Accelerated reversal of pancuronium blockade with divided administration of neostigmine

Key words  reversal of neuromuscular blockade pancuronium - neostigmine     

Flow cytometric DNA analysis of vascular soft tissue tumors, including African endemic-type Kaposi's sarcoma.

Vascular tumors of the soft tissue display a wide spectrum of histologic features and biologic behavior. Flow cytometric DNA analysis was performed on 40 vascular tumors, including nine African endemic-type Kaposi's sarcomas, nine angiosarcomas, seven hemangiopericytomas, six glomus tumors, and nine capillary hemangiomas. Six of the nine angiosarcoma cases (67%) and one of the seven hemangiopericytomas cases (14%) were aneuploid. All benign vascular tumors and Kaposi's sarcomas were diploid. Clinically, five of the six angiosarcoma patients with aneuploidy died within 2 to 28 months, while the remaining patient, who had the smallest tumor (2 x 1 cm), survived more than 4 years after the initial diagnosis was made. All three angiosarcoma patients with diploidy died within 10 to 14 months. One hemangiopericytoma patient with aneuploidy died within 1 month. No cases of benign tumor recurred. These results suggest that most vascular tumors, which generally follow a benign clinical course, were diploid and that the majority of those with a poor outcome were aneuploid. However, flow cytometrically assessed DNA ploidy has no prognostic value in angiosarcomas or hemangiopericytomas.     

Rapid development of renal lesions in diabetic DBA mice infected with the D-variant of encephalomyocarditis virus (EMC-D).

Marked hyperglycaemia and renal lesions developed rapidly in DBA mice infected with 10 plaque-forming units of the D-variant of encephalomyocarditis virus (EMC-D). Renal alterations were demonstrated in the glomeruli, tubular epithelium and small vessels 2 months after infection. Glomerular changes were characterized by mesangial thickening due to an increase of basement membrane-like material in the mesangial matrix. Nodular glomerular lesions were commonly observed 3 months after infection, whereas distinct thickening of the glomerular basement membrane was rarely seen. Besides these glomerular changes, glycogen inclusions in the distal tubular epithelium and medial degeneration in the arterioles were also noticed. The EMC-D-infected DBA mouse appears to be a useful experimental model for the study of human diabetic nephropathy.     

The Role of Cathepsin D in the Pathogenesis of Tuberculosis: A Histochemical Study Employing Unlabeled Antibodies and the Peroxidase-Antiperoxidase Complex

Cathepsin D was visualized in free pulmonary alveolar macrophages (AM), in oil-induced peritoneal macrophages (MN) and in rabbit pulmonary and dermal BCG lesions with unlabeled antibodies and the peroxidase-antiperoxidase (PAP) complex. Large amounts of cathepsin D were present in AM and lower amounts in MN. In the lung this enzyme was richest in the alveolar macrophages that accumulated around the BCG lesions. In the dermal lesions, cathepsin D was in highest concentration in macrophages at the border of the necrotic (liquefying) centers. It was also found in high concentration in keratinizing cells of the dermal epithelium and hair follicles. It did not, however, increase appreciably in many of the activated macrophages that stained intensely for the lysosomal enzyme β-galactosidase. In fact, many epithelioid cells with high β-galactosidase activity contained no visible cathepsin D. This proteinase does not, therefore, seem to be primarily involved in the lymphocyte-mediated macrophage activation associated with acquired cellular resistance to tubercle bacilli. It is probably more involved with cell autolysis, with the digestion of ingested necrotic debris and, in all likelihood, with the process of liquefaction, the most adverse event in the pathogenesis of tuberculosis in man.     

ADENOID SQUAMOUS CELL CARCINOMA OF THE SKIN OVERLYING THE RIGHT BREAST: An Autopsy Case Clinically Manifested with Rapid Growth and Widely Spreading Metastases

An autopsy case of a 62-year-old woman with a poorly differentiated, aggressive form of adenoid squamous cell carcinoma arising in the skin overlying the right breast was studied. The tumor, 9×8cm in diameter, had rapidly enlarged since one year before admission from a verrucous lesion of 20 years duration. The histologic features of the tumor showed a well-differentiated squamous cell carcinoma mainly in the superficial areas, which transformed into, with a zone of transition in between, an alveolar or adenoid structure in the deep invading portion. The adenoid tumor cells exhibited an undifferentiated appearance with prominent nucleoli and frequent mitotic figures. These cells partly showed dyskeratotic or acantholytic features. Mucin was negative. The patient died at 8 months after the operation. Autopsy revealed widely spreading metastases in which an adenoid structure was outstanding. These unusual pathological features and an aggressive behavior of this tumor, which were hitherto rarely described for adenoid squamous cell carcinoma, seemed to be a poorly differentiated variant of the tumor. This malignant transformation might be derived from loss of cohesion of the pre-existing usual well-differentiated squamous cell carcinoma in the basal and parabasal layers, inparting marked invasiveness of these cells into the supporting connective tissue.     

A CASE OF ALPORT'S SYNDROME

A 19-year-old female belonging to a family of Alport's syndrome was autopsied and her kidneys were examined in detail light and electron microscopically. The basement membrane was examined chiefly and the laminated thickening and/or splitting, looseness, irregularity and rail-like appearance of lamina densa were found in the glomerular, Bowman's capsular, tubular and interstitial capillary basement membranes. These findings were strongly suggestive of Alport's syndrome, whether or not the particles are seen in the basement membrane. In addition, Japanese reports on Alport's syndrome (total 48 families) were summarized and renal lesions were examined in comparison. It has been said that the prognosis is worse in the male than in the female, but according to our Investigation on case reports in Japan, the prognosis showed no difference between male and female.     

Biological properties and gene expression associated with metastatic potential of human osteosarcoma

Lung metastasis has a great influence on the prognosis of patients with osteosarcoma. We previously established two high-metastatic sublines, M112 and M132, from the HuO9 human osteosarcoma cell line by in vivo selection. In this study, we newly isolated a high-metastatic subline, H3, and three low-metastatic sublines, L6, L12 and L13, from HuO9 by the dilution plating method. Three high-metastatic sublines produced more than 200 metastatic nodules in the lung, while three low-metastatic sublines produced no or few nodules after injection of 2 × 10⁶ cells into the tail vein of nude mice. There were significant differences in the motility and invasiveness between high- and low-metastatic sublines, whereas the growth rates in vitro and the tumorigenicity in vivo showed no correlation with their metastatic abilities. Early adherence to culture plates was significantly lower in two of three low-metastatic sublines, which occupied smaller surface areas on the culture plates than other sublines did. Comparison of the expression of 637 cancer-related genes by cDNA microarray revealed that seven genes were differentially expressed between high- and low-metastatic sublines. Among them, five genes (AXL, TGFA, COLL7A1, WNT5A, and MKK6) were associated with adherence, motility, and/or invasiveness. These results suggest that the differences in motility/invasiveness and adhesive abilities are key determinants of lung metastasis in osteosarcoma. This revised version was published online in July 2006 with corrections to the Cover Date.     

Retrospective study on amplification of N-myc and c-myc genes in pediatric solid tumors and its association with prognosis and tumor differentiation

DNA was extracted from formalin-fixed and paraffin-embedded tissues of 85 patients with pediatric malignant solid tumors which had been resected at surgery or obtained at autopsy during a 24-year period. The tumors examined included 25 rhabdomyosarcomas, 12 Wilms' tumors, 10 hepatoblastomas and 37 neuroblastoma group tumors. Neuroblastoma group tumors were subclassified into 25 neuroblastomas and 12 ganglioneuroblastomas among which 6 composite ganglioneuroblastomas were included. Sample blocks were selected from both tumors and normal tissues in the majority of cases. We were able to reliably detect N- and c-myc gene amplification in tumor DNA by dot blot-hybridization. The N-myc gene showed approximately from 3- to 500-fold amplification in 19 of 33 cases of stage IV neuroblastoma group tumor. All of these 33 patients had been intensively treated with chemotherapy and/or radiotherapy. The c-myc was amplified 8-fold in 1 case of rhabdomyosarcoma, but neither N-myc nor c-myc was amplified in any cases of Wilms' tumor or hepatoblastoma. We retrospectively examined the association among N-myc gene amplification, prognosis, and histologic subtype in 33 patients with stage IV neuroblastoma group tumors. The survival of the patients with N-myc gene amplification was shorter than that of the patients without amplification of N-myc (p less than 0.05). There was no significant difference in prognosis between the 2 histologic subtypes; neuroblastoma and ganglioneuroblastoma, and the cases of tumors with amplified N-myc showed shorter survivals for each subtype (p less than 0.05). In every case of neuroblastoma group tumor, the copy number of the N-myc gene was the same among primary site and multiple metastatic tumors, even when the lesions showed differences in histologic subtype like neuroblastoma and ganglioneuroblastoma.