Placement of anterior cervical instrumentation without intraoperative radiography.

Adequate fixation with several commonly used anterior cervical plate systems requires that the screws penetrate both the anterior and posterior cortices of the vertebral bodies. This report emphasizes the shortcomings of plain film and fluoroscopic examinations in confirming screw position through the posterior vertebral cortex in three patients with lower cervical trauma or tumor. These cases and radiographs of isolated vertebrae from the cervicothoracic region demonstrate the inadequacy of plain film/fluoroscopy for determination of the position of anterior cervical plate screws in relation to the posterior cortex. Only axial images such as those obtained with computed tomography are able to show the exact relationship of the screws to the posterior cortical curvature in C7 and T1.     

The role of angiotensin II in regulation of cerebrospinal fluid formation in rabbits.

The effect of central and peripheral administrations of angiotensin II (AII) on cerebrospinal fluid (CSF) formation was investigated in rabbits anesthetized with intravenous alpha-chloralose and urethane. CSF production was measured by the ventriculo-cisternal perfusion method with Blue dextran 2000 used as an indicator substance. AII infused intracerebroventricularly (i.c.v.) at rates of 5.5 and 55 pg min-1 significantly decreased CSF formation rate by 27% and 36%, respectively. This AII action could be completely blocked by simultaneously administered specific AII antagonist, [Sar1,Ala8]AII (saralasin), given i.c.v. at a rate of 5.5 ng min-1. Intracerebroventricular infusion of AII at a rate of 5.5 ng min-1 did not change CSF production. Saralasin, when given alone into the ventricular system (5.5 ng min-1), non-significantly increased CSF production by 12%. However, in 4 of the 6 animals studied, the rise in CSF production was statistically significant (by 23%). Intravenous infusion of AII at rates of 30 and 100 ng kg-1 min-1 was found not to change CSF formation rate. Also, i.c.v. administration of angiotensin I converting enzyme inhibitor, captopril (10 microliters min-1), did not influence CSF production. It is concluded that the centrally released AII can control CSF production. Our results suggest that under normal conditions, AII exerts a tonic inhibitory effect on CSF formation. In contrast, the blood-borne peptide seems not to influence this physiological process.     

Inferior eyelid reconstruction. Various technics as a function of the length of substance loss

The authors expose the three technics for the inferior eyelid reconstruction which seem them now the most certain. If the defect is inferior at the quarter of the eyelid: suture with only one junction; if it is included between the quarter and the half of this length: tarso-conjunctival graft and cutaneous flap if it surpasses the half of the eyelid length: nasal chondromucous graft and temporojugal flap.     

Effects of interleukins on connective tissue type mast cells co-cultured with fibroblasts.

We investigated the effects of interleukin-2 (IL-2), interleukin-3 (IL-3) and interleukin-4 (IL-4) on mouse and rat peritoneal mast cells (MC) co-cultured with 3T3 fibroblasts (MC/3T3). The continuous presence of these cytokines for 7-9 days in the culture media was neither toxic nor caused proliferation of MC, as determined by the stability of MC numbers in culture. Long-term incubation of mouse MC/3T3 with IL-2 (100 U/ml), IL-3 (50 U/ml), IL-4 (50 U/ml) or a mixture of IL-3 and IL-4 (25 U/ml) induced an increase in basal histamine release of 79.3 +/- 19.0%, 41.0 +/- 17.3%, 25.2 +/- 10.4% and 30.2 +/- 3.2%, respectively, over control cells incubated with medium alone. When rat MC/3T3 were incubated for 7 days with the various interleukins an enhancement in histamine release similar to that observed with mouse MC/3T3 was found. Preincubation (1 hr) of rat MC/3T3 with interleukins prior to immunological activation with anti-IgE antibodies enhanced histamine release. The highest effect was observed with IL-3 + IL-4 (60.4 +/- 10.8% increase) followed by IL-2 (51.5 +/- 4.5%), IL-4 (28.6 +/- 10.3%) and IL-3 (13.2 +/- 4.2%). This study demonstrates that when mouse and rat peritoneal MC are cultured with fibroblasts in the presence of interleukins they do not proliferate, suggesting that they preserve their connective tissue type MC phenotype. Moreover, interleukins display a pro-inflammatory effect on these cells by enhancing both basal and anti-IgE-mediated histamine release.     

Psychotherapy for depression: current and future directions in research, theory, practice and public policy

This article is based on a symposium held at the 1998 Annual Meeting of Society for Psychotherapy Research (Snow Bird, Utah). Recognized experts addressed current and future directions in psychotherapy for depression from the perspectives of process and outcome research, basic research, theoretical models, clinical practice and training, and public policy. The specific issues discussed at the symposium included the strengths and limitations of major forms of psychotherapy; the therapeutic factors common and unique to different approaches; the future viability of current theories of depression; the role of treatment manuals in clinical practice and training; the development of new interventions based on basic research; and the priorities that should guide federal funding.     

Lactic dehydrogenase virus (LDV) impairs the antigen-presenting capacity of macrophages yet fails to affect their phagocytic activity

The effect of acute infection of mice with lactic dehydrogenase virus (LDV) on two major functions of peritoneal macrophages was tested. Using a macrophage-dependent T cell proliferative assay to test the antigen-presenting capacity of LDV-infected macrophages we found that LDV impairs the capacity of antigen-presenting cells to trigger memory T lymphocytes. Endocytosis of antigen by LDV-infected macrophages was similar to that of uninfected cells. In addition, the proportion of intracellular antigen versus membrane-bound antigen in LDV-infected cells were similar to that observed in uninfected mice. It appears therefore, that the impaired immunogenic effect of LDV-infected macrophages results from reduced immunogenicity of the membrane-bound antigen.Testing the phagocytic activity of peritoneal macrophages we found that the uptake of radiolabeled antibody-coated sheep erythrocytes or bacteria (E. coli) by infected cells was similar to that by uninfected macrophages. In addition, LDV failed to affect the ability of peritoneal macrophages in a nitroblue tetrazolium reduction reaction which serves as an alternative parameter for measuring phagocytic activity. Our results support the assumption that LDV, which probably propagates in the cells of the reticuloendothelial system, impairs some of the immunogenic functions of macrophages and thereby affects macrophage-dependent immune responses.     

Induction of a stable hapten-specific immunosuppression by a hapten conjugated to poly(N-vinylpyrrolidone) (PVP).

The ability of a hapten coupled to a clinically permissive synthetic polymer (NIP-PVP) to induce suppression was investigated. NIP coupled to the low molecular weight non-immunogenic form of poly(N-vinylpyrrolidone) (PVP) was found to be capable of inducing a hapten-specific longlasting suppression of both primary and secondary responses. The previous use of PVP as a plasma expander in humans makes this polymer a potentially suitable tool for the induction of specific immunosuppression to a variety of clinically important drug and tissue specific epitopes. The possible use of low molecular weight PVP for that purpose will be investigated further, specifically with larger antigenic components.     

Adaptive modification of the vestibulo-ocular reflex by mental effort in darkness

Summary The vestibulo-ocular reflex (VOR) can be suppressed in darkness if a subject tries to imagine that he looks at a head fixed target. This mental suppression of VOR was used to induce adaptive changes in VOR gam during 3 h of active head oscillations in complete darkness. VOR gain changes were tested by asking the subject to look at a visual target; then passively or actively the head was turned in darkness while the subject fixated the same target. Corrective saccades occurring at the end of the movement when lights were turned on give an elegant measure of VOR gain. Three hours of training induced in 3 subjects a mean of 10.9% and 11.4% decrease of VOR gain for passive and active conditions, respectively. This demonstrates that reflex adaptation can be obtained without external cues, and probably with only an internal reconstruction of target and eye movement.     

Interaction between sympathetic nerve activation and muscle fibre contraction in resistance vessels of hamster retractor muscle

The interaction between skeletal muscle contraction and sympathetic nerve activation (SNA) on blood flow during exercise has remained ambiguous due to indirect estimates of vasomotor control. In the hamster retractor muscle (   n = 54  ), interactions between three levels of SNA (∼3, 6 and 12 Hz) and of contractile activity (2.5, 10 and 20 % duty cycle) were studied in feed arteries (FA) and first- (1A), second- (2A), and third-order (3A) arterioles using intravital microscopy. During functional dilatation with rhythmic muscle contractions, sympathetic vasoconstriction was sustained in FA and 1A but impaired in 2A and 3A (   P < 0.05  ), where vessels 'escaped' from responding to SNA. To account for changes in baseline diameter and blood flow during contractions, vasodilatation was induced passively (2–3 levels) in resting muscles with papaverine or sodium nitroprusside. Compared to functional dilatation, the range of passive dilatation was similar in 3A and progressively greater in 2A, 1A and FA. With passive dilatation, SNA responses were sustained in 2A and increased with baseline diameter in 3A. Blood flow through FA (rest, ∼20 nl s⁻¹) increased ∼5-fold during contractile activity and ∼10-fold during passive dilatation. Absolute flow reductions (nl s⁻¹) with SNA increased during contractile activity and during passive dilatation; relative flow reductions were impaired during functional dilatation (   P < 0.05  ) and remained constant during passive dilatation. Thus, SNA can restrict blood flow to exercising muscle by constricting FA and 1A while dilatation prevails in 2A and 3A. Such concerted interaction will promote oxygen extraction when blood flow is restricted to maintain arterial pressure.