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Biomedical subjects

P T Wang

Publications and source records attributed to P T Wang.

7 recordsLinked to original sources

Multiple-revolution spiral osteotomy for cranial reconstruction. Technical note.

Various combinations of cranial remodeling techniques are used in an attempt to provide optimal cosmetic results and to reduce possible sequelae associated with craniosynostosis. One element of deformity that is difficult to correct directly is an overly flattened area such as that found in the parietal area in sagittal synostosis, unilaterally in lambdoid synostosis, or even in severe positional molding. The authors present a novel application for recontouring cranial bone, namely the multiple-revolution spiral osteotomy. The advantages of this technique include the avoidance of large areas of craniectomy and immediate correction of the cranial deformity. The surgical procedure, illustrative cases, early results, and apparent benefits of this technique are discussed.

Craniosynostoses↗

[Inhibitory activity of Dianthus superbus L. and 11 kinds of diuretic Traditional Chinese medicines for urogenital Chlamydia trachomatis in vitro].

OBJECTIVE: To detect the susceptibility of urogenital chlamydia trachomatis(CT) to 12 kinds of diuretic traditional Chinese medicines. METHODS: The inhibitory activity of these medicines for CT was detected by microculture technique of McCoy cell in vitro. RESULTS: All the 12 kinds of diuretic traditional Chinese medicines had inhibitory activities for urogenital CT, with minimal inhibitory concentrations (MICs) from 0.122 mg.ml-1 to 62.5 mg.ml-1. The activities of Dianthus superbus L., Poria cocos(Shcw.) Woft, Polyporus umbellatus and Artemissia capillaris were stronger. The number and volume of CT inclusions reduced gradually and disappeared finally with the rise of concentration. CONCLUSION: All the 12 kinds of diuretic traditional Chinese medicines possess some inhibitory activity for urogenital CT.

Artemisia↗

Ultrasonic assistance in the diagnosis of hand flexor tendon injuries.

In contrast to routine flexor tendon injuries, flexor tendon ruptures following blunt injury or re-ruptures following repair can be difficult to diagnose. The authors investigated the efficacy of using ultrasound to assist in the diagnosis. From 1996 to 1997, 8 patients underwent evaluation of the flexor tendons using an ATL HDI-3000 ultrasound machine with a high-resolution, 5 to 9-MHz hockey stick linear probe. Dynamic evaluation was performed in real time, simulating clinical symptoms. Six patients underwent surgical exploration. Sonographic diagnosis and intraoperative findings were correlated. Ultrasound was used to diagnose 3 patients with ruptured flexor digitorum profundus tendons. Mechanisms of injury included forceful extension, penetrating injury, and delayed rupture 3 weeks after tendon repair. Subsequent surgical exploration confirmed the ruptures and location of the stumps. Five patients had intact flexor tendons by ultrasound after forceful extension, penetrating injury, phalangeal fracture, crush injury, and unknown etiology. In 3 patients who underwent surgery for tenolysis, scar release, or arthrodesis, the flexor tendons were found to be intact, as predicted by ultrasound. The authors found ultrasound to be accurate in diagnosing the integrity of flexor tendons and in localizing the ruptured ends. They conclude that ultrasound is helpful in evaluating equivocal flexor tendon injuries.

Adult↗

Abnormal T cells from MRL/Mp-lpr/lpr mice do not respond to anti-T-cell-receptor antibody or tumor promoter and calcium ionophore A23187 despite the presence of the T-cell-receptor complex and protein kinase c.

Abnormal T cells from autoimmune MRL/Mp-lpr/lpr mice express T-cell-receptor complexes on their surfaces. These receptors are nonfunctional, since monoclonal anti-T-cell-receptor antibody-conjugated beads, which normally activate receptor-bearing T cells, were unable to activate these abnormal T cells. In addition, these abnormal T cells are unresponsive to the synergistic effect of phorbolmyristate acetate (PMA) and calcium ionophore A23187, as quantitated by proliferation, interleukin-2(IL-2) production, and the expression of IL-2 receptors. The failure of abnormal T cells to respond to PMA is not due to the absence of PMA receptors since Scatchard plot analysis reveals that there are 1-1.5 X 10(5) PMA-binding sites/cell with a Kd of 6-10 nM on these abnormal T cells. Similar to normal T lymphocytes, protein kinase c activity can be readily detected in the cytosolic fraction of these abnormal T cells. More importantly, in vitro culture of the abnormal T cells with PMA results in translocation of protein kinase c activity from the cytosolic fraction to the membrane fraction. From these experiments we concluded that the defect in the signal-transducing machinery in MRL/Mp-lpr/lpr T cells is not due to the lack of PMA receptors or the absence of protein kinase c activity, but may result from events which occur after the activation and translocation of protein kinase c. However, whether defects in response to a physiological stimulus (i.e., anti-receptor antibody) could occur in a step prior to protein kinase c activation remains to be determined.

Animals↗

Selective down modulation of L3T4 molecules on murine thymocytes by the tumor promoter, phorbol 12-myristate 13-acetate.

Treatment of murine thymocytes, but not mature peripheral T cells, with the tumor promoter, phorbol 12-myristate 13-acetate (PMA), 3 results in a rapid disappearance of L3T4 molecules from the surface of thymocytes. The effect of PMA on L3T4 molecules persists in vitro for at least 72 hr. Down modulation of L3T4 molecules was PMA dose-dependent and temperature-dependent. L3T4 molecules on cortisone-resistant thymocytes were significantly less sensitive to the effect of PMA than were L3T4 molecules on cortisone-sensitive thymocytes. Down modulation of L3T4 molecules on thymocytes did not interfere with their capacity to respond to concanavalin A or activation signals delivered via their T cell receptors. The difference in the ability of thymocytes and peripheral T cells to respond to PMA cannot be explained by differences in the number of PMA receptors. Both thymocytes and peripheral T cells have PMA receptors in the range of 1 to 1.5 X 10(5) receptors/cell. However, there is a small difference in the affinity (Kd) of the receptors on thymocytes (Kd = 30 to 40 nM) and peripheral T cells (Kd = 10 to 15 nM). Immunofluorescent staining revealed that the down modulation of L3T4 molecules by PMA was a result of internalization of L3T4 molecules. After down modulation, L3T4 could be readily detected on the cytoplasm of thymocytes. These findings suggest that L3T4 molecules on thymocytes may be subject to different regulatory signals than L3T4 molecules on peripheral T cells.

Animals↗