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Unique Mechanism (unique + mechanism)
Selected AbstractsEruptive Epidermoid Cysts Resulting from Treatment with ImiquimodDERMATOLOGIC SURGERY, Issue 7 2005Chelsy L. Marty MD Background Because of its unique mechanism of action and safety profile, imiquimod, a topical immune response modifier, is used for many benign and malignant dermatologic conditions. Adverse effects are typically limited to treatment site erythema and erosion. Objective To describe a newly recognized adverse effect of imiquimod. Methods A 79-year-old woman being treated with imiquimod 5 days per week for a nodular basal cell developed a verrucous plaque over the treatment area after 7 weeks of therapy. Results Scouting biopsies demonstrated multiple comedones and ruptured epidermoid cysts. There was no evidence of residual basal cell carcinoma. Conclusions Imiquimod is a new and novel treatment option for cutaneous malignancies. We report its successful use in the treatment of a nodular basal cell carcinoma. The multiple comedones and ruptured epidermoid cysts are newly reported adverse effects of imiquimod therapy. [source] The role of calcimimetics in the treatment of hyperparathyroidismEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2007R. P. Wüthrich Abstract Calcimimetics reduce serum levels of parathyroid hormone (PTH) and calcium, with a leftward shift in the set-point for calcium-regulated PTH secretion. The aim of this publication is to review the data available for calcimimetics in primary, secondary and tertiary hyperparathyroidism (HPT). Parathyroidectomy (PTX) is currently the only curative treatment for primary HPT, and recommended for patients with moderate-to-severe disease, as defined by a 2002 National Institute's of Health summary statement. In general, patients with primary HPT not meeting these surgical criteria, as well as those with contraindication or refusal for surgery, are monitored for signs and symptoms of primary HPT. There are currently no non-surgical therapies approved for use in primary HPT, although bisphosphonates are used in some patients, in an effort to control serum calcium levels. Calcimimetics decrease PTH and calcium levels and are a potential alternative for patients contraindicated for PTX, or who have failed previous PTX and have recurrent primary HPT. Secondary HPT develops early in chronic kidney disease and is present virtually in all patients with end-stage renal disease (ESRD). Secondary HPT is a progressive disease and is associated with several systemic complications, including renal osteodystrophy, soft tissue and vascular calcifications, and adverse cardiovascular outcomes. In ESRD patients, calcimimetics were shown to simultaneously reduce PTH, calcium, phosphate and calcium × phosphate product. In addition, observational analyses of use of calcimimetics in the ESRD population have shown a reduction of important clinical outcomes. In renal allograft recipients with tertiary HPT and hypercalcaemia, calcimimetics are a promising treatment option to control the parameters of calcium phosphate metabolism and may be a valid alternative to PTX. Based on its unique mechanism of action, the calcimimetic cinacalcet may play a role in the medical treatment of primary and tertiary forms of HPT, in addition to the registered indication for the treatment of secondary HPT. [source] IL-10 modulates cytokine gene transcription by protein synthesis-independent and dependent mechanisms in lipopolysaccharide-treated neutrophilsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2007Marzia Rossato Abstract We have recently reported that the ability of IL-10 to rapidly exert its anti-inflammatory effects on human neutrophils is dependent upon exposure of these cells to LPS for at least 3,4,h. Here, we demonstrate that, in neutrophils "preconditioned" by LPS, IL-10 primarily targets the transcription of TNF-,, CXCL8 and IL-1ra genes, as revealed by primary transcript real-time RT-PCR. We also show that IL-10-induced transcriptional repression of TNF-, and CXCL8 genes consists of two distinct phases: an early one, occurring rapidly and in a protein synthesis-independent manner, followed by a second phase, more delayed and dependent on protein synthesis. Interestingly, the protein synthesis dependence of the latter phase coincides with a reduced ability of IL-10 to induce STAT3 tyrosine phosphorylation. Importantly, inhibition of IL-10-induced STAT3 activation and IL-10-suppressive action by a prolonged exposure to cycloheximide (CHX) was observed to occur also in human monocytes and was caused by a defective IL-10-mediated activation of Jak1 and Tyk2 kinases. Taken together, our findings suggest that CHX interferes with the IL-10-mediated intracellular signaling pathway by interrupting events upstream of STAT3 activation. These data question the concept of the requirement of an IL-10-induced mediator as the unique mechanism to execute IL-10 anti-inflammatory program. [source] Asymmetric Reduction of Ketones Under Mild Conditions Using NaBH4 and TarB-NO2: An Efficient and Unusual Chiral Acyloxyborohydride Reducing System,EUROPEAN JOURNAL OF ORGANIC CHEMISTRY, Issue 24 2005David B. Cordes Abstract High enantioselectivities are obtained for the reduction of a series of ketones using the inexpensive and mild reducing agent NaBH4 with TarB-NO2 (1). This easily prepared tartaric acid-based reagent combines a Lewis acid with carboxylic acids in a single bifunctional reagent. When combined with NaBH4, the resulting chiral acyloxyborohydride mediates the reduction of aromatic ketones to provide the product alcohols in enantiomeric excesses of 93,98,%. Several aliphatic ketones were also reduced with moderate to excellent enantioselectivity. A unique mechanism is provided with supporting calculations for the proposed active species and transition state. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005) [source] Cooperation of two carotene desaturases in the production of lycopene in Myxococcus xanthusFEBS JOURNAL, Issue 16 2007Antonio A. Iniesta In Myxococcus xanthus, all known carotenogenic genes are grouped together in the gene cluster carB,carA, except for one, crtIb (previously named carC). We show here that the first three genes of the carB operon, crtE, crtIa, and crtB, encode a geranygeranyl synthase, a phytoene desaturase, and a phytoene synthase, respectively. We demonstrate also that CrtIa possesses cis -to- trans isomerase activity, and is able to dehydrogenate phytoene, producing phytofluene and ,-carotene. Unlike the majority of CrtI-type phytoene desaturases, CrtIa is unable to perform the four dehydrogenation events involved in converting phytoene to lycopene. CrtIb, on the other hand, is incapable of dehydrogenating phytoene and lacks cis -to- trans isomerase activity. However, the presence of both CrtIa and CrtIb allows the completion of the four desaturation steps that convert phytoene to lycopene. Therefore, we report a unique mechanism where two distinct CrtI-type desaturases cooperate to carry out the four desaturation steps required for lycopene formation. In addition, we show that there is a difference in substrate recognition between the two desaturases; CrtIa dehydrogenates carotenes in the cis conformation, whereas CrtIb dehydrogenates carotenes in the trans conformation. [source] Bacterial cell death induced by human pro-apoptotic Bax is blocked by an RNase E mutant that functions in an anti-oxidant pathwayGENES TO CELLS, Issue 3 2000Rika Nanbu-Wakao Background Bax is a member of the Bcl-2 family and induces apoptosis of mammalian cells. We have shown that a trace amount of human Bax induces the cell death of Escherichia coli, accompanied by damage to DNA, and that the region of Bax which is lethal to E. coli is also responsible for apoptosis-inducing activity in the mammalian cells. Results We isolated a Bax-resistant mutant from E. coli cells that survive in the presence of paraquat, a generator of superoxide, by screening a library constructed from the random insertion of a transposon. Psb1 (paraquat-resistant, suppressor of Bax-1) mutant had a Tn 10 transposon inserted in the rne gene of E. coli, splitting the RNase E gene (rne) into N- and C-terminal halves. The introduction of the truncated 5, end of rne specifically enhanced resistance to paraquat, prevented cell death induced by Bax and decreased the intracellular H2O2 concentration. The region responsible for the paraquat- and Bax-resistance was not the catalytic site for the endoribonuclease activity of RNase E. Conclusions The N-terminal region of the RNase E protein inhibits bacterial death induced by human Bax as well as paraquat through a unique mechanism that is distinct from RNA digestion. This study implies that the protection of bacterial death induced by Bax is associated with an anti-oxidant pathway and that a mutant RNase E has a novel function as an anti-oxidant. [source] Modeling of partial oxidation in gas,solids downer reactorsAICHE JOURNAL, Issue 8 2010S. Vaishali Abstract Selective partial oxidations represent an important class of reactions in the process industry. Of particular interest is the partial oxidation of n-butane to maleic anhydride (MAN), which is arguably the largest commercialized alkane partial oxidation process. Partial oxidation of n-butane, which uses vanadium phosphorous oxide (VPO) as a heterogeneous catalyst, is believed to operate through a unique mechanism in which lattice oxygen oxidizes n-butane selectively to MAN. Past work has shown that performing partial oxidation reactions in gas,solids riser configuration is realizable and commercially viable, which has lead to commercialization of this technology in the last decade. Though the riser configuration allows optimal and independent control of the oxidation and reduction steps, the riser unit suffers from solid backmixing at walls, which in turn result into lower conversion, nonoptimal selectivity and diminished overall yield of desired product. In recent years, there has been growing interest in downers involving cocurrent downflow of both solids and gas phases, hence offering relatively uniform flow characteristics. In this contribution, we explore through modeling the implications of effecting partial oxidation reactions in a downer (gas,solids cocurrent downflow) compared to that in a conventional riser reactor (gas,solids cocurrent up flow) operated under equivalent operating conditions. Further, we explore the operational space of downers for these reactions, suggesting ways for improving the productivity of downer for partial oxidation applications. © 2009 American Institute of Chemical Engineers AIChE J, 2010 [source] How many symbionts are provided by mothers, acquired by offspring, and needed for successful vertical transmission in an obligate insect,bacterium mutualism?MOLECULAR ECOLOGY, Issue 24 2007TAKAHIRO HOSOKAWA Abstract Vertical symbiont transmission is among the most pivotal processes for maintenance of symbiotic associations. However, it is poorly understood whether and how the levels of resource allocation and investment upon vertical transmission are regulated. The stinkbug Megacopta punctatissima is obligatorily associated with the gut symbiotic bacterium ,Candidatus Ishikawaella capsulata', whose transmission is mediated by a unique mechanism called ,symbiont capsule'. We investigated the population dynamics of the symbiont during vertical transmission in the host,symbiont mutualism. The stinkbug mothers produced one capsule for around 3.6 eggs irrespective of clutch size, suggesting a strict maternal control over symbiont supply for the offspring. However, experimental manipulation of egg/capsule ratios revealed that one capsule is sufficient for symbiont transmission to six nymphs. Quantitative polymerase chain reaction analyses demonstrated that a capsule contains 1.2 × 108 symbionts, a newborn nymph possesses 2 × 107 symbionts from a capsule, and thus one capsule certainly contains a sufficient amount of symbiont cells for six nymphs. These results indicated that the stinkbug mothers produce 1.7 times more symbiont capsules than needed. The newborn nymphs consistently harboured around 2 × 107 symbionts, also suggesting a nymphal control over symbiont transmission. The threshold symbiont titre minimally needed for successful vertical transmission was estimated to be 1.9 × 106 symbionts, which is only 1/10 of the actual symbiont titre detected in a newborn nymph. These results illuminate several ecological factors that may be relevant to parental and offspring controls over symbiotic resource allocation through host insect generations. [source] Repeat-induced point mutation (RIP) in Magnaporthe grisea: implications for its sexual cycle in the natural field contextMOLECULAR MICROBIOLOGY, Issue 5 2002Ken-ichi Ikeda Summary Repeat-induced point mutation (RIP) is a process that detects DNA duplications and peppers their sequences with C:G to T:A transitions in the sexual phase of the life cycle. So far, this unique mechanism has been identified as a currently active process in only two fungal species, Neurospora crassa and Podospora anserina. To determine whether a RIP-like process operates in the plant pathogenic fungus Magnaporthe grisea, the retrotransposon MAGGY and the hygromycin B phosphotransferase gene were introduced into the fungus as multiple transgenes and examined for sequence alterations after a cross. Frequent C:G to T:A transitions in the transgenes were found in the descendants, preferentially in (A/Tp)Cp(A/T) contexts, suggesting that a process similar to RIP functions in M. grisea. We also examined the sequence of another retrotransposon Pyret in six field isolates of M. grisea. Even though no perfect stage has been known in M. grisea under field conditions to date, RIP-like transitions were found in all the field isolates tested. Interestingly, the frequency of the transitions mostly correlated with the fertility of the isolates examined under laboratory conditions. These results imply that the sexual cycle of this fungus exists or existed in the natural field context. [source] A unique mechanism for cyclic adenosine 3,,5,-monophosphate-induced increase of 32-kDa tyrosine-phosphorylated protein in boar spermatozoa,MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 2 2004Hiroshi Harayama Abstract A cAMP-induced increase of tyrosine-phosphorylated proteins is involved in the expression of fertilizing ability in mammalian spermatozoa. We (Harayama, 2003: J Androl 24:831,842) reported that incubation of boar spermatozoa with a cell-permeable cAMP analog (cBiMPS) increased a 32-kDa tyrosine-phosphorylated protein (TyrP32). The purpose of this study is to characterize the signaling cascades that regulate the cAMP-induced increase of TyrP32. We examined effects of tyrosine kinase inhibitor (lavendustin A), tyrosine phosphatase inhibitor (Na3VO4), cell-permeable calcium chelator (BAPTA-AM), and cholesterol acceptor (methyl-,-cyclodextrin: MBC) on the increase of TyrP32 and the change and loss of acrosomes in boar spermatozoa. The spermatozoa were used for detection of tyrosine-phosphorylated proteins by Western blotting and indirect immunofluorescence and for examination of acrosomal integrity by Giemsa staining. At least eight tyrosine-phosphorylated proteins including TyrP32 exhibited the cAMP-dependent increase during incubation with cBiMPS. In many proteins of them, this increase was reduced by lavendustin A but was enhanced by Na3VO4. In contrast, the cAMP-induced increase of TyrP32 was abolished by Na3VO4 but was hardly affected by lavendustin A. Giemsa staining showed that the increase of spermatozoa with weakly Giemsa-stained acrosomes (severely damaged acrosomes) or without acrosomes was correlative to the cAMP-induced increase of TyrP32. Moreover, the lack of calcium chloride in the incubation medium or pretreatment of spermatozoa with BAPTA-AM blocked the change and loss of acrosomes and the increase of TyrP32, suggesting these events are dependent on the extracellular and intracellular calcium. On the other hand, incubation of spermatozoa with MBC in the absence of cBiMPS could mimic the change and loss of acrosomes and increase of TyrP32 without increase of other tyrosine-phosphorylated proteins. Based on these results, we conclude that the cAMP-induced increase of TyrP32 is regulated by a unique mechanism that may be linked to the calcium-dependent change and loss of acrosomes. Mol. Reprod. Dev. 69: 194,204, 2004. © 2004 Wiley-Liss, Inc. [source] Gas-phase formation of protonated benzene during collision-induced dissociation of certain protonated mono-substituted aromatic molecules produced in electrospray ionizationRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 11 2010Min Li Protonated benzene, C6H, has been studied extensively to understand the structure and energy of a protonated organic molecule in the gas phase. The formation of C6H is either through direct protonation of benzene, i.e., chemical ionization, or through fragmentation of certain radical cations produced from electron ionization or photon ionization. We report a novel observation of C6H as a product ion formed in the collision-induced dissociation (CID) of protonated benzamide and related molecules produced via electrospray ionization (ESI). The formation of C6H from these even-electron precursor ions during the CID process, which has not been previously reported, is proposed to occur from the protonated molecules via a proton migration in a five-membered ring intermediate followed by the cleavage of the mono-substituent CC bond and concurrent formation of an ion-molecule complex. This unique mechanism has been scrutinized by examining some deuterated molecules and a series of structurally related model compounds. This finding provides a convenient mean to generate C6H, a reactive intermediate of considerable interest, for further physical or chemical investigation. Further studies indicate that the occurrence of C6H in liquid chromatography/electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS) appears to be a rather common phenomenon for many compounds that contain ,benzoyl-type' moieties. Hence, the observation of the C6H ion in LC/ESI-MS/MS can be used as an informative fragmentation pathway which should facilitate the identification of a great number of compounds containing the ,benzoyl-type' and similar structural features. These compounds are frequently present in food and pharmaceutical products as leachable impurities that require strict control and rapid elucidation of their identities. Copyright © 2010 John Wiley & Sons, Ltd. [source] Endotoxin-Induced Myeloid-Derived Suppressor Cells Inhibit Alloimmune Responses via Heme Oxygenase-1AMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2009V. De Wilde Inflammation and cancer are associated with impairment of T-cell responses by a heterogeneous population of myeloid-derived suppressor cells (MDSCs) coexpressing CD11b and GR-1 antigens. MDSCs have been recently implicated in costimulation blockade-induced transplantation tolerance in rats, which was under the control of inducible NO synthase (iNOS). Herein, we describe CD11b+GR-1+MDSC-compatible cells appearing after repetitive injections of lipopolysaccharide (LPS) using a unique mechanism of suppression. These cells suppressed T-cell proliferation and Th1 and Th2 cytokine production in both mixed lymphocyte reaction and polyclonal stimulation assays. Transfer of CD11b+ cells from LPS-treated mice in untreated recipients significantly prolonged skin allograft survival. They produced large amounts of IL-10 and expressed heme oxygenase-1 (HO-1), a stress-responsive enzyme endowed with immunoregulatory and cytoprotective properties not previously associated with MDSC activity. HO-1 inhibition by the specific inhibitor, SnPP, completely abolished T-cell suppression and IL-10 production. In contrast, neither iNOS nor arginase 1 inhibition did affect suppression. Importantly, HO-1 inhibition before CD11b+ cell transfer prevented the delay of allograft rejection revealing a new MDSC-associated suppressor mechanism relevant for transplantation. [source] Police Pay and Bargaining in the UK, 1978,2000BRITISH JOURNAL OF INDUSTRIAL RELATIONS, Issue 1 2003Laurie Hunter Police pay and conditions in the UK are governed by a unique mechanism, the Police Negotiating Board. This paper reviews the circumstances in which it was set up and examines the outcomes, relative to other public service workers, over the first twenty years of its operation. Recent developments highlight the role of ministerial intervention and raise questions about the relationship between the PNB negotiating system and working practice at police force level. [source] Antiepileptic drug discovery: lessons from the past and future challengesACTA NEUROLOGICA SCANDINAVICA, Issue 2005H. Klitgaard Historically, most antiepileptic drugs (AEDs) have been discovered either by serendipity, or the screening of compounds using acute seizure models. However, an increasing understanding of the molecular mechanisms underlying epileptogenesis has led to more rational approaches to drug discovery, which have focused on either enhancing inhibitory , -amino butyric acid (GABA)-ergic, or antagonizing excitatory glutamatergic, neurotransmission. Unfortunately, AEDs generated using such strategies have poor efficacy and safety profiles, as they interfere with normal cell processes, while ignoring the complex underlying pathophysiology of epilepsy. Recently, however, the use of new epilepsy models has led to the discovery of levetiracetam, an AED with a truly unique mechanism of action, devoid of anticonvulsant activity in normal animals, but with potent seizure suppression in genetic and kindled chronic epilepsy models, and an unusually high safety margin. The recent identification of brivaracetam and seletracetam, which optimize this unique mechanism of action, may further improve the medical management of epilepsy. The experience with levetiracetam, brivaracetam and seletracetam reveals that new experimental epilepsy models can detect AEDs possessing a unique mechanism of action and thereby target the future challenge of providing clinicians novel additions to the current armamentarium of AEDs. [source] Potent antitumor effect elicited by superantigen-linked tumor cells transduced with heat shock protein 70 geneCANCER SCIENCE, Issue 2 2004Changxin Huang Heat shock proteins (HSP) induce antitumor-specific immunity via a unique mechanism, but HSP alone fails to produce a satisfactory antitumor efficacy. We considered that the potent immune-activation of superantigen (SAg) might assist HSP to elicit a strong tumor-antigen-specific immunity. We initially prepared B16 melanoma cells linked to SAg SEA via a fusion protein with a trans-membrane sequence (TM), and demonstrated that SEA thus anchored on the tumor cell surface could elicit strong antitumor immunity. We then prepared cells transduced with an inducible heat shock protein 70 (HSP70) gene, and bearing SEA-TM fusion protein on the cell surface, and used these cells as a dual-modified vaccine. In this study, either in a therapeutic setting or in a pre-immune model, the SEA-anchored vaccine or the HSP70 gene-modified vaccine induced marked tumor suppression, prolonged survival, augmented lymphocyte proliferation and higher NK and CTL activity in C57BL/6 mice compared with their controls (P<0.01), though they were less effective than the dual-modified vaccine. Among these vaccines, the dual-modified vaccine showed the best therapeutic efficacy in B16 melanoma-bearing mice and gave the greatest protection against wild-type B16 melanoma challenge. The results indicated that the dual-modified vaccine could induce a potent tumor-antigen-specific immune response in addition to an increase of non-specific immunity. This study offers a novel approach to bridging specific and non-specific immunity for cancer therapy. [source] Pyroptosis and host cell death responses during Salmonella infectionCELLULAR MICROBIOLOGY, Issue 11 2007Susan L. Fink Summary Salmonella enterica are facultatively intracellular pathogens causing diseases with markedly visible signs of inflammation. During infection, Salmonella interacts with various host cell types, often resulting in death of those cells. Salmonella induces intestinal epithelial cell death via apoptosis, a cell death programme with a notably non-inflammatory outcome. In contrast, macrophage infection triggers caspase-1-dependent proinflammatory programmed cell death, a recently recognized process termed pyroptosis, which is distinguished from other forms of cellular demise by its unique mechanism, features and inflammatory outcome. Rapid macrophage pyroptosis depends on the Salmonella pathogenicity island-1 type III secretion system (T3SS) and flagella. Salmonella dynamically modulates induction of macrophage pyroptosis, and regulation of T3SS systems permits bacterial replication in specialized intracellular niches within macrophages. However, these infected macrophages later undergo a delayed form of caspase-1-dependent pyroptosis. Caspase-1-deficient mice are more susceptible to a number of bacterial infections, including salmonellosis, and pyroptosis is therefore considered a generalized protective host response to infection. Thus, Salmonella -induced pyroptosis serves as a model to understand a broadly important pathway of proinflammatory programmed host cell death: examining this system affords insight into mechanisms of both beneficial and pathological cell death and strategies employed by pathogens to modulate host responses. [source] Somatic microindels: analysis in mouse soma and comparison with the human germline,,HUMAN MUTATION, Issue 1 2007Kelly D. Gonzalez Abstract Microindels, defined as mutations that result in a colocalized microinsertion and microdeletion with a net gain or loss of between 1 and 50 nucleotides, may be an important contributor to cancer. We report the first comprehensive analysis of somatic microindels. Our large database of mutations in the lacI transgene of Big Blue® mice contains 0.5% microindels, 2.8% pure microinsertions, and 11.5% pure microdeletions. There appears to be no age, gender, or tissue-type specificity in the frequency of microindels. Of the independent somatic mutations that result in a net in-frame insertion or deletion, microindels are responsible for 13% of protein expansions and 6% of protein contractions. These in-frame microindels may play a crucial role in oncogenesis and evolution via "protein tinkering" (i.e., modest expansion or contraction of proteins). Four characteristics suggest that microindels are caused by unique mechanisms, not just simple combinations of the same mechanisms that cause pure microinsertions and pure microdeletions. First, microinsertions and microdeletions commonly occur at hotspots, but none of the 30 microindels are recurrent. Second, the sizes of the deletions and insertions in microindels are larger and more varied than in pure microdeletions and pure microinsertions. Third, microinsertions overwhelmingly repeat the adjacent base (97%) while the insertions in microindels do so only infrequently (17%). Fourth, analysis of the sequence contexts of microindels is consistent with unique mechanisms including recruitment of translesion DNA synthesis polymerases. The mouse somatic microindels have characteristics similar to those of human germline microindels, consistent with similar causative mechanisms in mouse and human, and in soma and germline. Hum Mutat 28(1), 69,80, 2007. Published 2006 Wiley-Liss, Inc. [source] The Pathophysiology of Chronic Graft Failure in the Cardiac Transplant PatientAMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2009U. A. Khan Following cardiac transplantation, many patients develop chronic deterioration of graft function, which may lead to a clinical syndrome similar to native chronic heart failure (CHF). This condition of chronic cardiac graft failure (CGF) may also share pathophysiological processes comparable with that of CHF. However, the unique environment following cardiac transplantation may also contribute with a variety of unique mechanisms, deserved of special attention. This review article discusses the complex pathophysiology of CGF after cardiac transplantation, an important yet neglected condition of transplant medicine. [source] | ||||||||||||||||