我正在使用 citavi 结合 bibtex 和 bibstyle plain。我的问题是，有时作者姓名前面有一到两个空格/空白（比较作者 Albert 的空格和 Al-Hashimi 的空格，如图所示）。这看起来很奇怪，并且是由对齐引起的。当我删除对齐并将其更改为左对齐时，问题就解决了。但是，我更喜欢论文的对齐。
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这些是 bibfile 中的书目条目： 以下是书目条目：
@article{Adams.2009,
abstract = {Haematopoietic stem and progenitor cells (HSPCs) change location during development and circulate in mammals throughout life, moving into and out of the bloodstream to engage bone marrow niches in sequential steps of homing, engraftment and retention. Here we show that HSPC engraftment of bone marrow in fetal development is dependent on the guanine-nucleotide-binding protein stimulatory alpha subunit (Galpha(s)). HSPCs from adult mice deficient in Galpha(s) (Galpha(s)(-/-)) differentiate and undergo chemotaxis, but also do not home to or engraft in the bone marrow in adult mice and demonstrate a marked inability to engage the marrow microvasculature. If deleted after engraftment, Galpha(s) deficiency did not lead to lack of retention in the marrow, rather cytokine-induced mobilization into the blood was impaired. Testing whether activation of Galpha(s) affects HSPCs, pharmacological activators enhanced homing and engraftment in vivo. Galpha(s) governs specific aspects of HSPC localization under physiological conditions in vivo and may be pharmacologically targeted to improve transplantation efficiency.},
author = {Adams, Gregor B. and Alley, Ian R. and Chung, Ung-Il and Chabner, Karissa T. and Jeanson, Nathaniel T. and {Lo Celso}, Cristina and Marsters, Emily S. and Chen, Min and Weinstein, Lee S. and Lin, Charles P. and Kronenberg, Henry M. and Scadden, David T.},
year = {2009},
title = {Haematopoietic stem cells depend on Galpha(s)-mediated signalling to engraft bone marrow},
keywords = {0 (Adjuvants, Immunologic);143011-72-7 (Granulocyte Colony-Stimulating Factor);9012-63-9 (Cholera Toxin);Adjuvants, Immunologic/pharmacology;Animals;Bone Marrow Transplantation/physiology;Bone Marrow/drug effects/embryology/physiology;Cell Movement/drug effects/physiology;Cholera Toxin/pharmacology;EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gs);Granulocyte Colony-Stimulating Factor/metabolism;GTP-Binding Protein alpha Subunits, Gs/genetics/metabolism;Hematopoietic Stem Cells/physiology;Mice;Mice, Inbred C57BL;Signal Transduction/physiology},
pages = {103--107},
pagination = {page},
volume = {459},
number = {7243},
issn = {0028-0836},
doi = {\url{10.1038/nature07859}},
journal = {Nature}
}
@article{Afonina.2010,
abstract = {The caspase family of cysteine proteases becomes activated in response to diverse cellular insults and coordinates apoptosis through proteolysis of hundreds of cellular substrates. Cytotoxic lymphocytes are adept at promoting apoptosis of virally infected or transformed cells through delivery of cytotoxic enzymes, such as granzyme B, into target cells via the granule exocytosis pathway. Granzyme B promotes apoptosis of target cells through direct processing of certain caspases, which leads to their autoactivation. Granzyme B can also activate caspases indirectly through proteolysis of Bid, a protein that promotes mitochondrial permeabilization and consequent activation of the apoptosome pathway to caspase activation. Evidence also indicates that granzyme B may contribute to antiviral immunity by directly suppressing viral replication through direct proteolysis of viral proteins that are essential for pathogenicity. Recent reports also suggest that granzyme B may have additional non-cytotoxic roles under certain circumstances and may also function in the extracellular space. Here, we discuss the cytotoxic and putative non-cytotoxic functions of granzyme B within the immune system.},
author = {Afonina, Inna S. and Cullen, Sean P. and Martin, Seamus J.},
year = {2010},
title = {Cytotoxic and non-cytotoxic roles of the CTL/NK protease granzyme B},
keywords = {Animals;Apoptosis;BH3 Interacting Domain Death Agonist Protein/metabolism;Caspases/metabolism;Cytotoxicity, Immunologic;Granzymes/immunology/metabolism;Humans;Inflammation Mediators/metabolism;Inflammation/enzymology/immunology;Killer Cells, Natural/enzymology/immunology/virology;T-Lymphocytes, Cytotoxic/enzymology/immunology/virology;Virus Diseases/enzymology/immunology;Virus Replication},
pages = {105--116},
pagination = {page},
volume = {235},
number = {1},
issn = {0105-2896},
doi = {\url{10.1111/j.0105-2896.2010.00908.x}},
journal = {Immunol Rev}
}
@article{Aggarwal.2005,
abstract = {Mesenchymal stem cells (MSCs) are multipotent cells found in several adult tissues. Transplanted allogeneic MSCs can be detected in recipients at extended time points, indicating a lack of immune recognition and clearance. As well, a role for bone marrow-derived MSCs in reducing the incidence and severity of graft-versus-host disease (GVHD) during allogeneic transplantation has recently been reported; however, the mechanisms remain to be investigated. We examined the immunomodulatory functions of human MSCs (hMSCs) by coculturing them with purified subpopulations of immune cells and report here that hMSCs altered the cytokine secretion profile of dendritic cells (DCs), naive and effector T cells (T helper 1 [T(H)1] and T(H)2), and natural killer (NK) cells to induce a more anti-inflammatory or tolerant phenotype. Specifically, the hMSCs caused mature DCs type 1 (DC1) to decrease tumor necrosis factor alpha (TNF-alpha) secretion and mature DC2 to increase interleukin-10 (IL-10) secretion; hMSCs caused T(H)1 cells to decrease interferon gamma (IFN-gamma) and caused the T(H)2 cells to increase secretion of IL-4; hMSCs caused an increase in the proportion of regulatory T cells (T(Regs)) present; and hMSCs decreased secretion of IFN-gamma from the NK cells. Mechanistically, the hMSCs produced elevated prostaglandin E2 (PGE(2)) in co-cultures, and inhibitors of PGE(2) production mitigated hMSC-mediated immune modulation. These data offer insight into the interactions between allogeneic MSCs and immune cells and provide mechanisms likely involved with the in vivo MSC-mediated induction of tolerance that could be therapeutic for reduction of GVHD, rejection, and modulation of inflammation.},
author = {Aggarwal, Sudeepta and Pittenger, Mark F.},
year = {2005},
title = {Human mesenchymal stem cells modulate allogeneic immune cell responses},
pages = {1815--1822},
pagination = {page},
volume = {105},
number = {4},
issn = {0006-4971},
doi = {\url{10.1182/blood-2004-04-1559}},
journal = {Blood}
}
@article{Akagi.2013,
abstract = {BACKGROUND
Pulmonary vascular remodeling with idiopathic pulmonary arterial hypertension (IPAH) is associated with impaired apoptosis of pulmonary artery smooth muscle cells (PASMCs). We have reported that high-dose prostaglandin I2 (PGI2) therapy markedly improved hemodynamics in IPAH patients. The therapy is thought to reverse vascular remodeling, though the mechanism is unclear. The aim of this study is to assess proapoptotic effects of PGI2 on PASMCs obtained from IPAH patients.
METHODS
We investigated proapoptotic effects of PGI2 in PAH-PASMCs by TUNEL assays, caspase-3,-7 assays and transmission electron microscopy. We examined the expression of Fas ligand (FasL), an apoptosis-inducing member of the TNF cytokine family, in PAH-PASMCs. We measured the serum FasL levels in IPAH patients treated with PGI2.
RESULTS
TUNEL-positive, caspase-3, 7-active cells and fragmentation of the nucleus were detected in PAH-PASMCs treated with PGI2. The percentage of apoptotic cells induced by PGI2 at a high concentration was higher than that induced by PGI2 at a low concentration. PCR-array analysis revealed that PGI2 upregulated the FasL gene in PAH-PASMCs, and we measured the FasL expression by quantitative RT-PCR and Western blotting. PGI2 significantly increased the mRNA level of FasL by 3.98 fold and the protein level of FasL by 1.70 fold. An IP receptor antagonist inhibited the induction of apoptosis, elevation of cyclic AMP and upregulation of FasL by PGI2. Serum FasL level had a significant positive correlation with PGI2 dose in IPAH patients treated with PGI2.
CONCLUSIONS
PGI2 has proapoptotic effects on PAH-PASMCs via the IP receptor and upregulation of FasL.},
author = {Akagi, Satoshi and Nakamura, Kazufumi and Matsubara, Hiromi and Kusano, Kengo Fukushima and Kataoka, Noriyuki and Oto, Takahiro and Miyaji, Katsumasa and Miura, Aya and Ogawa, Aiko and Yoshida, Masashi and Ueda-Ishibashi, Hatsue and Yutani, Chikao and Ito, Hiroshi},
year = {2013},
title = {Prostaglandin I2 induces apoptosis via upregulation of Fas ligand in pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension},
pages = {499--505},
pagination = {page},
volume = {165},
number = {3},
doi = {\url{10.1016/j.ijcard.2011.09.004}},
journal = {Int J Cardiol}
}
@article{Akpek.2001,
abstract = {The disease-specific survival (DSS) of 151 patients with chronic graft-versus-host disease (cGVHD) was studied in an attempt to stratify patients into risk groups and to form a basis for a new grading of cGVHD. The data included the outcome and 23 variables at the diagnosis of cGVHD and at the primary treatment failure (PTF). Eighty-nine patients (58{\%}) failed primary therapy for cGVHD. Nonrelapse mortality was 44{\%} after a median follow-up of 7.8 years. The probability of DSS at 10 years after diagnosis of cGVHD (DSS1) and after PTF (DSS2) was 51{\%} (95{\%} confidence interval [CI] = 39{\%}, 60{\%}) and 38{\%} (95{\%} CI = 28{\%}, 49{\%}), respectively. According to multivariate analysis, extensive skin involvement (ESI) more than 50{\%} of body surface area; hazard ratio (HR) of 7.0 (95{\%} CI = 3.6-13.4), thrombocytopenia (TP) ({\textless} 100 000/microL; HR, 3.6; 95{\%} CI = 1.9-6.8), and progressive-type onset (PTO) (HR, 1.7; 95{\%} CI = 0.9-3.0) significantly influenced DSS1. These 3 factors and Karnofsky Performance Score of less than 50{\%} at PTF were significant predictors for DSS2. The DSS1 at 10 years for patients with prognostic factor score (PFS) at diagnosis of 0 (none), 1.9 and below [corrected] (ESI only or TP and/or PTO), above 1.9 and not above 3.5 [corrected] (ESI plus either TP or PTO), and more than 3.5 (all 3 factors) was 82{\%}, 68{\%}, 34{\%}, and 3{\%} (P =.05, {\textless}.001, {\textless}.001), respectively. The DSS2 at 5 years for patients with PFS at PTF of 0, 2 or less, 2 to 3.5, and more than 3.5 were 91{\%}, 71{\%}, 22{\%}, and 4{\%} (P =.2,.005, and {\textless}.001), respectively. It was concluded that these prognostic models might be useful in grouping the patients with similar outcome.},
author = {Akpek, G. and Zahurak, M. L. and Piantadosi, S. and Margolis, J. and Doherty, J. and Davidson, R. and Vogelsang, G. B.},
year = {2001},
title = {Development of a prognostic model for grading chronic graft-versus-host disease},
pages = {1219--1226},
pagination = {page},
volume = {97},
number = {5},
issn = {0006-4971},
journal = {Blood}
}
@article{AlHashmi.2011,
abstract = {Hematopoietic stem cell transplantation (HSCT) is a curative treatment for otherwise incurable diseases. Conditioning regimen is an important part of HSCT and consists of chemotherapy with or without irradiation. Conditioning exerts myelosuppressive, immunosuppressive and antitumor effects, but also contributes to HSCT-related complications including graft-versus-host disease (GVHD). Since almost 50{\%} of the transplanted patients are conditioned with cytostatics without irradiation, we developed and characterized a GVHD mouse model following conditioning with busulphan and cyclophosphamide. Recipient Balb/c female mice were treated with busulphan (20 mg/kg/day for 4 days) and cyclophosphamide (100 mg/kg/day for two days). After one day of rest, recipient mice were transplanted with 2$\times$107 bone marrow and 3$\times$107 spleen cells from male C57BL/6 (allogeneic group) or female Balb/c (syngeneic/control group) mice. The allogeneic, but not syngeneic transplanted mice developed GVHD. Histopathology of the major internal organs (liver, pancreas, spleen, lungs, heart and kidney) was examined before conditioning start, after conditioning's end and 5, 7 and 21 days after transplantation using hematoxylin-eosin staining. Decreased spleen cellularity and diminished glycogen content in the liver were observed after conditioning regimen. Histopathological changes such as vasculitis, inflammation and apoptotic cell forms in liver, spleen, pancreas, lungs and heart were observed in allogeneic transplanted mice, however, only hypocellular spleen and extramedullar hematopoiesis were detected in syngeneic transplanted animals. No morphological changes were observed in kidney in either HSCT setting. This is the first study describing early histopathological changes after conditioning regimen with busulphan/cyclophosphamide and dynamics of GVHD development in several major internal organs.},
author = {Al-Hashmi, Sulaiman and Hassan, Zuzana and Sadeghi, Behnam and Rozell, Bj{\"o}rn and Hassan, Moustapha},
year = {2011},
title = {Dynamics of early histopathological changes in GVHD after busulphan/cyclophosphamide conditioning regimen},
pages = {596--605},
pagination = {page},
volume = {4},
number = {6},
issn = {1936-2625},
journal = {Int J Clin Exp Pathol}
}
@article{Albert.2005,
abstract = {Successful hematopoietic cell transplantation (HCT) from an allogeneic donor ideally should produce tolerance to recipient alloantigens while preserving anti-infectious and antitumor immunity. Rapamycin together with costimulation blockade can induce tolerance in organ allograft models by inhibiting G(1) --{\textgreater} S-phase progression and promoting T-cell apoptosis. In contrast to blocking costimulation through CD28, administration of agonistic CD28-specific antibody 37.51 partially prevents lethal graft-versus-host disease (GVHD) by selective depletion of alloreactive T cells in mice. We hypothesized that combining rapamycin with agonistic CD28 treatment would improve GVHD control by tolerizing a small subset of alloreactive T cells that might escape effects of the CD28-specific antibody. A short course of rapamycin plus agonistic CD28 treatment showed synergism at suboptimal doses, was highly effective in preventing lethal GVHD, and was superior to rapamycin plus CD28 blockade in a major histocompatibility complex class I- and II-mismatched HCT model. The combination treatment reduced the number of proliferating, alloreactive cells in the recipient, promoted donor B- and T-cell reconstitution, and reduced inflammatory cytokine levels. Administration of rapamycin plus agonistic CD28 antibodies offers a promising new therapeutic approach to facilitate tolerance after HCT.},
author = {Albert, Michael H. and Yu, Xue-Zhong and Martin, Paul J. and Anasetti, Claudio},
year = {2005},
title = {Prevention of lethal acute GVHD with an agonistic CD28 antibody and rapamycin},
keywords = {Animals;Antibodies, Monoclonal/therapeutic use;Antibody Specificity;CD28 Antigens/immunology;Graft vs Host Disease/prevention {\&} control;Immunosuppression/methods;Lymphocyte Depletion;Mice;Mice, Inbred C57BL;Mice, Inbred Strains;Sirolimus/therapeutic use;T-Lymphocytes/immunology},
pages = {1355--1361},
pagination = {page},
volume = {105},
number = {3},
issn = {0006-4971},
doi = {\url{10.1182/blood-2004-08-3305}},
journal = {Blood}
}