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Li Bo

Publications and source records attributed to Li Bo.

2 recordsLinked to original sources

Anatomy and clinical significance of pectoral fascia.

BACKGROUND: The submuscular or subglandular plane for breast augmentation is widely used. Recently, the subfascial plane for breast augmentation was reported by some authors who achieved satisfactory results. The anatomy of the pectoral fascia in Chinese female corpses was investigated to explore the possibility for a location of augmentation mammaplasty under the pectoral fascia. METHODS: The anatomy of 30 side pectoral fascias on 15 corpses was studied. The thicknesses of the pectoral fascias were measured. RESULT: The pectoral fascia is attached to the clavicle and sternum and covers the pectoralis major muscle. It is continuous inferiorly with the fascia of the abdominal wall. Furthermore, the pectoral fascia extends laterally to be continuous with the fascia of the back. The pectoral fascia, which can be successfully dissected bluntly along the subfascial plane, varies in thickness from 0.2 to 1.14 mm. Perforating branches of vessels and nerves emerging from the pectoral fascia are located mainly at the medial lateral and lower fascias. CONCLUSIONS: The pectoral fascias can be dissected bluntly along a subfascial plane with the pectoral fascia intact. The potential pocket between the pectoralis major muscle and the pectoral fascia can be used as a place for breast augmentation. The pectoral fascia may provide the breast implant with more soft-tissue coverage.

Adult↗

[Collagen type III glomerulopathy: a morphologic study].

OBJECTIVE: To study the morphologic changes of collagen type III glomerulopathy and to investigate the possible cellular origin for collagen III production. METHODS: Light microscopy, immunofluorescent staining, immunohistochemistry (for collagen I, III and IV and alpha-SMA) and electron microscopy studies on 3 renal biopsy cases of collagen type III glomerulopathy were performed. RESULTS: Two cases presented with nephrotic syndrome, one of which was associated with systemic hypertension. The third case showed renal impairment and renal hypertension. None had any known family history of renal diseases. Light microscopy showed diffuse thickened glomerular basement membrane and expanded mesangium with deposition of weakly PAS-positive homogeneous material not associated with mesangial cell proliferation. Electron microscopy revealed massive collagen fiber deposits in the subendothelial spaces and mesangium. The mesangial cells also contained bundles of microfilaments in the subplasmalemmal regions. Immunohistochemically, the diffuse positivity for type III collagen corresponded to the homogeneous material seen under light microscopy. The staining for type I and IV collagens was negative. Alpha-SMA was expressed in many mesangial cells. CONCLUSIONS: The diagnosis of collagen type III glomerulopathy can be made on the basis of detailed morphologic examination and ancillary investigations. It is possible that activated mesangial cells may be the cellular origin of collagen III.

Actins↗