Preliminary dielectric studies of knee swelling fluid in the case of arthritis, which is hard to diagnose

This study addresses the problems connected with knee joint inflammatory swelling diagnosis, especially cases which have difficulty meeting rheumatic and laboratory criteria. A percentage of patients were considered who met the clinical criteria of the Association of Rheumatoid Arthritis (ARA), proceeded without any deviations within the range of rheumatoid factor (RF) laboratory results, and where only serum non-specific immuno-complexes (CIC) increased. The decision to execute a more effective treatment variant (salazopirin, for example, instead of NSAID), required criterial reliability in practice. The purpose of the study was to attempt to find physiochemical distinguishing features in the exudative liquid taken from the knee joints of two groups of patients: group A meeting the clinical criteria of immunological inflammation and a negative rheumatoid factor, and group B with other inflammation concerned with degenerative changes and with negative rheumatoid factor tests. The main area of interest was the question of whether dielectric scanning enables the distinction between immunology and degenerative inflammatory liquid. Analyses of dielectric joint liquid parameters in the domains of frequency and temperature made it possible to observe recurring changes in the shapes of diagrams in the event of the existence of immunological complexes in the studied environment. We found that (1) dielectric scanning diagrams after joint liquid analyses showed similar negative dielectric parameters in group A (inflammatory), B (degenerative) and C (post-accident) with scanning frequencies of about 10,000,000-3501,300 Hz and similar positive parameters of about 3501,300-1593,700 Hz, but qualitative difference dielectric parameters in group A with a frequency of 1593,700-1225,900 Hz, probably dependent on the inflammatory gamma-globulin concentration; (2) higher dielectric parameters (groups B, C) at a scanning frequency of 94,300-57,600 Hz probably dependent on ion concentration; (3) parametric changes of frequency scanning differentiating the diagrams between groups A and B, C, defining the outline pilot study recommended ranges of frequency and temperature testing for further investigations.     

Epstein-Barr virus (EBV) infection and p53 protein expression in gastric carcinoma

In the presented studies p53 protein expression was evaluated in samples of gastric carcinoma originating from 32 selected adult patients (with documented diagnosis of adenocarcinoma of the stomach and without the presence of Helicobacter pylori infection). Among the patients 14 individuals carried EBV-positive gastric carcinoma (group 1) while the 18 remaining patients carried EBV-negative gastric carcinoma (group 2). EBV infection was detected testing the tissue material for the presence of EBER by RNA in situ hybridization (ISH) and testing sera of the patients for EBV-specific antibodies. Expression of p53 protein was analysed using immunohistochemistry. Presence of p53 protein was noted in 9 (64.3%) cases of EBV-positive gastric cancer (group 1) and in 10 (55.5%) cases of EBV-negative gastric cancer (group 2). No significant differences were detected in the frequencies of p53 protein expression in the two studied groups. The results permit to conclude that abnormalities in p53 in gastric cancer are independent of EBV infection, even if EBV may participate in development of the tumour.     

Secondary amyloidosis connected with neoplasma of urinary bladder and acquired disorders of blood coagulation. Case report

Amyloidosis is a general term encompassing a group of disorders morphologically characterized by a deposition of proteinaceous fibrillar material in the tissues. The secondary amyloidosis is associated with systemic inflammatory processes, chronic infections or neoplasm. These processes are associated with elevated levels of circulating serum amyloid protein A (SAA). We have described a unique case of led to systemic amyloidosis associated with tumor of urinary bladder with significant renal involvement and acquired disorders of blood coagulation factor IX and X deficiency. A renal biopsy specimen with Congo red stain showed diffuse deposits of amyloidosis. Immunohistochemical examination was not done. Factor IX and X was determinated and to be 10-16% of normal values. Timely patient has failed to response to fresh frozen plasma and vitamin K and favorable responded to once weekly administrated factor IX and X concentrate. Progressive deterioration of renal function required hemodialysis, but he died one year later.     

Genetic background of ADHD: genes of the serotonergic system, other candidate genes, endophenotype

Recent studies have shown that in the aetiology of attention-deficit hyperactivity disorder (ADHD) genetic factors may be of importance. Biochemical and pharmacological studies reveal a connection between abnormalities of dopaminergic, adrenergic and serotonergic system and ADHD. Therefore genes for enzymes synthesizing or degrading proper neurotransmitters, genes for adequate transporters and receptors and genes for other substances, which altered the level of neurotransmitters, are studied. Many authors describe the connection between ADHD development and the synaptosomal-associated protein 25 (SNAP-25) gene. This protein plays a role in catecholamine secretion. Its higher expression is specific for neurones. SNAP-25 gene mutation may change this protein level, function of synapse and neurotransmitters storage. Acetylcholine receptor alpha4 subunit gene stimulation increases the dopamine level. Therefore this receptor gene may be important in the aetiology of ADHD studies. Other possible factors in ADHD background are substance influence on brain maturation, including N-methyl-D aspartate glutamate receptor 2A gene polymorphism (GRIN2A) and brain derived neurotrophic factor (BDNF) gene. One of the greatest challenges in studying the genetic basis of psychiatric disorders is to find appropriate ways to define the relevant endophenotype. ADHD often coexists with other psychiatric disorders, including specific developmental disorders, conduct disorders, obsessive-compulsive disorder and early onset of bipolar disorder.     

Genetic background of ADHD: population studies, genes of the catecholamine system

Attention-deficit hyperactivity disorder (ADHD) begins in early childhood. In this article we review the studies supporting a genetic background of this disorder. ADHD occurs in 3-10% of the general population. Family studies reveal a 5 times more likely frequency of ADHD among first-degree relatives than in the general population. Monozygotic twin concordance rate for ADHD is 81%, whereas for dizygotic twins it is 29%. One of the ADHD predisposing factors is dopaminergic neurotransmission abnormality. According to other studies there is a relationship between polymorphism of dopamine transporter gene (DAT), dopamine receptors genes: DRD2, DRD3, DRD4, DRD5, dopamine-beta-hydroxylase gene (DBH) and catechol-O-methyltransferase gene (COMT) and ADHD. In other articles authors describe abnormalities of the serotonergic system, such as the polymorphism of the serotonin transporter gene (5HTT/SERT), serotonin receptors genes 5HT2A and 5HT1B in the development ofADHD. Another possible factor in ADHD background is the dysregulation of the adrenergic system. The most frequently studied is the connection between polymorphism of norepinephrine transporter gene (NET), adrenergic receptors genes: alpha 2A (ADRA2A), alpha 1C (ADRA1C), alpha 2C and monoamine oxidase A gene (MAO-A).     

Increased plasma fibrinogen predicts one-year mortality in patients with acute ischemic stroke

BACKGROUND AND PURPOSE: Increased plasma fibrinogen is a risk factor for vascular diseases related to atherosclerosis. Its long-term predictive value in stroke survivors is not established. We conducted this study to establish the significance of hyperfibrinogenemia as the possible predictor of 30-day and one-year mortality in patients with acute ischemic stroke. METHODS: We studied 900 unselected patients with ischemic stroke admitted to the hospital within 24 h after onset of symptoms. We noted demographic data, risk factors for stroke, neurological deficit and disturbances of consciousness on admission. We measured plasma concentration of fibrinogen and the body temperature on day 1 and registered vital status at 1, 3, 6 and 12 months after stroke. RESULTS: Mean concentration of plasma fibrinogen was 2.9 g/L and 25.2% of patients had increased plasma concentration of fibrinogen (i.e. > or = 3.5 g/L) on day 1. Patients with hyperfibrinogenemia were more likely to die after 1, 3, 6 and 12 months than those with normal plasma fibrinogen (21.1% vs. 15.6%, 36.4% vs. 24.6%, 42.6% vs. 27.3%, 45.7% vs. 31.2%, respectively; P < 0.001 for the last three differences). Hyperfibrinogenemia did not predict short-term case-fatality, but increased concentration of plasma fibrinogen was an independent predictor of one-year case-fatality (P = 0.013; OR: 1.69 (95% CI 1.12-2.55)). Other independent predictors of one-year case-fatality were: neurological deficit on admission, age, white blood cell count, and body temperature on day 1. CONCLUSIONS: Increased concentration of plasma fibrinogen shortly after ischemic stroke independently increases risk of death within one year after stroke.