Investigation of Precipitins to Human Brain in Sera of Psychotic Patients

1965 ◽  
Vol 111 (479) ◽  
pp. 1003-1006 ◽  
Author(s):  
Robert T. Rubin

Altered serum proteins in mental illness have been reported by workers in various parts of the world, and a review of these studies has led to the consideration of an autoimmune mechanism in the pathogenesis of some functional psychoses (Fessel, 1962a). Several reports have appeared in recent years which suggest the presence of antibodies in the serum of certain psychiatric patients to central nervous system tissue. Many of these have been reviewed by Vartanyan (1963). Fessel (1962b, 1963) demonstrated agglutination of latex particles coated with monkey brain extract and agglutination of tanned sheep red blood cells coated with human brain extract, but no precipitins in double diffusion in agar of the sera against monkey brain extract. As an alternative to antibrain antibodies he suggested a less specific physicochemical abnormality of the serum which caused the agglutination. Yokoyama, Trams, and Brady (1962), using a sheep red blood cell haemagglutination technique, showed the presence of anti-asialoganglioside antibodies in the sera of 3 of 14 schizophrenic patients and anti-ganglioside antibody in the serum of another. Kuznetzova and Semenov (1961), by complement fixation, demonstrated antibodies in the sera of 22 of 84 schizophrenics, mainly to human brain and not to other organs. The antibodies appeared more frequently in the later stages of the illness (Semenov, Morozov, and Kuznetzova, 1961). Skalickova and Jezkova (1961), also with a complement fixation technique, demonstrated blood and cerebrospinal fluid antibodies to grey and white matter during the “infectious” onset of schizophrenia, but not in the chronic, demented phase.

1978 ◽  
Vol 132 (4) ◽  
pp. 342-348 ◽  
Author(s):  
E. Fuller Torrey ◽  
Michael R. Peterson ◽  
William L. Brannon ◽  
William T. Carpenter ◽  
Robert M. Post ◽  
...  

SummaryThe serum and CSF of 66 patients with functional psychoses were tested for immunoglobulins and antibodies to measles, HSV-1, CMV, and rubella viruses. Ten surgical and 80 neurological patients were controls. There were no significant findings in the serum, consistent with most previous studies. In the CSF 6 of 17 multiple admission schizophrenic patients had definite elevations of IgG or measles antibody and differed significantly from the surgical controls. Immunologically this group resembled the seriously ill neurological patients. No previous study has been made of immunoglobulins or viral antibodies in the CSF of psychiatric patients. It is concluded that further work is warranted in a search for biological subgroups of schizophrenia.


1978 ◽  
Vol 16 (14) ◽  
pp. 55-56

Neuroleptic drugs cause many forms of extra-pyramidal syndromes. One of these, tardive dyskinesia,1 occurs only after the patient has been taking the drug for some time (‘tardive’ refers to the late onset). The movements are involuntary and repetitive usually involving the face and tongue, but they may also affect the limbs and trunk. Tongue protrusion, licking and smacking of the lips, sucking and chewing movements, grimacing, grunting, blinking and furrowing of the forehead have all been described and attributed to long-continued medication with neuroleptic drugs of the phenothiazine, butyrophenone and thioxanthene groups. The patient can inhibit the movements, but anxiety makes them worse. Many of these symptoms were noticed in schizophrenic patients before neuroleptic drugs were introduced2 and they can occur in otherwise normal untreated elderly people. Nevertheless it is generally accepted that in most cases tardive dyskinesia is an unwanted effect of neuroleptic medication. Despite suggestions to the contrary, the abnormal movements are not necessarily associated with high dosage of neuroleptic drugs or with pre-existing brain damage.3 4 Tardive dyskinesia has been reported in 3–6% of a mixed population of psychiatric patients5 and over half of a group of chronic schizophrenics on long-term treatment.4 The more careful the neurological examination, the greater the apparent incidence.


PEDIATRICS ◽  
1972 ◽  
Vol 49 (1) ◽  
pp. 133-136
Author(s):  
Dale E. Dietzman ◽  
Luiz Horta-Barbosa ◽  
Helen M. Krebs ◽  
David L. Madden ◽  
David A. Fuccillo ◽  
...  

A double-diffusion gel precipitation test is described which provides an easy, rapid, and reliable procedure for assistance in the diagnosis of subacute sclerosing penencephalitis by detecting measles antibody in concentrated cerebrospinal fluid. The test is based on the precipitation of rubeola antibodies with a high titered SSPE measles-virus antigen. The sensitivity of the test is comparable to the sensitivity of rubeola complement-fixation and hemagglutination-inhibition determinations on unconcentrated spiral fluid. The method could be available to hospitals or institutions if the antigen were prepared commercially or by a national center.


1967 ◽  
Vol 21 (1) ◽  
pp. 24-26 ◽  
Author(s):  
Robert H. Goldstein ◽  
Leonard F. Salzman

Tests of vocabulary and abstraction administered to groups of schizophrenic and non-schizophrenic patients at time of hospital admission and at time of clinical remission and discharge home revealed some evidence of general cognitive impairment in both groups, with significant improvement by time of discharge, as well as evidence of continuing specific conceptual impairment among schizophrenics.


Gesnerus ◽  
1993 ◽  
Vol 50 (1-2) ◽  
pp. 96-112
Author(s):  
Semir Zeki

In 1888, Louis Verrey, a Swiss ophthalmologist, stated emphatically that there is a "centre for the chromatic sense" in the human brain and that it is located in the lingual and fusiform gyri. He did not, however, consider the “colour centre” to be a separate area but a large sub-division of the primary visual cortex. His evidence was quickly dismissed and forgotten. It was not to be taken seriously again until after the experimental discovery of functional specialization in the monkey brain. This paper considers why it is that Verrey did not consider the “colour centre” to be a separate cortical area, distinct from the primary visual cortex, why his evidence was so quickly and effectively dismissed, and why it is that Verrey did not pursue the logic of his findings.


1958 ◽  
Vol 104 (437) ◽  
pp. 1123-1129 ◽  
Author(s):  
Anne Broadhurst

It has been clinically observed that psychiatric patients in general (6, 11) and schizophrenic patients in particular (1, 4) show abnormalities of mental speed, being “retarded” or slower than normals on many measures. Confirmatory evidence on this point is to be found but much of the early work on speed of schizophrenic reactivity used measures of speed of motor performance (12, 13) or of reaction time under various conditions (6), ignoring more fundamental slowness of thought processes. The present studies are concentrated on the recent finding that schizophrenics show abnormally slow mental speed measured in a problem-solving situation (4, 18, 19). The aim of the investigation was to discover the exact conditions under which this abnormality appears, and, thence, by manipulating the experimental conditions, to be able to bring speed of mental functioning under experimental control. This paper describes the attempt to bring speed under control by means of drugs. A second paper (2) deals with the effect of practice upon mental speed.


2019 ◽  
Vol 21 (Supplement_4) ◽  
pp. iv7-iv7
Author(s):  
Mohammed Diksin ◽  
Jonathan Rowlinson ◽  
Alexandar Kondrashov ◽  
Chris Denning ◽  
Jamie Hughes ◽  
...  

Abstract Glioblastoma therapeutic challenges are in considerable part due to myriad survival adaptations and mechanisms, which allow malignant cells to repurpose signalling pathways within discreet microenvironments. These Darwinian adaptations facilitate invasion into brain parenchyma and perivascular space or promote evasion from repressive factors that represent anti-cancer defence mechanisms. We hypothesised that pre-clinical modelling of glioma invasion by recapitulating early events occurring immediately after surgery at the glioblastoma invasive margin, could reveal the cross-talk between malignant cells and the surrounding healthy astrocytes, which facilitates tumour recurrence. We first generated transgenic H1-derived neural stem cells using CRISPR/Cas9-mediated knock-in of the YFP reporter gene under the control of the GFAP promoter. Reproducible ultrahigh-throughput AggreWells™ (19,200 micro-wells per 24-well plate) were used to create astrocyte-glioblastoma organoids, which we term ‘Gliomasphere Matrices’. YFP-labelled astrocytes were co-cultured with 10 treatment-naïve patient-derived cell lines isolated from the 5-aminolevulinic (5ALA)-determined glioblastoma invasive margin. Co-cultures were seeded upon on a sequentially constructed, time-of-flight secondary ion mass spectrometry (ToF-SIMS)-characterised 3D scaffold, composed of decellularised human brain extract with defined PEGDA hydrogel. YFP-astrocytes were purified from each of the 10 Gliomasphere Matrices using fluorescence-activated cell sorting (FACS) after 6- and 10-days co-culture. RNAseq profiling to address both putative astrocytic reprogramming by invasive glioblastoma cells and gene expression changes intrinsic to tumour cells will be discussed in relation to RNAseq data from patient-derived 5ALA FACS-purified glioblastoma invasive margin tissue. This novel multi-faceted model offers a unique opportunity to recapitulate early molecular cross-talk which facilitates glioblastoma recurrence and may be utilised for high-throughput drug screening.


2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi264-vi265
Author(s):  
Mohammed Diksin ◽  
Jonathan Rowlinson ◽  
Alexander Kondrashov ◽  
Chris Denning ◽  
Jaime Hughes ◽  
...  

Abstract Glioblastoma therapeutic challenges are in considerable part due to myriad survival mechanisms which allow malignant cells to repurpose signalling pathways within discreet microenvironments. These Darwinian adaptations facilitate invasion into brain parenchyma and perivascular space. We hypothesised that pre-clinical modelling of glioma invasion by recapitulating early events occurring immediately after surgery at the glioblastoma invasive margin, could reveal the cross-talk between malignant cells and surrounding healthy astrocytes. We first generated transgenic H1-derived neural stem cells using CRISPR/Cas9-mediated knock-in of the YFP reporter gene under the control of the GFAP promoter at the AAVS1 safe harbour locus. Reproducible ultrahigh-throughput AggreWells™ (7200 mini-wells per plate) were used to create astrocyte-glioblastoma organoids, which we term ‘Gliomasphere Matrices’. YFP-labelled astrocytes were co-cultured with 10 treatment-naïve patient-derived cell lines isolated from the 5-aminolevulinic (5ALA)-determined glioblastoma invasive margin. Co-cultures were seeded upon a sequentially constructed, time-of-flight secondary ion mass spectrometry (ToF-SIMS)-characterised decellularised human brain extract. YFP-astrocytes were purified from each of the 10 Gliomasphere Matrices using fluorescence-activated cell sorting (FACS) after 6- and 10-days co-culture. RNA-sequencing of the putatively reprogrammed YFP-astrocytes showed the characteristic expression of canonical key regulators of multiple malignant diseases including high-grade glioma such as SND1 and EFNB2 in addition to the identification of a single novel marker located at chromosome 1 (C1orf61), highly expressed in malignant glioma when compared to somatic cancers according to TCGA RNA-sequencing data. Differentiated YFP-astrocytes also overexpressed IFITM2 and IFITM10, known to be involved in priming resistance against pathogenic microorganisms. This ultimately suggests a fluctuating state between malignant transformation imposed by the highly infiltrative glioma cells and the counter-action of the normal astrocytes to these deleterious invasive cells. This multi-faceted model offers a unique opportunity to recapitulate early molecular cross-talk which facilitates glioblastoma recurrence and may be utilised for high-throughput drug screening.


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