Efficacy of TachoSil® patches in controlling Dacron suture-hole bleeding after abdominal aortic aneurysm open repair

<p>Abstract</p> <p>Purpose</p> <p>The aim of this study is evaluate the efficacy of TachoSil^®patches in controlling suture-hole bleeding after elective infrarenal abdominal aortic aneurysm (AAA) replacement with Dacron graft.</p> <p>Materials and methods</p> <p>Patients undergoing elective replacement of infrarenal AAA with Dacron grafts were prospectively randomized to TachoSil^®patches (Group I) or standard compression with surgical swabs (Group II).</p> <p>We evaluated time to haemostasis, blood loss during the operation, blood loss after cross-clamp removal, duration of operation, drain volume, requirement for blood transfusion and surgeons rating of efficacy.</p> <p>Results</p> <p>Twenty patients were randomized (10 patients in each treatment Group). The mean time to haemostasis was 264 ± 127.1 s (range: 180-600 s) in Group I and 408 ± 159.5 s (range: 120-720 s) in Group II (p = 0.026); mean blood loss during the operation was 503.5 ± 20.7 cc (range: 474-545 cc) in Group I and 615.7 ± 60.3 cc (range: 530-720 cc) in Group II (p < 0.001); mean blood loss after cross-clamp removal was 26.5 ± 4 g (range: 22-34 g) in Group I and 45.4 ± 4.6 (range: 38-52 g) in Group II (p < 0.001) and mean drain volume was 116.7 ± 41.4 cc (range: 79-230 cc) in Group I and 134.5 ± 42.8 cc (range: 101-250 cc) in Group II (p = 0.034). There were no serious adverse events associated with use of TachoSil^®patches.</p> <p>Conclusion</p> <p>For patients undergoing aortic reconstruction with Dacron grafts, TachoSil^®patches were found to be safe and effective for the control of suture-hole bleeding.</p

Eradication of multidrug-resistant Acinetobacter baumannii in a female patient with total hip arthroplasty, with debridement and retention: a case report

<p>Abstract</p> <p>Introduction</p> <p>Multidrug-resistant <it>Acinetobacter baumannii </it>has become a significant cause of healthcare-associated infections, but few reports have addressed <it>Acinetobacter baumannii </it>infections associated with orthopedic devices. The current recommended treatment for complicated infections due to orthopedic devices, including resistant gram-negative rods, consists of antimicrobial therapy with debridement and removal of implants.</p> <p>Case presentation</p> <p>The patient, a 47-year-old woman, had previously had a prior total hip arthroplasty at 16 years of age for a complex femoral neck fracture, and multiple subsequent revisions. This time, she underwent a fifth revision secondary to pain. Surgery was complicated by hypotension resulting in transfer to the intensive care unit and prolonged respiratory failure. She received peri-operative cefazolin but postoperatively developed surgical wound drainage requiring debridement of a hematoma. Cultures of this grew ampicillin-sensitive <it>Enterococcus </it>and <it>Acinetobacter baumannii </it>(sensitive only to amikacin and imipenem). The patient was started on imipenem. Removal of the total hip arthroplasty was not recommended because of the recent surgical complications, and the patient was eventually discharged home. She was seen weekly for laboratory tests and examinations and, after 4 months of therapy, the imipenem was discontinued. She did well clinically for 7 months before recurrent pain led to removal of the total hip arthroplasty. Intra-operative cultures grew ampicillin-sensitive <it>Enterococcus </it>and coagulase-negative <it>Staphylococcus </it>but no multidrug-resistant <it>Acinetobacter baumannii</it>. The patient received ampicillin for 8 weeks and had not had recurrent infection at the time of writing, 37 months after discontinuing imipenem.</p> <p>Conclusion</p> <p>We describe the successful treatment of an acute infection from multidrug-resistant <it>Acinetobacter baumannii </it>with debridement and retention of the total hip arthroplasty, using monotherapy with imipenem. This case challenges the general assumption that all orthopedic-device infections due to multidrug-resistant gram-negative organisms will require hardware removal. Further studies are needed to determine if organisms such as multidrug-resistant <it>Acinetobacter baumannii </it>are amenable to treatment with hardware retention.</p

Eradication of multidrug-resistant Acinetobacter baumannii in a female patient with total hip arthroplasty, with debridement and retention: a case report

<p>Abstract</p> <p>Introduction</p> <p>Multidrug-resistant <it>Acinetobacter baumannii </it>has become a significant cause of healthcare-associated infections, but few reports have addressed <it>Acinetobacter baumannii </it>infections associated with orthopedic devices. The current recommended treatment for complicated infections due to orthopedic devices, including resistant gram-negative rods, consists of antimicrobial therapy with debridement and removal of implants.</p> <p>Case presentation</p> <p>The patient, a 47-year-old woman, had previously had a prior total hip arthroplasty at 16 years of age for a complex femoral neck fracture, and multiple subsequent revisions. This time, she underwent a fifth revision secondary to pain. Surgery was complicated by hypotension resulting in transfer to the intensive care unit and prolonged respiratory failure. She received peri-operative cefazolin but postoperatively developed surgical wound drainage requiring debridement of a hematoma. Cultures of this grew ampicillin-sensitive <it>Enterococcus </it>and <it>Acinetobacter baumannii </it>(sensitive only to amikacin and imipenem). The patient was started on imipenem. Removal of the total hip arthroplasty was not recommended because of the recent surgical complications, and the patient was eventually discharged home. She was seen weekly for laboratory tests and examinations and, after 4 months of therapy, the imipenem was discontinued. She did well clinically for 7 months before recurrent pain led to removal of the total hip arthroplasty. Intra-operative cultures grew ampicillin-sensitive <it>Enterococcus </it>and coagulase-negative <it>Staphylococcus </it>but no multidrug-resistant <it>Acinetobacter baumannii</it>. The patient received ampicillin for 8 weeks and had not had recurrent infection at the time of writing, 37 months after discontinuing imipenem.</p> <p>Conclusion</p> <p>We describe the successful treatment of an acute infection from multidrug-resistant <it>Acinetobacter baumannii </it>with debridement and retention of the total hip arthroplasty, using monotherapy with imipenem. This case challenges the general assumption that all orthopedic-device infections due to multidrug-resistant gram-negative organisms will require hardware removal. Further studies are needed to determine if organisms such as multidrug-resistant <it>Acinetobacter baumannii </it>are amenable to treatment with hardware retention.</p

Fluxes and Warping for Gauge Couplings in F-theory

We compute flux-dependent corrections in the four-dimensional F-theory effective action using the M-theory dual description. In M-theory the 7-brane fluxes are encoded by four-form flux and modify the background geometry and Kaluza-Klein reduction ansatz. In particular, the flux sources a warp factor which also depends on the torus directions of the compactification fourfold. This dependence is crucial in the derivation of the four-dimensional action, although the torus fiber is auxiliary in F-theory. In M-theory the 7-branes are described by an infinite array of Taub-NUT spaces. We use the explicit metric on this geometry to derive the locally corrected warp factor and M-theory three-from as closed expressions. We focus on contributions to the 7-brane gauge coupling function from this M-theory back-reaction and show that terms quadratic in the internal seven-brane flux are induced. The real part of the gauge coupling function is modified by the M-theory warp factor while the imaginary part is corrected due to a modified M-theory three-form potential. The obtained contributions match the known weak string coupling result, but also yield additional terms suppressed at weak coupling. This shows that the completion of the M-theory reduction opens the way to compute various corrections in a genuine F-theory setting away from the weak string coupling limit.Comment: 46 page

Antioxidant activities and phenolic contents of the methanol extracts of the stems of Acokanthera oppositifolia and Adenia gummifera

Abstract Background Acokanthera oppositifolia Lam (family: Apocynaceae) is a shrub or small tree with white latex, and the leaves of this plant are used in the form of a snuff to treat headaches and in infusions for abdominal pains and convulsions and septicaemia. Adenia gummifera Harv of the family Passifloraceae is a distinctive woody climber whose infusions are used as emetics and are said to help with some forms of depression. Lipid peroxidation has gained more importance today because of its involvement in pathogenesis of many diseases. Free radicals are the main agents in lipid peroxidation. Antioxidants thus play an important role of protecting the human body against damage by the free radicals. Plants containing phenolic compounds have been reported to possess strong antioxidant properties. Methods The antioxidant activities and phenolic contents of the methanol extracts of the stems of Acokanthera oppositifolia and Adenia gummifera were evaluated using in vitro standard procedures. Spectrophotometry was the basis for the determinations of total phenol, total flavonoids, flavonols, and proanthocyanidins. Tannins, quercetin and catechin equivalents were used for these parameters. The antioxidant activities of the stem extract of Acokanthera oppositifolia were determined by the 2,2'-azinobis-3- ethylbenzothiazoline-6-sulfonic acid (ABTS), 1,1-Diphenyl-2-picrylhydrazyl (DPPH), and ferrous reducing antioxidant property (FRAP) methods. Results The results from this study showed that the antioxidant activities of the stem extract of Acokanthera oppositifolia as determined by the 1,1-Diphenyl-2-picrylhydrazyl (DPPH), and ferrous reducing antioxidant property (FRAP) methods, were higher than that of Adenia gummifera. The levels of total phenols and flavonols for A. oppositifolia were also higher. On the other hand, the stem extract of Adenia gummifera had higher level of total flavonoids and proanthocyanidins than that of Acokanthera oppositifolia. The 2, 2'-azinobis-3- ethylbenzothiazoline-6-sulfonic acid (ABTS) activities of the 2 plant extracts were similar and comparable to that of BHT. Conclusion Thus, the present results indicate clearly that the extracts of Acokanthera oppositifolia and Adenia gummifera possess antioxidant properties and could serve as free radical inhibitors or scavengers, acting possibly as primary antioxidants. This study has to some extent validated the medicinal potential of the stems of Acokanthera oppositifolia and Adenia gummifera.</p

Nutritional upgrading for omnivorous carpenter ants by the endosymbiont Blochmannia

<p>Abstract</p> <p>Background</p> <p>Carpenter ants (genus <it>Camponotus</it>) are considered to be omnivores. Nonetheless, the genome sequence of <it>Blochmannia floridanus</it>, the obligate intracellular endosymbiont of <it>Camponotus floridanus</it>, suggests a function in nutritional upgrading of host resources by the bacterium. Thus, the strongly reduced genome of the endosymbiont retains genes for all subunits of a functional urease, as well as those for biosynthetic pathways for all but one (arginine) of the amino acids essential to the host.</p> <p>Results</p> <p>Nutritional upgrading by <it>Blochmannia </it>was tested in 90-day feeding experiments with brood-raising in worker-groups on chemically defined diets with and without essential amino acids and treated or not with antibiotics. Control groups were fed with cockroaches, honey water and Bhatkar agar. Worker-groups were provided with brood collected from the queenright mother-colonies (45 eggs and 45 first instar larvae each). Brood production did not differ significantly between groups of symbiotic workers on diets with and without essential amino acids. However, aposymbiotic worker groups raised significantly less brood on a diet lacking essential amino acids. Reduced brood production by aposymbiotic workers was compensated when those groups were provided with essential amino acids in their diet. Decrease of endosymbionts due to treatment with antibiotic was monitored by qRT-PCR and FISH after the 90-day experimental period. Urease function was confirmed by feeding experiments using ¹⁵N-labelled urea. GC-MS analysis of ¹⁵N-enrichment of free amino acids in workers revealed significant labelling of the non-essential amino acids alanine, glycine, aspartic acid, and glutamic acid, as well as of the essential amino acids methionine and phenylalanine.</p> <p>Conclusion</p> <p>Our results show that endosymbiotic <it>Blochmannia </it>nutritionally upgrade the diet of <it>C. floridanus </it>hosts to provide essential amino acids, and that it may also play a role in nitrogen recycling via its functional urease. <it>Blochmannia </it>may confer a significant fitness advantage via nutritional upgrading by enhancing competitive ability of <it>Camponotus </it>with other ant species lacking such an endosymbiont. Domestication of the endosymbiont may have facilitated the evolutionary success of the genus <it>Camponotus</it>.</p

Patterns of co-speciation and host switching in primate malaria parasites

<p>Abstract</p> <p>Background</p> <p>The evolutionary history of many parasites is dependent on the evolution of their hosts, leading to an association between host and parasite phylogenies. However, frequent host switches across broad phylogenetic distances may weaken this close evolutionary link, especially when vectors are involved in parasites transmission, as is the case for malaria pathogens. Several studies suggested that the evolution of the primate-infective malaria lineages may be constrained by the phylogenetic relationships of their hosts, and that lateral switches between distantly related hosts may have been occurred. However, no systematic analysis has been quantified the degree of phylogenetic association between primates and their malaria parasites.</p> <p>Methods</p> <p>Here phylogenetic approaches have been used to discriminate statistically between events due to co-divergence, duplication, extinction and host switches that can potentially cause historical association between <it>Plasmodium </it>parasites and their primate hosts. A Bayesian reconstruction of parasite phylogeny based on genetic information for six genes served as basis for the analyses, which could account for uncertainties about the evolutionary hypotheses of malaria parasites.</p> <p>Results</p> <p>Related lineages of primate-infective <it>Plasmodium </it>tend to infect hosts within the same taxonomic family. Different analyses testing for congruence between host and parasite phylogenies unanimously revealed a significant association between the corresponding evolutionary trees. The most important factor that resulted in this association was host switching, but depending on the parasite phylogeny considered, co-speciation and duplication may have also played some additional role. Sorting seemed to be a relatively infrequent event, and can occur only under extreme co-evolutionary scenarios. The concordance between host and parasite phylogenies is heterogeneous: while the evolution of some malaria pathogens is strongly dependent on the phylogenetic history of their primate hosts, the congruent evolution is less emphasized for other parasite lineages (e.g. for human malaria parasites). Estimation of ancestral states of host use along the phylogenetic tree of parasites revealed that lateral transfers across distantly related hosts were likely to occur in several cases. Parasites cannot infect all available hosts, and they should preferentially infect hosts that provide a similar environment for reproduction. Marginally significant evidence suggested that there might be a consistent variation within host ranges in terms of physiology.</p> <p>Conclusion</p> <p>The evolution of primate malarias is constrained by the phylogenetic associations of their hosts. Some parasites can preserve a great flexibility to infect hosts across a large phylogenetic distance, thus host switching can be an important factor in mediating host ranges observed in nature. Due to this inherent flexibility and the potential exposure to various vectors, the emergence of new malaria disease in primates including humans cannot be predicted from the phylogeny of parasites.</p

Calcium Homeostasis and Cone Signaling Are Regulated by Interactions between Calcium Stores and Plasma Membrane Ion Channels

Calcium is a messenger ion that controls all aspects of cone photoreceptor function, including synaptic release. The dynamic range of the cone output extends beyond the activation threshold for voltage-operated calcium entry, suggesting another calcium influx mechanism operates in cones hyperpolarized by light. We have used optical imaging and whole-cell voltage clamp to measure the contribution of store-operated Ca2+ entry (SOCE) to Ca2+ homeostasis and its role in regulation of neurotransmission at cone synapses. Mn2+ quenching of Fura-2 revealed sustained divalent cation entry in hyperpolarized cones. Ca2+ influx into cone inner segments was potentiated by hyperpolarization, facilitated by depletion of intracellular Ca2+ stores, unaffected by pharmacological manipulation of voltage-operated or cyclic nucleotide-gated Ca2+ channels and suppressed by lanthanides, 2-APB, MRS 1845 and SKF 96365. However, cation influx through store-operated channels crossed the threshold for activation of voltage-operated Ca2+ entry in a subset of cones, indicating that the operating range of inner segment signals is set by interactions between store- and voltage-operated Ca2+ channels. Exposure to MRS 1845 resulted in ∼40% reduction of light-evoked postsynaptic currents in photopic horizontal cells without affecting the light responses or voltage-operated Ca2+ currents in simultaneously recorded cones. The spatial pattern of store-operated calcium entry in cones matched immunolocalization of the store-operated sensor STIM1. These findings show that store-operated channels regulate spatial and temporal properties of Ca2+ homeostasis in vertebrate cones and demonstrate their role in generation of sustained excitatory signals across the first retinal synapse

SnoRNA Snord116 (Pwcr1/MBII-85) Deletion Causes Growth Deficiency and Hyperphagia in Mice

Prader-Willi syndrome (PWS) is the leading genetic cause of obesity. After initial severe hypotonia, PWS children become hyperphagic and morbidly obese, if intake is not restricted. Short stature with abnormal growth hormone secretion, hypogonadism, cognitive impairment, anxiety and behavior problems are other features. PWS is caused by lack of expression of imprinted genes in a ∼4 mb region of chromosome band 15q11.2. Our previous translocation studies predicted a major role for the C/D box small nucleolar RNA cluster SNORD116 (PWCR1/HBII-85) in PWS. To test this hypothesis, we created a ∼150 kb deletion of the >40 copies of Snord116 (Pwcr1/MBII-85) in C57BL/6 mice. Snord116del mice with paternally derived deletion lack expression of this snoRNA. They have early-onset postnatal growth deficiency, but normal fertility and lifespan. While pituitary structure and somatotrophs are normal, liver Igf1 mRNA is decreased. In cognitive and behavior tests, Snord116del mice are deficient in motor learning and have increased anxiety. Around three months of age, they develop hyperphagia, but stay lean on regular and high-fat diet. On reduced caloric intake, Snord116del mice maintain their weight better than wild-type littermates, excluding increased energy requirement as a cause of hyperphagia. Normal compensatory feeding after fasting, and ability to maintain body temperature in the cold indicate normal energy homeostasis regulation. Metabolic chamber studies reveal that Snord116del mice maintain energy homeostasis by altered fuel usage. Prolonged mealtime and increased circulating ghrelin indicate a defect in meal termination mechanism. Snord116del mice, the first snoRNA deletion animal model, reveal a novel role for a non-coding RNA in growth and feeding regulation

Transcriptional Activation of TINF2, a Gene Encoding the Telomere-Associated Protein TIN2, by Sp1 and NF-κB Factors

The expression of the telomere-associated protein TIN2 has been shown to be essential for early embryonic development in mice and for development of a variety of human malignancies. Recently, germ-line mutations in TINF2, which encodes for the TIN2 protein, have been identified in a number of patients with bone-marrow failure syndromes. Yet, the molecular mechanisms that regulate TINF2 expression are largely unknown. To elucidate the mechanisms involved in human TINF2 regulation, we cloned a 2.7 kb genomic DNA fragment containing the putative promoter region and, through deletion analysis, identified a 406 bp region that functions as a minimal promoter. This promoter proximal region is predicted to contain several putative Sp1 and NF-κB binding sites based on bioinformatic analysis. Direct binding of the Sp1 and NF-κB transcription factors to the TIN2 promoter sequence was demonstrated by electrophoretic mobility shift assay (EMSA) and/or chromatin immunoprecipitation (ChIP) assays. Transfection of a plasmid carrying the Sp1 transcription factor into Sp-deficient SL2 cells strongly activated TIN2 promoter-driven luciferase reporter expression. Similarly, the NF-κB molecules p50 and p65 were found to strongly activate luciferase expression in NF-κB knockout MEFs. Mutating the predicted transcription factor binding sites effectively reduced TIN2 promoter activity. Various known chemical inhibitors of Sp1 and NF-κB could also strongly inhibit TIN2 transcriptional activity. Collectively, our results demonstrate the important roles that Sp1 and NF-κB play in regulating the expression of the human telomere-binding protein TIN2, which can shed important light on its possible role in causing various forms of human diseases and cancers