Mycoplasma leachii sp. nov. as a new species designation for Mycoplasma sp. bovine group 7 of Leach, and reclassification of Mycoplasma mycoides subsp. mycoides LC as a serovar of Mycoplasma mycoides subsp. capri

The Mycoplasma mycoides cluster consists of six pathogenic mycoplasmas causing disease in ruminants, which share many genotypic and phenotypic traits. The M. mycoides cluster comprises five recognized taxa: Mycoplasma mycoides subsp. mycoides Small Colony (MmmSC), M. mycoides subsp. mycoides Large Colony (MmmLC), M. mycoides subsp. capri (Mmc), Mycoplasma capricolum subsp. capricolum (Mcc) and M. capricolum subsp. capripneumoniae (Mccp). The group of strains known as Mycoplasma sp. bovine group 7 of Leach (MBG7) has remained unassigned, due to conflicting data obtained by different classification methods. In the present paper, all available data, including recent phylogenetic analyses, have been reviewed, resulting in a proposal for an emended taxonomy of this cluster: (i) the MBG7 strains, although related phylogenetically to M. capricolum, hold sufficient characteristic traits to be assigned as a separate species, i.e. Mycoplasma leachii sp. nov. (type strain, PG50(T) = N29(T) = NCTC 10133(T) = DSM 21131(T)); (ii) MmmLC and Mmc, which can only be distinguished by serological methods and are related more distantly to MmmSC, should be combined into a single subspecies, i.e. Mycoplasma mycoides subsp. capri, leaving M. mycoides subsp. mycoides (MmmSC) as the exclusive designation for the agent of contagious bovine pleuropneumonia. A taxonomic description of M. leachii sp. nov. and emended descriptions of M. mycoides subsp. mycoides and M. mycoides subsp. capri are presented. As a result of these emendments, the M. mycoides cluster will hereafter be composed of five taxa comprising three subclusters, which correspond to the M. mycoides subspecies, the M. capricolum subspecies and the novel species M. leachii.

Modulating bioreductive drug activity with antivascular agents

Modulation of tumor hypoxia to increase bioreductive drug antitumor activity was investigated. The antivascular agent 5,6-dimethylxanthenone acetic acid (DMXAA) was used in combination studies with the bioreductive drugs Tirapazamine (TPZ) and Mitomycin C (MMC). Blood perfusion studies with DMXAA showed a maximal reduction of 66% in tumor blood flow 4 hours post drug administration. This tumor specific decrease in perfusion was also found to be dose-dependent, with 25 and 30 mg/kg DMXAA yielding greater than 50% reduction in tumor blood flow. Increases in antitumor activity with combination therapy (bioreductive drugs $+$ DMXAA) were significant over individual therapies, suggesting an increased activity due to increased hypoxia induced by DMXAA. Combination studies yielded the following significant tumor growth delays over control: MMC (5mg/kg) $+$ DMXAA (25mg/kg) = 20 days, MMC (2.5mg/kg) $+$ DMXAA (25 mg/kg) = 8 days, TPZ (21.4mg/kg) $+$ DMXAA (17.5mg/kg) = 4 days. The mechanism of interaction of these drugs was investigated by measuring metabolite production and DNA damage. 'Real time' microdialysis studies indicated maximal metabolite production at 20-30 minutes post injection for individual and combination therapies. DNA double strand breaks induced by TPZ $\pm$ DMXAA (20 minutes post injection) were analyzed by pulsed field gel electrophoresis (PFGE). Southern blot analyses and quantification showed TPZ induced DNA double strand breaks, but this effect was not evident in combination studies with DMXAA. Based on these data, combination studies of TPZ $+$ DMXAA showed increased antitumor activity over individual drug therapies. The mechanism of this increased activity, however, does not appear to be due to an increase in TPZ bioreduction at this time point. ^

Sphingosine kinase 2 deficiency increases proliferation and migration of renal mouse mesangial cells and fibroblasts

Both of the sphingosine kinase (SK) subtypes SK-1 and SK-2 catalyze the production of the bioactive lipid molecule sphingosine 1-phosphate (S1P). However, the subtype-specific cellular functions are largely unknown. In this study, we investigated the cellular function of SK-2 in primary mouse renal mesangial cells (mMC) and embryonic fibroblasts (MEF) from wild-type C57BL/6 or SK-2 knockout (SK2ko) mice. We found that SK2ko cells displayed a significantly higher proliferative and migratory activity when compared to wild-type cells, with concomitant increased cellular activities of the classical extracellular signal regulated kinase (ERK) and PI3K/Akt cascades, and of the small G protein RhoA. Furthermore, we detected an upregulation of SK-1 protein and S1P3 receptor mRNA expression in SK-2ko cells. The MEK inhibitor U0126 and the S1P1/3 receptor antagonist VPC23019 blocked the increased migration of SK-2ko cells. Additionally, S1P3ko mesangial cells showed a reduced proliferative behavior and reduced migration rate upon S1P stimulation, suggesting a crucial involvement of the S1P3 receptor. In summary, our data demonstrate that SK-2 exerts suppressive effects on cell growth and migration in renal mesangial cells and fibroblasts, and that therapeutic targeting of SKs for treating proliferative diseases requires subtype-selective inhibitors.

Modifying Post-Operative Medical Care after EBV Implant May Reduce Pneumothorax Incidence.

OBJECTIVE Endoscopic lung volume reduction (ELVR) with valves has been shown to improve COPD patients with severe emphysema. However, a major complication is pneumothoraces, occurring typically soon after valve implantation, with severe consequences if not managed promptly. Based on the knowledge that strain activity is related to a higher risk of pneumothoraces, we asked whether modifying post-operative medical care with the inclusion of strict short-term limitation of strain activity is associated with a lower incidence of pneumothorax. METHODS Seventy-two (72) emphysematous patients without collateral ventilation were treated with bronchial valves and included in the study. Thirty-two (32) patients received standard post-implantation medical management (Standard Medical Care (SMC)), and 40 patients received a modified medical care that included an additional bed rest for 48 hours and cough suppression, as needed (Modified Medical Care (MMC)). RESULTS The baseline characteristics were similar for the two groups, except there were more males in the SMC cohort. Overall, ten pneumothoraces occurred up to four days after ELVR, eight pneumothoraces in the SMC, and only two in the MMC cohorts (p=0.02). Complicated pneumothoraces and pneumothoraces after upper lobe treatment were significantly lower in MMC (p=0.02). Major clinical outcomes showed no significant differences between the two cohorts. CONCLUSIONS In conclusion, modifying post-operative medical care to include bed rest for 48 hours after ELVR and cough suppression, if needed, might reduce the incidence of pneumothoraces. Prospective randomized studies with larger numbers of well-matched patients are needed to confirm the data.

Galactofuranose in Mycoplasma mycoides is important for membrane integrity and conceals adhesins but does not contribute to serum resistance.

Mycoplasma mycoides subsp. capri (Mmc) and subsp. mycoides (Mmm) are important ruminant pathogens worldwide causing diseases such as pleuropneumonia, mastitis and septicaemia. They express galactofuranose residues on their surface, but their role in pathogenesis has not yet been determined. The M. mycoides genomes contain up to several copies of the glf gene, which encodes an enzyme catalysing the last step in the synthesis of galactofuranose. We generated a deletion of the glf gene in a strain of Mmc using genome transplantation and tandem repeat endonuclease coupled cleavage (TREC) with yeast as an intermediary host for the genome editing. As expected, the resulting YCp1.1-Δglf strain did not produce the galactofuranose-containing glycans as shown by immunoblots and immuno-electronmicroscopy employing a galactofuranose specific monoclonal antibody. The mutant lacking galactofuranose exhibited a decreased growth rate and a significantly enhanced adhesion to small ruminant cells. The mutant was also 'leaking' as revealed by a β-galactosidase-based assay employing a membrane impermeable substrate. These findings indicate that galactofuranose-containing polysaccharides conceal adhesins and are important for membrane integrity. Unexpectedly, the mutant strain showed increased serum resistance.

STUDIES OF THE MOLECULAR MECHANISMS OF CHROMOSOME ABERRATION FORMATION (DNA REPAIR, CROSSLINKS, MITOMYCIN C)

The objective of this research has been to study the molecular basis for chromosome aberration formation. Predicated on a variety of data, Mitomycin C (MMC)-induced DNA damage has been postulated to cause the formation of chromatid breaks (and gaps) by preventing the replication of regions of the genome prior to mitosis. The basic protocol for these experiments involved treating synchronized Hela cells in G(,1)-phase with a 1 (mu)g/ml dose of MMC for one hour. After removing the drug, cells were then allowed to progress to mitosis and were harvested for analysis by selective detachment. Utilizing the alkaline elution assay for DNA damage, evidence was obtained to support the conclusion that Hela cells can progress through S-phase into mitosis with intact DNA-DNA interstrand crosslinks. A higher level of crosslinking was observed in those cells remaining in interphase compared to those able to reach mitosis at the time of analysis. Dual radioisotope labeling experiments revealed that, at this dose, these crosslinks were associated to the same extent with both parental and newly replicated DNA. This finding was shown not to be the result of a two-step crosslink formation mechanism in which crosslink levels increase with time after drug treatment. It was also shown not to be an artefact of the double-labeling protocol. Using neutral CsCl density gradient ultracentrifugation of mitotic cells containing BrdU-labeled newly replicated DNA, control cells exhibited one major peak at a heavy/light density. However, MMC-treated cells had this same major peak at the heavy/light density, in addition to another minor peak at a density characteristic for light/light DNA. This was interpreted as indicating either: (1) that some parental DNA had not been replicated in the MMC treated sample or; (2) that a recombination repair mechanism was operational. To distinguish between these two possibilities, flow cytometric DNA fluorescence (i.e., DNA content) measurements of MMC-treated and control cells were made. These studies revealed that the mitotic cells that had been treated with MMC while in G(,1)-phase displayed a 10-20% lower DNA content than untreated control cells when measured under conditions that neutralize chromosome condensation effects (i.e., hypotonic treatment). These measurements were made under conditions in which the binding of the drug, MMC, was shown not to interfere with the stoichiometry of the ethidium bromide-mithramycin stain. At the chromosome level, differential staining techniques were used in an attempt to visualize unreplicated regions of the genome, but staining indicative of large unreplicated regions was not observed. These results are best explained by a recombinogenic mechanism. A model consistent with these results has been proposed.^

FANCM AND FAAP24 MAINTAIN GENOMIC STABILITY THROUGH COOPERATIVE AND UNIQUE FUNCTIONS

Fanconi anemia (FA) is a rare recessive genetic disease with an array of clinical manifestations including multiple congenital abnormalities, progressive bone marrow failure and profound cancer susceptibility. A hallmark of cells derived from FA patients is hypersensitivity to DNA interstrand crosslinking agents such as mitomycin C (MMC) and cisplatin, suggesting that FA- and FA-associated proteins play important roles in protecting cells from DNA interstrand crosslink (ICL) damage. Two genes involved in the FA pathway, FANCM and FAAP24, are of particular interest because they contain DNA interacting domains. However, there are no definitive patient mutations for these two genes, and the resulting lack of human genetic model system renders their functional studies difficult. In this study, I established isogenic human FANCM- and FAAP24-null mutants through homologous replacement-mediated gene targeting in HCT-116 cells, and systematically investigated the functions of FANCM and FAAP24 inchromosome stability, FA pathway activation, DNA damage checkpoint signaling, and ICL repair. I found that the FANCM-/-/FAAP24-/- double mutant was much more sensitive to DNA crosslinking agents than FANCM-/- and FAAP24-/- single mutants, suggesting that FANCM and FAAP24 possess epistatic as well as unique functions in response to ICL damage. I demonstrated that FANCM and FAAP24 coordinately support the activation of FA pathway by promoting chromatin localization of FA core complex and FANCD2 monoubiqutination. They also cooperatively function to suppress sister chromatid exchange and radial chromosome formation, likely by limiting crossovers in recombination repair. In addition, I defined novel non-overlapping functions of FANCM and FAAP24 in response to ICL damage. FAAP24 plays a major role in activating ICL-induced ATR-dependent checkpoint, which is independent of its interaction with FANCM. On the other hand, FANCM promotes recombination-independent ICL repair independently of FAAP24. Mechanistically, FANCM facilitates recruitment of nucleotide excision repair machinery and lesion bypass factors to ICL damage sites through its translocase activity. Collectively, my studies provide mechanistic insights into how genome integrity is both coordinately and independently protected by FANCM and FAAP24.

Molecular mechanism of the relaxin signaling pathways: Activation of cAMP, PI3K, and PKCzeta

Relaxin is a polypeptide hormone that has diverse effects on reproductive and non-reproductive tissues. Relaxin activates the G-protein coupled receptors, LGR7 and LRG8. Early studies described increased cAMP and protein kinase A activity upon relaxin treatment, but cAMP accumulation alone could not account for all of the relaxin-mediated effects. We utilized the human monocyte cell line THP-1 to study the mechanism of relaxin-stimulated CAMP production. ^ Relaxin treatment in THP-1 cells produces a biphasic time course in cAMP accumulation, where the first peak appears as early as 1–2 minutes with a second peak at 10–20 minutes. Selective inhibitors for phosphoinositide 3-kinase (P13K), such as wortmannin and LY294002, show a dose-dependent inhibition of relaxin-stimulated cAMP accumulation, specific for the second peak of the relaxin time course. Neither the effects of relaxin nor the inhibition of relaxin by LY294002 is mediated by the activity of phosphodiesterases. Furthermore, LY294002 blocks upregulation of vascular endothelial growth factor transcript levels by relaxin. ^ To further delineate relaxin signaling pathways, we searched for downstream targets of PI3K that could activate adenylyl cyclase (AC). Protein kinase C ζ (PKCζ) was a prime candidate because it activates types II and V AC. Chelerythrine chloride (a general PKC inhibitor) inhibits relaxin-induced cAMP production to the same degree as LY294002 (∼40%). Relaxin stimulates PKCζ translocation to the plasma membrane in THP-1, MCF-7, PHM1-31, and MMC cells, as shown by immunocytochemistry. PKCζ translocation is P13K-dependent and independent of cAMP production. Antisense PKCζ oligodeoxynucleotides (PKCζ-ODNs) deplete both PKCζ transcript and protein levels in THP-1 cells. PKCζ-ODNs abolish relaxin-mediated PKCζ translocation and inhibit relaxin stimulation of cAMP by 40%, as compared to mock and random ODN controls. Treatment with LY294002 in the presence of PKCζ-ODNs results in little further inhibition. Taken together, we present a novel role for PI3K and PKCζ in relaxin stimulation of cAMP and provide the first example of the PKCζ regulation of AC in an endogenous system. Furthermore, we have identified higher order complexes of AC isoforms and PKA anchoring proteins in attempts to explain the differential coupling of relaxin to cAMP and PI3K-signaling pathways in various cell types. ^

La 'Conexión mexicana' en la ruta de la efedrina : Prejuicios racistas y estereotipos acerca de los mexicanos en Argentina en el discurso de Clarín

Durante varias semanas de mediados de 2008 distintos medios masivos de comunicación (MMC) argentinos -con Clarín a la Cabeza - impulsaron en las audiencias imágenes estereotipadas del mexicano al tratar cierto tema de la agenda noticiosa del momento. Luego de repetidas imágenes de la violencia de los carteles mexicanos de la droga -del Golfo, de Sinaloa, los Zetas entre otros - los MMC contribuyeron a generalizar el prejuicio a los extranjeros mexicanos como peligrosos, riesgosos para la comunidad local y presuntos sospechosos para las autoridades. En esta ponencia se aborda el caso del llamado "triple crimen de General Rodríguez", en el que Clarín durante su cobertura involucró a mexicanos lo cual derivó en rechazo o desconfianza generalizada hacia los mexicanos in-migrantes que se tradujo en discriminación inculcada por los MMC particularmente por Clarín, el cual en días previos al suceso objeto de estudio presentó otro acontecimiento, la captura de una "banda de narcos mexicanos" ocurrida en Ingeniero Maschwitz, igualmente de modo tendencioso. Clarín al igual que el sistema de MMC del que forma parte opera en una nación en la que culturalmente rige un "sistema de dominio étnico o racial" (Van Dijk, 2008) para un sector considerable de la comunidad

La 'Conexión mexicana' en la ruta de la efedrina : Prejuicios racistas y estereotipos acerca de los mexicanos en Argentina en el discurso de Clarín

Durante varias semanas de mediados de 2008 distintos medios masivos de comunicación (MMC) argentinos -con Clarín a la Cabeza - impulsaron en las audiencias imágenes estereotipadas del mexicano al tratar cierto tema de la agenda noticiosa del momento. Luego de repetidas imágenes de la violencia de los carteles mexicanos de la droga -del Golfo, de Sinaloa, los Zetas entre otros - los MMC contribuyeron a generalizar el prejuicio a los extranjeros mexicanos como peligrosos, riesgosos para la comunidad local y presuntos sospechosos para las autoridades. En esta ponencia se aborda el caso del llamado "triple crimen de General Rodríguez", en el que Clarín durante su cobertura involucró a mexicanos lo cual derivó en rechazo o desconfianza generalizada hacia los mexicanos in-migrantes que se tradujo en discriminación inculcada por los MMC particularmente por Clarín, el cual en días previos al suceso objeto de estudio presentó otro acontecimiento, la captura de una "banda de narcos mexicanos" ocurrida en Ingeniero Maschwitz, igualmente de modo tendencioso. Clarín al igual que el sistema de MMC del que forma parte opera en una nación en la que culturalmente rige un "sistema de dominio étnico o racial" (Van Dijk, 2008) para un sector considerable de la comunidad

La 'Conexión mexicana' en la ruta de la efedrina : Prejuicios racistas y estereotipos acerca de los mexicanos en Argentina en el discurso de Clarín

Durante varias semanas de mediados de 2008 distintos medios masivos de comunicación (MMC) argentinos -con Clarín a la Cabeza - impulsaron en las audiencias imágenes estereotipadas del mexicano al tratar cierto tema de la agenda noticiosa del momento. Luego de repetidas imágenes de la violencia de los carteles mexicanos de la droga -del Golfo, de Sinaloa, los Zetas entre otros - los MMC contribuyeron a generalizar el prejuicio a los extranjeros mexicanos como peligrosos, riesgosos para la comunidad local y presuntos sospechosos para las autoridades. En esta ponencia se aborda el caso del llamado "triple crimen de General Rodríguez", en el que Clarín durante su cobertura involucró a mexicanos lo cual derivó en rechazo o desconfianza generalizada hacia los mexicanos in-migrantes que se tradujo en discriminación inculcada por los MMC particularmente por Clarín, el cual en días previos al suceso objeto de estudio presentó otro acontecimiento, la captura de una "banda de narcos mexicanos" ocurrida en Ingeniero Maschwitz, igualmente de modo tendencioso. Clarín al igual que el sistema de MMC del que forma parte opera en una nación en la que culturalmente rige un "sistema de dominio étnico o racial" (Van Dijk, 2008) para un sector considerable de la comunidad

The human papilloma virus 16E6 gene sensitizes human mammary epithelial cells to apoptosis induced by DNA damage.

Programmed cell death (apoptosis) is a normal physiological process, which could in principle be manipulated to play an important role in cancer therapy. The key importance of p53 expression in the apoptotic response to DNA-damaging agents has been stressed because mutant or deleted p53 is so common in most kinds of cancer. An important strategy, therefore, is to find ways to induce apoptosis in the absence of wild-type p53. In this paper, we compare apoptosis in normal human mammary epithelial cells, in cells immortalized with human papilloma virus (HPV), and in mammary carcinoma cell lines expressing wild-type p53, mutant p53, or no p53 protein. Apoptosis was induced with mitomycin C (MMC), a DNA cross-linking and damaging agent, or with staurosporine (SSP), a protein kinase inhibitor. The normal and HPV-transfected cells responded more strongly to SSP than did the tumor cells. After exposure to MMC, cells expressing wild-type p53 underwent extensive apoptosis, whereas cells carrying mutated p53 responded weakly. Primary breast cancer cell lines null for p53 protein were resistant to MMC. In contrast, two HPV immortalized cell lines in which p53 protein was destroyed by E6-modulated ubiquitinylation were highly sensitive to apoptosis induced by MMC. Neither p53 mRNA nor protein was induced in the HPV immortalized cells after MMC treatment, although p53 protein was elevated by MMC in cells with wild-type p53. Importantly, MMC induced p21 mRNA but not p21 protein expression in the HPV immortalized cells. Thus, HPV 16E6 can sensitize mammary epithelial cells to MMC-induced apoptosis via a p53- and p21-independent pathway. We propose that the HPV 16E6 protein modulates ubiquitin-mediated degradation not only of p53 but also of p21 and perhaps other proteins involved in apoptosis.

Sensibilização ao látex em pacientes com mielomeningocele na urologia do HC-FMUSP: prevalência e fatores associados

INTRODUÇÃO: A alergia ao látex é um importante problema de saúde pública, especialmente em grupos de risco que têm contato frequente com este potente alérgeno. Este estudo estimou a prevalência e os fatores de risco para sensibilização ao látex em pacientes com mielomeningocele (MMC) submetidos a procedimentos cirúrgicos urológicos no HC-FMUSP. MÉTODOS: Foram selecionados pacientes com MMC submetidos a pelo menos uma cirurgia urológica, entre 2009 e 2014.Todos foram entrevistados e seus prontuários revisados. Uma amostra de sangue permitiu que a IgE específica ao látex, a K82, e seus recombinantes fossem investigados pelo método lmmunoCAP100 (kUa/L -1). A associação entre a exposição e o desfecho foi avaliada por meio de regressão logística de Poisson, Quiquadrado ou o teste exato de Fischer, para variáveis categóricas. O teste t de Student foi utilizado para comparar variáveis contínuas (nível de significância de 5%). Foram calculados a razão de prevalência (RP) e o intervalo de confiança de 95%. RESULTADOS: Foram identificados Duzentos e doze pacientes (51% do sexo masculino, 20,4 ± 6,4 anos de idade), 68 foram submetidos a pelo menos um procedimento urológico e 51 aceitaram participar (87,9%). Vinte e nove pacientes foram considerados não-sensibilizados (IgE específica para o látex :: a 0,7 kUa/L) e 22 sensibilizados ao látex com IgE > 0,7 kUa/L. Quando comparados os dois grupos, o sensibilizado apresentou um número de procedimentos cirúrgicos maior (11,6 ± 5,9 vs 7,2 ± 5,6) e dentre eles 48,3% apresentaram alguma alergia anterior contra 27,6% no grupo não sensibilizado. A sensibilização ao látex foi independentemente associada com alergia a produtos de látex (p = 0,014) e com o número de cirurgias anteriores (p = 0,032). A alergia ao látex tinha uma razão de prevalência de 2,87 (95% Cl: 1,24 a 6,65) ajustado para o número de cirurgias. Para cada procedimento cirúrgico, ajustado à alergia a produtos que contém látex, aumentou o risco para sensibilização em 4% (PR = 1,04; 95% CI: 1,00-1,09). CONCLUSÕES: A história de alergia ao látex e o número de cirurgias foram fatores de risco independentes para sensibilização ao látex

Efeitos da soldagem por laser de fibra de Yb na microestrutura do compósito A356/SiCp

Materiais compósitos são projetados e fabricados para várias aplicações de alto desempenho, incluindo componentes para os segmentos automobilístico, aeroespacial, aeronáutico, naval, de defesa, de óleo e gás, energia eólica e até equipamentos esportivos. Porém, a união por soldagem de Compósitos de Matriz Metálica de Alumínio (Al-CMM) ainda é um grande obstáculo para a maior disseminação desta classe de materiais estruturais. As mudanças microestruturais decorrentes do ciclo de soldagem e/ou do tratamento térmico afetam sensivelmente as propriedades mecânicas e físico-químicas finais da junta e do metal base nas proximidades de mesma, daí a importância de se estudar a evolução microestrutural que prospera nestas etapas. O presente trabalho caracterizou a microestrutura do compósito liga-A356/SiCp soldado por laser de fibra de Itérbio, empregando-se nessa tarefa técnicas de microscopia óptica, radiografia e microscopia eletrônica de varredura, assim como difração de raios-X e de elétrons retroespalhados, ensaio instrumentado de dureza e microtomografia computadorizada. O foco das análises realizadas restringiu-se à geometria dos cordões de solda, à expulsão de SiC particulado da zona soldada, à volatilização de elementos químicos da poça de soldagem, à formação de precipitados fragilizantes de Al4SiC4 em formato de agulhas no cordão de solda e à determinação das regiões com concentração de poros, todos estes fenômenos tendo efeitos nocivos, em maior ou menor extensão, no desempenho global da junta do Al-CMM soldada a laser, notadamente em suas propriedades mecânicas e eletroquímicas.

Commerce, Justice, science, and related agencies appropriations for 2012 : hearings before a subcommittee of the Committee on Appropriations, House of Representatives, One Hundred Twelfth Congress, first session /

Shipping list number: 2011-0317-P (pt. 2A), 2011-0318-P (pt. 2B), 2011-0285-P (pt. 3, 4), 2011--0325-P (pt. 5), 2011-0410-P (pt. 6), 2012-0013-P (pt. 7), 2011-0383-P (pt. 8), 2011-0295-P (pt. 9).