Humanitarian Surgical Missions: Guidelines for Successful Anesthesia Support.

Many anesthesiologists and CRNAs are provided little training in preparing for a humanitarian surgical mission. Furthermore, there is very little published literature that outlines how to plan and prepare for anesthesia support of a humanitarian surgical mission. This article attempts to serve as an in-depth planning guide for anesthesia support of humanitarian surgical missions.

Advances in Anesthesia Delivery in the Deployed Setting.

Lessons learned over the past decade and a half of combat casualty management has brought about numerous advances in trauma anesthesia practice. In the post-Vietnam era, deployable anesthesia equipment centered on the capability to provide a balanced anesthetic technique, utilizing a combination of volatile gas and intravenous anesthetic adjuncts. The evolution of the modern battlefield has forced anesthesia providers across the military to adapt to mission requirements that often dictate a surgical capability that is more rapidly mobile and less reliant on logistical support.

Mouse models of Helicobacter-induced gastric cancer: use of cocarcinogens.

The human pathogen Helicobacter pylori causes inflammation in the stomach of infected hosts, leading in some cases to the development of gastric cancer. Several mouse models have been developed to study Helicobacter-induced carcinogenesis with similarities to gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (MALToma) in humans. These models require chronic infection of animals with mouse-colonizing isolates of H.

Chronic Helicobacter pylori infection with Sydney strain 1 and a newly identified mouse-adapted strain (Sydney strain 2000) in C57BL/6 and BALB/c mice.

The mouse model of Helicobacter pylori-induced disease using Sydney strain 1 (SS1) has been used extensively in Helicobacter research. Herein we describe the isolation and characterization of a new mouse-colonizing strain for use in comparative studies. One strain capable of persistent mouse colonization was isolated from a total of 110 clinical isolates and is named here SS2000 (Sydney strain 2000).

Selective depletion of the Type I, Type II, and Type III isozymes of hexokinase in mammalian cells using small interfering RNAs.

Constructs based on the pSUPER vector [Science 296 (2002) 550] and encoding small interfering RNAs specific for the Type I, Type II, or Type III isozymes of mammalian (rat) hexokinase were prepared. Transfection of Chinese hamster ovary and HeLa cells with these vectors resulted in selective depletion of the respective isozymes. A Zeocin marker was incorporated into the modified pSUPER vector, permitting isolation of stably transfected cell lines selectively depleted of the respective isozyme.

All three isoforms of the voltage-dependent anion channel (VDAC1, VDAC2, and VDAC3) are present in mitochondria from bovine, rabbit, and rat brain.

All three isoforms of the voltage-dependent anion channel (VDAC) were detected by immunoblot analysis of mitochondria isolated from rat, rabbit, and bovine brain. All three isoforms were associated with mitochondria after fractionation of rat brain extracts on sucrose density gradients. No VDAC isoforms were detected in non-mitochondrial fractions.

Isozymes of mammalian hexokinase: structure, subcellular localization and metabolic function.

The first step in metabolism of glucose (Glc) is usually phosphorylation, catalyzed by hexokinase. However, the Glc-6-P produced can then enter one or more of several alternative pathways. Selective expression of isozymic forms of hexokinase, differing in catalytic and regulatory properties as well as subcellular localization, is likely to be an important factor in determining the pattern of Glc metabolism in mammalian tissues/cells.

Catalase (KatA) and KatA-associated protein (KapA) are essential to persistent colonization in the Helicobacter pylori SS1 mouse model.

Helicobacter pylori infects the human gastric mucosa and elicits an aggressive inflammatory response. Despite the severity of the inflammatory response, the bacterium is able to persist and cause a chronic infection. It is believed that antioxidant defence mechanisms enable this organism to persist.

Functional interactions between the noncovalently associated N- and C-terminal halves of mammalian Type I hexokinase.

The 100 kDa Type I isozyme of mammalian hexokinase has evolved by duplication and fusion of a gene encoding an ancestral 50 kDa hexokinase. Although the N- and C-terminal halves are similar in sequence, they differ in function, catalytic activity being associated only with the C-terminal half while the N-terminal half serves a regulatory role. The N- and C-terminal halves of rat Type I hexokinase have been coexpressed in M + R 42 cells.

Kinetic and regulatory properties of HK I(+), a modified form of the type I isozyme of mammalian hexokinase in which interactions between the N- and C-terminal halves have been disrupted.

A modified form (HK I(+)) of rat Type I hexokinase (HK I) has been expressed. HK I(+) contains a centrally located polyalanine insert which, along with the known helical propensity of adjacent sequence, was expected to lead to alpha-helix formation, with resulting distension of the molecule and disruption of interactions between the N- and C-terminal halves. The properties of HK I(+) are consistent with this expectation and with previous proposals that (1) inhibition of HK I by Glc-6-P or its analogs and antagonism of this inhibition by P(i) result from competition of these ligands for a binding site in the N-terminal half of HK I, with resulting conformational changes propagated through interactions with the catalytic C-terminal half, and (2) binding of Glc-6-P to a site in the C-terminal half of HK I is obstructed by interactions between the halves, present in HK I but not HK I(+).

Purification of the Type II and Type III isozymes of rat hexokinase, expressed in yeast.

C-terminally His-tagged versions of the Type II and Type III isozymes of rat hexokinase were expressed in Pichia pastoris and Schizosaccharomyces pombe, respectively. Milligram amounts of the homogeneous isozymes were readily obtained in good yield by chromatography on Ni-NTA columns. The specific activities were 133 +/- 4 and 76 +/- 3 u/mg for the purified Type II and Type III isozymes, respectively.

In vivo behavior of a Helicobacter pylori SS1 nixA mutant with reduced urease activity.

Helicobacter pylori mutants devoid of urease activity fail to colonize the gastric mucosa of mice; however, the effect of decreased levels of urease on colonization has not been examined. The nixA gene, required for full urease activity, encodes a cytoplasmic membrane nickel transporter that imports nickel ions and leads to incorporation of nickel ions into apourease. A nixA mutant of the Sydney strain of H.

Functional characteristics of hexokinase bound to the type a and type B sites of bovine brain mitochondria.

Hexokinase is released from Type A sites of brain mitochondria in the presence of glucose 6-phosphate (Glc-6-P); enzyme bound to Type B sites remains bound. Hexokinase of freshly isolated bovine brain mitochondria (Type A:Type B, approximately 40:60) selectively uses intramitochondrial ATP as substrate and is relatively insensitive to the competitive (vs ATP) inhibitor and Glc-6-P analog, 1,5-anhydroglucitol 6-phosphate (1,5-AnG-6-P). After removal of hexokinase bound at Type A sites, the remaining enzyme, bound at Type B sites, does not show selectivity for intramitochondrial ATP and has increased sensitivity to 1,5-AnG-6-P.