The Gendered Worlds of Latin American Women Workers

The Gendered Worlds of Latin American Women Workers. John D. French and Daniel James. eds. Durham, NC: Duke University Press, 1998. 320 pp.     

A novel postpriming regulatory check point of effector/memory T cells dictated through antigen density threshold-dependent anergy

CTLs act as the effector arm of the cell-mediated immune system to kill undesirable cells. Two processes regulate these effector cells to prevent self reactivity: a thymic selection process that eliminates autoreactive clones and a multistage activation or priming process that endows them with a license to kill cognate target cells. Hitherto no subsequent regulatory restrictions have been ascribed for properly primed and activated CTLs that are licensed to kill. In this study we show that CTLs possess a novel postpriming regulatory mechanism(s) that influences the outcome of their encounter with cognate target cells. This mechanism gauges the degree of Ag density, whereupon reaching a certain threshold significant changes occur that induce anergy in the effector T cells. The biological consequences of this Ag-induced postpriming control includes alterations in the expression of cell surface molecules that control immunological synapse activity and cytokine profiles and induce retarded cell proliferation. Most profound is genome-wide microarray analysis that demonstrates changes in the expression of genes related to membrane potential, TCR signal transduction, energy metabolism, and cell cycle control. Thus, a discernible and unique gene expression signature for anergy as a response to high Ag density has been observed. Consequently, activated T cells possess properties of a self-referential sensory organ. These studies identify a new postpriming control mechanism of CTL with anergenic-like properties. This mechanism extends our understanding of the control of immune function and regulation such as peripheral tolerance, viral infections, antitumor immune responses, hypersensitivity, and autoimmunity.     

The expanded supraclavicular flap, prefabricated with thoracoacromial vessels, for reconstruction of postburn anterior cervical contractures

Mentosternal contractures are well-known complications after burns, scald injuries, and injuries with acid or lye. These contractures may cause severe deformities that are both functionally and aesthetically crippling. Reconstruction of the neck requires the transfer of large flaps of thin, pliable skin to optimally match the texture and color of the recipient region. With the introduction of free tissue transfer, the availability of flaps for reconstruction of large neck defects has greatly increased. Unfortunately, many of these flaps are bulky and are not well matched to the thin and pliable skin of the neck. This article introduces the expanded supraclavicular flap prefabricated with the thoracoacromial vessels for reconstruction of anterior cervical contractures. Their anatomic location, length, and arc of rotation make the thoracoacromial vessels an excellent choice for prefabricating the supraclavicular skin for its subsequent interpolation into the anterior neck. Skin expansion in the donor region not only allows coverage of the larger unit of the anterior neck but also modifies the morphologic characteristics of the transferred flap through capsule formation and fatty tissue atrophy, which is beneficial for obtaining an optimal neck reconstruction.     

Morphological analysis of young and old pellicles of Salmonella Typhimurium

A wide variety of microorganisms are able to form biofilms at the interface between air and liquid (pellicles). In this study changes during the maturation of the pellicle of Salmonella Typhimurium were analysed and the role of cellulose in the pellicle structure and morphology evaluated. The morphology of both sides of the pellicle was characterised using atomic force microscopy and scanning electron microscopy. Overall, there was a marked difference in the morphology of the water-facing (WF) and air-facing (AF) biofilm surfaces. While the AF side appeared to be uniform, and extensively covered with an exocellular coating, cells in the WF side were distributed into clusters and were less covered. However, the similarity in size and shape of single cells from both sides of the pellicle may indicate that the bacterial cells across the pellicle have a similar physiological status. During maturation, porous structures with multiple cracks and channels were created in the pellicle, leading to disintegration. By comparison with the structure of pellicles of a cellulose-deficient mutant, it was demonstrated that the observed disintegration of mature pellicles probably occurred in part by self-hydrolysis of components of the matrix.     

Specification of Arabidopsis floral meristem identity by repression of flowering time genes

Flowering plants produce floral meristems in response to intrinsic and extrinsic flowering inductive signals. In Arabidopsis, the floral meristem identity genes LEAFY (LFY) and APETALA1 (AP1) are activated to play a pivotal role in specifying floral meristems during floral transition. We show here that the emerging floral meristems require AP1 to partly specify their floral identities by directly repressing a group of flowering time genes, including SHORT VEGETATIVE PHASE (SVP), AGAMOUS-LIKE 24 (AGL24) and SUPPRESSOR OF OVEREXPRESSION OF CO1 (SOC1). In wild-type plants, these flowering time genes are normally downregulated in emerging floral meristems. In the absence of AP1, these genes are ectopically expressed, transforming floral meristems into shoot meristems. By post-translational activation of an AP1-GR fusion protein and chromatin immunoprecipitation assays, we further demonstrate the repression of these flowering time genes by induced AP1 activity and in vivo AP1 binding to the cis-regulatory regions of these genes. These findings indicate that once AP1 is activated during the floral transition, it acts partly as a master repressor in floral meristems by directly suppressing the expression of flowering time genes, thus preventing the continuation of the shoot developmental program.     

Chemokines in hepatitis C virus infection: pathogenesis, prognosis and therapeutics

Hepatitis C virus infection and its associated liver inflammatory disease is a major global health problem affecting over 170 million people worldwide. Following viral infection, multiple pro-inflammatory mediators contribute to recruitment of immune cells to the liver and to the generation of an anti-viral immune response. However, when this vigorous immune response fails to eliminate the virus, chronic infection is established. This in turn, results in an ongoing process of inflammation, regeneration and fibrosis that in many cases leads to the development of cirrhosis and of hepatocellular carcinoma. Multiple recent publications mark chemokines and their receptors as key players in leukocyte recirculation through the inflamed liver. Furthermore, chemokines may also be involved in liver regeneration, fibrosis, and in malignant transformation, which is induced by the persistence of inflammation. Accumulating data indicates that distinct chemokines and chemokine receptors may be associated with different stages of the chronic hepatitis C virus infection-associated liver disease. Multiple small molecules and peptide antagonizing chemokines and their receptors are in advanced phase 3 and phase 2 clinical trials. In the near future, such drugs are expected to enter clinical use raising the question whether they may be applicable for the treatment of chronic viral infection-associated liver disease. In this review, recent advances in understanding the role of chemokines and their receptors in the pathogenesis of chronic viral infection-associated liver disease are presented. Furthermore, the clinical implications of these novel findings, which mark chemokines as prognostic markers and therapeutic targets for immune-modulation during chronic liver viral infection, are documented.     

Modern Processing and Insights on Selenium Solar Cells: The World's First Photovoltaic Device

The first solid‐state solar cells, fabricated ≈140 years ago, were based on selenium; these early studies initiated the modern research on photovoltaic materials. Selenium shows high absorption coefficient and mobility, making it an attractive absorber for high bandgap thin film solar cells. Moreover, the simplicity of a single element absorber, its low‐temperature processing, and intrinsic environmental stability enable the utilization of selenium in extremely cheap and scalable solar cells. In this paper, a detailed study of selenium solar cell fabrication is presented, and the key factors that affect the selenium film morphology and the resulting device efficiency are presented. Specifically, the crystallization process from amorphous film into functional crystalline device is studied. The importance of controlling the process is shown, and methods to align the growth orientation are suggested. Finally, the crystallization process under illumination, which has general importance for the fabrication of thin film photovoltaics, is investigated. Specifically for selenium, the illumination significantly improves the film morphology and leads to device efficiency of 5.2%, with open‐circuit voltage of 0.911 V, short‐circuit current density of 10.2 mA cm^?2, and fill factor of 55.0%. These findings form a solid foundation for future improvements of the photovoltaic material and device architecture.     

Association of pre-admission statin therapy and the inflammatory response in ST elevation myocardial infarction patients

Purpose: To demonstrate the possible association of statin therapy with C reactive protein (CRP) serial measurements in ST elevation myocardial infarction (STEMI) patients.

Materials and methods: STEMI patients between 2008 and 2016 with available CRP data from admission were divided into two groups according to pre-admission statin therapy. A second CRP measurement was noted following primary coronary intervention (within 24?h from admission). The difference between the two measurements was designated ΔCRP.

Results: The cohort consisted of 1134 patients with a median age of 61 (IQR52–70), 81% males. Patients on statins prior to admission (336/1134, 26%) were more likely to have CRP levels within normal range (≤5?mg/l) compared to patients without prior treatment, both at admission (75 vs. 24%, p?=?0.004) and at 24?h (70 vs. 48%, p?=?0.029). The prevalence of patients with pre-admission statin therapy decreased as ΔCRP increased (p?=?0.004; n?=?301). The likelihood of ΔCRP to be above 5?mg/l in patients with pre-admission statin therapy was reduced after age and gender adjustments (OR 0.54, 95% CI 0.32–0.92, p?=?0.023) and in multivariate (OR 0.57, 95% CI 0.33–0.99, p?=?0.048) analysis.

Conclusions: Pre-admission statin therapy is associated with a less robust inflammatory response in STEMI patients, highlighting statin’s pathophysiological importance.