Modification of Insulin Resistance

1956 ◽  
Vol 102 (428) ◽  
pp. 576-588 ◽  
Author(s):  
Edward Marley
Keyword(s):  
Deep Coma ◽  
Insulin Dosage ◽  
Insulin Resistant ◽  
Significant Difference ◽  
High Insulin ◽  
Insulin Coma ◽  
The Central Nervous System ◽  
Resistance To Insulin ◽  
High Doses ◽  
Special Instance

Sakel (1938a) drew attention to the difficulty of establishing satisfactory comas in a minority of patients attending for Deep Insulin therapy. This phenomenon has since been confirmed by other workers including Tillim (1938) whose patient received 500 units of insulin without the production of deep coma, by Hall (1940) who reported an instance in which 1,000 units of insulin was equally unsuccessful, by Reznikoff and Scott (1942) who described how neither 120 nor 1,000 units of insulin when injected intravenously produced any significant difference in hypoglycaemia in insulin resistant patients, and more recently by Fogarty (1953) whose case required 5,000 units of insulin for the production even of sopor. Other recorded examples of resistance to massive doses of insulin include those of Bantinget al.(1938) and Tennent (1944).Various explanations of this perverse response to insulin have been formulated, including that of Jones (1939) who proposed that resistance to insulin was both a problem of true insulin insensitivity and also of an anomalous response of the central nervous system to hypoglycaemia. Medunaet al.(1942) preferred to ascribe it to anti-insulin factors in the blood, but a more interesting interpretation derived from Freudenberg (1952) who suggested that if the effects of high insulin dosage employed in insulin coma treatment were regarded as a special instance of a stress response, then the fluctuations and differences in response could be equated in terms of the General Adaptation Syndrome of Selye. High doses were thus an index of an effective “alarm stage” characterized by a discharge from plentiful adrenocortical reserves.

Markers of Hemostatic Activation in Affected Coronary Arteries during Angioplasty

1994 ◽  
Vol 72 (05) ◽  
pp. 672-675 ◽  
Author(s):  
Nicolas W Shammas ◽  
Michael J Cunningham ◽  
Richard M Pomearntz ◽  
Charles W Francis
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Venous Blood ◽  
Balloon Inflation ◽  
Blood Samples ◽  
Hemostatic System ◽  
Significant Difference ◽  
Hemostatic Markers ◽  
Artery Disease ◽  
High Doses

SummaryTo characterize the extent of early activation of the hemostatic system following angioplasty, we obtained blood samples from the involved coronary artery of 11 stable angina patients during the procedure and measured sensitive markers of thrombin formation (fibrino-peptide A, prothrombin fragment 1.2, and soluble fibrin) and of platelet activation ((3-thromboglobulin). Levels of hemostatic markers in venous blood obtained from 14 young individuals with low pretest probability for coronary artery disease were not significantly different from levels in venous blood or intracoronary samples obtained prior to angioplasty. Also, there was no translesional (proximal and distal to the lesion) gradient in any of the hemostatic markers before or after angioplasty in samples obtained between 18 and 21 min from the onset of the first balloon inflation. Furthermore, no significant difference was noted between angioplasty and postangioplasty intracoronary concentrations. We conclude that intracoronary hemostatic activation does not occur in the majority of patients during and immediately following coronary angioplasty when high doses of heparin and aspirin are administered.

PENENTUAN NILAI PARAMETER LIPOFILITAS SENYAWA 4-KLOROBENZOILTIOUREA DAN UJI POTENSIASI TERHADAP TIOPENTAL PADA MENCIT PUTIH (Mus musculus)

2019 ◽  
Vol 4 (1) ◽  
pp. 1
Author(s):  
Dini Kesuma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electronic Properties ◽  
Mus Musculus ◽  
Log P ◽  
P Value ◽  
Lead Compounds ◽  
Significant Difference ◽  
Central Nervous System Depressant ◽  
The Central Nervous System

Synthesis of the 4-chlorobenzoylthiourea compound was carried out by acylating thiourea with 4-chlorobenzoyl chloride. The 4-chlorobenzoylthiourea compound  will increase the lipophilic and the electronic properties other than the lead compounds of benzoylthiourea in order to, by expectation, raise the central nervous system depressant as well. The lipophilic would affect the ability of the compounds in penetrating biological membranes, which is highly dependent on the solubility of the drug within lipid/water. Log P is the most common method used in determining the parameter value. This experiment was to mix two dissolvents (octanol and water) which are immissible. The both levels of the compounds were carefully observed by a spectrophotometer UV-Vis. From the test, the result of log P value of the 4-chlorobenzoylthiourea compound was 2.32, while the theoretical log P value of the compounds, by using the π Hansch-Fujita method is 1.62 and the f Rekker-Mannhold method is 2.225. Consequently, the result of the test shows that there is a significant difference between the progress experiment and both theoretical log P methods. Moreover, in the test of the central nervous system depressant through the potentiation test to thiopental using mice indicates that the 4-chlorobenzoylthiourea compound have potentiation effects to thiopental compared to the lead compounds of benzoylthiourea.

Irreversible Hypoglycaemic Coma in Islet-Cell Adenoma and in Schizophrenia

1955 ◽  
Vol 101 (424) ◽  
pp. 673-682 ◽  
Author(s):  
D. N. Parfitt
Keyword(s):  
Personal Experience ◽  
Islet Cell ◽  
Severe Hypoglycaemia ◽  
Insulin Dosage ◽  
Cell Adenoma ◽  
After Effects ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Trained Staff ◽  
Hypoglycaemic Coma

As an approach to the problem of schizophrenia it is proposed to compare the effects and after-effects of severe hypoglycaemia due mainly to islet-cell adenoma of the pancreas in otherwise healthy people with the effects and after-effects of severe hypoglycaemia therapeutically induced in schizophrenics.The difficulties are plain. Personal experience of patients with functioning islet-cell adenoma is limited almost always to a few cases, whereas average experience of insulin coma treatment covers some hundreds of cases; moreover, there is little overlap of experience except in the post-mortem room or in the laboratory for morbid histology. During insulin treatment there is constant supervision by a trained staff, medical and nursing, so that serious developments can be met by immediate intravenous sugar and investigations are continual; with adenomata there is no observation until, perhaps, a general practitioner is called in about alarming symptoms of one kind or another and sometimes months or even years elapse before a patient gets into hospital, where the intensity of observation and even more so of investigation may exceed that available in mental hospitals. Insulin coma treatment has a more or less standard aim, to produce coma of increasing duration up to a maximum of something like an hour which is then repeated thirty times or more; dosage is built up with the greatest care. Adenomata produce conditions varying from the hardly serious to the fatal under the influence of an insulin dosage which is quite unknown.This comparison is based chiefly on an analysis of 290 serial courses of insulin coma treatment given to schizophrenic patients at Holloway Sanatorium during the four years 1950 to 1953 inclusive, and on the 258 cases of islet-cell adenoma reported by Crain and Thorn (1949) and the 398 cases, all that could be traced up to that date and including the Crain and Thorn cases, analysed by Howard, Moss and Rhoads (1950). Many separate papers have been consulted for more detailed approaches and for extra information, although of course those published before 1950 were included in the reviews already mentioned. Despite the difficulties of this comparison, it can be shown that the similarities between the two groups follow expectation and are very strong indeed, so that the differences which emerge have at least possible significance.

Some Aspects of the Psychopharmacological Activity of Maprotiline (Ludiomil®): Effects of Single and Repeated Treatments

1978 ◽  
Vol 6 (6) ◽  
pp. 421-429 ◽  
Author(s):  
A Delini-Stula ◽  
E Radeke ◽  
A Vassout
Keyword(s):  
Nervous System ◽  
Chronic Treatment ◽  
Conditioned Fear ◽  
Conditioned Avoidance ◽  
Repeated Treatment ◽  
Antidepressant Effects ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
High Doses ◽  
Psychopharmacological Activity

Three different aspects of the psychopharmacological activity of the antidepressant maprotiline were investigated: its influence on serotoninergic functions the effects produced by chronic treatment its central nervous depressant and anxiolytic properties. Study of the effects of maprotiline on 5-HTP-induced head-twitch in mice pre-treated with pargyline or on hyperpyrexia in rats provided no evidence that the drug interferes with serotonin-mediated functions in the central nervous system even after quite high doses. These findings corroborate the results of extensive neurobiochemical investigations, which failed to demonstrate any influence of maprotiline on the metabolism of serotonin. Chronic studies showed that classical effects of maprotiline such as antagonism against reserpine-induced ptosis or tetrabenazine-induced catalepsy do not change in their intensity after daily administration of the drugs in a dose of 30 mg/kg p.o.for 11 days. A new component of the action of the compound, not detectable after one single dose, seems to appear, however, after repeated treatment (8 days). This effect is manifested in the restoration of conditioned avoidance behaviour after its suppression by pre-treatment with reserpine. The same effect is produced by imipramine. It is suggested that this restorative effect may be due to an additional activation of the dopaminergic nervous system and may have a bearing on the appearance of clinical antidepressant effects. Maprotiline was found to potentiate central nervous depressant effects of drugs like chlorpromazine, phenobarbitone and propranolol. This affords further confirmation that, in addition to its antidepressant qualities, it possesses sedative actions. An anxiolytic component was also demonstrated in rats in which maprotiline suppressed the conditioned, fear-induced rise in body-temperature.

INCIDENCE OF CRANIAL NERVE PARALYSIS IN POLIOMYELITIS IN RELATION TO PRESENCE OR ABSENCE OF TONSILS

PEDIATRICS ◽  
1958 ◽  
Vol 21 (1) ◽  
pp. 94-105
Author(s):  
F. H. Top
Keyword(s):  
Facial Nerve ◽  
Cranial Nerves ◽  
Age Group ◽  
Real Difference ◽  
Satisfactory Explanation ◽  
Nerve Paralysis ◽  
Cranial Nerve Paralysis ◽  
Significant Difference ◽  
The Central Nervous System ◽  
The Common

Evidence is presented from data covering the period 1940 to 1952 which corroborates the conclusion of previous studies that prior tonsillectomy probably adversely affects the occurrence of brainstem paralysis (bulbar and bulbospinal) in poliomyelitis. Neither this study nor any preceding studies relating to this problem have proved the contention. On the basis that the hypothesis is correct, an attempt is made to find an answer by studying the incidence of the common paralysis of cranial nerves (VII, IX and X and XI) in bulbar and bulbospinal cases of poliomyelitis on the basis of presence or absence of tonsils. Rates of incidence of paralysis of cranial nerves, not adjusted for age, indicate a decidedly higher proportion of paralysis of the facial nerve (VII) among nontonsillectomized patients whereas tonsillectomized persons are preportionately more affected by palatal and pharyngeal paralysis (nerves IX and X). Paralysis of the facial nerve appears from two studies to occur more commonly at earlier ages, particularly in the age group 0 to 4 years. However, age adjustment did not erase, although it did somewhat lower, the TR/TP ratio. This finding lends credence to a real difference but can only be applied to this study, as Paffenbarger in a smaller study found no significant difference in frequencies of paralysis of the facial nerve between groups with tonsils removed and tonsils present, and Southcott, also in a small study, found paralysis of the facial nerve more common among tonsillectomized patients with bulbar (includes bulbospinal) involvement. The differences noted for palatal and pharyngeal paralyses (nerves IX and X) in the unadjusted rates as between tonsillectomized and nontonsillectomized patients remain statistically different and in some instances significant when corrections for age are made. The results of this study are suggestive but give no entirely satisfactory explanation for the differences noted. Various explanations previously offered are cited and briefly discussed. Perhaps more definitive studies in animals along the approach suggested by Southcott will prove more fruitful, namely, labelling virus by some radioactive element in order to trace the route it takes to the central nervous system.

scholarly journals Systematic Review and Meta-analysis of Eculizumab, Inebilizumab, Tocilizumab, and Satralizumab for Neuromyelitis Optica

2021 ◽  
Author(s):  
Rajan Chamlagain ◽  
Sangam shah ◽  
Suman Gaire ◽  
Anuj Krishna Paudel ◽  
Krishna Dahal ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
Neuromyelitis Optica ◽  
Treatment Guidelines ◽  
Meta Analysis ◽  
Cochrane Central Register ◽  
Central Register ◽  
Significant Difference ◽  
Quantitative Synthesis ◽  
The Central Nervous System

Neuromyelitis optica is rare, autoimmune-mediated inflammation and demyelination of the central nervous system with a prevalence of 1-2 persons per 100,000 populations. We aim to generate a head-to-head comparison of these drugs with appropriate evidence to guide future trials and treatment guidelines in a patient with recurrent attacks of NMO. We searched the databases like PubMed, MEDLINE, Cochrane Central Register of Controlled Trials (CENTRAL) and Embase for studies published prior to April 2021 using the keywords. Over all 929 patients from 11 different publications were included in the study. Five studies were included for quantitative synthesis. Pooling of studies showed significant mean reduction of ARR in the monoclonal antibody group (-0.26 [-0.35, -0.17], P <0.00001, I2=0%) and the mean difference in EDSS score from baseline in monoclonal antibodies was -0.23(95% CI [-0.43, -0.03], P=0.02, I2=0%). There was no significant difference in frequency of total reported adverse events between monoclonal antibody and the comparator arm (RR: 1.01 [0.95, 1.07], P=0.74, I2=14%). Our findings, particularly seen from the context of a few RCTs, support the pursuit of larger, multi-center RCTs that evaluate the effectiveness of each of the currently available monoclonal antibodies and better describe their adverse risk profile.

Development of adrenomedullary function in suckling rats: Effects of high doses of thyroxine and cortisol

1990 ◽  
Vol 123 (1) ◽  
pp. 100-107
Author(s):  
L. Goya ◽  
C. Aláez ◽  
A. M. Pascual-Leone
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adrenal Glands ◽  
Normal Development ◽  
Insulin Administration ◽  
Newborn Rats ◽  
Short Intervals ◽  
Slowing Down ◽  
The Central Nervous System ◽  
High Doses

Abstract. The development of epinephrine, norephinephrine, and total catecholamine secretion in plasma and andrenal glands was studied in newborn rats at short intervals: at day 2, 4, 6, 8, 10, 12 and 23. The increase in the plasma level of epinephrine represents a maturation of the secretion of the adrenal medulla. The increase in plasma of epinephrine and norepinephrine and the content of catecholamines in the adrenal glands of both normal animals and those treated with either high doses of T4 or cortisol at birth suggest a slowing down of the normal development of epinephrine secretion. This was confirmed by inducing hypoglycemia in these three groups of animals by a 20-h fast or by insulin administration (0.1436 μmol/kg). We conclude that both high doses of T4 and cortisol administered at birth seem to retard the development of the autonomic nervous system similar to the effect on the central nervous system.

scholarly journals Neuromyelitis optica spectrum disorder in pediatrics. Case report

Case reports ◽  
2019 ◽  
Vol 5 (1) ◽  
pp. 11-18
Author(s):  
Jhon Camacho ◽  
Sebastian Zuleta ◽  
Maria Paula Alba ◽  
Andrea Hernandez ◽  
Carlos Navas
Keyword(s):  
Neuromyelitis Optica ◽  
Interesting Case ◽  
Spectrum Disorder ◽  
Demyelinating Diseases ◽  
Inflammatory Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
The Central Nervous System ◽  
High Doses ◽  
Aqp4 Antibody ◽  
Timely Treatment

Introduction: Neuromyelitis optica is an inflammatory disorder of the central nervous system that accounts for 5% of demyelinating diseases in pediatrics. Its clinical presentation is variable and associated to the involved area of the central nervous system.Case presentation: This is the case of a 15-year-old patient who consulted several times for nonspecific neurological symptoms. During his last visit to the Clínica Universitaria Colombia in Bogotá, he presented with bilateral optic neuritis, associated with frontal and parietal headache. Immunophenotyping studies were carried out, reporting positive IgG anti-aquaporin 4 antibodies (anti-AQP4 antibody), thus leading to a diagnosis of seropositive neuromyelitis optica spectrum disorder (NMOSD). Management with methylprednisolone pulses was initiated with subsequent outpatient management with rituximab that allowed stabilizing the disease.Discussion: This is an interesting case due to its insidious and uncertain onset in a pediatric patient. It was possible to evaluate clinical and diagnostic differences in relation to its presentation in adults. NMOSD mediated by anti-AQP4 is rare; brain and bone marrow MRI are essential for diagnosis. The treatment of choice for acute conditions consists of high doses of methylprednisolone.Conclusion: This disorder may result in irreversible neurological damage; for this reason, high suspicion is required for early diagnosis and timely treatment.

scholarly journals EPID-12. IMPACT OF RACE AND GEOGRAPHIC LOCATION ON IDH MUTATIONS AND GLIOBLASTOMA SURVIVAL

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi76-vi77
Author(s):  
Ryan McCormack ◽  
Ping Zhu ◽  
Takeshi Takayasu ◽  
Gabriella Hines ◽  
Hussein Zeineddine ◽  
...  
Keyword(s):  
Geographic Location ◽  
Relative Survival ◽  
Population Based ◽  
Future Studies ◽  
Mixed Heritage ◽  
Idh Mutations ◽  
Significant Difference ◽  
The Central Nervous System ◽  
The City ◽  
Generation Sequencing

Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor of the central nervous system with a 5-year survival of < 5%. Population studies have demonstrated that among all ethnicities, non-Hispanic whites (NHW) have the worst prognosis; however, differences within the oncogenome based on ethnicity have not been assessed. We utilized the Texas Cancer Registry (TCR) for population-based analysis including 4,134 GBM patients between the years of 1995 to 2013 with 75.6% NHW and 16.5% Hispanics. In accordance with previously published findings, within the TCR we detected a 12% relative survival improvement in Hispanics compared to NHW when controlling for known survival mediators including age, resection, chemotherapy, and radiation. In order to assess for oncogenic differences, we utilized a prospectively maintained database of 257 GBM patients within the city of Houston, TX (14.9% Hispanic) and 48 GBM patients from the National Institute of Neurology and Neurosurgery in Mexico City, Mexico (100% Hispanic) to assess for oncogenomic differences attributable to ethnicity. Next generation sequencing of GBM within the Houston cohort, for 315 tumor-related genes, identified no significant differences in genomic alterations owing to ethnicity. However, when we compared the multigenerational, mixed-heritage Hispanics present in the Houston cohort to the Mexico cohort (Sanger sequencing), a significant difference was found in the frequency of IDH1and IDH2mutations (29.8 % Mexico Hispanics, 7.9% Houston Hispanics; p=0.014). In particular, the rate of IDH2mutations is significantly enriched in the Mexico population (19%) when compared to the Houston population (0%) or to previously published rates of IDH2 mutations in GBM (~3%). Ultimately, these findings highlight the need for multiethnic trial enrollment as well as the need for improved testing of IDH2 mutations in patients of distinct ethnicities. Future studies are needed to identify the mechanisms promoting the increased frequency of IDH2 mutations in Mexican Hispanics.

Recombinant human thyrotropin stimulated 131I treatment for multinodular goiter

2016 ◽  
Vol 55 (06) ◽  
pp. 228-235 ◽  
Author(s):  
Limin Tang ◽  
Tiekun Ma ◽  
Fengyu Wu
Keyword(s):  
Adverse Effects ◽  
Data Extraction ◽  
Thyroid Volume ◽  
131I Therapy ◽  
Cochrane Library ◽  
131I Treatment ◽  
Significant Difference ◽  
High Doses ◽  
Recombinant Human Thyrotropin ◽  
The Cochrane Library

SummaryThe aim of the study was to investigate the effects of rhTSH stimulation before 131I treatment in patients with MNG. Methods: Sources included the Cochrane Library, MEDLINE, EMBASE, and SCOPUS database (all until January 2016). Randomized controlled trials (RCTs) that assessed the efficacy of rhTSH-stimulated 131I treatment compared to placebo or 131I treatment alone were collected. Two authors performed the data extraction independently. Results: Six RCTs involving 294 patients with MNG were included in this review. Altogether 168 patients were randomized to rhTSH-stimulated 131I therapy, and 126 to either placebo and 131I or 131I alone. rhTSH-stimulated 131I vs placebo and 131I or 131I alone for MNG showed no statistically significant difference in quality of life and all-cause mortality. rhTSH- (at a dose of 0.03 mg and above) stimulated 131I treatment for MNG showed significant benefits in thyroid volume reduction. 131I treatment with rhTSH stimulation at high doses (0.03 mg, 0.1 mg, 0.3 mg and 0.45 mg) for MNG caused significantly higher adverse effects and hypothyroidism. Conclusions: The overall results indicated that using rhTSH at high doses of 0.03–0.45 mg before 131I therapy resulted in a greater TVR than 131I therapy alone for patients with non-toxic MNG. However, an increased incidence of adverse effects and hypothyroidism was observed in patients receiving highdose of rhTSH pretreatment than in patients who received low-dose rhTSH pretreatment. Therefore, a dose of 0.03 mg rhTSH pretreatment before 131I therapy may be more potent than 131I alone in treating patients with non-toxic MNG who either had a contraindication for or declined surgery.

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