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PubMedDate not supplied

Information-sharing in out-of-hospital disaster response: the future role of information technology.

Numerous examples exist of the benefits of the timely access to information in emergencies and disasters. Information technology (IT) is playing an increasingly important role in information-sharing during emergencies and disasters. The effective use of IT in out-of-hospital (OOH) disaster response is accompanied by numerous challenges at the human, applications, communication, and security levels. Most reports of IT applications to emergencies or disasters to date, concern applications that are hospital-based or occur during non-response phases of events (i.e., mitigation, planning and preparedness, or recovery phases). Few reports address the application of IT to OOH disaster response. Wireless peer networks that involve ad hoc wireless routing networks and peer-to-peer application architectures offer a promising solution to the many challenges of information-sharing in OOH disaster response. These networks offer several services that are likely to improve information-sharing in OOH emergency response, including needs and capacity assessment databases, victim tracking, event logging, information retrieval, and overall incident management system support.

Computer Communication Networks↗

PubMed1979

The use of in vitro technics to study drug-induced pancytopenia.

The confirmation of drug-induced marrow aplasia is difficult since rechallenging the patient can lead to serious morbidity. We used marrow-culture technics to challenge in vitro the bone marrow of a patient with marrow aplasia after ingestion of quinidine. There was no clinical or laboratory evidence of quinidine-mediated destruction of erythrocytes, leukocytes or platelets. By contrast, use of quinidine in combination with the patient's serum substantially inhibited in vitro growth of allogeneic marrow granulocytic and erythroid series. Furthermore, use of quinidine in combination with acute-phase serum (but not acute-phase serum alone or quinidine in combination with recovery-phase serum) inhibited growth of the patient's marrow. This observation suggests that both a transient serum factor and quinidine were responsible for the marrow aplasia. These technics could be applied with minimal risk to similar patients and would permit in vitro rechallenge with the suspected drug.

Aged↗

PubMed1990

Voltage-dependent gating of gap junction channels in embryonic chick ventricular cell pairs.

The dependence of macroscopic gap junctional conductance (Gj) on transjunctional voltage (Vj) was studied in paired myocytes after enzymatic dissociation of 7-day-old embryonic chick ventricles. The membrane voltage of both cells was independently controlled by separate patch-clamp circuits in the whole cell configuration. Two distinctive unitary junctional conductances were identified in recordings from seven different cell pairs. The larger channel had a mean conductance of 166 +/- 37 pS (n = 6 pairs), whereas a second channel averaged 58 +/- 10 pS (n = 3). Instantaneous Gj remained linear over a Vj range of -100 to +100 mV, whereas the steady-state Gj declined when voltages exceeded +/- 30 mV. Both decay and recovery phases of Gj follow exponential time courses, with the recovery time constant being four times slower than inactivation, requiring 1.1 s at 80 mV. The normalized steady-state Gj-Vj curve could be defined by a two-state Boltzmann distribution, assuming an effective gating charge of 1.72, a half-inactivation voltage of 45 mV, and a residual voltage-insensitive Gj of 27% of maximum. Single-channel recordings revealed closure of 160-pS channels on a Vj step to 80 mV, and the ensemble average of five such records produced an exponentially decaying junctional current with a time constant of 184 ms. The single-channel current-voltage relationship remains linear with a slope of 145 pS over the entire Vj range. The results support the hypothesis that a population of 160-pS gap junction channels is gated by transjunctional potentials.

Animals↗

PubMed2006

Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury.

In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin-binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidney injury, stathmin-deficient (OP18-/-) and wild-type (WT) animals were subjected to experimental IRI. At 3, 7, and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology, and recovery. Our studies indicate that on day 14 after reperfusion OP18-/- mice have significant renal failure, whereas the creatinine levels of WT animals have returned to baseline. Compared with WT animals OP18-/- mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen expression indicated that OP18-/- animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18-/- animals also had an increased number of tubules with apoptotic cells. These results suggest that in stathmin-deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.

Animals↗

PubMed2006

Neuroprotection and stroke rehabilitation: modulation and enhancement of recovery.

Recent advances in research are modifying our view of recovery after nervous system damage. New findings are changing previously held concepts and providing promising avenues for treatment of patients after stroke. This review discusses mechanisms of neuronal injury after brain ischemia and the attempts to study neuroprotection options based on such mechanisms. It also considers measures available at present to improve outcome after stroke and presents new areas of research, particularly stimulation techniques, neurogenesis and trophic factors to enhance recovery. In order to improve outcomes, medications that may be detrimental to recovery should be avoided, while symptomatic therapy of problems such as depression, pain syndromes and spasticity may contribute to better results. Continued surveillance and early treatment of complications associated with acute stroke, along with supportive care remain the mainstay of treatment for stroke patients in the recovery phase. Present research on limiting brain damage and improving recovery and plasticity enhance the prospects for better clinical treatments to improve recovery after stroke.

Brain Damage, Chronic↗

PubMed1993

[The importance of neuromuscular monitoring during anesthesia for neuroradiologic diagnosis].

Muscle relaxants are essential in anaesthesia for neuroradiological diagnosis. In addition, neurosurgical and neurological patients often face, because of their basic illness, respiratory danger, which can increase postoperatively through the use of muscle relaxants during anaesthesia. Because of their pharmacodynamic properties and side-effects, muscle relaxants must be clearly differentiated from one another and used selectively for the different phases of anaesthesia-intubation, calmness during examination and recovery from neuromuscular block with extubation. During planned extubation in particular, no residual relaxation or danger of recurarization must exist during the recovery stage from neuromuscular block. For investigations with planned extubation, only the muscle relaxants atracurium and vecuronium with their medium-long effect should be applied. A high degree of safety is provided by neuromuscular block and especially in the recovery phase. Using relaxometers it is possible to determine individual relaxant requirements, avoid under- and overdoses, carry out an antagonism at the correct time and prevent residual relaxation situations so that respiratory insufficiency can be reliably excluded.

Anesthesia↗

PubMed1992

Neurological rehabilitation.

Increasingly, neurologists are participating in the rehabilitation of disorders of the nervous system. Compelling reasons why neurologists, especially those with academic interests, should become involved in rehabilitation include the opportunity to observe patients in the recovery phases of their illnesses and to study issues relating to functional recovery, exposure to patients (such as those with spinal cord injury) who are often not seen by neurologists in the acute phase, and the opportunity to help establish a scientific base for rehabilitation medicine. Many areas of investigation can contribute to the scientific basis of neurological rehabilitation. Among the most promising are regeneration in the central (CNS) and peripheral nervous systems, adaptive mechanisms following CNS injury, computational neuroscience, neuromuscular physiology of chronic denervating conditions (e.g., the post-polio syndrome), and outcome studies of both physical and pharmacological therapeutic modalities. While there may be financial advantages to involvement in neurological rehabilitation, these are probably overestimated and interest in this field would continue to grow without them. There is a need for enhanced training in this subspecialty, including the development of dual certification programs in neurology and rehabilitation medicine.

Certification↗

PubMed1996

Circulating tumor necrosis factor (TNF)-alpha and soluble TNF-alpha receptors in patients with Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is an inflammatory disorder that may implicate proinflammatory cytokines such as TNF-alpha in its pathogenesis. We determined serum levels of TNF-alpha and the specific antagonists sTNF-Rs p55 and p75 in 24 patients with GBS at days 1, 15 and 30 of hospitalization. Patients were in the progression phase of the disease at day 1, and in the recovery phase at day 30. They were classified as able to walk (stage A), confined to bed (B), or under assisted ventilation (C). All patients underwent plasma exchange within day 1-12. At day 1, TNF-alpha levels were elevated in 15/24 patients, and sTNF-Rs were elevated in 21/23. TNF-alpha levels had not decreased at day 15, and dropped at day 30 (p < 0.04), whereas sTNF-R p55 remained elevated at day 15 and day 30. The TNF-alpha/sTNF-Rs ratio, estimating active TNF-alpha unbound to sTNF-Rs, decreased from day 1 to day 30 (p < 0.05). A positive correlation was found between disease severity and sTNF-R serum levels (p < 0.01). In conclusion, elevated circulating sTNF-Rs assesses activation of the TNF-alpha system in almost all patients with GBS and correlates positively with disease severity. Drop of TNF-alpha contrasting with sustained elevation of sTNF-R p55 during recovery suggests that sTNF-R p55 may be important in the fading of the neural inflammatory effect of TNF-alpha in GBS.

Antibody Specificity↗

PubMed1996

Hopping and swimming in the leopard frog, Rana pipiens: I. Step cycles and kinematics.

This study presents a model for the step cycle patterns used during both hopping and swimming by the leopard frog, Rana pipiens. The two behaviors are essentially similar in movement pattern and in the ways they are modified from quadrupedal gaits. In hopping, there is marked hind limb extension throughout stance. The swing begins with a suspension equivalent to the leap that occurs in a galloping or bounding quadruped. Following suspension, as the frog descends from the apex of its leap, the hind limbs remain posterior and in line with the spine while they flex. Near the end of flexion, there is a rapid downward rotation of the hindquarters to bring the hind feet underneath the body. This movement utilizes the planted forelimb as a pivot. A similar pattern of movement occurs in swimming; the stance (propulsion) phase involves extension at all hind limb joints. The swing (recovery) phase begins with the hind feet fully extended and includes a protracted gliding phase, equivalent to the suspension in the hop. The hind limb then recovers to its initial position during a flexion phase. Since there is no landing and the hind limbs remain lateral rather than ventral to the pelvis, less flexion occurs in the spine or the limb joints. In both behaviors, the extensor muscles of hip (M. semimembranosus), knee (M. cruralis), and ankle (M. plantaris longus) achieve their longest lengths, when they likely can produce near maximal force, at the beginning of extension. All three muscles shorten during extension, but, because they are multiple-joint muscles, the amount of shortening is relatively small (approximately 15%). Hopping and swimming in frogs are comparable asymmetrical gaits with the same relative contact intervals (25% of stride). The step cycles in both gaits are modified from quadrupedal locomotion in the same ways: by 1) loss of knee and ankle extension toward the ground prior to landing (or end of flexion in swimming), 2) loss of a yield phase on landing (or end of flexion in swimming), and 3) inclusion of extended suspensions in both gaits.

Animals↗

PubMed1992

Electrogenic Na-independent HCO3 transport in OK cells.

We have shown previously that OK cells recover from an acid load in a medium nominally CO2-free by extruding H via a Na/H exchanger and a passive H-conductive pathway. In this work, the regulation of cell pH (pHi) was studied after addition or withdrawal of CO2/HCO3 (5% CO2, 95 mM HCO3, pH = 8) using the fluoroprobe BCECF. In the presence of Na and amiloride to inhibit Na/H exchange, the recovery of pHi after CO2 entry and CO2 exit were found to depend in part on HCO3 entry and exit, respectively. Efflux of H per se also contributed to restoring pHi after CO2 addition, whereas H influx may have played a smaller role to normalize pHi after CO2 removal. DIDS, 0.5 mM, significantly inhibited both recovery phases of pHi. Removal of Na failed to inhibit the recovery of pHi after CO2 addition and removal. Cl removal also failed to inhibit pHi recovery after CO2 removal. Cell depolarization in the presence of Na moderately stimulated the pHi recovery rate after CO2 addition whereas it markedly inhibited the normalization of pHi after CO2 removal. Cell depolarization in the absence of sodium had only a slight effect to increase pHi recovery after CO2 addition but markedly prevented the pHi recovery after CO2 removal. These results indicate that OK cells lack Na or Cl-dependent HCO3 transport systems. The OK cell possesses a novel stilbene-sensitive electrogenic HCO3 transport system that is involved in the regulation of cell pH.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed2005

Diabetes insipidus, secondary hypoadrenalism and hypothyroidism after traumatic brain injury: clinical implications.

Adequate ADH secretion, adrenal and thyroid functions are vital during the acute and post-acute phases of TBI. Deficiencies of these functions as a result of TBI are increasingly recognized. During the acute phase of TBI the incidence of severe DI is 2.9%; the incidence of less severe forms of DI is 21.6-26%. The development of DI seems to correlate with the severity of trauma. In most occasions DI is transient, but persisting DI may develop with an incidence of 6.9-7.5% amongst TBI victims. The assessment of the adequacy of adrenal function during the acute phase of TBI remains a diagnostic challenge. A few studies demonstrated an incidence of hypoadrenalism of 15-16% during the early phase of TBI. It should be noted that early hypoadrenalism may be due to either a structural damage at the level of the hypothalamo-pituitary unit or it may develop in the context of the so-called "relative adrenal insufficiency", a functional abnormality that is currently increasingly recognized during the course of severe illness. Secondary hypoadrenalism during the late phases of TBI appears with an incidence of 7.1-12.7%. The "low-T3 syndrome" compromises the assessment of thyroid function during the acute phase of TBI; the incidence of TSH insufficiency during the recovery phase varies widely between 1-21%. In summary, diabetes insipidus, secondary hypoadrenalism and hypothyroidism may develop in a small albeit significant proportion of patients during the course of TBI. Therefore, assessment of the integrity of ADH secretion, hypothalamic-pituitary adrenal (HPA) axis and thyroid axis is crucial to ensure survival and optimal rehabilitation of TBI patients.

Adrenal Insufficiency↗

PubMed1991

Clinical signs in severe Guillain-Barré syndrome: analysis of 63 patients.

Clinical data are presented of 63 artificially ventilated Guillain-Barré patients. About half of them had an antecedent event. In 57% the disease was heralded by sensory symptoms. The mean progressive phase lasted 12 days, the plateau 12 days and the recovery phase 568 days. In all patients one or more cranial nerves were involved, most often leading to facial palsy or difficulties in swallowing. Three-quarters of the patients had sensory signs, proprioceptive more often than superficial. Autonomic disturbances were common, especially hypertension and tachycardia. Twenty-two percent of the patients were severely confused in the first weeks of the disease. Laboratory examination showed atypical lymphocytes in the blood of 37% of patients and disturbed hepatic function tests in 79%. CSF protein level was elevated in all patients, with a mean value of 1.5 g/l.

Adolescent↗

PubMed1993

The induction of lipid peroxidation by E. coli lipopolysaccharide on rat hepatocytes as an important factor in the etiology of endotoxic liver damage.

Oxygen-derived radicals have been suggested to produce tissue injury during endotoxic shock by initiating lipid peroxidation. In order to investigate the induction of lipid peroxidation by Escherichia coli 0111:B4 lipopolysaccharide (LPS) on hepatocytes, malondialdehyde (MDA) and superoxide dismutase (SOD) activity have been evaluated in vivo and in vitro using two experimental models: rat liver after the establishment of endotoxic reversible shock, and cultured hepatocytes after treatment with LPS. Liver MDA levels were increased in vivo during the acute-phase of endotoxic shock, decreasing below control values in the recovery phase. An inverse pattern was obtained when SOD activity was measured, consistent with an active system of cellular protection. Similar results were obtained in vitro after treatment of cultured hepatocytes with LPS (50 micrograms/ml), thus indicating that a direct LPS cytotoxic effect on hepatocytes exits during the endotoxic process. The direct LPS interaction induced alterations in Ca2+ permeability of hepatocyte plasma membrane as detected by flow cytometry using the fluorescent probe Indo-1.

Animals↗

PubMed2000

Helper T cell and antibody responses to infection of CBA mice with Babesia microti.

Helper T cell cytokine and antibody responses were investigated in mice after infection with Babesia microti (King strain). Infection of CBA mice with 106 parasitized erythrocytes resulted in the development of a transitory high parasitaemia which peaked 14 days post infection (DPI), and was resolved at 24 DPI. Th1 responses were activated predominately during the acute phase (6-18 DPI) whereas Th2 responses predominated during the recovery phase (14-28 DPI) as detected by the reverse transcriptase polymerase chain reaction. Increased expression of Th1 cytokines was first detected at 6 DPI (IL-2) and 8 DPI (IFN-gamma) and their peak levels were reached at 12 DPI. After the peak levels were reached, they progressively declined and fell to baseline levels (22 DPI). Increased expression of Th2 cytokines (IL-4 and IL-10) first appeared at 14 DPI, peaked at 20 DPI and Th2 cytokine levels were elevated till the end of the study (28 DPI). Levels of serum IFN-gamma detected by a sandwich ELISA correlated well with IFN-gamma gene expression and were detectable at 8-18 DPI. IgM against B. microti was first detected in serum by ELISA at 4 DPI, and peaked at 10 DPI. The levels of IgM subsequently declined but remained positive at low titre till the end of study. IgG against B. microti was first detected at 8 DPI and peak levels were reached at 24 DPI and remained at that level until the end of study. The results of the present study show that Th1 cytokines predominated in the early inflammatory response and might be involved in control of levels of acute parasitaemia whereas the Th2-associated responses, including expression of IL-4 and IL-10 and the production of parasite-specific IgG, might be the functional means for the reduction and clearance of the parasite from the body. It was concluded that an effective vaccine against Babesia spp. should be designed to induce Th1 responses to maintain the parasitaemia at unfulminating levels and also maintain Th2 responses to clear the parasite from the body.

Animals↗

PubMedDate not supplied

[Acute leukemia after aplastic anemia in childhood].

Only few reports about ALL after aplastic anaemias in childhood exist. It remains still unclear which immunophenotypes of the leukaemias must be expected thereafter. Here it is reported about two children with quite different immunophenotypes of the leukaemic cells. In the first one the most common type was found, the constellation of a c-ALL, whereas in the other the precise classification was impossible at all. Myeloic and T-cell markers were present at the same time. This form of leukaemia was not influenced therapeutically in a sufficient manner. The patient died after recovery phases of only short duration. After aplastic anaemias with fast recovery by prednisolone ALL of different constellation has to be expected. Therefore the antileukaemic treatment immediately after recovery of the aplastic anaemia should be taken into consideration.

Anemia, Aplastic↗

PubMed1983

Asynchronous transmural perfusion during coronary reactive hyperaemia.

Dynamic variation in the transmural distribution of myocardial blood flow was studied in 36 anaesthetised open-chest dogs during the course of the reactive hyperaemia following a 90 s occlusion of the left anterior descending coronary artery. Myocardial blood flow was estimated from tissue uptake of radioactive microspheres, 9 to 10 micrometers in diameter. Endo/epi flow ratios indicated asynchronous reactive hyperaemic responses across the free wall of the left ventricle; flow was preferentially to subepicardium during the initial (pre-peak) phase, whereas flow was preferentially to subendocardium during the prolonged recovery phase. The mean of endo/epi flow ratios obtained during the peak plateau of coronary artery reactive hyperaemia indicated essentially uniform transmural distribution. However, further analysis indicated that this was result of ratios less than 1 early in the peak plateau and ratios greater than 1 late in the peak plateau. Reversal of the endo/epi flow ratios due to regionally asynchronous maximum flows is responsible for the prolonged plateau at peak flow observed in measurements of coronary artery reactive hyperaemia. Transmural asynchrony of peak reactive hyperaemic flow may also account for underestimates in vasodilator capability of ischaemia based on measurements of either coronary artery or myocardial blood flow.

Animals↗

PubMed1985

Effect of complement on the viscoelastic properties of human erythrocyte membrane.

Using the micropipette technique, we examined the viscoelastic properties of the red blood cell (RBC) membrane which had been strongly coated with various components of complement (primary C3b, C3d, C4b, C4d) in vitro. The membrane elastic modulus (E), the viscosity index of the initial rapid phase of deformation (eta D1), the viscosity of the later slow phase of deformation (eta D2) and the viscosity of the recovery phase (eta R) were determined. Compared to control non-complement coated RBCs, RBCs coated with C3d, either alone or with other complement components, showed significant increase in the values for elasticity and viscosities. Thus C3d fixation resulted in decreased membrane deformability. Changes in membrane viscoelasticity due to bound C3d were not enhanced by bound C4b, C4d, C5, factor Bb or p; presence on RBC membrane of the latter two complement components may partially reverse the effect of C3d fixation. Lipid fluidity of RBC membrane, examined by fluorescence depolarization, increased with fixation of all complement components except C5. These complement-induced changes in membrane viscoelastic properties have potential pathophysiological and clinical implications. The data suggest that extravascular sequestration of human RBCs may be explained in part by increased membrane rigidity resulting from C3d fixation.

Complement C3↗

PubMed1980

Photostress recovery times in cases of central serous retinopathy.

Photostress recovery times were measured in 50 normal individuals in the age group 20-50 years and in 27 patients who had developed central serous retinopathy. A flash generator of a commercially available fundus camera was used to provide the appropriate stimulus. The results showed that photostress recovery times were grossly abnormal in patients with central serous retinopathy for the first few weeks after the onset of symptoms, but gradually returned to normal values by 5 months and remained so thereafter. In a few patients during the recovery phase a transient paradoxical response was noted, whereby the photostress recovery times became less than in the unaffected control eye.It appears that the use of a fundus camera to provide photostress stimulus has merit because the light source is subject only to slight variation in intensity, standardization of responses is possible and the technique can be employed on patients about to have fluorescein angiographic studies for diagnostic or documentation purposes.

Adult↗