After cardiopulmonary resuscitation in this pediatric CICU, the rate of success was 63% and the rate of survival was 42%. Prior cardiac surgery and use of epinephrine before arrest did not influence the outcome of CPR. The availability of effective mechanical cardiopulmonary support can improve the outcome of CPR.

We compared the pungency and tolerability of three inhaled anaesthetics in a randomized, double-blind study. Eighty-one unpremedicated patients (n = 27, each group) inhaled 2 MAC of isoflurane (2.3%), desflurane (12%) or sevoflurane (4%) for 60 s from an anaesthetic breathing circuit via a mask. Two blinded observers recorded coughing, complaints of burning and irritation, and how long the inhalation was tolerated. One sevoflurane patient coughed, but completed the study period, whereas 11 isoflurane patients and 20 desflurane patients coughed, objected verbally or removed the mask forcefully. All sevoflurane, 20 isoflurane and seven desflurane patients completed the study period (average 60, 49 and 33 s, respectively, P < 0.05). The irritability grading was: desflurane > isoflurane > sevoflurane (P < 0.05). Sevoflurane is the least irritating agent for inhalation at 2 MAC concentration.

Species B human adenoviruses (Ads) are increasingly associated with outbreaks of acute respiratory disease in U.S. military personnel and civil population. The initial interaction of Ads with cellular attachment receptors on host cells is via Ad fiber knob protein. Our previous studies showed that one species B Ad receptor is the complement receptor CD46 that is used by serotypes 11, 16, 21, 35, and 50 but not by serotypes 3, 7, and 14. In this study, we attempted to identify yet-unknown species B cellular receptors. For this purpose we used recombinant Ad3 and Ad35 fiber knobs in high-throughput receptor screening methods including mass spectrometry analysis and glycan arrays. Surprisingly, we found that the main interacting surface molecules of Ad3 fiber knob are cellular heparan sulfate proteoglycans (HSPGs). We subsequently found that HSPGs acted as low-affinity co-receptors for Ad3 but did not represent the main receptor of this serotype. Our study also revealed a new CD46-independent infection pathway of Ad35. This Ad35 infection mechanism is mediated by cellular HSPGs. The interaction of Ad35 with HSPGs is not via fiber knob, whereas Ad3 interacts with HSPGs via fiber knob. Both Ad3 and Ad35 interacted specifically with the sulfated regions within HSPGs that have also been implicated in binding physiologic ligands. In conclusion, our findings show that Ad3 and Ad35 directly utilize HSPGs as co-receptors for infection. Our data suggest that adenoviruses evolved to simulate the presence of physiologic HSPG ligands in order to increase infection.

The efficacy of cancer-immunotherapy is limited because of central and peripheral immune-tolerance towards tumor-antigens. We propose a novel approach based on the fact that the immune-system has not evolved tolerance towards adenoviruses (Ads) and that Ads have not evolved efficient mechanisms for immune-escape. The host-response to intratumoral Ad-vector-injection in mice that were immunologically tolerant to neu-positive syngeneic mammary-cancer (MMC) was investigated. Intratumoral injection with replication-deficient, transgene-devoid Ad induced immune-responses at two different anatomical sites: the tumor-draining lymph-nodes and the tumor-microenvironment. The lymph-nodes supported the generation of both neu- and Ad-specific T-effector-cells, while inside the tumor-microenvironment only Ad-specific T-cells expanded. Importantly, Ad-specific T-cells were anti-tumor-reactive despite the presence of active regulatory-T-cell-mediated immune-tolerance inside MMC-tumors and anti-tumor efficacy of Ad was increased by pre-immunization against Ad despite the production of Ad-neutralizing antibodies.

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