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At least 379 records · Page 21Linked to original sources
PubMed1984

[Coma and praecoma diabeticum. Physiopathology, clinical aspects and therapy].

The diabetic coma is characterized by fundamental metabolic changes. Apart from the hyperglycaemia, exsiccosis and the disturbed electrolyte metabolism are considerable factors contributing to the coma. The treatment of diabetic coma puts great demands on the doctors, since the prognosis can only be improved by systematic and correct intervention. A fast filling up of the volume and a specific electrolyte (potassium) substitution are very important. In cases of ketoacidotic diabetic coma the acidosis must be carefully balanced, whereby the "rest-acidosis" up to pH 7.1 can be tolerated. The administration of insulin can only begin, when the volume and electrolyte substitution is guaranteed, otherwise dangerous insulin-induced hypokalaemia is unavoidable. By no means may the first treatment for the insulinisation be carried out ambulatory.

Bicarbonates↗
PubMed1981

[Prognostic value of EEG in acute posttraumatic coma (author's transl)].

To evaluate the prognostic power of a single EEG-record, the recordings of 50 patients with posttraumatic coma performed within 48 hours after the injury were compared with the outcome after 6 months. A 5-point scale comprising 2 EEG-patterns being notorious for their dismal prognostic significance (suppression bursts, alpha-coma) and changes of vigilance were used as a mean of visual assessment of the recordings. In 24 out of the 28 patients with a bad outcome, the EEG had shown the patterns of category I, II and III (suppression bursts, alpha coma, no changes of vigilance). Of the 22 patients with a good outcome, the EEG had been classified as IV or V (clearly discernible changes of vigilance, sleep patterns). Further findings of particular dismal prognostic significance were focal epileptic discharges, as 9 out of the 11 patients with this EEG pattern had not survived the posttraumatic coma for more than 6 months.

Adolescent↗
PubMed1982

Prognosis after cardiac arrest based on age and duration of coma.

In an attempt to determine the relation between duration of coma and neurologic recovery following cardiac resuscitation 163 survivors of cardiac arrest from Winnipeg, Manitoba and Aarhus, Denmark were studied. The age of the patients did not influence the outcome. Of the 153 patients who had awakened from the coma within 24 hours, only 11 suffered brain damage, compared with all of the 10 patients who wakened after 24 hours. The three who wakened after 72 hours had severe brain damage and required permanent care in an institution. It was concluded that recovery of communicative brain function is unlikely if coma persists longer than 72 hours after cardiac arrest and that full recovery cannot be expected after 24 hours of coma.

Adult↗
PubMed1993

[Conscious, unconscious and not conscious in coma].

In this work, the relation between the consciousness and the unconsciousness was studied in patients presenting a neurosurgical coma state. The study includes 29 patients with clinical observations during their hospitalisation period and a follow up for one year after the emergence from the state of coma. The psychoanalytic methods were used, taking in consideration the emotional and personal history of each patient. We attempted to demonstrate the persistence of the unconscious psychic life during coma and the early period after awakening from the coma. In addition, we felt the existence of a sort of direct confrontation with the unconscious psychic life in some patients emerging from a comatose state. The question is also what are the effects of such experience and how would they affect the life of the patients in the future?

Coma↗
PubMed1994

[Intracranial hypertension in severe diabetic ketoacidosis with coma. Two cases].

We observed two cases of severe diabetic ketoacidosis with coma and shock. In one case, coma was present at admission and in the second occurred within 15 hours. In both cases, intracranial hypertension was confirmed with an extradural captor. These findings are in agreement with observations of brain oedema in diabetic ketoacidosis with coma. Clinical data suggest that brain oedema may occur after a latency period but that clinical expression is much more rare, perhaps favoured by treatment (excessive rehydratation, alkalinization, too sharp drop in blood glucose level). In our cases, despite major fluid infusion, shock persisted requiring norepinephrine. This shock could have been the expression of the severe ketoacidosis or have resulted from an underlying infection. In case of sudden onset coma, a regularly encountered manifestation of brain oedema, respiratory assistance and mannitol infusion must be instituted rapidly. With this type of management, it should be possible to improve the severe prognosis of brain oedema in diabetic ketoacidosis.

Blood Glucose↗
PubMed1993

[Use of the Glasgow Coma Scale in pediatric craniocerebral trauma].

Over five years the applicability of a modified Glasgow Coma Scale was analysed in 38 children (mean age 7.2 +/- 3.8 years) with head and associated injuries (47.4%). The score was estimated after the accident and in the course of intensive therapy. At the beginning of the treatment on the intensive care unit, the cases were staged according to the severity of the head injuries (Glasgow Coma Scale: 4-8, 9-12 and 13-19 points). At the stage evaluated as between 4 and 8 points, 50% of the patients died and the survivors were ventilated (11.7 +/- 10.7 days) and intensively treated (45.7 +/- 31.5 days). All patients had had neurological damage. Additional injuries worsened the prognosis in the acute phase. 42.9% of the patients received intracranial pressure monitoring. In the patients between 9 and 12 points, the time of ventilation (3.7 +/- 2.9 days) and of intensive therapy (19.5 +/- 13.3 days) decreased. Over 13 points, all patients had a shorter duration of treatment (10.8 +/- 8.8 days) and a quick and good recovery. The Glasgow Coma Scale has the advantage of an examination with a quantitative analysis and resulting effective diagnostic and therapeutic measures. Even the inexperienced physician can use the Glasgow Coma Scale with success at the site of the accident.

Adolescent↗
PubMed1997

Attempt to establish a classification of patients suffering from coma and admitted to a hospital structure for short or medium term treatment: medical aspects and costs of hospital care.

We dispose of a database, constituted between 1987 and 1993, containing medical and cost information concerning 515 patients suffering from coma and admitted, after a period of resuscitation, to a French hospital establishment--Etablissement Hélio-Marin of Berck-sur-Mer (EHMB)--for short and medium term treatment, between 1974 and 1986. From this base, which contains demographic and clinical data (age, sex, condition upon admission, duration of consciousness disorders, Glasgow Outcome Scale (GOS) upon discharge) we devised a hierarchical classification analysis following a factorial analysis of multiple correspondences, on 2 sets: a sample of 515 patients (all causes of coma being merged) and a sample of 266 patients suffering from brain injuries. Four groups were determined for each typology. These groups were first described on the basis of the variables used for their construction, and later by considering other available variables: origin of coma, duration of stay at EHMB, future evolution of patients and cost of treatment (cost of specific care, average daily cost, total cost of hospitalization). Thus, typical clinical situations were identified in each classification, depending on age of patient, origin of coma and condition upon admission. These situations led to extremely different treatment costs (ratio from 1 to 5 in the general typology and 1 to 2.85 in the classification of brain injuries.

Adult↗
PubMed1976

Treatment of diabetic coma with low-dose injections of insulin.

Twenty-one patients in severe diabetic coma were treated with small doses of insulin at a rate of 4.1 units per hour (total dose about 100 units per 24 hours). Using single doses of 4 to 10 units by the intravenous or intramuscular routes the fall of blood glucose was steady in all cases. In the treatment of diabetic coma this regimen of insulin administration has proved simple, safe and effective since 1946. Main dangers during recompensation of diabetic coma are: hypovolaemia with oliguria -- anuria, dysequilibrium syndrome with cerebral edema and hypokalaemia. Therefore early intensive and adequate intravenous fluid and electrolyte replacement is the most important part of treatment. Most of the cases in this study were undiagnosed diabetics (14) and elderly patients (9). Three patients older than 65 years and a 56-year old diabetic died. In this context the most important aspects of treatment to avoid death are: prevention of diabetic coma and adequate fluid and electrolyte replacement especially in geriatric patients.

Adolescent↗
PubMed1989

[Functional neurologic studies in the diagnosis of coma].

Despite the development of medical imaging, functional exploration of the central nervous system by means of EEG and evoked potentials still plays an important role in the diagnosis and monitoring of coma. Together with clinical examination, these techniques contribute to the assessment of coma depth and inform, sometimes earlier than clinical signs, on the course of the coma. Finally, the data supplied by paraclinical explorations have a diagnostic value in cases of acute encephalitis, dysmetabolic diseases, drug poisoning or severe cerebral anoxia.

Coma↗
PubMed1982

Histopatological findings of the liver before and during hepatic coma in fulminant hepatitis.

The histopathological findings of the liver taken by needle biopsy before and during hepatic coma of fulminant hepatitis were studied in 3 patients; two died and one survived. In the first fatal case, massive hepatic necrosis was already present 7 days before the development of hepatic coma. In the second fatal case, submassive hepatic necrosis was seen during coma grade IV. In both cases, histological findings of the biopsy liver specimens were in accord with those of the autopsied liver. In the third survived case, diffuse degeneration and multilobular liver cell necrosis were found on the biopsy specimen taken immediately after the development of hepatic coma, grade IV.

Adolescent↗
PubMed1975

Methionine-induced hepatic coma in dogs.

Oral methionine is noncomatogenic in normal dogs, but it is consistently comatogenic in dogs with portacaval shunts in the presence of elevated ammonia levels. Such action appears to be enhanced by the ammonia itself, since relatively small doses of oral methionine can induce coma when baseline levels of ammonia are above 1,000 mug/100 ml; much higher doses are nesessary for near normal ammonemia. The methionine-induced coma closely reproduces the clinical and electroencephalographic picture of coma in other canine models. Oral methionine does not significantly increase the ammonia levels, but its action is probably mediated by the release of methanethiol (and other less active compounds) from the bowel. Methanethiol levels tend to increase in proportion to the amount of methionine administered, and its comatogenic action may be amplified, up to one hundredfold, by high ammonia levels. Methanethiol levels in comatose patients and the concept of the synergistic effect with ammonia may lead to a clearer understanding of certain enterogenous and dietetic forms of hepatic encephalopathy in cirrhotic patients. The lowering of ammonia levels by hemodialysis or methanethiol levels by activated charcoal hemoperfusion, as attempts to reverse such forms of coma, warrants further investigation.

Administration, Oral↗
PubMed1985

Hepatic coma and amino acids in the nerve endings of the central nervous system.

The levels of amino acids in the cerebral cortex and synaptosomes of 6 autopsied patients who had died of chronic liver diseases with portasystemic shunt were examined and compared with those of controls. The level of threonine in the cerebral cortex and synaptosomes of the 6 patients, who had developed hepatic coma before death, was significantly higher than that of 9 patients without hepatic coma. However, the levels of the neurotransmitters, aspartate, glutamate, and glycine, showed no significant difference between the two groups. In animal experiments, threonine uptake into the synaptosomes was enhanced by an increase of threonine concentration in the cerebral cortex, and at the same time ammonia further promoted threonine uptake. The high level of threonine in the synaptosomes was released just like a neurotransmitter on potassium stimulation in the patients with hepatic coma. Since threonine has no post-synaptic action, it is thought that threonine released in this way somehow interferes with brain action. This phenomenon may play an important role in the development of hepatic coma.

Amino Acids↗
PubMed1986

Lack of evidence for impaired dopamine receptor function in experimental hepatic coma in the rabbit.

In order to determine whether hepatic coma is associated with an altered sensitivity of the dopamine (DA) receptor in the brain, the activity of DA-sensitive adenylate cyclase was assayed in homogenates from the corpus striatum of normal rabbits and rabbits with galactosamine-induced fulminant hepatic failure by measuring cyclic adenosine monophosphate production from adenosine triphosphosphate radioimmunochemically. The kinetic properties of adenylate cyclase in control rabbits and rabbits with hepatic coma were similar (Km, 17 +/- 2.9 (S.E.M.) vs 20 +/- 6.4 mM; Vmax, 816 +/- 58 vs 1054 +/- 233 pmol/mg protein/5 min, respectively). Hepatic coma was not associated with any changes in the responses of the DA receptor-adenylate cyclase system to DA (maximum stimulation 60% vs 57%), sodium fluoride (maximum stimulation 104% vs 132%), or a D-2 DA receptor agonist (maximum inhibition 18% vs 12%). These findings make it unlikely that alterations of dopaminergic neurotransmission play an important role in the pathogenesis of hepatic coma.

Adenylyl Cyclases↗
PubMed2006

Overlapping 3q28 amplifications in the COMA cell line and undifferentiated primary sarcoma.

Historically, amplicon mapping and characterization of double minute (dmin) chromosomes content have been the ways to pinpoint important oncogenes. The COMA cell line established from a sarcoma contains DMs, some of them composed of material of the long arm of chromosome 3. To identify putative oncogenes on 3q that may be included in these dmins, we have analyzed the COMA cell line by microarray-based comparative genomic hybridization (array-CGH). We have detected the amplification of 1-Mb segment at 3q28, which contains the genes LPP, FLJ42393, and hsa-mir-28. Fluorescence in situ hybridization experiments confirmed the presence of numerous copies of 3q28 segment included in dmins. Further screening of eight undifferentiated primary sarcomas with 3q gains previously detected by chromosome CGH disclosed, in two cases, amplifications at 3q28 overlapping the 1-Mb segment amplified in COMA. To isolate target genes upregulated by gene dosage effect, we measured the transcription levels of every gene (in the RefSeq collection) located in the common region of amplification, selected expressed sequence tags (ESTs) and the micro-RNA hsa-mir-28 in the COMA cell line compared to one MFH cell line without alteration at 3q28. Expression levels of all transcripts were almost similar in both cell lines, except for two ESTs (AI338598 and BX118304) showing a 20-fold increase. These two transcripts are poorly characterized and their contribution to MFH carcinogenesis is difficult to evaluate.

Adult↗
PubMed2004

Dissecting chill coma recovery as a measure of cold resistance: evidence for a biphasic response in Drosophila melanogaster.

Cold resistance in insects has traditionally been measured in terms of survival following a stress, but alternative methods are increasingly being used because of their relevance to the ecology of organisms and their utility in characterizing variation among species, populations and individuals. One such method capable of discriminating among Drosophila species and conspecific Drosophila populations from different environments is adult chill coma recovery time, the time taken for adults to become active again after being knocked down by a cold stress. Here we characterized the chill coma response of D. melanogaster in detail. Adults were exposed to a range of temperatures and stressful periods prior to measuring recovery. Recovery from chill coma in D. melanogaster was biphasic; as flies were stressed under cooler temperatures, recovery times leveled off and then decreased before sharply increasing again as mortality starts to occur. This biphasic response has previously been observed in D. subobscura where it has a somewhat different shape. A second mechanism therefore acts at relatively lower temperatures to ameliorate the effects of the cold stress. When D. melanogaster were reared at 19 and 25 degrees C for two generations, the shape of the curve relating temperature to recovery time was similar, but flies from the warmer temperature had longer recovery times and showed responses that leveled off and then decreased at relatively higher temperatures. As exposure time to cold stress was increased, recovery times also increased except at mild stress levels. Chill coma recovery in D. melanogaster is a complex trait and likely to reflect multiple underlying components.

Acclimatization↗
PubMed1984

Substance P is markedly increased in plasma of patients with hepatic coma.

Substance P (determined as immunoreactive substance P [i-SP]), noradrenaline, and adrenaline were measured in plasma of 18 patients with hepatic coma (stage I-IV), 16 healthy controls, and 10 critically ill patients without evidence of hepatocellular disease. Plasma i-SP (119 +/- 13 fmol/ml) was significantly higher in patients with hepatic coma than in healthy controls (13 +/- 2 fmol/ml) or control patients (23 +/- 4 fmol/ml). Plasma i-SP rose in parallel with plasma noradrenaline and adrenaline. There was a significant direct correlation between plasma i-SP and noradrenaline. Increase in plasma i-SP and noradrenaline was associated with a decrease in systemic vascular resistance and an increase in cardiac index and was most pronounced in those patients who finally died in coma. Deterioration in the dying patients was accompanied by a further significant increase in plasma i-SP. Immunoreactivity was identified as authentic SP by high performance liquid chromatography in 3 representative patients. Accumulation of the vasodilating peptide SP in plasma of patients with hepatic coma may be important in the pathogenesis of the cardiovascular disturbances associated with this disease.

Adolescent↗
PubMed2003

Practical procedure for coma-free alignment using caustic figure.

The practical procedure for coma-free alignment using a single defocused transmission electron microscopy (TEM) image is presented. Caustic figures observed in the defocused TEM image of a focused probe are utilized. Coma-free alignment can be carried out by coinciding a bright-field spot with the center of a caustic curve as observed in an underfocus TEM image. With this method, beam tilt misalignment is reduced to the sub-mrad order (e.g. 0.3mrad for 300kV FEG-TEM). This can be done without intentional beam tilting, an amorphous specimen, high-resolution TEM images, or fast Fourier transform for diffractogram or cross-correlation, which are used in previous methods. Residual coma aberration is detected using the multiple Bragg images of a known crystal. Similarity between the present coma-free alignment and well-known STEM alignment using shadow image is discussed.

Journal Article↗
PubMedDate not supplied

ComA-dependent transcriptional activation of lichenysin A synthetase promoter in Bacillus subtilis cells.

ComA is a DNA-binding activator protein which is required for the transcription of several late-growth phase expressed genes including srfA, an operon needed for the development of genetic competence, efficient sporulation, and surfactin production in Bacillus subtilis (B. subtilis). We show here that the ComA protein can also recognize the promoter regulatory region of the lchA, lichenysin A synthetase operon, found in. Bacillus licheniformis (B. licheniformis) when introduced into B. subtilis cells. Mutational analysis of this region suggests that a palindromic sequence upstream of the lchA promoter may be the target for ComA-dependent transcriptional activation. Considering that the comA operon is present in the B. licheniformis chromosome, we propose the similar mechanism of transcriptional activation of the lichenysin A synthetase operon.

Amino Acid Sequence↗