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C Metz

Publications and source records attributed to C Metz.

At least 55 records · Page 3Linked to original sources

Jugular bulb monitoring of cerebral oxygen metabolism in severe head injury: accuracy of unilateral measurements.

To investigate the accuracy of unilateral jugularvenous monitoring, we performed bilateral jugularvenous monitoring in 22 comatose head injured patients. Fiberoptic catheters were placed upstream in both internal jugular veins and advanced into the jugular bulbs. Arterial and bilateral jugularvenous blood samples were obtained simultaneously for in vitro determination of jugularvenous oxygen saturation (SJO2), arterial minus jugularvenous lactate content difference (AJDL) and modified lactate-oxygen-index (mLOI). Ischemia was assumed, if one of the following pathologies occurred at least unilaterally: SJO2 < 55%, AJDL < -0.37 mmol/L, mLOI > 0.08. The mean and maximum bilateral SJO2 differences varied between 1.4% to 21.0%, and 8.1% to 44.3% respectively. The bias and limits of agreement (mean differences +/- 2SD) between paired samples were -0.4% +/- 12.8%. Regarding AJDL bias and limits of agreement were -0.01 mmol/L +/- 0.18 mmol/L. At best 87% of defined ischemic events could be evaluated by monitoring at the side of predominant lesion or, in diffuse injuries, at the side of the larger jugular foramen in CT scan (CT approach). We conclude, due to the wide limits of agreement in bilateral SJO2 and AJDL the reliability of unilateral jugularvenous monitoring in patients with intracranial pathology is questionable. For diagnosing ischemia the CT approach has the highest sensitivity and is therefore recommended.

Brain↗

Acute effects of continuous rotational therapy on ventilation-perfusion inequality in lung injury.

OBJECTIVE: To investigate ventilation-perfusion (VA/Q) relationships, during continuous axial rotation and in the supine position, in patients with acute lung injury (ALI) using the multiple inert gas elimination technique. DESIGN: Prospective investigation. SETTING: Eighteen-bed intensive care unit in a university hospital. PATIENTS AND INTERVENTIONS: Ten patients with ALI (PaO2/FIO2 ratio < 300 mm Hg) were mechanically ventilated in a pressure controlled mode and placed on a kinetic treatment table. MEASUREMENTS AND RESULTS: Distributions of VA/Q were determined 1) during rotation (after a period of 20 min) and 2) after a resting period of 20 min in the supine position. During axial rotation, intrapulmonary shunt (19.1 +/- 15% of cardiac output) was significantly reduced in comparison with when in the supine position (23 +/- 14%, p < 0.05), areas with "low" VA/Q were not affected by the positioning maneuver. General VA/Q mismatch (logarithmic distribution of pulmonary blood flow) was decreased during rotation (0.87 +/- 0.37) in comparison with when the patient was in the supine position (0.93 +/- 0.37, p < 0.05). Arterial oxygenation was significantly improved during continuous rotation (PaO2/FIO2 = 217 +/- 137 mm Hg) as compared with in the supine position (PaO2/FIO2 = 174 +/- 82 mm Hg, p < 0.05). The positive response of the continuous rotation on arterial oxygenation was only demonstrated in patients with a Murray Score of 2.5 or less, indicating a "mild to moderate" lung injury, while in patients presenting with progressive ARDS (Murray Score > 2.5), the acute positive response was limited. CONCLUSIONS: Continuous axial rotation might be a method for an acute reduction of VA/Q mismatch in patients with mild to moderate ALI, but this technique is not effective in late or progressive ARDS. Further studies including a large data collection are needed.

Adult↗

Mouse glycosylphosphatidylinositol-specific phospholipase D (Gpld1) characterization.

Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) is an 110-kDa monomeric protein found in the circulation that is capable of degrading the GPI anchor utilized by dozens of cell-surface proteins in the presence of detergent. This protein is relatively abundant (5-10 microgram/ml in human serum), yet its sites of synthesis, gene structure, and overall function are unclear. It is our purpose to use the mouse system to determine its putative roles in lipid transport, pathogen control, and diabetes. We have isolated murine full-length cDNA for GPI-PLD from a pancreatic alpha cell library. The deduced amino acid sequence shows 74% homology to bovine and human GPI-PLD. There is a single structural gene (Gpld1) mapping to mouse Chromosome (Chr) 13, and among nine tissues, liver showed the greatest abundance of GPI-PLD mRNA. Genetic differences in serum GPI-PLD activity were seen among four mouse strains, and no correlation was seen between GPI-PLD activity and circulating levels of high density lipoproteins in these mice. This is the first report of map position and genetic regulation for Gpld1. This information will enable us to further study the expression and function of GPI-PLD in normal and pathological conditions.

Amino Acid Sequence↗

Clinical evaluation of the InnerSpace fibreoptic intracranial pressure monitoring device.

OBJECTIVE: The aim of this study is the clinical evaluation of the intraparenchymal ICP monitor InnerSpace OPX 100. METHODS: Sixty-four Inner Space OPX 100 transducers in 51 patients with severe head injury (42), intracranial spontaneous bleeding (6) or hypoxia (3) were studied. The transducer was placed in the frontal white matter. Thirty-nine patients received one catheter, eleven patients two catheters and one patient three catheters. The study period ranged from 10 hours-25 days; total study time was 421.5 days (mean duration 6.6 days). RESULTS: In nine cases (14.1%) an inadequate location of the ICP transducer was found, but the accuracy of the measurement was not influenced. Dislocation of the transducer occurred in eight cases (12.5%) due to inadequate handling. A failed transducer was observed in four cases (6.3%) because of a damaged optical fibre (1) or inadequate handling (3). In one patient (1.9%) a minor local infection developed. In eleven cases (17%) a haematoma around the ICP sensor was observed. Six haematomas were small; five haematomas were larger than 1 cm in diameter. In two patients a large frontal haematoma developed after exchange of the transducer. Operative evacuation was necessary in both cases. Zero shift was below 2 mmHg in all catheters. CONCLUSION: It is concluded that the InnerSpace intraparenchymal ICP monitor is a reliable device: the rate of catheter related intracerebral haematomas, however, is not acceptable. This could be improved by a better fixation of the catheter in the burr hole in order to avoid micromovements of the transducer.

Adult↗

Local regulation of macrophage subsets in the adult rat testis: examination of the roles of the seminiferous tubules, testosterone, and macrophage-migration inhibitory factor.

In the adult rat testis, macrophages belong to one of two subsets differentiated by expression or lack of expression of the resident macrophage surface antigen recognized by monoclonal antibody ED2. Local regulation of the testicular macrophage subsets was investigated in normal and 4-wk experimentally cryptorchid adult rats with and without s.c. testosterone implants (T-implants). Macrophage subsets ED2(+) (resident-type) and ED2(-) (monocyte-like) were identified immunohistochemically and counted in perfusion-fixed frozen testis sections. Depletion of the spermatogenic cells by cryptorchidism had no effect on testicular macrophage numbers. Inhibition of Leydig cell and seminiferous tubule function by low-dose (3 cm) T-implants caused a 40% reduction in ED2(+) resident macrophages in both scrotal and abdominal testes. High-dose (24 cm) T-implants, which inhibit Leydig cell function while maintaining normal seminiferous tubule function, also reduced the number of resident macrophages by approximately 40%, although this reduction was at least partially prevented in the abdominal testes. In the scrotal testis only, the ED2(-) monocyte/macrophage subset was significantly reduced in number by low-dose, but not high-dose, T-implants. The concentration of the Leydig cell-secreted cytokine macrophage-migration inhibitory factor (MIF) in testicular fluid was reduced by cryptorchidism, but not by the T-implants. When data from all experimental groups were combined, ED2(+) resident macrophage numbers showed a significant positive correlation with parameters of Leydig cell function (serum LH and testicular testosterone levels) but a negative correlation with MIF levels. This study indicates that Leydig cells regulate testicular macrophage numbers directly, rather than via an effect upon the seminiferous epithelium, in the adult rat testis. The data also suggest that testosterone and MIF play only a minor role, if any, in this regulation.

Animals↗

Monitoring of cerebral oxygen metabolism in the jugular bulb: reliability of unilateral measurements in severe head injury.

To investigate the reliability of unilateral jugular venous monitoring and to determine the appropriate side, we performed bilateral jugular venous monitoring in 22 head-injured patients. Fiberoptic catheters were placed in both jugular bulbs. Arterial and bilateral jugular venous blood samples were obtained simultaneously for in vitro determination of jugular venous oxygen saturation (SJO2), arterial minus jugular venous lactate content difference (AJDL), and modified lactate-oxygen index (mLOI). Ischemia was assumed if one of the following pathologic values occurred at least unilaterally: SJO2 <54%, AJDL <-0.37 mmol/L, mLOI >0.08. The sensitivity of calculated unilateral monitoring in detecting ischemia was evaluated by comparing the incidence detected unilaterally with that disclosed bilaterally. The mean and maximum bilateral SJO2 differences varied between 1.4% and 21.0%, and 8.1% and 44.3%, respectively. The bias and limits of agreement (mean differences +/- 2 SD) between paired samples were 0.4% +/- 12.8%. There was no significant variation in bilateral SJO2 differences with time. Decreasing cerebral perfusion pressure (r = -0.559, P < 0.001) and arterial PCO2 (r = -0.342, P < 0.001) were associated with increasing bilateral SJO2 differences. Regarding AJDL, the maximum bilateral differences varied between 0.04 mmol/L and 1.52 mmol/L. The bias and limits of agreement were -0.01 +/- 0.18 mmol/L. At best, 87% of ischemic events were disclosed by monitoring on the side of predominant lesion or, in diffuse injuries, on the side of the larger jugular foramen (computed tomographic [CT] approach). We conclude that in severe head injury, even calculated unilateral jugular venous monitoring has an unpredictable risk for misleading or missing data. Therefore, the reliability of unilateral jugular venous monitoring appears suspicious. For diagnosing ischemia the CT approach is recommended.

Adult↗

S-100 serum levels after minor and major head injury.

BACKGROUND: S-100, a protein of astroglial cells, is described as a marker for central nervous system damage. The aim of this study was to evaluate whether the marker could give information about the severity and possibility of functional recovery after minor and severe head injury. METHODS: Thirty patients after severe head injury (Glasgow Coma Scale score < 9) and 11 patients after minor head injury (Glasgow Coma Scale score > 12) were included. In each case, blood samples were drawn within 6 hours after injury. Outcome was estimated at hospital discharge using the Glasgow Outcome Scale. RESULTS: All patients who sustained minor head injury had reached a favorable outcome by the time they were discharged from the hospital. Their mean S-100 serum level was 0.35 microg/L. Patients who sustained severe head injury and were classified as having an unfavorable outcome (31%) showed a mean serum concentration of 4.9 microg/L, whereas patients classified as having a favorable outcome (69%) had a mean S-100 level of 1.2 microg/L. All groups differed significantly (p < 0.05). CONCLUSION: S-100 appears to be a promising marker for the severity of head injury and neuronal damage.

Adolescent↗

Filarial nematode parasites secrete a homologue of the human cytokine macrophage migration inhibitory factor.

Filarial nematode parasites establish long-term chronic infections in the context of an antiparasite immunity that is strongly biased toward a Th2 response. The mechanisms that lead to this Th2 bias toward filarial antigens are not clear, but one possibility is that the parasites produce molecules that have the capacity to proactively modify their immunological environment. Here we report that filarial parasites of humans secrete a homologue of the human proinflammatory cytokine macrophage migration inhibitory factor (MIF) that has the capability of modifying the activity of human monocytes/macrophages. A cDNA clone isolated from a Brugia malayi infective-stage larva expression library encoded a 12.5-kDa protein product (Bm-MIF) with 42% identity to human and murine MIF. MIF homologues were also found to be expressed in the related filarial species Wuchereria bancrofti and Onchocerca volvulus. Bm-mif was transcribed by adult and larval parasites, and the protein product was found in somatic extracts and in the parasite's excretory-secretory products. Immunohistocytochemistry revealed that Bm-MIF was localized to cells of the hypodermis/lateral chord, the uterine wall, and larvae developing in utero. Unexpectedly, the activities of recombinant Bm-MIF and human MIF on human monocytes/macrophages were found to be similar. When placed with monocytes/macrophages in a cell migration assay, Bm-MIF inhibited random migration. When placed away from cells, Bm-MIF induced an increase in monocyte/macrophage migration that was specifically inhibited by neutralizing anti-Bm-MIF antibodies. Bm-MIF is the first demonstration that helminth parasites produce cytokine homologues that have the potential to modify host immune responses to promote parasite survival.

Amino Acid Sequence↗

Reversal of established rat crescentic glomerulonephritis by blockade of macrophage migration inhibitory factor (MIF): potential role of MIF in regulating glucocorticoid production.

Macrophage migration inhibitory factor (MIF) is a potent pro-inflammatory cytokine that also counter-regulates glucocorticoid action. We investigated whether immunoneutralization of MIF could reverse established experimental crescentic glomerulonephritis and if this treatment could modulate endogenous glucocorticoid levels. Accelerated anti-GBM glomerulonephritis was induced in six littermate pairs of rats. Once crescentic disease was established on day 7, one animal in each pair was given a daily injection of neutralizing anti-MIF antibody (Ab) or irrelevant isotype control Ab for 14 days and then killed on day 21. In addition, a group of 6 animals was killed on day 7 of disease without any treatment. Animals receiving the control Ab exhibited a rapidly progressive glomerulonephritis with severe renal injury (proteinuria), loss of renal function (creatinine clearance), anemia, and marked histologic damage (including glomerular crescent formation), compared with animals killed on day 7 without treatment. In contrast, anti-MIF Ab treatment partially reversed the disease by restoring normal renal function and reducing histological damage compared with untreated animals killed on day 7 (p < 0.05). Interestingly, anti-MIF Ab treatment also prevented severe anemia (p < 0.05). Reversal of disease was associated with a significant reduction in leukocyte infiltration and activation and renal interleukin-1 (IL-1) production. Importantly, anti-MIF Ab treatment caused a significant increase in endogenous serum corticosterone levels, which correlated with the reversal of disease parameters. In conclusion, this study has demonstrated that blocking MIF activity can partially reverse established crescentic glomerulonephritis and suggests that MIF operates by both enhancing the cellular immune response and suppressing the endogenous anti-inflammatory glucocorticoid response.

Animals↗

Scintigraphic screening prior to visceral arteriography in acute lower gastrointestinal bleeding.

UNLABELLED: We evaluated the effect on the diagnostic yield of visceral arteriography in patients with acute gastrointestinal bleeding of a protocol requiring a positive 99mTc-red blood cell scintiscan before the performance of arteriography (scintigraphic screening). METHODS: A retrospective review was conducted of 249 scintiscans and 271 arteriograms obtained over 99 mo, with scintigraphic screening implemented during the final 18 mo. RESULTS: Before the implementation of scintigraphic screening, arteriograms detected bleeding at a rate of 22%. After its implementation, 53% of the arteriograms detected bleeding. This represented a statistically significant increase (0.53 versus 0.22, p = 0.015). CONCLUSION: Scintigraphic screening appears to increase by a factor of 2.4 the diagnostic yield of arteriography by screening out patients who are not actively bleeding at the time of the examination, thus sparing them the risks and costs of a nondiagnostic invasive study.

Acute Disease↗

The pathogenic role of macrophage migration inhibitory factor in immunologically induced kidney disease in the rat.

Macrophage migration inhibitory factor (MIF) plays a pivotal role in the inflammatory response in endotoxemia and in the delayed-type hypersensitivity response, but its potential as a regulator of immunologically induced disease is unknown. We have addressed this issue by administering a neutralizing anti-MIF antibody in a rat model of immunologically induced crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Six individual experiments using paired inbred littermates were performed. Rats were primed with rabbit immunoglobulin on day -5 and then injection with rabbit anti-rat GBM serum on day 0. Pairs of animals were treated with anti-MIF or a control monoclonal antibody from the time of anti-GBM serum administration until being killed 14 d later. Control antibody-treated animals developed severe proteinuria and renal function impairment with severe histological damage due to marked leukocytic infiltration and activation within the kidney. In contrast, anti-MIF treatment substantially reduced proteinuria, prevented the loss of renal function, significantly reduced histological damage including glomerular crescent formation, and substantially inhibited renal leukocytic infiltration and activation (all P <0.001 compared with control treatment). Inhibition of renal disease by anti-MIF treatment was attributed to preventing the marked upregulation of interleukin-1beta, leukocyte adhesion molecules including intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and inducible nitric oxide synthase expression seen in the control antibody-treated animals. This inhibition of progressive renal injury was mirrored by the complete suppression of the skin delayed-type hypersensitivity response to the challenge antigen (rabbit IgG). Interestingly, anti-MIF treatment did not effect the secondary antibody response or immune deposition within the kidney, indicating that MIF participates in cellular-based immunity in this primed macrophage-dependent anti-GBM glomerulonephritis. In conclusion, this study has demonstrated a key regulatory role for MIF in the pathogenesis of immunologically induced kidney disease. These results argue that blocking MIF activity may be of benefit in the treatment of human rapidly progressive glomerulonephritis, and suggest that MIF may be important in immune-mediated disease generally.

Animals↗

Comparison of serial S-100 and NSE serum measurements after severe head injury.

We investigated the time course of neuron specific enolase (NSE) and S-100 protein after severe head injury in correlation to outcome. We included 30 patients (GCS < 9), who had been admitted within 5 hours after injury, in a prospective study. Blood samples were taken on admission, 6, 12, and 24 hours and every 24 hours up to the fifth day after injury. The outcome was estimated on discharge using the Glasgow Outcome Scale. 70% reached a good outcome. All concentrations of NSE and 83% of the S-100 samples were elevated concerning the first probe (30.2 micrograms/l NSE mean and 2.6 micrograms/l S-100 mean). Patients with bad outcome had an NSE concentration of 38 micrograms/l (mean) compared with 26.9 micrograms/l (mean) in patients with good outcome. Patients with bad outcome had an S-100 concentration of 4.9 micrograms/l (mean) compared with 1.7 micrograms/l (mean) in patients with good outcome (p < 0.05). The mean values of NSE and S-100 decreased during the first 5 days. Four patients with increasing intracranial pressure showed a quick increasing concentration of NSE, in two patients the S-100 level showed a slower rise. The NSE serum levels did not correlate with intracranial pressure values. Our results show that the first serum concentration of S-100 seems to be predictive for outcome after severe head injury.

Adolescent↗

Comparison of changes in cerebral blood flow and cerebral oxygen saturation measured by near infrared spectroscopy (NIRS) after acetazolamide.

The present study compares the change of cerebral blood flow and HbO2 measured by near-infrared spectroscopy (NIRS) after administration of 1000 mg acetazolamide intravenously. CBF studies in 21 patients with ischaemic cerebrovascular disease were performed routinely with the 133Xenon technique. Additionally the local HbO2 was recorded by NIRS. A rest study was followed by a second study after the administration of 1000 mg acetazolamide. In 18 patients we observed an increase of 30.8% of CBF and 4.7% of HbO2, 3 patients showed a decrease of CBF and 2 patients a simultaneous decrease of HbO2. We did not find a correlation between the absolute values of CBF and HbO2 at rest or after stimulation. However, a positive correlation (r = 0.71, p < 0.05) between the change of CBF and HbO2 could be detected. Assuming a threshold value of normal CBF reactivity of 30% and 4% HbO2 reactivity we found for NIRS a sensitivity of 0.88 and a specificity of 0.75. The results demonstrate that changes of CBF can be detected with NIRS and the algorithm of the used monitor is able to calculate the intracranial part of the signal. So, NIRS can be used as non-invasive screening method to test the cerebrovascular reserve capacity.

Acetazolamide↗

Relationship of Beck Depression Inventory factors to depression among adolescents.

Beck Depression Inventory (BDI) scores of 328 adolescents referred to a depression clinic were factor analyzed to test the discriminant validity of each factor. Three of the four factors (Negative Self Attitude. Performance Difficulty, and Somatic Symptoms) discriminated depressed adolescents from those with a behavior disorder or no diagnosis; the Negative Self Attitude and Performance Difficulty factors also discriminated depressed from anxious adolescents. The fourth factor, Physical Worry, failed to discriminate diagnostic groups. Diagnostic efficiency statistics are reported for both the BDI and for items comprising the 13-item BDI Short Form. Results indicate the BDI is a valid screening tool for adolescent depression in a clinical setting, regardless of the presence of comorbid conditions.

Adolescent↗

[Transitory hyperinsulinism with hypoglycemia in asphyxia neonatorum].

BACKGROUND: Hypoglycemia is a well-known complication in neonates small for gestational age and in those with diabetic mothers. Birth asphyxiated infants can develop severe hypoglycemia due to reduced glycogen stores. CASE REPORTS: The first patient was born at 41 weeks, weighing 3,780 g by emergency cesarean section because of fetal distress. He developed a pneumothorax and hypoglycemia. He was given glucose infusion (at day 4: 20 mg/kg/d). Hyperinsulinism was confirmed: blood levels at 18.3 mU/L on day 1 and 11.7 mU/L on day 2. The infusion rate was gradually decreased. The second patient was born at 39 weeks, weighing 2,780 g by emergency cesarean section because of fetal distress. She needed glucose infusion (24 g/kg/d) because of hypoglycemia with hyperinsulinism (12.8 mU/L on day 2 and 11.7 mU/L on day 3). After 5 days, the infusion of glucose was replaced by oral feeding only. CONCLUSION: Transient hypoglycemia in asphyxiated newborn infants with hyperinsulinism must be considered even when hypoglycemia may be difficult to prove.

Asphyxia Neonatorum↗

[Neonatal detection of central hypothyroidism].

BACKGROUND: Congenital hypothyroidism is very rare compared to primary hypothyroidism. Its early diagnosis may escape neonatal mass screening using TSH assay. CASE REPORT: Anthony was born at 37 weeks, weighing 3,060 g. He presented with hypotony, jaundice, tongue protrusion evoking congenital hypothyroidism. Thyroid function tests favored hypothyroidism central in origin, while the systematic neonatal screening was normal. CONCLUSION: Clinical signs of congenital hypothyroidism must lead to more specific tests when neonatal screening is normal.

Congenital Hypothyroidism↗

Dynamic changes of cerebral oxygenation measured by brain tissue oxygen pressure and near infrared spectroscopy.

The aim of this study was to find out whether a correlation exists between changes in brain tissue oxygen pressure (ti-pO2) and hemoglobin oxygenation (HbO2) measured by near-infrared spectroscopy. We studied 10 patients with severe head injury. A ti-pO2 monitoring device was introduced in the frontal white matter as soon as possible after administration. Additionally a NIRS sensor was placed at the forehead. All data were recorded simultaneously. Changes of the ti-pO2 curve were defined as events with the following criteria: > 10% change from the baseline value, > 3 min duration, clearly not an artifact. 137 events were found with a mean change of ti-pO2 of 8.3 +/- 10.2 mmHg. In 77.4% we observed a corresponding change of the HbO2. In 7 patients we found a good correlation (r > 0.7) between change ti-pO2 and change HbO2. In 3 patients the correlation was poor. The reason for poor correlation might be poor signal quality of the NIRS sensor or inhomogenous distribution of ischemic areas in the whole brain. We conclude that under the condition of a stable NIRS signal and a diffuse brain lesion, changes of ti-pO2 are well reflected by NIRS.

Adult↗