Duodenal leiomyosarcoma presenting as a pulmonary lesion.
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Biomedical subjects
Publications and source records attributed to P S Lin.
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This study was undertaken to explore whether we could provide supportive laboratory evidence for the clinical observations that a stroke patient has lost functional mobility/locomotion capability based on dynamic balance responses (center of force sway patterns) and motor control activities (electromyography patterns) during the motor task of sit-to-stand. A computerized controlled dynamic postural control assessment system was developed and used in this study. Various dynamic balance indexes were introduced and derived from center of force sway patterns expressed in four domains (space, time, force, and frequency). Motor control was assessed by multichannel surface electromyography of each side of the lower limb during the same motor task. The functional mobility capability was evaluated using the traditional FIM method. Fourteen stroke patients with right hemiplegia and nine healthy elderly individuals were recruited as the experimental and control groups, respectively. Muscle activity was recorded for quadriceps, hamstrings, anterior tibialis, and triceps surae muscles and was used for analysis. Center of force sway patterns and ground reaction forces were registered. All signals were synchronized at "seat-off." Surface electromyographic patterns of activities recorded during sit-to-stand and dynamic balance indexes computed from center of force sway patterns were categorized and compared with the functional mobility scores. Results show that both the motor control patterns and dynamic balance indexes correlated well to the extent of mobility impairment evaluated using the traditional FIM method. An important conclusion for rehabilitation medicine is that the functional mobility capability of stroke patients may be expressed numerically using dynamic balance indexes and visualized graphically through electromyographic motor patterns.
Normal blood vessels are leakage proof, non-adherent to blood cell elements, and participate actively in directional blood flow. These properties rely on the shape of endothelial cells and the integrity of the endothelial cell monolayer. The often observed effects of tumour necrosis factor-alpha (TNF) and hyperthermia on tumour tissue are the disruption of blood flow and an increase of vascular permeability. These agents are also known to affect the cytoskeletal organization and the cytoskeleton-dependent cellular functions. We observed that TNF (100 U/ml for 60 min) or heat (43 degrees C for 60 min) treatment causes the collapse of actin filaments in human umbilical vein endothelial cells (HUVEC). The combined treatment of TNF and hyperthermia intensifies the change of shape and loss of actin filaments. However, these changes are reversible within 24 h. These transient changes may contribute to the dysfunction and increased leakage of the microvasculature in tumours during and after these treatments despite the fact that the viability determined by MTT assay did not show a significant interaction between TNF and hyperthermia. Radiation (5 Gy) and TNF interact to a lesser extent compared with heat and TNF on cell shape and actin filament organization in HUVEC. Heat or radiation treatment enhances the expression of ELAM-1 mRNA in HUVEC while TNF produces the strongest effect on ELAM-1 mRNA expression. Our study suggests that radiation and heat affect endothelial cells and their subsequent functions differently. Result of an interaction between heat and TNF on endothelial cells supports the common notion that the anti-tumour effect by heat plus TNF treatments may benefit due to the increased disruption of vasculature function in the tumour.
The antitumour effects of flavone acetic acid (FAA) against a broad spectrum of established experimental tumours has been demonstrated. Damage to the vasculature, which rapidly disrupts blood flow and induces haemorrhagic necrosis, is believed to be a major mechanism contributing to the observed antitumour effects. Despite these established observations, FAA has shown little effect against human tumours. However, other applications of FAA, for examples, for an extended period of treatments or in combination with other antitumour modalities, have not been sufficiently explored. In order to test the direct effects of FAA on vasculature, endothelial cells isolated from human umbilical vein (HUVEC) and bovine pulmonary artery (CPAEC) were used in this study. FAA at the concentrations of 50 to 200 micrograms/ml causes reduction in cell number (from 20 to > 30% of the cells) of HUVEC as measured by MTT assay after 1, 3, and 5 h of treatment at 37 degrees C. FAA did not produce significant effects on similarly treated human squamous cell carcinoma, cell line UM-SCC-2. After 1 h treatment of FAA at 300 micrograms/ml, a large number of HUVECs failed to react with an actin stain, NBD-phallacidin. The growth of HUVECs and CPAEC in the presence of FAA for 1-3 days was progressively reduced. The number of HUVEC treated for 3 days at the concentrations of 100, 200, and 300 micrograms/ml were reduced by 75-86% in comparison with the control culture. The experiments with CPAEC showed similar results. The inhibition of the growth of endothelial cells by FAA was enhanced when it combines with tumour necrosis factor-alpha but not with interleukin-1, interferon-gamma, heat, or radiation. We observed that FAA can initiate both immediate effects and growth inhibition on cultured endothelial cells. These results support the notion that FAA rapidly induces vasculature damage. Furthermore, cytokines such as tumour necrosis factor-alpha can enhance the toxicity of FAA on endothelial cells.
The purpose of this study was to explore whether we could provide supportive laboratory evidence for clinical observations that a stroke patient has lost functional mobility/locomotion capability based on dynamic balance responses (centre of pressure, COP sway patterns) and motor control activities (EMG patterns) during the motor task of sit-to-stand. A computerized controlled dynamic postural control assessment system was developed and used in this study. Various dynamic balance indices were introduced and derived from COP sway patterns expressed in four domains (i.e. space, time, force, and frequency). Motor control was assessed by multi-channel surface electromyography of each side of the lower limb during the same motor task. The functional mobility capability was evaluated using a traditional FIM method. Fourteen stroke patients with right hemiplegia and nine healthy elderly were recruited as the experimental and control groups respectively. Muscle activity was recorded for quadriceps, hamstrings, anterior tibialis, and triceps surae muscles and used for analysis. Centre of pressure sway patterns and ground reaction forces were registered. All signals were synchronized at 'seat-off'. Surface electromyographic patterns of activities recorded during sit-to-stand and dynamic balance indices computed from centre of pressure sway patterns were categorized and compared with the functional mobility scores. The results show that both the motor control patterns and dynamic balance indices correlated well to the extent of mobility impairment evaluated using the traditional FIM method. An important conclusion for rehabilitation medicine is that the functional mobility capability of stroke patients may be quantified analytically using dynamic balance indices and visualized graphically through EMG motor patterns.