Author Correction: Sex-specific innate immune selection of HIV-1 in utero is associated with increased female susceptibility to infection.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Sex-specific innate immune selection of HIV-1 in utero is associated with increased female susceptibility to infection.

Female children and adults typically generate more efficacious immune responses to vaccines and infections than age-matched males, but also suffer greater immunopathology and autoimmune disease. We here describe, in a cohort of > 170 in utero HIV-infected infants from KwaZulu-Natal, South Africa, fetal immune sex differences resulting in a 1.5-2-fold increased female susceptibility to intrauterine HIV infection.

Effectiveness of the South African expanded program of immunization against hepatitis B in children infected with human immunodeficiency virus-1 living in a resource-limited setting of Kwazulu-Natal.

Prevalence of Human-Immunodeficiency-Virus/Hepatitis-B-virus (HIV/HBV) coinfection and HBV vaccination response in children are unknown in Kwazulu-Natal. This study included 183 HIV-infected and 108 HIV-uninfected children aged between 5 and 15 years screened for HBV infection and vaccination. HBV infection occurred in 2.

Role of ATM in bystander signaling between human monocytes and lung adenocarcinoma cells.

The response of a cell or tissue to ionizing radiation is mediated by direct damage to cellular components and indirect damage mediated by radiolysis of water. Radiation affects both irradiated cells and the surrounding cells and tissues. The radiation-induced bystander effect is defined by the presence of biological effects in cells that were not themselves in the field of irradiation.

Differential response of three cell types to dual stress of nitric oxide and radiation.

The perception of toxicity to nitric oxide (NO) and irradiation (IR) by three different cell types has been studied. The three cell types are the macrophage like RAW264.7 cells, EL4 lymphoma cells, and splenocytes, which represent the different components of a tumor.

Ionizing radiation induced signaling of DNA damage response molecules in RAW 264.7 and CD4⁺ T cells.

Ionizing radiation (IR) treatment results in activation of several DNA damage response molecules, such as ataxia telangiectasia, mutated (ATM), and DNA-dependent protein kinase (DNAPK) in mammals that are increasingly recognized for their potential roles in the sensing of DNA damage and initiating the subsequent protein kinase cascade. In vitro evidence indicates that both ATM and DNA-PK are responsible for efficient repair of DNA double strand breaks in response to IR exposure. To unravel the role of ATM and DNA-PK, we studied the mRNA and protein levels of ATM, DNA-PK and their downstream substrates in two different cell types after irradiation viz.

Role of Rad52 in fractionated irradiation induced signaling in A549 lung adenocarcinoma cells.

The effect of fractionated doses of γ-irradiation (2Gy per fraction over 5 days), as delivered in cancer radiotherapy, was compared with acute doses of 10 and 2Gy, in A549 cells. A549 cells were found to be relatively more radioresistant if the 10Gy dose was delivered as a fractionated regimen. Microarray analysis showed upregulation of DNA repair and cell cycle arrest genes in the cells exposed to fractionated irradiation.

DNA damage response signaling in lung adenocarcinoma A549 cells following gamma and carbon beam irradiation.

Carbon beams (5.16MeV/u, LET=290keV/μm) are high linear energy transfer (LET) radiation characterized by higher relative biological effectiveness than low LET radiation. The aim of the current study was to determine the signaling differences between γ-rays and carbon ion-irradiation.

Activation of DNA damage response signaling in lung adenocarcinoma A549 cells following oxygen beam irradiation.

Oxygen beams are high linear energy transfer (LET) radiation characterized by higher relative biological effectiveness than low LET radiation. The aim of the current study was to determine the signaling differences between γ- and oxygen ion-irradiation. Activation of various signaling molecules was looked in A549 lung adenocarcinoma cells irradiated with 2Gy oxygen, 2Gy or 6Gy γ-radiation.

Low energy proton beam induces efficient cell killing in A549 lung adenocarcinoma cells.

The aim of the current study was to determine the signaling differences between gamma- and proton beam-irradiations. A549 lung adenocarcinoma cells were irradiated with 2 Gy proton beam or gamma-radiation. Proton beam was found to be more cytotoxic than gamma-radiation.

Curcumin mediates time and concentration dependent regulation of redox homeostasis leading to cytotoxicity in macrophage cells.

The present study was designed to test a hypothesis that curcumin may be modulating oxidative stress parameters including reactive oxygen species, non-protein thiols and expression of antioxidant genes in a concentration and time dependent manner in exhibiting cytotoxic effects in macrophage cell line RAW 264.7. The results have shown that curcumin elevated the reactive oxygen species levels accompanied by a decrease in levels of intracellular non-protein thiols at 2 h after its addition to cells.

Differential activation of mitogen-activated protein kinases following high and low LET radiation in murine macrophage cell line.

Mitogen-activated protein kinases have been shown to respond to various stimuli including cytokines, mitogens and gamma irradiation, leading to cell proliferation, differentiation, or death. The duration of their activation determines the specificity of response to each stimulus in various cells. In this study, the crucial intracellular kinases, ERK, JNK, and p38 kinase involved in cell survival, death, or damage and repair were examined for their activity in RAW 264.

Role of iNOS in bystander signaling between macrophages and lymphoma cells.

Purpose: The present report describes the bystander effects of radiation between similar and dissimilar cells and the role of iNOS in such communication.

Materials And Methods: EL-4 and RAW 264.7 cells were exposed to 5 Gy gamma-irradiation.

Effect of nitric oxide donor and gamma irradiation on modifications of ERK and JNK in murine peritoneal macrophages.

Mitogen activated protein kinases (MAPKs) play an important role in activation, differentiation and proliferation of macrophages. Macrophages, upon activation, produce large amounts of nitric oxide that inhibit the growth of variety of microorganisms and tumor cells. This nitric oxide which is known to interfere with tyrosine phosphorylation may result in changes in the pattern of activation of MAPKs.

Effect of nitric oxide donor and gamma irradiation on MAPK signaling in murine peritoneal macrophages.

Irradiation (IR) of cells is known to activate enzymes of mitogen activated protein kinase (MAPK) family. These are known to be involved in cellular response to stress and are determinants of cell death or survival. When radiotherapy is delivered to malignant cells, macrophages, being radioresistant, survive, get activated, and produce large amounts of nitric oxide.

Fractionated and acute irradiation induced signaling in a murine tumor.

The effect of fractionated doses of Co(60) gamma-irradiation (2 Gy per fraction over 5 days), as is delivered in cancer radiotherapy, was compared with acute doses of 10 and 2 Gy, in a serially transplanted mouse fibrosarcoma grown in Swiss mice. The aspects that were studied included the three major mitogen-activated protein (MAP) kinases, namely p44 MAP kinase, p38 MAP kinase, and stress-activated protein (SAP) kinase, which are known to be involved in determining the cell fate following exposure to ionizing radiation. The response of dual specificity phosphatase PAC1 which is involved in the dephosphorylation of MAP kinases was also looked at.

MAP kinases: differential activation following in vivo and ex vivo irradiation.

Mitogen activated protein kinases (MAPK) play a critical role in controlling cell survival and repopulation following exposure to ionising radiation. Most investigations on these pathways have been done using cultured cells or by ex vivo treatments. The present study was carried out to determine whether the response of MAPKs in mouse lymphocytes differs following in vivo and ex vivo irradiation with 60Co gamma-rays.

Involvement of cytoplasmic membrane damage in the copper (II)-dependent cytotoxicity of a novel naturally occurring tripyrrole.

In the presence of a nonlethal concentration of Cu(II), washed Escherichia coli ATCC8739 cells were killed by a novel tripyrrole 1, isolated as a red pigment from the Serratia sp. Cell killing was accompanied by a depletion in the potassium pools of the cells due to the damage to the cytoplasmic membrane, without any detectable DNA damage as revealed by the transformed plasmid DNA and phage induction assay. This revealed that the bactericidal activity of compound 1 in the presence of Cu(II) results from membrane damage.

Radiation-induced bystander effect: activation of signaling molecules in K562 erythroleukemia cells.

Gap junction independent signaling mechanism was investigated using K562 human erythroleukemia cells. They were exposed to 2, 5, or 10 Gy of (60)Co gamma irradiation, the medium isolated 20 min post-irradiation and added to fresh cells. Evidence of radiation-induced bystander effect was observed wherein there was activation of p21, nuclear factor-kappaB (NF-kappaB), Bax, Bcl-2 and cleavage of poly(ADP-ribose) polymerase in bystander cells.

DNA damage induced nucleotide excision repair in Saccharomyces cerevisiae.

Nucleotide excision repair (NER) is the most versatile and universal pathway of DNA repair that is capable of repairing virtually any damages other than a double strand break (DSB). This pathway has been shown to be inducible in several systems. However, question of a threshold and the nature of the damage that can signal induction of this pathway remain poorly understood.

DNA strand breaks signal the induction of DNA double-strand break repair in Saccharomyces cerevisiae.

Genotoxic stress induces a checkpoint signaling cascade to generate a stress response. Saccharomyces cerevisiae shows an altered radiation response under different type of stress. Although the induction of repair has been implicated in enhanced survival after exposure to the challenging stress, the nature of the signal remains poorly understood.

Alteration in the expression of signaling parameters following carbon ion irradiation.

Ionizing radiation induces DNA damage, which generates a complex array of genotoxic responses. These responses depend on the type of DNA damage, which in turn can lead to unique cellular responses. High LET radiation results in clustered damages.

Inhibition of radiation induced nitration by curcumin and nicotinamide in mouse macrophages.

Nitric oxide plays an important role in inflammation and carcinogenesis and has now been implicated as an important signaling molecule under normal physiological conditions also. Increased nitric oxide (NO) results in increased nitration of proteins at tyrosine, which can cause protein dysfunction or alterations in signal transduction pathways. Irradiation of Lipopolysaccharide (LPS) activated mouse peritoneal macrophages was found to increase NO production, inducible nitric oxide synthase (iNOS) expression and nitration of proteins.

In vivo modulation of signaling factors involved in cell survival.

In vivo expression of cell survival factors protein kinase C (PKC), nuclear factor kappaB (NFkappaB), and extracellular signal-regulated kinase (Erk), which may contribute to the development of radioresistance following radiotherapy, was looked for. Their modulation with natural compounds (curcumin, rutin or nicotinamide) was attempted in mice bearing a serially transplanted fibrosarcoma. Expression of protein kinase C was isoform specific.