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La Fe es razonable: cómo comprender, explicar y defender la fe católica. Scott Hahn. Published by Ediciones Rialp, S.a.. ISBN / ISBN Many Hahn book titles have been translated into the following languages: . La Fe es razonable: Como comprender; explicar y defender la fe catolica. by Scott Hahn First published Sort by La Fe Es Razonable: Cómo Comprender, Explicar Y Defender La Fe Católica (Paperback). Published by.
Of 4 prospective randomized studies, 3 recommend HTS as a safe alternative to produce cerebral relaxation in patients with supratentorial tumours.
Fluid resuscitation in patients with TBI is of critical importance because of the need to avoid hypotension and secondary neurological injury, which result in increased mortality in these patients.
The Brain Trauma Foundation in its management guidelines for TBI is clear in stating that hypotension must be avoided because it is an isolated parameter of poor prognosis. This led Bulger et al. Observational studies have shown a relationship between PbtO2 reduction and poor outcomes80,81 and suggest that therapy targeted on maintaining PbtO2 may improve clinical outcomes. Of the 16 studies reviewed, including 4 prospective randomized studies and multiple observational studies, the data support the use of HTS as an effective means to lower ICP in patients with TBI.
Only 1 study out of the 36 articles reviewed found a better long-term result in patients treated with HTS, compared with mannitol. Oedema following an ischaemic stroke begins within 1—3 days, peaks within 3—5 days, and lasts up to two weeks. Schwarz et al. Moreover, there is the advantage of being able to use HS-HES successfully again after mannitol has failed.
Although it is 35 not appropriate to extrapolate data obtained in a cell culture models to clinical situations, these data show that HTS may potentially damage hippocampal neurons in vitro. Toung et al. Mannitol therapy was more effective at reducing water in the ischaemic hemisphere of the brain, but HTS was equally effective at dehydrating both hemispheres of the brain ischaemic and non-ischaemic. In a study in rodents in , Bhardwaj et al. Two years later, Toung et al.
Several theories have been proposed. One theory is that they reduce water content in the brain, and a second theory is that they reduce viscosity and cerebrovascular resistance, giving rise to compensatory vasoconstriction and reduced CBV. In , Diginger et al.
They found varying degrees of increased CBF in the contralateral hemisphere of patients with ischaemic stroke after osmotic therapy, apparently mediated by blood pressure.
However these measures have not been tested and, consequently, they are not recommended Class IIa, level C evidence. They administered He determined that In , the same group showed, in 44 patients with high grade SAH, that HTS increases CBF and improves cerebral oxygenation significantly during 4 h after the infusion. This favourable result is associated with improved cerebral tissue oxygenation for more than min.
The study by Bentsen et al. No ICP rebound effect was observed in any of the trials during their respective study periods. Intracerebral haemorrhage ICH Intracranial hypertension occurs during the acute phase of ICH and it is a predictor of poor prognosis in these patients.
There is no clear knowledge to date of which are the best modalities for the management of this condition. Still under the continuous HTS infusion, 48—96 h after the episode, the brain CT scan of both patients revealed extension of the cerebral oedema, suggesting a rebound effect similar to that already described with mannitol. After inducing haematomas, they measured ICP, cerebral perfusion pressure, cerebral oxygen extraction and oxygen consumption, as well as CBF in regions close to the haematoma and distant to it.
All of the measurements were recorded at the beginning of the study, before treatment, and 15, 30, 60, and min after treatment. They also showed increased CPP and a lower volume of hemispheric water compared to the animals that received These changes persisted for a period of 80— min.
Both mannitol and HTS have proven to be effective at controlling ICP, through different mechanisms; osmotic dehydration of the cerebral interstitium; reduction of blood viscosity; increased red blood cell deformation; and improved microcirculation.
The use of mannitol and hypertonic saline solution in neurocritical patients varies considerably among centres and there is no consensus regarding which of the two is the agent of choice. The majority of the data reviewed suggest that HTS offers more favourable results in the control of ICP and all types of IH, regardless of concentration.
A metaanalysis found 8 prospective randomized studies with a high failure rate of mannitol-based therapy. It is still to be determined whether HTS should be administered in the form of a drip or infusion; both are effective but there are more results, and none of them worse, with the use of bolus doses.
HTS produces less osmotic diuresis, thus maintaining more stable systemic and cerebral haemodynamics in the neurocritical patient, considering that it does not only lower ICP and maintain CPP, but it also increases PtbO2.
A large prospective randomized study is needed in order to answer this question. Hyperosmolar therapy for intracranial hypertension. Neurocrit Care. Osmotherapy: use among neurointensivists. The University of Toronto TBI treatment study: a prospective, randomized comparison of pentobarbital and mannitol.
Can J Neurol Sci. Silver S. The treatment of tromboangiitis obliterans by intravenous injection of hypertonic salt solution. J Neurol Sci. Experimental alteration of brain bulk.
Am J Physiol. Intraocular and intracranial pressure: an experimental study. Arch Neurol Psychiatr. Wise BL, Chater N. J Neurosurg. Zornow MH. J Neurosurg Anesthesiol. Cerebral effects of isovolemic hemodilution with hypertonic saline solution. Use of mannitol during neurosurgery: interpatient variability in the plasma and CSF levels. Eur J Clin Pharmacol. Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes.
The effects of mannitol on blood viscosity. J Neurochem. Guidelines for the management of severe traumatic brain injury. Hyperosmolar therapy. J Neurotrauma. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. James HE. Methodology for the control of intracranial pressure with hypertonic mannitol.
Acta Neurochir Wien. Dose—response relationship of mannitol and intracranial pressure: a meta analysis.
Rosner MJ, Coley I. Cerebral perfusion pressure: a hemodynamic mechanism of mannitol and the post-mannitol hemogram. Characterizing the dose—response relationship between mannitol and intracranial pressure in traumatic brain injury patients using a high-frequency physiological data collection system.
Osmole gap in neurologic-neurosurgical intensive care unit: its normal value, calculation, and relationship with mannitol serum concentrations. Crit Care Med.
Case report: mannitol nephrotoxicity syndrome: role of hemodialysis and postulate of mechanisms. Am J Med Sci. Mannitol-induced renal failure.
J Am Soc Nephrol. Mannitol induced acute renal failure. Medicine Baltimore.
The effect of high-dose mannitol on serum and urine electrolytes and osmolality in neurosurgical patients. Can J Anaesth. Mannitol-induced acute renal failure. Neth J Med. Rebound swelling of astroglial cells exposed to hypertonic mannitol.
BMC Neurosci. Aggravation of vasogenic cerebral edema by multiple-dose mannitol. Effects of single, repeated and massive mannitol infusion in the dog: structural and function changes in the kidney and brain.
Ann Surg. Anesth Analg. Comparison of peripheral and central infusions of 7. Hypertonic saline-dextran solutions for the prehospital management of traumatic hypotension.
Am J Surg. Comparison between hypertonic saline and mannitol in the reduction of elevated intracranial pressure in a rodent model of acute cerebral injury.
Discussion 86—7. Effect of mannitol and hypertonic saline on cerebral oxygenation in patients with severe traumatic brain injury and refractory intracranial hypertension.
J Neurol Neurosurg Psychiatr. Cerebral hemodynamic effects of 7. Hypertonic saline 7. Predictable reduction of intracranial hypertension with hypertonic saline hydroxyethyl starch: a prospective clinical trial in critically ill patients with subarachnoid hemorrhage.
Acta Anaesthesiol Scand.
Acta Neurochir Suppl. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure. Drobin D, Hahn RG. For better characterization of the structure-function relationships of the HCMV helicase-primase complex, we first compared the protein sequences of 18 herpesviruses homologs of pUL and pUL Finally, we used a mutational approach to investigate the importance of amino acids potentially involved in ATP binding pUL or zinc chelation pUL This allowed identification of amino acids in the helicase-primase complex that are crucial for viral replication.
Differences in the structural models of the HCMV and HSV-1 helicases that could explain specificity of antiviral drugs action were also highlighted.
To identify amino acids that might be involved in the catalytic activity of the HCMV helicase, we aligned pUL sequence to 18 herpesviruses homologs sequences of different origins 11 alpha, 4 beta, and 3 gamma herpesviruses; Supplementary Table S1. Our results confirmed and completed the previous alignment made on five herpesviruses motifs I and II Martignetti and Barrell, In order to determine which of these amino acids might be involved in ATP binding, we attempted to build a first homology model of pUL using CPHmodels To refine the model, we made the query with the N-terminal part of pUL residue 1— and obtained a model for pUL 2— score 5.
As shown in Figure 2A , the theoretical structure of pUL 2— superimposed neatly on the known Upf1 helicase domain structure. Theoretical structure of pUL E Superposition of homology modeling of pUL — in green and E. Cheng et al. As motifs V and VI are conserved among SF1 helicases, we attempted to build a homology model of the C-terminal part of pUL encompassing both domains.
We obtained a homology model of pUL — C-terminal domain 84 residues based on the coordinates of the crystal structure of the RecD helicase in the E. The mutations were chosen such as to change the side-chain length or the functional group, in order to determine whether the size or charge is important for the function.
In addition, to determine if histidine 82 might belong to the catalytic site see above , H82 was replaced by a lysine or an arginine H82K and H82R. To estimate the fitness impact of these mutations on virus replicative capacity, we then compared the growth curves of the wildtype and mutant viruses.
Both mutants grew more slowly than the wildtype virus Figure 3. Effect of the helicase pUL H82 mutations on viral growth. Fluorescent foci were counted daily from day 1 to day 7. Data are the average of three independent experiments. To assess this potential similarity of function at the structural level, we also built a first homology model of the HSV-1 helicase.
As expected from the models, the theoretical structures of pUL5 26— and pUL 2— superimposed neatly on each other Figure 4B.
Within the putative metal-binding pattern of pUL70, we identified three cysteines C, C, and C and one histidine H that are highly conserved among herpesviruses Figure 5A and that could be directly involved in zinc ion binding Figure 5B.
Conserved zinc finger region and amino acids in primase pUL A Sequences alignment of the zinc finger conserved region of pUL70 with homologs from 18 herpesviruses belonging to alpha, beta, and gamma sub-families of herpesviruses as indicated. Conserved key residues involved in the formation of the zinc-finger motif are shown in bold letters.
Amino acids involved in zinc ion binding are numbered. Unlike wildtype HCMV-BAC, none of the mutants formed infectious foci after 11 days of culture Table 2 and Supplementary Figure S2 , indicating that these mutations drastically impair viral replication and propagation in cell culture.
Discussion The helicase-primase of HCMV is essential for viral replication and thus represents a potential target for the development of new anti CMV compounds.
However, no crystal structure is available to date and structure-function relationships are not clearly defined. We propose that the potential metal-binding motif involving the cysteine and histidine residues within the sequence CX4-HXCX4-C is essential for proper pUL70 folding and might be required for DNA binding.
Interestingly, a single mutation, AT, conferring resistance to pritelivir, has been located near the zinc-finger domain of the pUL52 primase in HSV-1 Field and Biswas, , suggesting that this region might be one of the potential target for pritelivir. Our study proved that they are essential for viral replication and propagation. There is now a need for more studies focusing on a better characterization of the role of the identified conserved amino acids at the level of the enzymatic activity of pUL and pUL The homology model for both proteins was built through CPHmodels These models showed that the theoretical structures of pUL5 26— , pUL 2— and the helicase domain of Upf1 superimposed neatly on each other.
These models are strongly comforted by our functional results and others Graves-Woodward et al. Besides the similarities in the catalytic sites of the helicases, our theoretical homology models also highlighted some differences that could be important in differentiating the specificity of these helicases. Interestingly enough, alignment of herpesviruses helicase proteins sequences showed that the region 39 residues containing this amino acid in pUL is missing in pUL5 and other herpesviruses supplementary Figure S3.
As commonly observed in SF1 helicases Fairman-Williams et al. The presence of these insert might actually explain why, when trying to obtain a theoretical structure of the whole proteins, only the N-terminal portion of the proteins could be modeled.
The homology model for pUL encompassed residues 2—, i. The homology model for pUL5 contained amino acids residues 26— including protein sequence beyond motif IV Figure 1A.