Towards Simultaneous Noninvasive Arterial and Venous Oxygenation Monitoring with Wearable E-Tattoo.

While noninvasive arterial blood oxygenation is easily estimated using peripheral pulse oximeters, noninvasive venous blood oxygenation monitoring is still a critical unmet need. Critical conditions that lead to inefficient extraction of oxygen from the blood, such as sepsis or shock, can only be detected by analyzing the oxygen content of the venous blood. In this work, we introduce a soft wearable e-tattoo sensor that simultaneously measures the arterial and venous pulses from the wrist.

The use of curcumin as an effective adjuvant to cancer therapy: A short review.

Turmeric (Curcuma longa) is a popular spice that has been used in Ayurvedic medicine for its ability to treat various common ailments. There have been statistical correlations between turmeric consumption and lower incidences of cancer development, prompting research into its primary component curcumin. Several in vitro and in vivo studies over the last decade into cancer treatment have provided experimental evidence that curcumin contains antiproliferative, antiangiogenic, and apoptotic properties.

Prescribing Ceftolozane/Tazobactam for Pediatric Patients: Current Status and Future Implications.

Antibiotics are arguably the greatest medical development of the 20th century but these precious resources are being threatened by the continued rise in infections caused by multidrug-resistant bacteria. There is concern that we are on the precipice of a 'post-antibiotic era'. The situation is exacerbated by a stagnation in the pharmaceutical industry in developing new antibiotics, particularly those with activity against some of the most resistant Gram-negative organisms because of significant economic, scientific, and regulatory barriers.

Influence of polyunsaturated fatty acids on urologic inflammation.

Purpose: Studies demonstrate that polyunsaturated fatty acids, fish oils, and alpha-linoleic acid are beneficial anti-inflammatory agents, which suppress inflammatory mediators and their activity.

Methods: This review focuses on the effects of omega-3 fatty acids (O-3FAs) on three primary urologic organs (bladder, kidney, and prostate) and associated conditions such as urolithiasis, kidney transplantation, interstitial cystitis/bladder pain syndrome, bladder cancer, prostate cancer (CaP), and chronic prostatitis/chronic pelvic pain syndrome.

Results: The following themes emerged: the potential influence of O-3FA in suppressing urologic inflammation; the supportive role of O-3FA in therapeutic interventions; pro-inflammatory mechanisms of omega-6 fatty acids (O-6FAs) associated with disease progression; and the importance of the optimal ratio of O-6FAs/O-3FAs.

Complete Genome Sequences of Two Helicobacter pylori Strains from a Canadian Arctic Aboriginal Community.

We report here the complete genome sequences of two Amerind Helicobacter pylori strains from Aklavik, Northwest Territories, Canada. One strain contains extra iron-cofactored urease genes and ~140 rearrangements in its chromosome relative to other described strains (typically differing from one another by <10 rearrangements), suggesting that it represents a novel lineage of H. pylori.

Genome Sequences of Three hpAfrica2 Strains of Helicobacter pylori.

We present the genome sequences of three hpAfrica2 strains of Helicobacter pylori, which are postulated to have evolved in isolation for many millennia in people of San ethnicity. Although previously considered to be ancestral to Helicobacter acinonychis, the hpAfrica2 strains differ markedly from H. acinonychis in their gene arrangement.

Helicobacter pylori from Peruvian amerindians: traces of human migrations in strains from remote Amazon, and genome sequence of an Amerind strain.

Background: The gastric pathogen Helicobacter pylori is extraordinary in its genetic diversity, the differences between strains from well-separated human populations, and the range of diseases that infection promotes.

Principal Findings: Housekeeping gene sequences from H. pylori from residents of an Amerindian village in the Peruvian Amazon, Shimaa, were related to, but not intermingled with, those from Asia.

p38 MAPK plays a role in IL-4 synthesis in jacalin plus CD28-stimulated CD4+ T cells--II.

We have previously shown that jacalin, a CD4+ T cell lectin, induces phosphorylation of intracellular events, moderate levels of interleukin (IL)-2 secretion. We have also shown that in the presence of CD28 costimulation, jacalin induces IL-4 secretion. In the present study, we showed that stimulation of normal CD4+ T cells with jacalin plus CD28 cross-linking (CD28XL) resulted in phosphorylation of signal transducer and activator of transcription (STAT)-6 and expression of Bcl-2 and Bcl-xL, which were inhibited significantly when cells were cultured in the presence of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580.

The lectin jacalin plus costimulation with anti-CD28 antibody induces phosphorylation of p38 MAPK and IL-4 synthesis-I.

Costimulatory signals play an important role in the development of T helper cell type 1 (Th1) or Th2 type. Little is known about jacalin plus CD28-mediated signaling and cytokine secretion. In the present study, we analyzed the intracellular signaling events following stimulation of CD4+ T cells with jacalin plus CD28 cross-linking (CD28XL) with anti-CD28 antibody.

IgD-receptor (IgD-R) cross-linking partially protects murine T cells from dexamethasone-induced apoptosis.

Based on our previous findings that immunoglobulin D (IgD) receptor (IgD-R) cross-linking with oligomeric IgD (IgD-R-xL) led to T cell activation, we examined the effect of IgD-R-xL on the expression of Fas antigen and apoptosis induction. In splenic T cells, IgD-R-xL followed by dexamethasone (dex) treatment resulted in a decreased percentage of Fas-positive cells as well as a decreased mean fluorescence intensity (P<0.05) when compared with cells treated with dex alone.

The lectin jacalin induces phosphorylation of ERK and JNK in CD4+ T cells.

The CD4 molecule plays an essential role in mediating the transduction of intracellular signals by functioning as a coreceptor for the complex T cell receptor/CD3 and also acts as the primary receptor for human immunodeficiency virus (HIV). Several authors have shown evidence that jacalin, a plant lectin, binds to CD4 and inhibits in vitro HIV infection. We analyzed jacalin-induced intracellular signaling events in CD4(+) T cells and have shown that cell activation resulted in tyrosine phosphorylation of intracellular substrates p56(lck), p59(fyn), ZAP-70, p95 (vav), phospholipase C-gamma1, and ras activation, as assessed by conversion of ras guanosine 5'-diphosphate to ras guanosine 5'-triphosphate.

Chemokine pattern in relation to disease state in human immunodeficiency virus-infected children.

Although beta chemokines can block human immunodeficiency virus (HIV) entry into target cells, their role in HIV disease progression is controversial. To determine the association of RANTES with HIV disease state, we examined constitutive mRNA expression by reverse-transcribed polymerase chain reaction (RT-PCR) in peripheral blood mononuclear cells (PBMCs) and induction of RANTES secretion by enzyme-linked immunosorbent assay (ELISA) in anti-CD3 monoclonal antibody (MAb)-stimulated cultures of PBMCs, and in CD4+ and CD8+ T cell subsets of 17 HIV-infected children. In comparison with uninfected subjects, PBMCs of HIV-infected children were deficient in both constitutive RANTES mRNA expression as well as in stimulus-induced RANTES production.

Reduction in T cell apoptosis in patients with HIV disease following antiretroviral therapy.

Patients with HIV infection manifest increased T lymphocyte apoptosis. This study investigated the influence of antiretroviral therapy (ART) upon lymphocyte apoptosis in 23 HIV-infected adults naive to protease inhibitors. Patients were enrolled in a treatment trial consisting of Nelfinavir (NFV), d4T, or NFV + d4T for 24 weeks, followed by triple therapy (NFV + reverse transcriptase inhibitors) for an additional 24 weeks.

Human T cell IgD receptors react with O-glycans on both human IgD and IgA1.

Previous studies on murine T cell IgD-R have shown that these receptors recognize N-glycans of murine IgD, and not of other Ig isotypes. We have now studied the specificity of IgD-R on human T cells. Human IgD digested with proteinase K to fragments of < 5 kDa inhibit the ability of T cells to form rosettes with IgD-coated ox erythrocytes.

Signals transduced through the CD4 molecule interfere with TCR/CD3-mediated ras activation leading to T cell anergy/apoptosis.

It has been previously demonstrated that the occupancy of CD4 molecules by the HIV-1 envelope glycoprotein gp120 results in marked inhibition of T cell receptor-CD3 complex (TCR/CD3) activation-induced IL-2 secretion. To elucidate the mechanism of inhibitory effects of gp160 on T cell signaling, we have investigated the intracellular biochemical events and biological output in response to anti-CD3 mAb activation of purified peripheral blood CD4+ T cells from healthy donors with and without prior exposure to HIV-1 gp160. Pretreatment with gp160 resulted in marked inhibition of tyrosine phosphorylation of p59(fyn), PLC-gamma1, ras activation, and TNF-alpha secretion in anti-CD3 mAb activated CD4+ T cells, and a subset of CD4+ cells underwent activation-induced cell death.

CD4 cross-linking (CD4XL) induces RAS activation and tumor necrosis factor-alpha secretion in CD4+ T cells.

CD4 molecules are the primary receptors for human immunodeficiency virus (HIV) and bind the envelope glycoprotein gp120 of HIV with high-affinity. We have previously shown that cross-linking of CD4 molecules (CD4XL) in normal peripheral blood mononuclear cells (PBMC) results in secretion of cytokines tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), but not of interleukin-2 (IL-2) or IL-4. To investigate the intracellular signaling events associated with CD4-gp120 interaction, we incubated CD4+ T cells from peripheral blood of HIV-negative healthy donors with HIV envelope protein gp160 alone or performed CD4XL with gp160 and anti-gp160 antibody.

HIV-1 gp 120 blocks jacalin-induced proliferative response in CD4+ T cells: jacalin as a useful surrogate marker for qualitative and quantitative deficiency of CD4+ T cells in HIV-1 infection.

Jacalin is a plant lectin that induces mitogenic responses selectively in CD4+ T lymphocytes and has been shown to block infection by the human immunodeficiency virus type 1 (HIV-1) in a T lymphoid cell line, but the relationship of jacalin to the HIV envelope glycoprotein gp 120 in its interaction with the CD4 molecule is unclear. Here we demonstrate that pretreatment of normal T cells with native HIV-1 gp 120 impairs their ability to proliferate and secrete IL-2 in response to jacalin. This effect was not observed with deglycosylated gp 120, which fails to bind to CD4 molecule, or with gp 120 that has been premixed with soluble CD4.

Inhibition of sphingolipid synthesis down-modulates CD4 expression by peripheral blood T lymphocytes and T lymphoma cells.

Recent studies have demonstrated that L-cycloserine, an inhibitor of sphingolipid biosynthesis, interferes with the life cycle of HIV. Experiments with human T cells and CD4+ T lymphoma cells were performed to examine possible mechanisms. L-CS selectively down-modulated CD4 expression without affecting the expression of CD3 and CD8.

The immunoaugmenting properties of murine IgD reside in its C delta 1 and C delta 3 regions: potential role for IgD-associated glycans.

IgD receptor (IgD-R) bearing CD4+ T cells with immunoaugmenting properties in vivo are induced in mice within 24 h after a single injection of dimeric or aggregated IgD. In the present study, we sought to identify the region(s) of IgD responsible for upregulation of IgD-R and for the immunoaugmenting effect of IgD. IgD-R can be upregulated on CD4+ T cells in vitro and in vivo by glutaraldehyde-aggregated mutant IgD or by fragments of enzymatically digested IgD molecules possessing either the C delta 1 domain (Fd delta) or the C delta 3 domain (Fc delta).

IgD-receptor-positive human T lymphocytes. II. Identification and partial characterization of human IgD-binding factor.

Membrane receptors specific for IgD (IgD-R) have been identified on murine CD4+ and human CD4+ and CD8+ T lymphocytes. Up-regulation of these IgD-specific receptors can be achieved by exposure of such T cells to various stimuli, including oligomeric or Ag cross-linked IgD, IL-2, IL-4, and T cell mitogens, such as PHA. Previous studies with murine IgD-R+ splenic T cells and IgD-R+ T hybridoma cells have demonstrated the existence of soluble IgD-binding factors (IgD-BF) that are shed or released into the medium in which these cells are grown.

Specificity of the murine IgD receptor on T cells is for N-linked glycans on IgD molecules.

IgD receptors on murine T cells have been reported in this issue [Tamma, S. M. L.

IgD receptors on murine T-helper cells bind to Fd and Fc regions of immunoglobulin D.

Receptors for immunoglobulins on animal cells invariably show specificity for Fc regions of the protein and are hence called Fc receptors. The present study shows that immunoglobulin D receptors present an exception to this rule. Binding of IgD-coated erythrocytes to murine IgD-receptor-bearing T-helper cells is competitively inhibited by IgD, by its Fab delta fragments, and by deletion mutants of IgD lacking (i) the first constant domain of the delta heavy chain (KWD1), (ii) that region plus the delta heavy-chain-hinge region (KWD6), or (iii) the third constant domain of the delta heavy chain (Gen.

IgD-receptor-positive human T lymphocytes. I. Modulation of receptor expression by oligomeric IgD and lymphokines.

Studies with human myeloma-derived IgD have demonstrated the existence of IgD-R on peripheral blood T cells. These receptors, which are detected by rosetting with IgD-coated ox E (IgD-rosette-forming cells), are competitively inhibited by IgD, but not by IgM or IgG. Similar results were obtained with human T cell clones and T hybridomas derived from such clones either by rosetting assays or by staining with biotinylated-IgD.