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Planar cellular structure panels are affected by a series of factors, which can produce various types of initial damage within the structure and thus affect the service life as well as the starting point and path of crack propagation. Investigating the effect of different initial damage modes on crack expansion paths and failure modes in additively manufactured honeycomb cellular panel under quasi-static three-point bending load. Experimental tests and finite element simulations are used. The quasi-static three-point bending experiments are conducted by using the CMT5305 universal testing machine, and numerical simulations are carried out by combining finite element analysis software ANSYS Workbench. Two kinds of experimental specimens with prefabricated cracks (PFC) and plastic hinge truncation (PHT) are fabricated by using additive manufacturing technology to simulate the initial damage. The final failure of the specimens includes plastic failure dominated by type-I cracks and brittle failure dominated by type-I and type-II mixed cracks. T-0-60 and C-90-60 specimens have the strongest crack suppression and load-bearing ability. With the increase in load speed, the cracking displacement decreases, and peak load increases. The undamaged (UDD) specimens have the strongest crack suppression ability at loading speeds of 10mm/min and 50mm/min, while the damage mode has little effect on the peak load of the specimens. The damage mode affects the crack initiation point, propagation path and failure mode of the cellular structure, and the model with initial damage will enhance the crack suppression ability at a specific inclination angle. In practical engineering applications, as a load-bearing structure, such as the open beam of a truck, two types of structures, T-0-60, and C-90-60, should be given priority, while avoiding the design of C-0-60 structure. As an energy-absorbing structure, such as the front bumper of a car, the cushioning effect should be enhanced by adjusting the hole direction and the initial damage direction. [ABSTRACT FROM AUTHOR]

Our pre-clinical studies demonstrated that intratumoral vaccination with a recombinant oncolytic type 2 adenovirus overexpressing the heat shock protein (HSP)70 protein, designated as H103, can inhibit primary and metastatic tumors through enhanced oncolytic activity and HSP-mediated immune responses against shared and mutated tumor antigens. In the pre-clinical studies of local H103 administration, no significant toxicity was observed in the animal trials with mice, cavy or rhesus monkeys. A phase I clinical trial of intratumoral injection of H103 was conducted in the patients with advanced solid tumors. A total of 27 patients were injected intratumorally with H103 in a dose-escalation study from a dose of 2.5 × 107 to 3.0 × 1012 viral particles (VPs). The maximum tolerated dose of H103 was not defined. Two patients developed dose-limiting toxicities of grade III fever at the dose of 1.5 × 1012 VP and transient grade IV thrombocytopenia at the dose of 3.0 × 1012 VP. The common adverse events were mainly mild to moderate (grade I/II) in nature, including fever, mild injection-site reaction, leucopenia, lymphopenia, thrombocytopenia and hypochromia. The objective response (complete response+partial response) to H103-injected tumors was 11.1% (3/27), and the clinical benefit rate (complete response+partial response+minor response+stable disease) was 48.1%. Interestingly, transient and partial regression of distant, uninjected tumors was observed in three patients. The numbers of immune cells (CD4+ and CD8+ T cells, and natural killer cells) were elevated after H103 administration, but without statistical significance. This phase I trial demonstrates that intratumoral administration of H103 can be safely applied to cancer patients and shows promising clinical antitumor activity, warranting a further clinical investigation.Gene Therapy (2009) 16, 376–382; doi:10.1038/gt.2008.179; published online 25 December 2008 [ABSTRACT FROM AUTHOR]

The activation of hepatic stellate cells (HSCs) is the key event of the pathogenesis of hepatic fibrosis. Platelet-derived growth factor (PDGF) is the most potent mitogen for HSCs, and PDGF receptor-β subunit (PDGFR-β) is required for the proliferation of HSCs induced by PDGF. In this study, a high gene-silencing-efficacy PDGFR-β small interference RNA (siRNA) was synthesized that could suppress the PDGFR-β expression and inhibit the activation and proliferation but could not induce the apoptosis of HSCs in vitro. To avoid the side effect of nonspecific interference of PDGFR-β, we constructed an HSCs-specific short hairpin RNA (shRNA) expression plasmid in which PDGFR-β shRNA was driven by a glial fibrillary acidic protein (GFAP) promoter. The double-staining immunofluorescence examination indicated that GFAP promoter could target the transgene expression into HSCs in carbon tetrachloride induced acute injured rat's liver and bile duct ligation (BDL)-induced chronic injured rat's liver. Furthermore, HSCs-specific PDGFR-β shRNA could relieve liver injury and hepatic fibrosis in the rat's model induced by BDL. This study demonstrates that PDGFR-β siRNA may be presented as an antifibrogenic agent. The application of HSCs-specific RNA interference induced by the GFAP promoter might supply a new powerful tool for cell-specific gene therapy of hepatic fibrogenesis.Gene Therapy (2008) 15, 1424–1435; doi:10.1038/gt.2008.93; published online 29 May 2008 [ABSTRACT FROM AUTHOR]

The relationship between chronic prostatitis and fertility has been disputed for many years. Several groups have shown infection and autoimmune response against prostate antigens could have a deleterious effect on semen quality and fertility. This study was conducted to test the hypothesis that Omi/HtrA2-induced apoptosis in chronic prostatitis could be a mechanism underlying the observed clinical benefit. The Omi/HtrA2 serine protease is a nuclear-encoded mitochondrial protein, which can be released from mitochondria into the cytosol after apoptosis stimuli, inducing apoptosis in caspase-dependent and independent manners. Forty-one patients diagnosed as suffering from chronic prostatitis were included. Healthy normal individuals were included as controls. Human spermatozoa in the semen were purified by Percoll-gradient technique to separate the seminal plasma and other round cells. Measurements for sperm concentration, motility, morphology, proinflammatory cytokines, Omi/HtrA2 mRNA and protein levels in spermatozoa of chronic protatitis patients, were performed accordingly. Significantly increased levels of proinflammatory cytokines were detected in seminal plasma from these prostatitis patients. Omi/HtrA2 mRNA and protein levels were significantly higher in prostatitis men than in normal men. This study shows that chronic prostatitis patients present important alterations in their semen quality parameters, Omi/HtrA2 mRNA and protein levels of spermatozoa. We speculate that the inflammatory process involved may affect male fertility by release of proapoptotic protein Omi/HtrA2.Prostate Cancer and Prostatic Diseases (2007) 10, 104–108. doi:10.1038/sj.pcan.4500919; published online 17 October 2006 [ABSTRACT FROM AUTHOR]

It has been demonstrated that femtosecond laser pulses can be used to process dielectric materials such as optical glass. One of the applications of this process is to produce sub-diffraction-limit structures whose index of refraction is different from that of the host medium. Due to the small size of these ‘bits’, it has been proposed to use this technique for high-density optical data storage. This paper is concerned with the mechanisms of the change of the index of refraction in such a small domain. We propose that the laser-induced strain field is responsible for the localized change of the index of refraction. It is demonstrated that the compressive strain field could be smaller than the area where the laser energy is absorbed in the glass. [ABSTRACT FROM AUTHOR]

Upon activation, naïve T helper cells can differentiate into two major distinct subsets, T helper 1 (Th1) and T helper 2 (Th2), as defined by their effector functions and cytokine secretion patterns. Cytokine milieu and costimulatory molecules have been shown to play an essential role in determining T helper differentiation. However, it is still unclear how the effects of signals of costimulatory molecules and cytokines are exerted during T helper differentiation. We show evidence suggesting that while cytokine signals initiate the differentiation program, the selective action of death effectors determines the end point balance of differentiating T helper subsets. We examined the expression of TNF-related apoptosis-inducing ligand (TRAIL) and CD95L in cloned and in vitro differentiated Th1 and Th2 cells. We found that activation-induced expression of TRAIL is exclusively observed in Th2 clones and primary T helper cells differentiated under the Th2 condition, while the expression of CD95L is mainly in Th1 cells. Furthermore, these two subsets exhibit distinct susceptibilities to TRAIL- and CD95L-mediated apoptosis. Th2 cells are more resistant to either TRAIL- or CD95L-induced apoptosis than Th1 cells. More importantly, both Th1 and Th2 cells could induce apoptosis in labeled Th1 but not Th2 cells. Blocking TRAIL and CD95L significantly enhance IFN-c production in vitro. Likewise, young MRL/MpJ-lpr/lpr mice also showed more Th1 response to ovalbumin immunization as compared to MRL/MpJ+/+. Therefore, apoptosis mediated by CD95L and TRAIL is critical in determining the fate of differentiating T helper cells. [ABSTRACT FROM AUTHOR]

The formation of self-organized assemblies by CnH2n+1NH2·HCl and C12H25SO4 Na in polar solvents was studied. By adding 1-propanol or 2-propanol, the precipitation formed in aqueous solution was resolved and a bilayer structure was discovered. Furthermore, multilamellar vesicle formation could be observed by methods of adjusting the molar ratio of CnH2n+1NH2·HCl to C12H25SO4Na, changing the length of the hydrocarbon chain of CnH2n+1NH2·HCl, or adding 1-octanol to the mixed surfactant systems. [ABSTRACT FROM AUTHOR]

A correction to the article "Reduced semen Quality in Chronic Prostatitis Patients That Induce the Release of Apoptotic Protein Omi/HtrA2 From Spermatozoa," that was published in the 2007 issue of this journal.