Biomedical subjects

L Lim

Publications and source records attributed to L Lim.

256 records · Page 15Linked to original sources

PubMedDate not supplied

Saccadic velocity analysis in patients with divergence paralysis.

Twelve patients with clinical findings of divergence paralysis underwent horizontal saccadic velocity testing. Peak velocities were measured using digitally sampled electro-oculography during 10 degrees, 20 degrees, and 30 degrees saccades. Results were compared with those of 12 age-matched controls. The peak saccadic velocities of each eye in adduction and 10 degrees abduction did not differ from those of age-matched controls (P > .05). The 20 degrees and 30 degrees abducting saccades showed mildly reduced saccadic velocities when compared with controls (P < .05). The finding of only mildly reduced abduction saccadic velocities bilaterally is not consistent with bilateral lateral rectus palsy. The data support the hypothesis that divergence paralysis represents a distinct clinical entity unrelated to abducens nerve paresis and argues for the existence of an active divergence center. We further report the surgical results of five patients who were treated with strabismus surgery. A 4.0 to 6.0 mm bilateral lateral rectus muscle resection corrected 16 to 30 delta of esotropia at distance without resulting in an overcorrection at near. Bilateral lateral rectus muscle resection is an effective therapy for divergence paralysis.

Abducens Nerve↗

PubMedDate not supplied

Manganese mineral interactions in brain.

Manganese (Mn) is an essential mineral but is toxic when taken in excess. However, whether its interactions with other minerals in organs and cells are involved in mechanisms underlying Mn toxicity is poorly understood. We designed a developmental rat model of chronic Mn treatment (Group A: 1 mg MnCl2.4H2O per ml of drinking water; Group B: 10 mg MnCl2.4H2O per ml of drinking water; Group C: 20 mg MnCl2.4H2O per ml of drinking water; Control Group given water without manganese addition). Employing the model and instrumental neutron activation analysis, we investigated two hypotheses: (i) chronic manganese treatment alters the brain regional distribution of manganese and this altered manganese distribution also leads to region-specific changes of other metals; (ii) chronic manganese treatment induces differential changes in subcellular distributions of metals and electrolytes. In the treated rats, brain Mn level showed dose-related increases, the most pronounced being noted in striatum, hypothalamus, and hippocampus: these increases also led to alterations in regional distribution pattern of Mn. In the treated rats, Fe level was increased in hypothalamus, cerebellum, hippocampus, pons and medulla, and striatum. Cu level was increased in pons and medulla, hippocampus, midbrain, and striatum. Se level was increased in cerebellum, striatum, midbrain, hypothalamus, and pons and medulla. Zn level was increased in hypothalamus and striatum. Ca level was increased in midbrain but decreased in cerebellum; however, Mg and Al levels were not markedly affected. In brains of Mn-treated rats, Mn levels in subcellular fractions were all increased, being especially marked in nuclei, mitochondria, and synaptosomes; the subcellular distributions of Fe, Cu, Zn, and Mg were differentially altered although those of Al and Ca were minimally affected. These results are consistent with our hypotheses and may have implications in manganese neurotoxicity. The cellular and molecular mechanisms underlying manganese-mineral interactions in brain are still poorly defined and merit further investigation.

Administration, Oral↗

PubMedDate not supplied

Signal therapy for RAS-induced cancers in combination of AG 879 and PP1, specific inhibitors for ErbB2 and Src family kinases, that block PAK activation.

BACKGROUND: Both EGF family ligands and ErbB family receptor kinases act upstream of RAS to induce mitogenesis of normal cells, such as NIH 3T3 fibroblasts. However, oncogenically mutated RAS, such as v-Ha-RAS is constitutively activated and therefore no longer requires these ligands or receptors for its activation. Nevertheless, it up-regulates the expression of these EGF family ligands. To understand the biologic significance of RAS-induced up-regulation of these ligands in both RAS-induced PAK activation and malignant transformation, we have conducted the following studies, based on the previous observations that (1) the N-terminal SH3 domain of PIX selectively binds a Pro-rich domain of 18 amino acids of PAKs, CDC42/Rac-dependent Ser/Thr kinase family, and (2) this specific interaction is essential for both PAK activation and membrane ruffling RESULTS: Using four distinct, cell-permeable, and highly specific inhibitors, namely WR-PAK18, which blocks the PAK-PIX interaction; AG 1478, which inhibits ErbB1 kinase activity; and AG 825 or AG 879, which inhibits ErbB2 kinase activity, we demonstrate that (1) the PAK-PIX interaction is essential for v-Ha-RAS-induced malignant transformation; (2) v-Ha-RAS requires not only ErbB1 but also ErbB2, which are activated through two independent autocrine pathways to induce both the PIX/Rac/CDC42-dependent PAK activation and malignant transformation in vitro; and (3) a combination of AG 879 and the Src family kinase-specific inhibitor PP1 suppresses almost completely the growth of RAS-induced sarcomas in nude mice. CONCLUSION: These findings not only change our conventional view on the role of these RAS-inducible ligands and ErbB family receptors (serving as RAS activators) but also suggest a new avenue for the treatment of RAS-associated cancers by a combination of inhibitors specific for ERbB, Src, or PAK family kinases.

3T3 Cells↗

PubMedDate not supplied

Infected late false aneurysm of the deep femoral artery.

A false aneurysm may mimic an abscess, but concomitant existence of the two lesions seems not to have been previously described. In a 32-year-old man, a false aneurysm of the deep femoral artery was found to be in communication with an abscess cavity in the posterolateral thigh. The false aneurysm was found in the proximity of the protruding tip of a Steinmann pin which had eroded the arterial wall. The abscess was a consequence of posttraumatic and postoperative osteomyelitis which had been previously debrided, bone grafted, and immobilize with an external fixator attached to four Steinmann pins. The condition was successfully treated by surgical drainage of te abscess cavity, excision of the false aneurysm, and ligation of the deep femoral artery.

Abscess↗