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Sleep bruxism (SB) is a common phenomenon defined as a masticatory muscle activity during sleep. Untreated severe SB can have significant dental and orofacial consequences. SB has often been linked with stress and maladaptive coping strategies. Therefore, in this study, a potential correlation between SB, perceived stress and coping strategies was evaluated. A total of 60 adults were enrolled into this study. Participants underwent a detailed intra- and extraoral exam focused on detecting bruxism symptoms. Additionally, the overnight Bruxism Index was recorded using the Bruxoff device. A total of 35 participants with symptoms of bruxism were assigned to the study group, whereas 25 asymptomatic participants were assigned to the control group. The Perceived Stress Scale (PSS-10) was used for stress assessment and Brief-COPE for coping strategies. Results showed that the higher the PSS-10 score, the higher the Bruxism Index was in the study group. Positive coping strategies were chosen most frequently in the control group, while maladaptive ones were chosen in the study group. It can be concluded that there is a relationship between perceived stress and sleep bruxism. Moreover, the type of coping strategies used by participants may have an impact on sleep bruxism, but the relationship should be further investigated.

Sleep bruxism (SB) is a masticatory muscle activity during sleep and a common phenomenon. Severe SB can have a serious impact on the success of dental treatment. Reliable methods of screening and diagnosing patients with SB are crucial. Therefore, in this study, a Bruxoff device as a potential screening and diagnostic method for sleep bruxism was evaluated. A total of 60 adults participated in this study: 35 patients with symptoms of bruxism (study group) and 25 asymptomatic patients (control group). Data were recorded using Bruxoff. All symptomatic patients participating in the study turned out to be bruxers, while not all asymptomatic patients turned out to be non-bruxers according to the Bruxoff device. Bruxoff is a simple screening device that can be safely used to evaluate masseter muscle activity during sleep. Since the device does not have a built-in microphone and/or video camera and, therefore, cannot record grinding sounds, the objective capabilities of Bruxoff as a single diagnostic device for sleep bruxism are limited.

The authors have made attempts to show analysis of cesarean section' indications in the Obstetric-Gynecological Ward of the provincial hospital in Ciechanów within the years 1986-1994. There have been 18,362 deliveries during this period of time, 2769 (15.1%) of which have been finished by c.s. We have made our tables and estimations basing mainly on the operation records and the records of labor. The analyses have revealed the increase of the c.s. number because of gestosis in multiple gestations and non-obstetric indications in our ward. The greatest group in this period of time were parturients with one or more c.s. in history. To diminish the number of this parturients could be possible when one would better analyse the indications to the first c.s., and making the attempt of a vaginal delivery in multigravidas after c.s. while the operation theater is standby.

Twenty nine patients (7 women, 22 men) with III and IV stage of Hodgkin's disease were treated according to alternating programme ChLVPP/ABV. The results were evaluated in 27 patients. Complete remission was obtained in 41% (11 patients), partial remission in 22% (6 patients). Applied treatment revealed a relatively small toxicity.

The authors report two cases of acute leukaemia in adults with development of sings central nervous system involvement at the time of full haematological remission. In the first case the diagnosis was: acute undifferentiated-cell leukaemia, in the second one: acute lymphoblastic leukaemia. In both cases in the first stage of the disease complete remission of neurological manifestations was obtained; in the second case it was also obtained after the following relapse. In the first case death occurred during successive haematological exacerbation. Ametopterin was given intrathecally or X-ray therapy was applied.

It has previously been shown that there are extensive idiotypic cross-reactions among antiphenylarsonate antibodies of A/J mice. The present work indicates that administration, into normal, adult A/J mice, of rabbit antiidiotypic antibody directed to A/J antiphenylarsonate antibody suppresses almost completely the subsequent production of antibody of the corresponding idiotype. No effect was noted on the formation of antibodies to the protein carrier or of antiphenylarsonate antibody of a different idiotype. The data are consistent with central suppression of production of the idiotypic antibody mediated through interaction with immunoglobulin receptors on lymphocytes.

The expression of an idiotype characteristic of anti-p-azophenylarsonate antibodies of all A/J mice was explored in F(1) progeny, in other inbred strains, and in congenic mice. Of the strains tested only those closely related to A/J produced antibodies with the cross-reactive idiotype (CRI). None of the mice synthesized intermediate levels of CRI. No relationship between H-2 type and idiotype was noted. Congenic mice with a strain A background but a different H-2 type produced CRI in amounts quantitatively equivalent to those of strain A mice. Conversely, the presence of the H-2 genotype of strain A on an unrelated background was not associated with the formation of CRI. Nearly all F(1) progeny of strain A mice formed CRI, indicating that failure of the other (non-A) parental strain to produce CRI is not attributable to the presence of a gene controlling the synthesis of a suppressor of CRI. NZB mice, which have the same heavy chain allotype as strain A, but are unrelated in origin, failed to produce CRI, although allotype has been shown to be linked to idiotype in congenic strains.

Anti-p-azophenylarsonate (anti-Ar) antibodies elicited in all strain A/J mice tested share one or more idiotypic specificities. These specificities are also found in the anti-Ar antibodies of mice of the closely related strain, AL/N, but not in those of BALB/c mice. Anti-Ar antibodies were elicited in congenic mice in which the IgC(H) locus of AL/N mice, which controls allotypic markers in the constant regions of heavy chains, had been introgressively backcrossed for nine generations onto a BALB/c background; the mice were then rendered homozygous for the AL/N allotypic determinant. On the average, these antibodies were quantitatively equivalent, with respect to content of the cross-reactive idiotype, to those of AL/N mice. This indicates that the gene controlling the idiotype is closely linked to the IgC(H) locus. Since idiotype must be a function of V region sequences, the results suggest close linkage of V(H) and C(H) genes. The cross-reactive idiotype was found in nearly all F(1) mice (C57/BL x A/J or BALB/c x A/J) tested.

The appearance of an idiotypic specificity, present in anti-p-azophenylarsonate (anti-Ar) antibodies of all immunized A/J mice, ran be suppressed in adult mice by prior administration of an IgG fraction of rabbit antiidiotypic (anti-D) antiserum; anti-Ar antibodies arise but are of different idiotype. Prolonged suppression was observed in earlier experiments, but antigen was first administered to adult mice only 2 wk or 9 wk after anti-D antibodies; subsequent escape from idiotypic suppression could have been masked by the capture of antigen by large numbers of memory cells having receptors of a different idiotype. In the present experiments antigen was first administered at intervals up to 22 wk after the antiidiotypic antibody. Suppression was maintained for 6 wk in all mice and for 5 mo in about half the mice tested. It thus appears that suppression of idiotype is less reversible if antigen is administered soon after the antiidiotypic antibody. The data suggest that escape from suppression is attributable to the generation of new precursor cells rather than to reactivation of suppressed cells. The minimum dosage of antiidiotypic IgG required for effective suppression was about 2 mg. The subcutaneous or intraperitoneal routes of inoculation of antiidiotypic IgG were equally effective. When antiidiotypic antibody was administered 3 days after antigen no suppressive effects were observed. There was partial suppression when antiidiotypic antibody was injected on the same day as the antigen. Fab' and F(ab')(2) fragments of antiidiotypic IgG had no suppressive effect. Quantitative measurements revealed no significant differences among control and suppressed mice with respect to total concentration of precipitable anti-Ar antibodies produced.