Mechanical stresses of primary branches: a survey of 40 woody tree and shrub species

Land plants have evolved a large number of growth forms and each plant species has a unique morphology. For many tall plants, main stems serve the function of vertical growth while primary and higher order branches are responsible for lateral growth for greater light interception. Herein we search for a mechanical constant for primary branches. Primary branches were sampled from 40 species of trees and shrubs. Among the species sampled, branch lengths ranged from 1.8 to 12.2 m, weights from 0.056 to 16.6 kg, base diameters from 17 to 150 mm, bending moments from 7.1 to 2,200 N-m, and section moduli from 0.039 to 29.0 × 10⁻³ m³. Primary branches of all 40 tree and shrub species exhibited relatively constant bending stresses along each branch. Moreover stress values among the 40 species were relatively constant at about 11 MPa (mean = 11.1 MPa [range 5.2–18.9]; standard deviation = 3.3 MPa). Furthermore, primary branches without secondary branches attached (1) had similar bending moment distributions as tapered cantilever beams, (2) exhibited relatively constant slope values of stress versus length among all species (stresses increased linearly with length), and (3) exhibited both relatively constant density and relatively constant taper within each species. We conclude that the relatively constant stress of about 11 MPa of primary branches was due solely to the numbers, weights, and distributions of secondary branches and associated higher order branches along primary branches for the 40 plant species. To our knowledge, this is the first publication that shows a unifying mechanical constant for primary branches of plants.

Recombinant IFN-alpha (2b) increases the expression of apoptosis receptor CD95 and chemokine receptors CCR1 and CCR3 in monocytoid cells.

IFN-alpha-2b, known as potent immune modulator, can either inhibit or enhance immune cell activity within the tightly regulated microenvironment of inflammation, depending upon the concentration of the cytokine and the activation stage of the cell. Chemokine receptors, which not only mediate chemotaxis of immune cells to the site of inflammation but also affect cellular activation by transferring corresponding signals, represent yet another level of immune regulation. Here we demonstrate that IFN-alpha increases the expression of CCR1 and CCR3 in primary mononuclear phagocytes, as well as in the monocytoid cell line U937. Enhanced receptor mRNA expression correlated with functional readouts such as increased intracellular calcium mobilization and cell migration in response to ligands. Expression of CCR2b, CCR4, CCR5, and CXCR4 was unchanged or decreased after IFN-alpha treatment. These observations indicate a differentially regulated cellular signaling relationship of IFN-alpha pathways and chemokine receptor expression. We also provide evidence that, under these conditions, IFN-alpha treatment increased the expression of CD95 (Fas, Apo1), resulting in enhanced susceptibility to apoptosis. Taken together, these data add important information for the rational application of IFN-alpha (2b) in immune and cancer therapies.     

Engagement of CD28 modulates CXC chemokine receptor 4 surface expression in both resting and CD3-stimulated CD4+ T cells

Optimal CD4+ T cell activation requires the cooperation of multiple signaling pathways coupled to the TCR-CD3 complex and to the CD28 costimulatory molecule. In this study, we have investigated the expression of surface CXC chemokine receptor 4 (CXCR4) in enriched populations of CD4+ T PBL, stimulated with anti-CD3 and anti-CD28 mAbs, immobilized on plastic. Anti-CD3 alone induced a progressive down-regulation of surface CXCR4, accompanied by a significant decline in the entry of the HXB2 T cell line-tropic (X4-tropic) HIV-1 clone in CD4+ T cells. Of note, this effect was strictly dependent on the presence in culture of CD14+ monocytes. On the other hand, anti-CD28 alone induced a small but reproducible increase in the expression of surface CXCR4 as well as in the entry of HXB2 HIV-1 clone in resting CD4+ T cells. When the two mAbs were used in combination, anti-CD28 potently synergized with anti-CD3 in inducing the expression of CD69 activation marker and stimulating the proliferation of CD4+ T cells. On the other hand, anti-CD28 counteracted the CXCR4 down-modulation induced by anti-CD3. The latter effect was particularly evident when anti-CD28 was associated to suboptimal concentrations of anti-CD3. Because CXCR4 is the major coreceptor for the highly cytopathic X4-tropic HIV-1 strains, which preferentially replicate in proliferating CD4+ T cells, the ability of anti-CD28 to up-regulate the surface expression of CXCR4 in both resting and activated CD4+ T cells provides one relevant mechanism for the progression of HIV-1 disease.     

Mitochondrial Changes in Platelets Are Not Related to Those in Skeletal Muscle during Human Septic Shock

Platelets can serve as general markers of mitochondrial (dys)function during several human diseases. Whether this holds true even during sepsis is unknown. Using spectrophotometry, we measured mitochondrial respiratory chain biochemistry in platelets and triceps brachii muscle of thirty patients with septic shock (within 24 hours from admission to Intensive Care) and ten surgical controls (during surgery). Results were expressed relative to citrate synthase (CS) activity, a marker of mitochondrial density. Patients with septic shock had lower nicotinamide adenine dinucleotide dehydrogenase (NADH)/CS (p = 0.015), complex I/CS (p = 0.018), complex I and III/CS (p<0.001) and complex IV/CS (p = 0.012) activities in platelets but higher complex I/CS activity (p = 0.021) in triceps brachii muscle than controls. Overall, NADH/CS (r² = 0.00; p = 0.683) complex I/CS (r² = 0.05; p = 0.173), complex I and III/CS (r² = 0.01; p = 0.485), succinate dehydrogenase (SDH)/CS (r² = 0.00; p = 0.884), complex II and III/CS (r² = 0.00; p = 0.927) and complex IV/CS (r² = 0.00; p = 0.906) activities in platelets were not associated with those in triceps brachii muscle. In conclusion, several respiratory chain enzymes were variably inhibited in platelets, but not in triceps brachii muscle, of patients with septic shock. Sepsis-induced mitochondrial changes in platelets do not reflect those in other organs.