Microelectrode findings and topographic reorganisation of kinaesthetic cells after gamma knife thalamotomy

Summary  A 64-year-old woman with Parkinson is disease had a severe resting tremor that was not completely relieved by right-sided gamma knife thalamotomy (GKT). We performed bilateral staged thalamic deep brain stimulation (DBS) and compared the right and left ventral intermediate nucleus (Vim) of the thalamus including the frequency of single units recorded with microelectrodes, and also the somatotopical distribution of kinaesthetic cells (Ki). The average frequency of units for the presumed left Vim exceeded that of the right (22.6 ± 19.2 Hz vs. 14.3 ± 8.8 Hz). Regarding the somatotopic distribution of Ki, the receptive field for the leg, which is usually situated in the dorsolateral Vim, was more widely scattered in the right Vim than the non-lesioned left side. Our findings raise the possibility that the specific properties of the neurons changed due to partial coagulation by GKT within both the coagulated and the surrounding thalamic lesions. Correspondence: Tohru Terao, Department of Neurosurgery, Tokyo Metropolitan Neurological Hospital, 2-6-1 Musashidai Fuchu-shi, Tokyo, Japan.     

Initial bone regeneration around fenestrated implants in Beagle dogs using basic fibroblast growth factor–gelatin hydrogel complex with varying biodegradation rates

PurposeThe purpose of this study was to compare the effectiveness of fast and slow biodegradation of basic fibroblast growth factor (bFGF)–gelatin hydrogel complex on bone regeneration around fenestrated implants as a new augmentation drug delivery system.MethodsNine titanium implants (3.3 mm diameter and 10 mm length) were placed into the edentulous areas of the mandibles of three adult beagle dogs with four screws exposed at the upper buccal side. The effectiveness of bFGF–gelatin hydrogel complexes of varying degradation types used to cover implant screws without membrane were compared with 1 μg and 10 μg bFGF–98 wt% gelatin as the fast degradation type and 10 μg bFGF–95 wt% gelatin as the slow degradation type. After 4 weeks, bone regeneration around the screws was evaluated histologically and histomorphometrically.ResultsWith use of 10 μg bFGF, regenerated bone around exposed screws was clearly seen in both the fast and slow degradation type groups. In contrast, little bone formation was seen in the fast degradation-type group with 1 μg bFGF. Height of regenerated bone for the slow degradation-type complex group was significantly greater than for the fast degradation-type group with 1 μg bFGF (P < 0.05).ConclusionThese results suggest that use of slow degradation-type bFGF–gelatin hydrogel complex may accelerate bone regeneration around fenestrated implants at an early stage of bone regeneration.     

An anti-inflammatory drug, propagermanium, may target GPI-anchored proteins associated with an MCP-1 receptor, CCR2.

Monocyte chemoattractant protein-1 (MCP-1) promotes the migration and activation of monocytes and plays a pivotal role in the development of chronic inflammation. Propagermanium (3-oxygermylpropionic acid polymer) has been used as a therapeutic agent against chronic hepatitis B in Japan. We report here that propagermanium specifically inhibits in vitro chemotactic migration of monocytes by MCP-1. Propagermanium did not inhibit binding of MCP-1 to a human monocytic cell line, THP-1 cells, or affect intracellular Ca(2+) mobilization or the cAMP concentration in MCP-1-treated THP-1 cells. The effect of propagermanium seems to require glycosylphosphatidylinositol (GPI)-anchored proteins, as cleavage of GPI anchors by phosphatidylinositol-phospholipase C (PI-PLC) eliminated the inhibitory activity of propagermanium. Anti-GPI-anchored protein antibodies, such as anti-CD55 and anti-CD59, reduced staining of C-C chemokine receptor 2 (CCR2) with an anti-CCR2 antibody against the N-terminus of CCR2 in a flow cytometric analysis, and these antibodies also selectively inhibited MCP-1-induced migration of THP-1 cells. Furthermore, under fluorescence microscopy, GPI-anchored proteins colocalized with CCR2 on THP-1 cells. These results suggest that propagermanium may target GPI-anchored proteins that are closely associated with CCR2 to selectively inhibit the MCP-1-induced chemotaxis, thus providing a mechanistic basis for the anti-inflammatory effects of the drug.     

A mutant of Escherichia coli enterotoxin inducing a specific Thl-type of T cells to varicella-zoster vaccine enhances the production of IL-12 by IFNgamma-stimulated macrophages

A mutant of Escherichia coli enterotoxin induces specific Thl-type T cells to varicella-zoster vaccine. The mutant increased IL-12p40, TNFalpha and nitric oxide production by IFNgamma-stimulated bone marrow macrophages but cholera toxin did not. Anti-TNFalpha antibodies blocked its stimulation of IL-12p40 production but iNOS inhibitor did not. IL-12p40 and IL-12p35 production was stimulated at the level of mRNA formation by the mutant. Cholera toxin suppressed IL-12beta1 expression by spleen T cells stimulated with anti-CD3 antibodies but the mutant did not. These findings indicate that the mutant may induce Thl-type response to the vaccine through its IL-12 and TNFalpha induction by macrophages.     

Lethal thrombus in the carotid artery during operation for acute aortic dissection with cerebral malperfusion

A drowsy patient with acute type A aortic dissection and cerebral malperfusion required emergency operation. Because the right carotid artery was totally obstructed, cerebral perfusion was first restored by cannulating it and the left femoral artery before midline sternotomy. However, a long fresh thrombus was found flowing backward from the obstructed carotid artery. This thrombus was removed, and both arteries were connected through a Y-shaped extracorporeal circulation circuit to reperfuse the brain. During the subsequent aortic procedure, both arteries were used for arterial inflow. Such thrombi can cause grave postoperative neurologic dysfunction. Carotid artery cannulation is mandatory in such cases.     

Interferon (IFN)-beta induces apoptotic cell death in DHL-4 diffuse large B cell lymphoma cells through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)

The effect of interferon (IFN)-alpha, beta and gamma on the growth of DHL-4 diffuse large B cell lymphoma cells was studied. IFN-beta significantly inhibited the cell growth, and the effect was stronger than that of IFN-alpha. IFN-gamma did not inhibit the cell growth because of lack of IFN-gamma receptors. IFN-beta caused apoptotic cell death which was accompanied by DNA fragmentation, caspase 3 activation and annexin V binding. IFN-beta lead to the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA. Anti-TRAIL antibody significantly prevented IFN-beta-induced apoptosis. It was suggested that IFN-beta might cause apoptosis in DHL-4 cells through TRAIL.