depsipeptides that are added to the precursor peptide chain by the enzyme MurF. Here we show that
L. plantarum
also encodes a
d
-Ala-
d
-Ala dipeptidase, Aad, which eliminates
d
-alanyl-
d
-alanine dipeptides that are produced by the Ddl ligase, thereby preventing their incorporation into the precursors. Although
d
-alanine-ended precursors can be incorporated into the cell wall, inactivation of Aad failed to suppress growth defects of
L. plantarum
mutants deficient in
d
-lactate-ended precursor synthesis.
Identification of an AU-rich Translational Enhancer within theEscherichia coli fepBLeader RNA
Authors: Hook-Barnard India G. , Brickman Timothy J. , McIntosh Mark A. 
Published: March 2007

ABSTRACTThefepBgene encodes a periplasmic binding protein that is essential for the uptake of ferric enterobactin byEscherichia coli. Its transcription is regulated in response to iron levels by the Fur repressor. ThefepBtranscript includes a 217-nucleotide leader sequence with several features suggestive of posttranscriptional regulation. To investigate thefepBleader for its contribution tofepBexpression, defined deletions and substitution mutations in the leader were characterized usingfepB-phoAtranslational fusions. ThefepBleader was found to be necessary for maximalfepBexpression, primarily due to the influence of an AU-rich translational enhancer (TE) located 5′ to the Shine-Dalgarno sequence. Deletions or substitutions within the TE sequence decreasedfepB-phoAexpression fivefold. RNase protection and in vitro transcription-translation assays demonstrated that the TE augmented translational efficiency, as well as RNA levels. Moreover, primer extension inhibition assays showed that the TE increases ribosome binding. In contrast to the enhancing effect of the TE, the naturalfepBGUG start codon decreased ribosome binding and reducedfepBexpression 2.5-fold compared with the results obtained with leaders bearing an AUG initiation codon. Thus, the TE-GUG organization infepBresults in an intermediate level of expression compared to the level with AUG, with or without the TE. Furthermore, we found that the TE-GUG sequence is conserved among the eight gram-negative strains examined that havefepBgenes, suggesting that this organization may provide a selective advantage.
In what ways can human skeletal remains be used to understand health and disease from the past?
Authors: Metcalfe Neil H 
Published: April 2007

Abstract
Disease and illness in previous generations can be investigated using palaeopathology. This article describes the commonly used techniques in palaeopathology, includes examples of how such techniques are able to formulate data on a variety of health issues that occurred in the past and suggests how these data can be relevant today.
DNA sequence variations of metalloproteinases: their role in asthma and COPD
Authors: Sampsonas Fotis , Kaparianos Alexander , Lykouras Dimosthenis , Karkoulias Kiriakos , Spiropoulos Kostas 
Published: April 2007

Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are complex genetic diseases that cause considerable morbidity and mortality worldwide. Genetic variability interacting with environmental and ethnic factors is presumed to cause tobacco smoke susceptibility and to influence asthma severity. A disintegrin and metalloproteinase 33 (ADAM33) and matrix metalloproteinase-9 (MMP9) appear to have important roles in asthma and COPD pathogenesis. ADAM33 and MMP9 genetic alterations could possibly contribute to the establishment and progression of these multifactorial diseases, although their association with the clinical phenotypes has not yet been elucidated. However, the occurrence of these alterations does not always result in clear disease, implying that either they are an epiphenomenon or they are in proximity to the true causative alteration. This review summarises the most recent literature dealing with the genetic variations of metalloproteinases and outlines their potential pathogenetic outcome.
THE EARLY HISTORY OF HAND SURGERY IN THE PHILIPPINES AND HIGHLIGHTS IN MY EXPERIENCE AT THE NATIONAL ORTHOPAEDIC HOSPITAL MANDALUYONG AND THE OUR LADY OF LOURDES HOSPITAL, MANILA
Authors: Inocentes Eugenio M. 
Published: April 2007

Several years ago, while attending a Philippines Orthopaedic Association (PDA) Annual Convention, held at the Westin Philippine Plaza Hotel, Manila in December, I had the opportunity to meet with Professor Yoshikazu Ikuta, a well-known microsurgery and hand surgeon from Japan and one of the foreign guest speakers. I had been invited to work with him at the Armed Forces of the Philippines (AFP) Medical Center on the case of a high ranking general of the AFP, with a hand contracture disability problem. The case was referred to him by Dr. Evaristo Sanchez, Chief of Orthopaedics and the Commanding General of the AFP Medical Center. He had been pre-scheduled for surgery the next day, a Sunday morning, the day before Prof. Ikuta was due to return to Japan. After a brief examination and evaluation of the generals affected hand, in the operating room with Prof. Ikuta, just before he was placed under general anaesthesia, we performed the operation together. The operation did not involve microsurgery. The procedures done were multiple combined Bunnell-Zancolli pulley advancements and MP-joint volar capsulorraphies plus flexor tendon releases in the volar forearm, which although quite extensive, were only palliative, to minimise and improve on the contracture deformities, in preparation for a final re-evaluation for possible later, more definitive tendon transfers for hand function. However, I never received any further information regarding the results of our surgery. Recently, I have been honoured and invited again by Prof. Ikuta, presently the Editor-in-Chief of the Hand Surgery Journal (Asian Volume), this time to write the history of hand surgery in the Philippines and add to it, "Highlights in my experience at the National Orthopaedic Hospital, Mandaluyong, and the Our Lady of Lourdes Hospital, Manila", the last portion of which is on paralytic disabilities of the Hand. I am deeply grateful to Prof. Ikuta for giving me this honour and opportunity to present the total experience, favourable and unfavourable, of a hand surgeon from a developing country, like the Philippines. Furthermore, this would afford me also, the chance to be able to make known to readers of this now prestigious journal, the philosophical thoughts which led me to unwittingly originate or come up with and develop a few of my own "Long Tendon Rerouting Procedures" which may possibly and hopefully merit as this author's title contribution to surgery of the hands.
Transfection with Anti-p65 Intrabody Suppresses Invasion and Angiogenesis in Glioma Cells by Blocking Nuclear Factor-κB Transcriptional Activity
Authors: Li Liang , Gondi Christopher S. , Dinh Dzung H. , Olivero William C. , Gujrati Meena , Rao Jasti S. 
Published: April 2007

Abstract
Purpose: The strategy of intracellular antibodies to neutralize the function of target proteins has been widely developed for cancer research. This study used an intrabody against p65 subunit to prevent nuclear factor κB (NF-κB) transcriptional activity in glioma cells and to inhibit the expression of its target genes involved in the invasion and angiogenesis of human gliomas.
Experimental Design: A single-chain fragment of antibody variable region (scFv) against p65 was prepared using phage display technique. We then prepared an anti-p65 intrabody construct (pFv/nu) by cloning the scFv-encoding sequence into the mammalian nuclear-targeting vector, pCMV/myc/nuc.
Results: p65 expression in human glioma cells (U251 and] U87) transfected with pFv/nu was significantly decreased. We showed that NF-κB nuclear translocation and its DNA binding activity were blocked via intrabody transfection in electrophoretic mobility shift assays and the inhibition of NF-κB activity in nucleus resulted in the decreasing expression and bioactivity of matrix metalloproteinase-9, urokinase-type plasminogen activator receptor, urokinase-type plasminogen activator, and vascular endothelial growth factor. The intrabody transfected glioma cells showed a markedly lower level of invasion in Matrigel invasion assay. The capillary-like structure formation of endothelial cells was also repressed by coculture with the intrabody transfected glioma cells or exposure to their conditional medium. Intrabody transfection neither induced apoptosis nor altered cell proliferation in U251 and U87 cells as compared with the control vector pCMV/nu. After the injection of pFv/nu-transfected glioma cells, preestablished tumors were almost completely regressed when compared with mock, pCMV/nu, and pGFP/nu.
Conclusion: Blocking NF-κB activity via the nuclear intrabody expression might be a potential approach for cancer therapy.
Mcl-1 Is a Relevant Therapeutic Target in Acute and Chronic Lymphoid Malignancies: Down-Regulation Enhances Rituximab-Mediated Apoptosis and Complement-Dependent Cytotoxicity
Authors: Hussain Syed-Rehan A. , Cheney Carolyn M. , Johnson Amy J. , Lin Thomas S. , Grever Michael R. , Caligiuri Michael A. , Lucas David M. , Byrd John C. 
Published: April 2007

Abstract
Purpose: The antiapoptotic Bcl-2 family member protein Mcl-1 is dynamically regulated in transformed B-cells, has a short mRNA and protein half-life, and is rapidly processed during apoptosis. Multiple therapies cause down-regulation of Mcl-1 in chronic and acute lymphoid leukemia (CLL and ALL) cells. Mcl-1 has also been reported to mediate resistance to rituximab in CLL. We therefore investigated whether direct reduction of Mcl-1 was sufficient to induce apoptosis and increase sensitivity to rituximab.
Experimental Design: We used Mcl-1–specific small interfering RNA in ALL cell lines and tumor cells from CLL patients to block transcription of Mcl-1.
Results: We show that Mcl-1 down-regulation alone is sufficient to promote mitochondrial membrane depolarization and apoptosis in ALL and CLL cells. Given the importance of rituximab in B-cell malignancies, we next assessed the influence of Mcl-1 down-regulation on antibody-mediated killing. Mcl-1 down-regulation by small interfering RNA increased sensitivity to rituximab-mediated killing both by direct apoptosis and complement-dependent cytotoxicity, but did not enhance antibody-dependent cellular cytotoxicity.
Conclusions: These results show that Mcl-1 is a relevant therapeutic target for ALL and CLL, and its down-regulation has the potential to enhance the therapeutic effect of rituximab in CD20-bearing lymphoid cells.
3q26 Amplification and Polysomy of Chromosome 3 in Squamous Cell Lesions of the Lung: A Fluorescence In situ Hybridization Study
Authors: Pelosi Giuseppe , Del Curto Barbara , Trubia Maurizio , Nicholson Andrew G. , Manzotti Michela , Veronesi Giulia , Spaggiari Lorenzo , Maisonneuve Patrick , Pasini Felice , Terzi Alberto , Iannucci Antonio , Viale Giuseppe 
Published: April 2007

Abstract
Purpose: An overlapping area of gain at 3q26 has been reported in lung squamous cell carcinoma (SCC), but whether this also occurs in preneoplastic/preinvasive squamous cell proliferations and early-stage invasive carcinomas of the lung is still unknown.
Experimental Design: We evaluated the prevalence and the clinicopathologic implications of 3q26 amplification and polysomy of chromosome 3 in 31 preneoplastic/preinvasive squamous cell lesions of the bronchial mucosa and in 139 early-stage invasive pulmonary SCC, both of limited growth within the bronchial wall [early hilar SCC (EHSCC)] and involving the pulmonary parenchyma [parenchyma-infiltrating SCC (PISCC)]. Moreover, mRNA expression of two candidate genes (h-TERC and SKI-like), both mapping to the minimal common amplification region, was also studied by quantitative real-time reverse transcription-PCR.
Results: 3q26 amplification and polysomy of chromosome 3 were confined to malignant samples, with 37% of invasive SCC, and 27% of severe dysplasias/in situ carcinomas showing these chromosomal abnormalities. Amplification (with minimal common amplification region at 3q26.2), polysomy 3, concurrent amplification and polysomy 3, or other changes (monosomy) were found in 25 SCC and 1 dysplasia, 24 and 2, 2 and 0, and 1 and 0, respectively. Amplification was significantly associated with EHSCC, polysomy 3 with PISCC. 3q26 amplification correlated with increased tumor diameter and a history of smoking, whereas polysomy 3 correlated with tumor diameter, pT class, and p53, p21, and fascin immunoreactivity. No relationship of either 3q26 gain or polysomy was found with patients' survival. Overexpression of h-TERC or SKI-like mRNA was found in 3q26-amplified or polysomic SCC, with higher levels of h-TERC in the former and of SKI-like in the latter.
Conclusions: 3q26 amplification and chromosome 3 polysomy may be related to the development of invasive SCC, with differential distribution in tumor subsets, despite substantial histologic uniformity. Both h-TERC and SKI-like may be involved in tumor progression.
The impact of Epstein-Barr virus status on clinical outcome in diffuse large B-cell lymphoma
Authors: Park Sarah , Lee Jeeyun , Ko Young Hyeh , Han Arum , Jun Hyun Jung , Lee Sang Chul , Hwang In Gyu , Park Yeon Hee , Ahn Jin Seok , Jung Chul Won , Kim Kihyun , Ahn Yong Chan , Kang Won Ki , Park Keunchil , Kim Won Seog 
Published: March 2007

AbstractTo define prognostic impact of Epstein-Barr virus (EBV) infection in diffuse large B-cell lymphoma (DLBCL), we investigated EBV status in patients with DLBCL. In all, 380 slides from paraffin-embedded tissue were available for analysis by EBV-encoded RNA-1 (EBER) in situ hybridization, and 34 cases (9.0%) were identified as EBER-positive. EBER positivity was significantly associated with age greater than 60 years (P = .005), more advanced stage (P < .001), more than one extranodal involvement (P = .009), higher International Prognostic Index (IPI) risk group (P = .015), presence of B symptom (P = .004), and poorer outcome to initial treatment (P = .006). The EBER+ patients with DLBCL demonstrated substantially poorer overall survival (EBER+ vs EBER− 35.8 months [95% confidence interval (CI), 0-114.1 months] vs not reached, P = .026) and progression-free survival (EBER+ vs EBER− 12.8 months [95% CI, 0-31.8 months] vs 35.8 months [95% CI, 0-114.1 months], respectively (P = .018). In nongerminal center B-cell–like subtype, EBER in situ hybridization positivity retained its statistical significance at the multivariate level (P = .045). Nongerminal center B-cell–like patients with DLBCL with EBER positivity showed substantially poorer overall survival with 2.9-fold (95% CI, 1.1-8.1) risk for death. Taken together, DLBCL patients with EBER in situ hybridization+ pursued more rapidly deteriorating clinical course with poorer treatment response, survival, and progression-free survival.
Rapid transit in the immune cells: the role of mRNA turnover regulation
Authors: Khabar Khalid S A 
Published: March 2007

AbstractThere have been recent, significant advances about the role of mRNA turnover in controlling gene expression in immune cells. Post-transcriptional regulation of gene expression contributes to the characteristics of many of the processes underlying the immune response by ensuring early, rapid, and transient action. The emphasis of this review is on current work that deals with the regulation of mRNA decay during innate immunity against microbes and T cell activation as a model of the adaptive response.
Protection of CD8+ T cells from activation-induced cell death by IL-18
Authors: Li Wen , Kashiwamura Shin-ichiro , Ueda Haruyasu , Sekiyama Atsuo , Okamura Haruki 
Published: March 2007

AbstractRole of IL-18 on proliferation and survival of CD8+ T cells, activated by immobilized anti-CD3 antibody (anti-CD3), was examined. Proliferation and survival of activated T cells, especially that of CD8+ T cells, were impaired by IL-18 deficiency [IL-18 knockout (KO)]. After 3 days of culture with anti-CD3, the number of living CD8+ T cells from IL-18KO mice was ∼25% of that from wild-type (WT) mice but was increased to the same level as WT cells by the addition of IL-18. The expression of IL-18 receptors (IL-18Rs), particularly IL-18Rβ chain, in naïve CD8+ T cells was very low but elevated after stimulation with anti-CD3. Blockade of IL-18R by anti-IL-18R antibody on activated WT CD8+ T cells resulted in reduction of living cells, suggesting that IL-18 promotes survival of proliferating CD8+ T cells. Levels of Bcl-2 in activated IL-18KO CD8+ T cells were lower than those in WT cells but were raised by exogenous IL-18. Blockade of IL-18R on WT CD8+ T cells decreased the expression of surface markers CD122 and CD94, which are related to cell viability, and the expression of these markers was increased by exogenous IL-18 in IL-18KO cells. These results suggest that IL-18 acts directly on activated CD8+ T cells through IL-18Rs and promotes their survival to expand the population.
Localization of hCAP-18 on the surface of chemoattractant-stimulated human granulocytes: analysis using two novel hCAP-18-specific monoclonal antibodies
Authors: Stie Jamal , Jesaitis Andrew V , Lord Connie I , Gripentrog Jeannie M , Taylor Ross M , Burritt James B , Jesaitis Algirdas J 
Published: March 2007

AbstractThe well-described antimicrobial and immunoregulatory properties of human cathelicidin antimicrobial protein 18 (hCAP-18) derive in part from the ability of its proteolytic fragment, LL-37 (a.k.a. CAP-37), to associate with activated immune and epithelial cells during inflammation. We now show a stable association between hCAP-18 and the cell surface of formyl-Met-Leu-Phe (fMLF)-stimulated neutrophils using two novel hCAP-18-specific mAb, H7 and N9, which recognize a single 16-kDa band, identified by N-terminal sequencing and mass spectrometry as hCAP-18. Phage display analysis of epitope-binding sites showed that both mAb probably recognize a similar five amino acid sequence near the C terminus of the prodomain. Immunoblot analysis of degranulated neutrophil supernatants resulted in mAb recognition of the 14-kDa prodomain of hCAP-18. Subcellular fractionation of unstimulated neutrophils on density gradients showed expected cosedimentation of hCAP-18 with specific granule lactoferrin (LF). fMLF stimulation resulted in an average 25% release of specific granule hCAP-18, with ∼15% of the total cellular hCAP-18 recovered from culture media, and ∼10% and ∼75%, respectively, codistributing with plasma membrane alkaline phosphatase and specific granule LF. Surface association of hCAP-18 on fMLF-stimulated neutrophils was confirmed by immunofluorescence microscopy and flow cytometry analysis, which also suggested a significant up-regulation of surface hCAP-18 on cytochalasin B-pretreated, fully degranulated neutrophils. hCAP-18 surface association was labile to 10 mM NaOH treatment but resistant to 1 M NaCl and also partitioned into the detergent phase following Triton X-114 solubilization, possibly suggesting a stable association with one or more integral membrane proteins. We conclude that fMLF stimulation promotes redistribution of hCAP-18 to the surface of human neutrophils.
A vacuolar-type H+-ATPase and a Na+/H+exchanger contribute to intracellular pH regulation in cockroach salivary ducts
Authors: Hille Carsten , Walz Bernd 
Published: March 2007

SUMMARYCells of the dopaminergically innervated salivary ducts in the cockroach Periplaneta americana have a vacuolar-type H+-ATPase(V-ATPase) of unknown function in their apical membrane. We have studied whether dopamine affects intracellular pH (pHi) in duct cells and whether and to what extent the apical V-ATPase contributes to pHiregulation. pHi measurements with double-barrelled pH-sensitive microelectrodes and the fluorescent dye BCECF have revealed: (1) the steady-state pHi is 7.3±0.1; (2) dopamine induces a dose-dependent acidification up to pH 6.9±0.1 at 1 μmol l–1 dopamine, EC50 at 30 nmol l–1dopamine; (3) V-ATPase inhibition with concanamycin A or Na+-free physiological saline (PS) does not affect the steady-state pHi; (4)concanamycin A, Na+ -free PS and Na+/H+exchange inhibition with 5-(N-ethyl-N-isopropyl)-amiloride(EIPA) each reduce the rate of pHi recovery from a dopamine-induced acidification or an acidification induced by an NH4Cl pulse; (5)pHi recovery after NH4Cl-induced acidification is almost completely blocked by concanamycin A in Na+-free PS or by concanamycin A applied together with EIPA; (6) pHi recovery after dopamine-induced acidification is also completely blocked by concanamycin A in Na+-free PS but only partially blocked by concanamycin A applied together with EIPA. We therefore conclude that the apical V-ATPase and a basolateral Na+/H+ exchange play a minor role in steady-state pHi regulation but contribute both to H+extrusion after an acute dopamine- or NH4Cl-induced acid load.
Mechanics of cutting maneuvers by ostriches (Struthio camelus)
Authors: Jindrich Devin L. , Smith Nicola C. , Jespers Karin , Wilson Alan M. 
Published: March 2007

SUMMARYWe studied the strategies used by cursorial bipeds (ostriches) to maneuver during running. Eight ostriches were induced to run along a trackway and execute turns. Ground reaction forces and three-dimensional kinematics of the body and leg joints were simultaneously recorded, allowing calculation of joint angles and quasi-static net joint torques. Sidesteps, where the leg on the outside of the turn changes the movement direction, and crossovers using the inside leg, occurred with nearly equal frequency. Ostriches executed maneuvers using a simple control strategy that required minimal changes to leg kinematics or net torque production at individual joints. Although ostriches did use acceleration or braking forces to control body rotation, their morphology allowed for both crossovers and sidesteps to be accomplished with minimal net acceleratory/braking force production. Moreover, body roll and ab/adduction of the leg shifted the foot position away from the turn direction, reducing the acceleratory/braking forces required to prevent under-or over-rotation and aligning the leg with the ground reaction force.