Frontiers in Biology
Cover Story   2014, Volume 9 Issue 2
Autism spectrum disorders (ASDs) are neurologic disorders of developmental origin that share a complex and heterogeneous etiology. ASDs are characterized by profound deficits in social interaction, communication skills, and repetitive and stereotypic behaviors. The prevalence of ASD has increased to >1% of U.S. children over the past a few decad [Detail] ...
   Online First

Administered by

, Volume 9 Issue 2

For Selected: View Abstracts Toggle Thumbnails
MINI-REVIEW
The effect of adjuvants on vaccine-induced antibody response against influenza in aged mice
Mark A. CONCANNON,Jiu JIANG
Front. Biol.. 2014, 9 (2): 89-94.  
https://doi.org/10.1007/s11515-014-1301-7

Abstract   HTML   PDF (117KB)

While influenza remains a major threat to public health, researchers continue to search for a universal solution to improving the efficacy of the influenza vaccine. Even though influenza affects people of all different ages, it can be extremely hazardous to people of 65 years of age or older since that is the population that makes up the high majority of the death toll caused by influenza-related diseases. Elderly individuals suffer the effects of immunosenescence as they age, which is the diminishing of the overall immune response. Immunosenescence occurs by specifically affecting the adaptive immune response which controls the establishment of immunity after vaccination or infection. There are many studies under way that are trying to find a resolution to the problem of the influenza vaccine not providing enough protection in the elderly population. One of the possible strategies is to seek the use of an optimal adjuvant, an immunological agent that can enhance immune responses, with the current vaccine formulation. Here, we used the murine model to review the effects of adjuvants on the antibody response to influenza vaccines in aged mice. Since adjuvants can enhance the production of important inflammatory cytokines and activation of dendritic cells, the stimulation of these cells are boosted to increase the effectiveness of the influenza vaccine in aged mice which would hopefully translate to the elderly.

References | Related Articles | Metrics
REVIEW
Growth arrest signaling of the Raf/MEK/ERK pathway in cancer
Jong-In PARK
Front. Biol.. 2014, 9 (2): 95-103.  
https://doi.org/10.1007/s11515-014-1299-x

Abstract   HTML   PDF (220KB)

The Raf/MEK/extracellular signal-regulated kinase (ERK) pathway has a pivotal role in facilitating cell proliferation, and its deregulated activation is a central signature of many epithelial cancers. However paradoxically, sustained activity of Raf/MEK/ERK can also result in growth arrest in many different cell types. This anti-proliferative Raf/MEK/ERK signaling also has physiological significance, as exemplified by its potential as a tumor suppressive mechanism. Therefore, significant questions include in which cell types and by what mechanisms this pathway can mediate such an opposing context of signaling. Particularly, our understating of the role of ERK1 and ERK2, the focal points of pathway signaling, in growth arrest signaling is still limited. This review discusses these aspects of Raf/MEK/ERK-mediated growth arrest signaling.

Figures and Tables | References | Related Articles | Metrics
Ribonucleotide reductase metallocofactor: assembly, maintenance and inhibition
Caiguo ZHANG,Guoqi LIU,Mingxia HUANG
Front. Biol.. 2014, 9 (2): 104-113.  
https://doi.org/10.1007/s11515-014-1302-6

Abstract   HTML   PDF (253KB)

Ribonucleotide reductase (RNR) supplies cellular deoxyribonucleotide triphosphates (dNTP) pools by converting ribonucleotides to the corresponding deoxy forms using radical-based chemistry. Eukaryotic RNR comprises α and β subunits: α contains the catalytic and allosteric sites; β houses a diferric-tyrosyl radical cofactor (FeIII2-Y•) that is required to initiates nucleotide reduction in α. Cells have evolved multi-layered mechanisms to regulate RNR level and activity in order to maintain the adequate sizes and ratios of their dNTP pools to ensure high-fidelity DNA replication and repair. The central role of RNR in nucleotide metabolism also makes it a proven target of chemotherapeutics. In this review, we discuss recent progress in understanding the function and regulation of eukaryotic RNRs, with a focus on studies revealing the cellular machineries involved in RNR metallocofactor biosynthesis and its implication in RNR-targeting therapeutics.

Figures and Tables | References | Related Articles | Metrics
Priming cancer cells for drug resistance: role of the fibroblast niche
Wei Bin FANG,Min YAO,Nikki CHENG
Front. Biol.. 2014, 9 (2): 114-126.  
https://doi.org/10.1007/s11515-014-1300-8

Abstract   HTML   PDF (294KB)

Conventional and targeted chemotherapies remain integral strategies to treat solid tumors. Despite the large number of anti-cancer drugs available, chemotherapy does not completely eradicate disease. Disease recurrence and the growth of drug resistant tumors remain significant problems in anti-cancer treatment. To develop more effective treatment strategies, it is important to understand the underlying cellular and molecular mechanisms of drug resistance. It is generally accepted that cancer cells do not function alone, but evolve through interactions with the surrounding tumor microenvironment. As key cellular components of the tumor microenvironment, fibroblasts regulate the growth and progression of many solid tumors. Emerging studies demonstrate that fibroblasts secrete a multitude of factors that enable cancer cells to become drug resistant. This review will explore how fibroblast secretion of soluble factors act on cancer cells to enhance cancer cell survival and cancer stem cell renewal, contributing to the development of drug resistant cancer.

Figures and Tables | References | Related Articles | Metrics
Surgical decompression in acute spinal cord injury: A review of clinical evidence, animal model studies, and potential future directions of investigation
Yiping LI,Chandler L. WALKER,Yi Ping ZHANG,Christopher B. SHIELDS,Xiao-Ming XU
Front. Biol.. 2014, 9 (2): 127-136.  
https://doi.org/10.1007/s11515-014-1297-z

Abstract   HTML   PDF (249KB)

The goal for treatment in acute spinal cord injury (SCI) is to reduce the extent of secondary damage and facilitate neurologic regeneration and functional recovery. Although multiple studies have investigated potential new therapies for the treatment of acute SCI, outcomes and management protocols aimed at ameliorating neurologic injury in patients remain ineffective. More recent clinical and basic science research have shown surgical interventions to be a potentially valuable modality for treatment; however, the role and timing of surgical decompression, in addition to the optimal surgical intervention, remain one of the most controversial topics pertaining to surgical treatment of acute SCI. As an increasing number of potential treatment modalities emerge, animal models are pivotal for investigating its clinical application and translation into human trials. This review critically appraises the available literature for both clinical and basic science studies to highlight the extent of investigation that has occurred, specific therapies considered, and potential areas for future research.

Figures and Tables | References | Related Articles | Metrics
Convergent synaptic and circuit substrates underlying autism genetic risks
Aaron MCGEE,Guohui LI,Zhongming LU,Shenfeng QIU
Front. Biol.. 2014, 9 (2): 137-150.  
https://doi.org/10.1007/s11515-014-1298-y

Abstract   HTML   PDF (299KB)

There has been a surge of diagnosis of autism spectrum disorders (ASD) over the past decade. While large, high powered genome screening studies of children with ASD have identified numerous genetic risk factors, research efforts to understanding how each of these risk factors contributes to the development autism has met with limited success. Revealing the mechanisms by which these genetic risk factors affect brain development and predispose a child to autism requires mechanistic understanding of the neurobiological changes underlying this devastating group of developmental disorders at multifaceted molecular, cellular and system levels. It has been increasingly clear that the normal trajectory of neurodevelopment is compromised in autism, in multiple domains as much as aberrant neuronal production, growth, functional maturation, patterned connectivity, and balanced excitation and inhibition of brain networks. Many autism risk factors identified in humans have been now reconstituted in experimental mouse models to allow mechanistic interrogation of the biological role of the risk gene. Studies utilizing these mouse models have revealed that underlying the enormous heterogeneity of perturbed cellular events, mechanisms directing synaptic and circuit assembly may provide a unifying explanation for the pathophysiological changes and behavioral endophenotypes seen in autism, although synaptic perturbations are far from being the only alterations relevant for ASD. In this review, we discuss synaptic and circuit abnormalities obtained from several prevalent mouse models, particularly those reflecting syndromic forms of ASD that are caused by single gene perturbations. These compiled results reveal that ASD risk genes contribute to proper signaling of the developing gene networks that maintain synaptic and circuit homeostasis, which is fundamental to normal brain development.

Figures and Tables | References | Related Articles | Metrics
Toxoplasma, testosterone, and behavior manipulation: the role of parasite strain, host variations, and intensity of infection
Amir ABDOLI
Front. Biol.. 2014, 9 (2): 151-160.  
https://doi.org/10.1007/s11515-014-1291-5

Abstract   HTML   PDF (202KB)

Toxoplasma gondii is an intracellular parasite involved in the etiology of various behavioral and hormonal alterations in humans and rodents. Various mechanisms, including induction changes of testosterone production, have been proposed in the etiology of behavioral alterations during T. gondii infection. However, controversy remains about the effects of T. gondii infection on testosterone production; in some studies, increased levels of testosterone were reported, whereas other studies reported decreased levels. This is a significant point, because testosterone has been shown to play important roles in various processes, from reproduction to fear and behavior. This contradiction seems to indicate that different factors—primarily parasite strains and host variations—have diverse effects on the intensity of T. gondii infection, which consequently has diverse effects on testosterone production and behavioral alterations. This paper reviews the role of parasite strains, host variations, and intensity of T. gondii infection on behavioral alterations and testosterone production, as well as the role of testosterone in the etiology of these alterations during toxoplasmosis.

References | Related Articles | Metrics
RESEARCH ARTICLE
Microbial diversity in coastal sediments during pre and post tsunami periods in the south east coast of India
Prince S. GODSON,N. CHANDRASEKAR,S. Krishna KUMAR,Vimi P.V
Front. Biol.. 2014, 9 (2): 161-167.  
https://doi.org/10.1007/s11515-014-1296-0

Abstract   HTML   PDF (309KB)

Sediment samples were collected from 12 beaches affected by the 2004 Asian Tsunami in the south-east coast of India between Vanagiri and Nagoor. The objective of the present study is to delineate the microbial diversity in pre- and post-tsunami disaster coastal sediments. The collected marine sediments indicate that the overall microbial diversity is higher in the pre-tsunami sediments. The increase in pathogenic bacteria and fungal species after the tsunami is obscured due to inundation and backwashing of seawater along the coast. The reduction of other microbial diversity after the tsunami is attributed that the coastal and shelf sediments play an important role in the demineralization of organic matter, which supports the growth of microbes. The continuous exchange of ocean water and backwashing of coastal sediments by the tsunami wave probably reduced the pathogenic bacterial diversity in the sediments.

Figures and Tables | References | Related Articles | Metrics
8 articles