Thus, transformation and recombinational repair appear to contribute to successful infection. Transformation (the transfer of DNA from one bacterial cell to another through the intervening medium) appears to be part of an adaptation for DNA repair. H. pylori is naturally competent for transformation. While many organisms are competent only under certain environmental conditions, such as starvation, H. pylori is competent throughout logarithmic growth. All organisms encode genetic programs for response to stressful conditions including those that cause DNA damage. In H. pylori, homologous recombination is required for repairing DNA double-strand breaks (DSBs). The AddAB helicase-nuclease complex resects DSBs and loads RecA onto single-strand DNA (ssDNA), which then mediates strand exchange, leading to homologous recombination and repair. The requirement of RecA plus AddAB for efficient gastric colonization suggests, in the stomach, H. pylori is either exposed to double-strand DNA damage that must be repaired or requires some other recombination-mediated event. In particular, natural transformation is increased by DNA damage in H. pylori, and a connection exists between the DNA damage response and DNA uptake in H. pylori, suggesting natural competence contributes to persistence of H. pylori in its human host and explains the retention of competence in most clinical isolates. RuvC protein is essential to the process of recombinational repair, since it resolves intermediates in this process termed Holliday junctions. H. pylori mutants that are defective in RuvC have increased sensitivity to DNA-damaging agents and to oxidative stress, exhibit reduced survival within macrophages, and are unable to establish successful infection in a mouse model.
Several studies have supported this theory by showing reduced mortality when treating refractory intracranial hypertension with a barbiturate coma.About 60% of the glucose and oxygen used by the brain is meant for its electrical activity and the rest for all other activities such as metabolism. When barbiturates are given to brain injured patients for induced coma, they act by reducing the electrical activity of the brain, which reduces the metabolic and oxygen demand. The infusion dose rate of barbiturates is increased under monitoring by electroencephalography until burst suppression or cortical electrical silence (isoelectric "flatline") is attained. Once there is improvement in the patients general condition, the barbiturates are withdrawn gradually and the patient regains consciousness. Controversy exists over the benefits of using barbiturates to control intracranial hypertension. Some studies have found that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage. Furthermore, the reduction in intracranial hypertension may not be sustained. Some randomized trials have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, head trauma, intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma. See also
Insulin shock therapy
Traumatic brain injury


== References ==