Search PubMed⌕ Search

Biomedical subjects

S A Sadiq

Publications and source records attributed to S A Sadiq.

45 records · Page 3Linked to original sources
PubMed1990

Autoantigens in human neuroblastoma cells.

Neuroblastoma cells are frequently used as targets in studies of autoimmune diseases of the nervous system. We examined the human neuroblastoma cell line, LAN-5, for the presence of autoantigens that react with naturally occurring autoantibodies in human sera. Antibodies to the HNK-1 and Gal(beta 1-3)GalNAc epitopes, which have been implicated in human autoimmune neuropathy and motor neuron disease, respectively, immunostained the surface of the neuroblastoma cells, and antibodies to the 200 kDa high molecular weight neurofilament protein (NFH) immunostained the cytoplasm and cell processes. The NHK-1 and Gal(beta 1-3)GalNAc epitopes were associated with several glycoprotein bands in Western blots of the neuroblastoma cells, and the HNK-1 epitope was also shared by a glycolipid which co-migrated with 3-sulfoglucuronyl paragloboside (SGPG) from peripheral nerve, indicating that SGPG is synthesized in neuronal cells. Northern blot analysis revealed a single RNA band of 4800 bp for NFH in normal brain but two RNA species of 4800 and 3800 bp in both neuroblastoma and adrenal cells, confirming their common origin. The neuroblastoma cells appear to contain antigens that bind to naturally occurring autoantibodies in human serum and might therefore be useful for detecting and investigating the effects of anti-neuronal antibodies. The antibody populations being investigated, however, should be distinguished from other autoantibodies which might be present in the patients' serum.

Antibodies, Monoclonal↗
PubMed1990

Human monoclonal IgM anti-Gal(beta 1-3)GalNAc autoantibodies bind to the surface of bovine spinal motoneurons.

An IgM monoclonal autoantibody (M-protein) with anti-Gal(beta 1-3)GalNAc activity from a patient with lower motor neuron disease bound to the surface of motoneurons isolated from bovine spinal cord. The Gal(beta 1-3)GalNAc epitope is shared by the gangliosides GM1 and GD1b and by several glycoproteins in the nervous system, and binding was abolished by preabsorbing the patient's serum with GM1. Antibodies specific for GM1, however, which do not bind to GaL(beta 1-3)GalNAc, did not bind to the motoneurons. This suggests that Gal(beta 1-3)GalNAc bearing glycoproteins or glycolipids other than GM1 are expressed on the surface of motoneurons, while GM1 may be absent or shielded, and that antibody binding to the cell surface might contribute to the development of the motor neuron disease.

Animals↗
PubMed1990

A monoclonal IgA in a patient with amyotrophic lateral sclerosis reacts with neurofilaments and surface antigen on neuroblastoma cells.

A 75-year-old woman had breast carcinoma, an IgA paraprotein and autopsy-proven amyotrophic lateral sclerosis. Autopsy tissues showed immune-reactive IgA within surviving motor neurons and deposits of IgA and C3 within renal glomeruli. By indirect immunofluorescence, the patient's serum contained high-titer IgA that bound to axons and to the perikarya of nerve cells in central and peripheral nervous system. The IgA paraprotein reacted with the 200 kDa, high molecular weight subunit of neurofilament protein (NFH) in Western blots of purified neurofilaments. It also reacted with dephosphorylated NFH and with NFH expressed as a fusion protein in E. coli, suggesting that the autoantibody recognized a peptide epitope. The IgA crossreacted with a surface antigen of cultured human neuroblastoma cells but mouse monoclonal antibodies to NFH did not. Absorption of the patient's serum with neurofilaments eliminated IgA binding to neuroblastoma cells, indicating that the same antibodies bound to both determinants. The IgA paraprotein seems to be an autoantibody with specificity for neurofilament protein and a cell surface component of neuronal cells; the antibody may have been important in the pathogenesis of neuronal degeneration.

Aged↗
PubMed1990

The spectrum of neurologic disease associated with anti-GM1 antibodies.

We compared anti-GM1 IgM antibody titers in patients with various neurologic diseases and in normal subjects. We found increased titers in patients with lower motor neuron disease, sensorimotor neuropathy, or motor neuropathy with or without multifocal conduction block. In patients with other diseases, titers are similar to those in normal individuals, suggesting that anti-GM1 antibody levels are not increased nonspecifically after neural injury or inflammatory diseases. Anti-GM1 antibodies in many of the patients occur as monoclonal gammopathies, predominantly of lambda light-chain type, but the antibodies are sometimes polyclonal with normal or increased serum IgM concentrations. Most of the anti-GM1 antibodies appear to react with the Gal(beta 1-3)GalNAc epitope which is shared with asialo-GM1 and GD1b, but in some patients the antibodies are more specific for GM1 and associated with motor neuropathy. Patients with motor or sensorimotor peripheral neuropathy or lower motor neuron disease should be tested for anti-GM1 antibodies or anti-Gal(beta 1-3)GalNAc antibodies, as therapeutic reduction in antibody concentrations was reported to result in clinical improvement in some patients.

Adult↗
PubMedDate not supplied

Unusual manifestations of Epstein-Barr virus encephalomyelitis.

A patient with atypical manifestations of Epstein-Barr Virus (EBV) encephalomyelitis is presented. The patient had unusual spinal fluid immunoglobulin abnormalities, the syndrome of inappropriate anti-diuretic hormone secretion, autonomic dysfunction and spinal arachnoiditis. The cisternal CSF, with a very high IgG level (34.3 mg/dl; normal less than 6.1) but a normal albumin content, displayed evidence of massive intrathecal immunoglobulin production. This was further confirmed by the presence of oligoclonal bands. These clinical manifestations have not previously been reported in encephalomyelitis associated with EBV infection.

Adult↗
PubMedDate not supplied

Pupillary dilation and axial length measurement for preoperative assessment of intraocular lens power.

Cataract extraction is now routinely followed by insertion of an intraocular lens (IOL) which requires preoperative biometry to determine the most accurate implant power required. Biometry is generally performed just prior to surgery and may even require the patient to make a special hospital visit when day case surgery is contemplated. A prospective study was undertaken to determine the accuracy of axial length (AL) measurement through a dilated pupil. The AL of one eye of 64 patients admitted for cataract surgery was measured before and after dilation with a drop of tropicamide 1%. Our results show that there was no significant difference in the ALs before and after dilation (p = 0.10), and neither was there a difference in the average range of measurements (p = 0.70), with 78% of eyes having a difference of < +/- 0.3 mm between pre and post dilation ALs. We conclude that AL measurement performed on a dilated pupil can give an accurate result, and suggest that performing biometry on a dilated pupil following ocular assessment may be an efficient and time saving exercise.

Aged↗
PubMedDate not supplied

The visual results and changes in retinopathy in diabetic patients following cataract surgery.

INTRODUCTION: A study was designed to investigate the visual improvement and incidence of progression of retinopathy in diabetic patients following extracapsular cataract extraction or phacoemulsification. They were compared to a matched group of non-diabetic patients. METHODS: A retrospective analysis of all diabetic patients (118) undergoing ECCE (90) or phacoemulsification (28) in 1995. These patients were operation and age matched with 118 non-diabetic patients who underwent surgery during the same year. RESULTS: There was no statistically significant difference in complications following ECCE in diabetic and non-diabetic patients (p = 0.2). Complications were however more common in non-diabetic patients undergoing phacoemulsification compared to diabetics undergoing the same procedure (p = 0.046). Although consultants performed 42% of the surgery in diabetics compared to 31% in non-diabetics, there was no significant difference in the rate of complications between consultants and residents (p = 0.8). Overall the visual improvement in non-diabetics was better than diabetic patients (p = 0.006). This was due to a better improvement amongst non-diabetic patients undergoing phacoemulsification (p = 0.02). Overall, cataract surgery was found to lead to a worsening in retinopathy in 19 operated eyes (15 had no retinopathy preoperatively) compared to a worsening in 8 fellow eyes. This was statistically significant (p = 0.04). However, ECCE was no more likely to cause worsening of retinopathy than phacoemulsification (p = 0.87). CONCLUSIONS: Diabetic patients due to undergo cataract surgery a) have a good chance of visual improvement but to a level less than if they were not diabetic, b) have a greater chance of visual loss, c) surgery may initiate or worsen any pre-existing retinopathy and this may affect their vision in the future.

Adult↗