bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cloning of a pine germin‐like protein (GLP) gene promoter and analysis of its activity in transgenic tobacco Bright Yellow 2 cells
Authors: Mathieu Mélanie , Neutelings Godfrey , Hawkins Simon , Grenier Emmanuel , David Hélène 
Published: March 2003

Germins and germin‐like proteins (GLPs) constitute a large and highly diverse family of ubiquitous plant cell wall proteins. These proteins seem to be involved in many developmental stages and stress‐related processes, but their exact participation in these processes generally remains obscure. In Pinus caribaea Morelet, the PcGER1 gene is expressed uniquely in embryo tissues, and encodes a GLP ionically bound to the walls of pine embryo cells maintained in 2,4‐D‐containing medium. We have cloned a genomic fragment including the 1520 bp 5′‐upstream promoter region of PcGER1. This sequence contains, in its 1200 bp distal part, several cis elements (e.g. SEF4, 60 kDa protein, ABA RE and Dof recognition sites) present in genes responding to hormones and/or expressed in embryo or seed tissues, or during germination. The PcGER1 promoter sequence was cloned upstream of the GUS (β‐glucuronidase) reporter gene and transferred to tobacco Bright Yellow 2 (BY‐2) cells via Agrobacterium tumefaciens‐mediated transformation. Promoter activity and growth performances of transgenic asynchronous cell suspensions were analysed in the presence or absence of 2,4‐D and/or BA. Optimal growth, maximum cell‐wall yield and PcGER1 promoter activity were observed in the presence of 2,4‐D and BA at day 4, the end of the exponential growth phase where 70–75% cells have a 2C DNA content. Analysis of promoter activity during the cell cycle in an aphidicoline‐synchronized culture suggested that the expression is maximum in G1 cells. We also showed that under optimal growth conditions, 5′ promoter deletions decreased the activity of the reporter gene. We discuss the function of this gene with regards to cell growth. Accession number: The PcGER1 promoter sequence was submitted to the genbank database under the accession number AY077704.
Cytomegalovirus infection and cardiac allograft vasculopathy
Authors: Koskinen P.K. , Kallio E.A. , Tikkanen J.M. , Sihvola R.K. , Häyry P.J. , Lemström K.B. 
Published: March 2003

Abstract:There is a wealth of clinical and experimental evidence indicating the interaction of cytomegalovirus (CMV) infection and rejection in cardiac and other solid organ allografts. A plausible explanation for this association comes from data showing that therapy with biologicals, sepsis, and rejection, all lead to the release of TNF‐α which, upon binding to its receptor, activates NF‐kB. TNF‐α is also able to stimulate the activity of the CMV‐IE enhancer/promoter region. CMV infection of several cell lines leads to NF‐kB activation. NF‐kB binding sites are present in regulatory regions of various cellular and viral genes, including the IE enhancer region of CMV. In a reciprocal situation, CMV infection, most likely via γ‐interferon, leads to upregulation of MHC antigens in the transplant and, thereby, to increased transplant immunogenicity. Thus, a vicious circle is induced. We have investigated in detail the pathobiology of CMV and allograft vasculopathy (chronic rejection) in experimental animals, using aortic and cardiac allografts as well as a trachea model. The results may be summarized as follows: Infection of the recipient with rat CMV results in an early inflammatory response in the aortic and cardiac allograft vascular adventitia and intima (endothelialitis) and in the airway wall of tracheal allografts. This early inflammatory response leads to enhanced intimal thickness in aortic and cardiac allografts and enhanced luminal occlusion of tracheal allografts. Timewise, this coincides with early activation of intragraft inflammatory leukocytes and increased mRNA of various growth factors and cytokines. When the recipients receive gancyclovir, the enhanced intimal response in aortic and cardiac allografts and luminal occlusion in tracheal allografts is entirely abolished. Gancyclovir treatment dramatically reduces the inflammatory response in the allograft, and thereby growth factor synthesis in response to injury. However, gancyclovir does not prevent the expression of IE antigen of CMV, suggested to inactivate tumor suppressor protein p53 predisposing smooth muscle cells to increased growth. Taken together, the effect of CMV infection on cardiac allograft dysfunction is bidirectional and biphasic. The bidirectional nature emerges from the observations that acute CMV infection may accelerate acute rejection, and, on the other hand, acute alloimmune response‐associated cytokine response may activate latent CMV infection. The biphasic effect of CMV on allograft dysfunction refers to its early and late detrimental effects, i.e. during the time of acute and chronic rejection. These two effects of CMV on allograft dysfunction emphasize the need for precise diagnosis of CMV infection in transplant recipients and pre‐emptive or prophylactic anti‐viral therapy. The benefits of this strategy may not be evident during the early post‐transplant period, but 5–10 years after transplantation they manifest as better graft survival
Note.
Emerging fungal pathogens: evolving challenges to immunocompromised patients for the twenty‐first century
Authors: Walsh T.J. , Groll A.H. 
Published: March 2003

Abstract:Opportunistic fungi have emerged during the past decade as important causes of morbidity and mortality in immunocompromised patients. Candida species constitute the third to fourth most common causes of nosocomial blood stream infections, and Aspergillus species have emerged as the most common infectious cause of pneumonic mortality in bone marrow/stem cell transplant recipients. Among HIV‐infected patients, meningoencephalitis due to Cryptococcus neoformans ranks among the most common AIDS‐defining infections. Hyaline septated filamentous fungi, such as Fusarium species, Acremonium species, Paecilomyces species, and Trichoderma species, are increasingly reported as causing invasive mycoses refractory to conventional therapy. Dematiaceous septated filamentous fungi, such as Pseudallescheria boydii, Bipolaris species, and Cladophialophora bantiana cause pneumonia, sinusitis, and CNS infection unresponsive to current therapy. An increasing number of different members of the class of Zygomycetes are reported as causing lethal infections, despite aggressive medical and surgical interventions. Yet the treatment for zygomycosis has not changed in approximately 40 years. The prevalence of the endemic mycoses, such as those due to Penicillium marneffei, Coccidioides immitis, and Histoplasma capsulatum, has been reported to expand rapidly in response to environmental exposures and increased numbers of vulnerable hosts in endemic regions of the world. Dermatophytoses are occurring with increasing prevalence and morbidity in elderly and immunocompromised patients. As we enter the next millennium, we may anticipate that emergent fungal infections will continue to develop in the settings of permissive environmental conditions, selective antifungal pressure, and an expanding population of immunocompromised hosts. Note
Aerosolized pentamidine prophylaxis for Pneumocystis carinii pneumonia after allogeneic marrow transplantation
Authors: Marras T.K. , Sanders K. , Lipton J.H. , Messner H.A. , Conly J. , Chan C.K. , Marras T.K. , Sanders K. , Lipton J.H. , Messner H.A. , Conly J. , Chan C.K. 
Published: March 2003

Abstract: Pneumocystis carinii pneumonia (PCP) poses a serious risk to allogeneic bone marrow transplant (BMT) patients, who are often intolerant of trimethoprim‐sulfamethoxazole (TMP‐SMX), the traditional first‐line prophylactic agents. There are limited published data supporting the use of aerosolized pentamidine (AP) prophylaxis in the BMT population. We assessed the effectiveness of AP in BMT recipients by reviewing the experience at our center. We divided our review into four time periods from January 1990 to March 2000, during which approximately 700 BMTs were performed. The first period includes patients receiving AP treatments from January 1990 to July 1997 (baseline), the second from August 1997 to July 1998 (pre‐outbreak), the third from August 1998 to October 1999 (outbreak), and the fourth from November 1999 to March 2000 (post‐outbreak). At our center, TMP‐SMX is the first‐line agent for PCP prophylaxis, which is routinely continued for at least one year, or for the duration of enhanced immunosuppression. During the baseline period, 505 BMTs were performed and 192 patients (38%) received AP for part of their time at risk. Six patients (3%) experienced toxicities requiring discontinuation of AP. Three cases of PCP were diagnosed over 1114 patient‐months of treatment in the baseline period. During the last 42 months of the baseline period, 2/154 patients receiving AP and 2 of an estimated 293 patients receiving exclusively oral prophylaxis developed breakthrough PCP (p = 0.61). During the outbreak period, 9 of 180 patients receiving AP developed PCP compared to none in the group receiving exclusively oral prophylaxis. Either changes in our AP protocol during the pre‐outbreak period or pentamidine resistance may have led to this failure of prophylaxis. There were no further cases during the 5‐month post‐outbreak period. Our observed overall breakthrough rate was 12 cases out of 439 patients (2.7%). Our study shows that AP is an effective and well‐tolerated second‐line agent in preventing PCP post BMT and we recommend its continued use in this regard. However, it should be administered using a well‐studied protocol, and only when TMP‐SMX is not tolerated.
Growth of porcine kidneys in their native and xenograft environment
Authors: Soin Bob , Ostlie Daniel , Cozzi Emanuele , Smith Kenneth G. C. , Bradley John R. , Vial Conrad , Masroor Saqib , Lancaster Richard , White David J. , Friend Peter J. 
Published: March 2003

Abstract: The increased survival of hDAF pig‐to‐primate renal xenografts for up to two months has afforded the opportunity to study physiological aspects such as organ growth. Experimental evidence exists of species restriction of the activity of growth hormone, although growth itself is also controlled by a number of other endocrine, paracrine and autocrine substances.This study consisted of four parts: (1) measurement of pig kidney size according to pig body weight; (2) measurement of pig kidney size according to pig age; (3) serial length measurement of pig‐to‐primate renal xenografts; (4) correlation of terminal weight of renal xenograft with age and histology.The xenografted pig kidneys in a primate recipient grow as they would in the pig for the first two weeks after transplantation. After this time there is a reduction in the rate of increase in the length of the xenograft. Over the same period, changes in weight are greatly increased by the presence of rejection. This observational study supports the notion that regulation of growth of a xenotransplanted porcine kidney occurs.
Concordant xenotransplantation –non‐vascularized pancreatic islets are more difficult to regraft than the vascularized heart
Authors: Bersztel Adam , Andersson Arne , Björkland Anna , Tufveson Gunnar , Johnsson Cecilia 
Published: March 2003

Abstract: We have previously demonstrated that it is possible to perform retransplantation of a xenogeneic heart (mouse‐to‐rat) using cyclosporine A as monotherapy, provided that the first heart is transplanted under a short course of deoxyspergualin (DSG). If DSG is omitted, the first heart is rejected within four days and the second heart succumbs to hyperacute rejection within minutes. A mouse heart as first graft does not protect a consecutive pancreatic islet graft, although the heart continues to function after rejection of the cellular graft. One explanation for this discrepancy may be the fact that cellular grafts, as pancreatic islets, lack an endothelial lining. We have, therefore, further investigated possible differences between vascularized and non‐vascularized xenografts regarding their capacity to induce unresponsiveness.The use of pancreatic islets as primary graft neither accelerated nor decelerated the speed of rejection of the vascularized heart used as secondary graft. Furthermore, hemagglutinating and cytotoxic antibody titres responded in the same manner as in naive rats transplanted with a mouse heart. Retransplantation with pancreatic islets also resulted in complete rejection of both the primary and secondary grafts. Thus, the lack of unresponsiveness cannot simply be explained by differences, between the pancreatic and cardiac tissues, in antigen expression. In addition, intraperitoneal transplantation of mouse heart cells as primary graft resulted in rejection of a secondary cardiac graft after three days. However, it cannot be totally excluded that the time of antigen exposure had an impact on these results.In conclusion, our previous and present studies suggest that the presence of an intact vascular bed, both in the first and second graft, is necessary to create a state of unresponsiveness. Because the pancreatic islets lack an endothelial lining, they do not benefit from an unresponsiveness of the immune system. Neither are they able to induce such an unresponsiveness.
Structure and flexibility of the multiple domain proteins that regulate complement activation
Authors: Kirkitadze Marina D. , Barlow Paul N. 
Published: March 2003

Summary:In this review we summarise more than 10 years of biophysical exploration into the structural biology of the regulators of complement activation (RCA). The five human proteins responsible for regulation of the early events of complement are homologous and are composed largely from building blocks called “complement control protein (CCP) modules”. Unlike most multiple domain proteins they do not contain any of the other widely occurring module types. This apparent simplicity of RCA structure, however, is belied by their sophistication of function. In fact, the structures of the individual CCP modules exhibit wide variations on a common theme while the extent and nature of intermodular connections is diverse. Some neighbouring modules within a protein stabilise each other and some co‐operate to form specific binding surfaces. The degree of true “modularity” of CCPs is open to debate. The study of RCA proteins clearly illustrates the value of combining complementary structural biology techniques. The results could have implications for folding, evolution, flexibility and structure–function relationships of other molecules in the large, diverse and little understood category of multiple domain proteins.Work in the Barlow laboratory was supported by the Medical Research Council and the Biotechnology and Biological Sciences Research Council of the UK and by the Wellcome Trust. MDK was supported by the Human Frontiers Science Program.
The ever‐expanding Ly49 gene family: repertoire and signaling
Authors: Anderson Stephen K. , Ortaldo John R. , McVicar Daniel W. 
Published: March 2003

Summary: The mouse lectin‐related Ly49 family and the human killer cell Ig‐like receptor (KIR) family represent structurally distinct, yet functionally analogous, class I MHC receptors that are expressed on natural killer cells and some T cells. The functional similarity of these two families has been borne out by the demonstration of identical signal transduction pathways associated with each receptor family. The Ly49 family therefore provides a useful model system to study the role of this class of receptors in the regulation of the immune system. Recent data relating to the Ly49 repertoire in several mouse strains has revealed an additional evolutionary parallel between KIR and Ly49 receptor families. There is now an appreciation of the variation in the number and type of Ly49s expressed in different mouse strains, similar to the previously demonstrated differences in the number of KIR genes found in humans. This review summarizes the current members of the Ly49 gene family, their MHC class I recognition and associated signal transduction pathways.This work was supported in part through NCI contract No. NO1‐CO‐56000.
Murine natural killer cell activation receptors
Authors: Smith Hamish R. C. , Idris Azza H. , Yokoyama Wayne M. 
Published: March 2003

Summary: Natural killer (NK) cells express two types of receptors involved in target recognition: inhibitory receptors for target cell MHC class I molecules and activation receptors. While there has been significant progress in understanding the inhibitory receptors, less is known about the activation receptors. Detailed analysis of several mouse NK‐cell activation receptors provides insight into the physiologic relevance of these receptors in the innate immune response.We gratefully acknowledge past and present members of our laboratory for their work on NK‐cell receptors and particularly Hubert Chuang for his recent efforts on Qa‐1 receptors mentioned in this manuscript. Work in the Yokoyama laboratory is supported by grants from the National Institutes of Health. H.R.C.S. is supported by a training grant from NIH. W.M.Y. is an investigator of the Howard Hughes Medical Institute.
Role of protein tyrosine phosphatases in T cell activation
Authors: Mustelin Tomas , Rahmouni Souad , Bottini Nunzio , Alonso Andres 
Published: March 2003

Summary:The last decade has seen an exponentially increasing interest in the molecular mechanisms of signal transduction. In T cells, much of the focus has been on protein tyrosine kinase (PTK)‐mediated signaling from the T cell receptor (TCR) and cytokine receptors, while the study of protein tyrosine phosphatases (PTPases) has lagged behind. However, recent discoveries have revealed that several PTPases play important roles in many different aspects of T cell physiology. We predict that the phosphatases will become a ‘hot topic’ in the field within the next few years. This review summarizes the current understanding of the regulation and biology of PTPases in T lymphocyte activation.
An evolutionary and structural perspective on T cell antigen receptor function
Authors: Malissen Bernard 
Published: March 2003

Summary:After a brief overview of the themes and variations that occur in the family of receptors containing immunoreceptor tyrosine‐based activation motifs (ITAMs), and of recent structural data on the ligand‐binding subunits of these receptors, we use these data to revisit how information on the state and quality of occupancy of the binding site of the T cell antigen receptor (TCR) is conveyed to the proximal components of the TCR transduction cassette.
Endometrial function in vervet monkeys (Cercopithecus aethiops): morphology, β3 integrin and insulin‐like growth factor binding protein‐1 expression during the menstrual cycle and pregnancy in the normal and disrupted endometrium
Authors: Seier J. V. , Chwalisz K. , Louw J. , Van Der Horst G. , De Kock M. , Du Toit D. , Laubscher J. A. 
Published: March 2003

Abstract: The expression of endometrial β3 integrin and insulin‐like growth factor binding protein‐1 (IGFBP‐1) was studied in cycling and pregnant vervet monkeys. There were clear changes of β3 integrin expression during the menstrual cycle, with the strongest immunostaining observed on day 26. Moderate to strong expression was observed during pregnancy. The expression of IGFBP‐1 during the menstrual cycle was weak but upregulated during pregnancy with moderate to strong staining. The administration of a single dose of onapristone at 10 mg/kg on days 17, 21 and 22 of the menstrual cycle, followed by a biopsy on days 22, 22 and 26, respectively, and during pregnancy (34–44 days menstrual age) 24 h before the biopsy, disrupted and desynchronized the endometrium. However, no effect on β3 integrin expression could be observed and staining reflected the untreated patterns. The same applied to IGFBP‐1 except that during pregnancy the expression of this protein was reduced or abolished. The results suggest that β3 integrin is associated with endometrial receptivity in vervet monkeys and that IGFBP‐1 plays an important role during pregnancy in this species. The administration of onapristone appeared to only influence IGFBP‐1 expression. To our knowledge, this is the first time that these endometrial proteins have been investigated in vervet monkeys. This study should therefore contribute to improving our understanding of the reproductive function of this species.
Rhesus rhadinovirus infection in healthy and SIV‐infected macaques at Tulane National Primate Research Center
Authors: Ruff K. , Baskin G.B. , Simpson L. , Murphey‐Corb M. , Levy L.S. 
Published: March 2003

Abstract:Rhesus rhadinovirus (RRV) infection was quantified in peripheral blood mononuclear cells (PBMC) from healthy and simian immunodeficiency virus (SIV)‐infected rhesus macaques (Macaca mulatta) at the Tulane National Primate Research Center and in a large collection of simian acquired immunodeficiency syndrome – (SAIDS)‐associated lymphomas. Quantification of RRV load was performed by real‐time PCR using amplification primers specific for the RRV interleukin‐6 homologue (RRV vIL‐6). RRV infection was detected infrequently and at low levels in PBMC of randomly selected healthy animals. Examination of longitudinally collected PBMC from 22 SIV‐infected animals throughout progression to SAIDS revealed similarly low RRV loads that sometimes increased with advancing disease. RRV infection was detected more frequently in the peripheral blood of SIV‐infected animals than in healthy animals. Examination of SAIDS‐associated lymphomas showed that RRV is rare within the tumor mass, likely representing infection in an occasional tumor‐infiltrating cell or contaminating blood. The results indicate that RRV infection in PBMC is not predictive of, and is apparently not required for, development of lymphoma or hyperplastic lymphadenopathy in SIV‐infected animals at TNPRC.
Comparison of HPV infection, p53 mutation and allelic losses in post‐transplant and non‐posttransplant oral squamous cell carcinomas
Authors: Zhang L. , Epstein J. B. , Poh C. F. , Berean K. , Lam W. L. , Zhang X. , Rosin M. P. 
Published: March 2003

AbstractBackground: Oral squamous cell carcinoma (SCC) is increasingly found in transplant recipients, although little is known of the natural history of the disease or the mechanism underlying this increase.Methods: In this article we describe the history of development of 5 oral post‐transplant SCCs (PSCCs) and compare their genetic profiles to 34 non‐posttransplant SCCs (NPSCCs).Results: Of the five patients with PSCCs, 3 had bone marrow transplants and two, kidney. All three PSCCs from bone marrow recipients were preceded locally by graft‐vs.‐host disease (GVHD). Two of the GVHD were biopsied and demonstrated dysplasia. Similar frequencies of loss of heterozygosity (LOH) occurred in PSCCs and NPSCCs at 3p, 9p, 17p and 8p, with lower frequencies in PSCCs at 4q (39% vs. 0%), 11q (53% vs. 20%) and 13q (45% vs. 20%), although the latter were not significantly different. Only 1 PSCC had ap53mutation, compared to historical values of 40–60% for NPSCC. Interestingly, human papillomavirus (HPV) DNA was detected in 3 (60%) PSCCs, in comparison to only 4 (12%) of the 34 NPSCCs (P = 0.0346).Conclusions: Dysplasia in oral GVHD may be a strong indicator of cancer risk and should not be regarded as reactive changes to lichenoid mucosites. The low level ofp53mutation and increased HPV infection support the involvement of HPV in the development of PSCC, while the similarity in LOH patterns suggests that other aspects of carcinogenesis may be comparable in these two types of SCCs.