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B Cruz

Publications and source records attributed to B Cruz.

10 recordsLinked to original sources
PubMed2001

Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity.

OBJECTIVE: In the prehospital setting, countershock terminates ventricular fibrillation (VF) in about 80% of cases. However, countershock is most commonly followed by asystole or pulseless electrical activity (PEA). The consequences of such a countershock outcome have not been well studied. The purpose of this investigation was to compare the outcome of prehospital VF victims shocked into asystole or PEA with that of patients whose first documented rhythm was asystole or PEA (primary asystole or PEA). DESIGN: Observational, retrospective study conducted over 5 yrs (1995-1999). SETTING: A municipal hospital with a catchment area of >200,000. PATIENTS: Consecutive adult patients with out-of-hospital nontraumatic cardiopulmonary arrest of cardiac origin. Patients found in VF who developed asystole or PEA after countershocks (group 1) and patients found in asystole or PEA (primary asystole or PEA) (group 2) were included if the reported downtime was <10 min. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Study end points included restoration of circulation (defined as a pulse for any duration), survival to hospital admission, and survival to hospital discharge. Ratios were determined, 95% confidence intervals were calculated, and observed differences were compared. For group 1 patients (n = 101), 61% of patients had a bystander-witnessed collapse and 34% received bystander cardiopulmonary resuscitation. For group 2 patients (n = 140), collapse was bystander witnessed in 71% and 45% received bystander cardiopulmonary resuscitation. These differences were not statistically significant. Restoration of circulation was significantly more frequent in group 2 than group 1 (42% vs. 16%, p <.001) as was survival to hospital admission (36% vs. 11%, p =.001). Survival to hospital discharge was greater in group 2 patients, but the difference failed to achieve statistical significance (10% vs. 3%, p =.062). CONCLUSIONS: Countershock of prolonged VF followed by a nonperfusing rhythm has a worse prognosis than primary asystole or PEA and may be related to myocardial electrical injury.

Adult↗
PubMed2000

Bacterial lipoprotein based expression vectors as tools for the characterisation of African swine fever virus (ASFV) antigens.

African swine fever virus (ASFV) is the causative agent of an important pig disease for which protective mechanisms are still poorly understood. The present work was aimed at the characterisation of ASFV antigens using previously reported vectors that allow their expression as fusion proteins with the bacterial lipoprotein OprI. Several recombinant clones induced SLA-restricted, ASFV-specific lymphoproliferation and one (A2) was demonstrated to stimulate ASFV-specific CTL activity in vitro, in opposition to the effect of UV inactivated virus. The nucleotide sequence of the fragment cloned in A2 showed 99% identity with a portion of the G1340L ORF of the BA71V isolate, and the expressed fusion lipoprotein induced specific antibodies in vivo. Blood mononuclear leukocytes from a pig immunised with outer membrane preparations from A2 showed to reduce strongly (99.6%) the ASFV yield in cultures of autologous macrophages. However, after inoculation with virulent virus the pig developed acute fatal ASF. Overall our results show that OprI based expression vectors are valuable tools to screen viral antigens in terms of their capacity to trigger immune competent cells.

African Swine Fever↗
PubMed2000

Immediate countershock versus cardiopulmonary resuscitation before countershock in a 5-minute swine model of ventricular fibrillation arrest.

STUDY OBJECTIVE: Prior laboratory and clinical studies demonstrate that cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation (VF) increases the likelihood of successful cardiac resuscitation. The lower limit of VF duration at which time preshock CPR provides no benefit has not been specifically studied. The purpose of this study was to compare countershock and cardiac resuscitation outcome between immediate countershock of VF of 5-minute duration and CPR without drug therapy before countershock in a swine model. METHODS: VF was induced in anesthetized and instrumented swine. After 5 minutes of VF, animals received 1 of 2 treatments. Animals in group 1, a "historical" control group (n=20), received immediate countershock followed by CPR and repeated shocks if needed. Group 2 animals (n=11) received CPR for 90 seconds preceding countershock, then continued CPR and repeated countershock if necessary. Drugs were not administered to either group, and resuscitation efforts were discontinued if a perfusing rhythm was not restored within 10 minutes of the first countershock. First shock success rate (defined as termination of VF), the number of shocks required to terminate VF, and the cardiac resuscitation rate were compared between groups. RESULTS: The first shock terminated VF in 13 of 20 group 1 animals and 2 of 11 group 2 animals (P =.023). All but 1 animal in group 1 developed pulseless electrical activity after countershock. All but 1 animal in group 1 were eventually successfully resuscitated with CPR and repeated shocks if necessary. Four group 2 animals could not be resuscitated (P =.042). CONCLUSION: Although effective in improving outcome of prolonged VF, CPR preceding countershock of VF of 5-minute duration does not improve the response to the first shock, decrease the incidence of postshock pulseless electrical activity, or the rate of return of circulation. In this study, CPR preceding countershock resulted in a significantly lower cardiac resuscitation rate.

Animals↗
PubMed2000

Experimental studies on precordial compression or defibrillation as initial interventions for ventricular fibrillation.

Countershock of prolonged ventricular fibrillation is usually followed by asystole or a nonperfusing rhythm. Data from three laboratory investigations indicate that administration of epinephrine and cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation significantly improves cardiac resuscitation outcome compared with immediate countershock (relative risk reduction of failed resuscitation, 0.61). Preliminary investigations indicate that a similar improvement is not observed when the ventricular fibrillation period is of shorter duration, e.g., 5 mins. This time interval is probably at the lower limit at which CPR preceding shock of ventricular fibrillation provides benefit in terms of cardiac resuscitation. A single clinical trial of "CPR first" supports the use of a brief period of CPR before countershock of prolonged ventricular fibrillation. Additional trials with and without epinephrine are anticipated.

Adrenergic Agonists↗
PubMed1998

Entry of African swine fever virus into Vero cells and uncoating.

African swine fever virus (ASFV) enters Vero cells by adsorptive endocytosis [Valdeira, M.L., Geraldes, A., 1985. Morphological study on the entry of African swine fever virus into cells, Biol Cell. 55, 35-40]. Electron microscopy of a lysosomotropic drug-controlled penetration indicated that this step takes place in the endosomes, after fusion between the viral envelope and the limiting membrane of the endosome. Inhibition studies with colcemid, cytochalasin B, sodium azide, dinitrophenol, lysosomotropic weak bases, and the ionophore monensin, showed that the virus uptake is largely independent of cytoskeletal and lysosomal function, but dependent on oxidative phosphorylation. Some protease inhibitors inhibited viral replication at an early step, indicating that the initiation of infection depends on a viral proteolytic cleavage.

2,4-Dinitrophenol↗
PubMed1998

Lingual ulceration.

Explore the source record for details and available documents.

Carcinoma, Squamous Cell↗
PubMed1995

Pattern of disease after murine hepatitis virus strain 3 infection correlates with macrophage activation and not viral replication.

Murine hepatitis virus strain (MHV-3) produces a strain-dependent pattern of disease which has been used as a model for fulminant viral hepatitis. This study was undertaken to examine whether there was a correlation between macrophage activation and susceptibility or resistance to MHV-3 infection. Peritoneal macrophages were isolated from resistant A/J and susceptible BALB/cJ mice and, following stimulation with MHV-3 or lipopolysaccharide (LPS), analyzed for transcription of mRNA and production of interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta), mouse fibrinogen-like protein (musfiblp), tissue factor (TF), leukotriene B4, and prostaglandin E2 (PGE2). Macrophages from BALB/cJ mice produced greater amounts of IL-1, TNF-alpha, TGF-beta, leukotriene B4, and musfiblp following MHV-3 infection than macrophages from resistant A/J mice, whereas in response to LPS, equivalent amounts of IL-1, TNF-alpha, TGF-beta, and TF were produced by macrophages from both strains of mice. Levels of mRNA of IL-1, TNF-alpha, and musfiblp were greater and more persistent in BALB/cJ than in A/J macrophages, whereas the levels and kinetics of IL-1, TNF-alpha, and TF mRNA following LPS stimulation were identical in macrophages from both strains of mice. Levels of production of PGE2 by MHV-3-stimulated macrophages from resistant and susceptible mice were equivalent; however, the time course for induction of PGE2, differed, but the total quantity of PGE2 produced was insufficient to inhibit induction of musfiblp, a procoagulant known to correlate with development of fulminant hepatic necrosis in susceptible mice. These results demonstrate marked differences in production of inflammatory mediators to MHV-3 infection in macrophages from resistant A/J and susceptible BALB/cJ mice, which may explain the marked hepatic necrosis and fibrin deposition and account for the lethality of MHV-3 in susceptible mice.

Animals↗
PubMed1994

A Th1 cell line (3E9.1) from resistant A/J mice inhibits induction of macrophage procoagulant activity in vitro and protects against MHV-3 mortality in vivo.

Induction of immune coagulants has been implicated in the pathogenesis of murine hepatitis virus strain 3 (MHV-3)-induced fulminant hepatic necrosis. Previous work from our laboratory has shown that the induction of procoagulant activity (PCA) correlates with the resistance/susceptibility to disease in inbred and recombinant inbred (RI) strains of mice. Macrophages from susceptible, but not resistant, strains of mice expressed increased levels of PCA in response to MHV-3 stimulation. T lymphocytes, however, had a marked regulatory role in the final expression of macrophage PCA. CD3+ CD4+ CD8- lymphocytes from RI H-2 compatible susceptible mice were able to instruct macrophages from susceptible mice to express significantly augmented levels of PCA, whereas CD3+ lymphocytes from RI H-2 compatible MHV-3-immunized resistant mice were able to suppress induction of PCA. In this present study, T-cell lines were derived from draining popliteal lymph nodes from resistant A/J mice, which had been immunized with MHV-3. All T-cell lines showed marked proliferation to MHV-3 and MHV-JHM which was major histocompatibility complex (MHC) restricted. All cell lines were CD3+, four of these were CD4+ and one was CD8+. All of the CD4+ cell lines produced IL-2 and two produced interferon-gamma (IFN-gamma), consistent with the Th1 cytokine profile. One cell line (3E9.1) was able to inhibit the induction of macrophage PCA through production of a soluble factor although cell-to-cell contact could not be excluded. This CD4+ T-cell line conferred protection to infected and susceptible AXB8 mice. These results demonstrate that the existence of a Th1 subpopulation of cells with a regulatory effect on macrophage PCA induction in MHV-3-infected mice contributes to the resistance of the A/J strain of mice to MHV-3 infection.

Animals↗
PubMed1989

Short trachea, a hazard in tracheal intubation of neonates and infants: syndromal associations.

Short trachea results from reduction in number of tracheal cartilage rings to 15 or fewer from normal mean of 17 rings in infants. In a review of radiologic and pathologic data, the thoracic vertebral level of tracheal bifurcation as seen in anteroposterior chest radiographs of infants with congenital malformations, cardiovascular anomalies, and skeletal dysplasias, was compared with numbers of tracheal cartilage rings demonstrated in postmortem specimens. Increased frequency of short trachea was seen in patients with DiGeorge anomaly (77%), skeletal dysplasias (55%), brevicollis (57%), diaplacental rubella (40%), and patients with congenital heart disease who did not have DiGeorge anomaly (36%, with range 25-83% for different types, the highest, 83%, being interrupted aortic arch). Preintubation high kilovoltage chest radiographs to establish the level of tracheal bifurcation in patients with increased risk of short trachea can be helpful in avoiding bronchial intubation and its complications. Postintubation chest films to assure the level of the endotracheal tube tip should be considered for such patients. Growth in length of the trachea with age is accomplished both by increase in size of tracheal cartilage rings and interring membranes, and by increase in ring number.

Bronchi↗