Proximal row carpectomy for chronic unreduced perilunate dislocations

We evaluated the results of proximal row carpectomy (PRC) for unreduced perilunate dislocation in 6 patients. The average period from the injury to the operation was 24 weeks. The modified Mayo wrist score was used for clinical evaluation. Radiological evaluation was based on the radius-capitate alignment. Pain disappeared in 4 cases; mild pain during activity persisted in 2 cases. The average flexion-extension are was 59% of the values on the unaffected side. The average grip strength was 72% of the unaffected side, and the average modified Mayo wrist score was 71 points. Three patients showed favourable radius-capitate alignment, while the other 3 patients showed poor radius-capitate alignment on the radiographs. The postoperative radius-capitate alignment was related to the preoperative position of the capitate on the lateral view. Those with poor radius-capitate alignment tended to obtain lower scores compared to those with favourable alignment.     

The role of STAT1 in activation of IL-3- and IL-5-induced eosinophils by interferon gamma

Tyrosine phosphorylation of STAT1alpha in eosinophils after IFN-gamma stimulation has been shown, but the biological significance of eosinophil STAT1alpha activation in transmitting the signals through the IFN-gamma receptor remains unknown. The purpose of this study is to determine whether STAT1 is involved in the regulation of eosinophils by IFN-gamma-IFN-gamma receptor interaction. rhIL-3- and rhIL-5-induced eosinophils from CD34+ cells of cord blood on day 28 of culture were used. The cells were washed and further incubated in IL-3- and IL-5-free medium for 48 h. The induced eosinophils constitutively expressed CD69 and lost this expression after a further 48-hour incubation without the cytokines. IFN-gamma significantly upregulated CD69 expression on the 48-hour incubated cells. In inhibitory experiments on STAT1, a phosphorothioate oligo antisense DNA against STAT1alpha was added to IL-3- and IL-5-containing medium from day 15 to day 28 of culture. The oligo DNAs altered neither the expressions of myeloid cell marker CD9 and 13 nor the expression of IFN-gamma receptor on the cells. The added STAT1alpha antisense, but not sense, DNA significantly reduced STAT1alpha mRNA expression in the cells. The STAT1 antisense also significantly inhibited IFN-gamma-induced CD69 expression on the 48-hour incubated eosinophils. In conclusion, these results indicate that IFN-gamma induces CD69 expression in the induced eosinophils through STAT1alpha, suggesting that STAT1alpha may play a significant role in eosinophil regulation by IFN-gamma.     

Trojan p16 peptide suppresses pancreatic cancer growth and prolongs survival in mice.

PURPOSE: The tumor suppressor gene p16INK4A is inactivated frequently in a large number of human cancers, and many investigators have attempted to restore the function of p16 using the p16 wild-type gene and viral vectors. In this study, we treated the tumor-bearing animals with the p16-derived synthetic peptide coupled with the Antennapedia carrier sequence, which we designated as Trojan p16 peptide. EXPERIMENTAL DESIGN: Injections (i.p.) of the Trojan p16 peptide (100 microg/mouse/day) were given for 3 weeks in the AsPC-1 and BxPC-3 s.c. tumor models. Tumor growth, histopathology, and TUNEL staining of the tumor and toxicity of the animals were evaluated. To examine its influence on the survival of tumor-bearing mice, Trojan p16 was administered in the AsPC-1 peritoneal dissemination model. RESULTS: In the AsPC-1 s.c. tumor model, a significant growth inhibition was obtained by the Trojan p16 treatment when compared with the three control treatments, i.e., vehicle, unconjugated form of p16, or Trojan peptide alone. Tumor growth inhibition was almost complete in the BxPC-3 tumor, a relatively slow growing tumor. Neither hematological cytotoxicity or body weight loss were observed. Histopathology of the BxPC-3 s.c. tumor in the Trojan p16 treatment group revealed marked vacuole formation and apoptotic death of cancer cells. In the AsPC-1 peritoneal dissemination model, the survival curve of mice treated with Trojan p16 was significantly longer than that of control. CONCLUSIONS: These results provide evidence that the Trojan p16 peptide system, a gene-oriented peptide coupled with a peptide vector, functions for experimental pancreatic cancer therapy.     

Inhibition of pRb phosphorylation and cell cycle progression by an antennapedia-p16(INK4A) fusion peptide in pancreatic cancer cells

In this study, we examined whether or not a small peptide derived from p16(INK4A) protein with the antennapedia carrier sequence could inhibit the growth of pancreatic cancer cells through the inhibition of cell cycle progression. Growth inhibition by the p16-derived peptide was observed in a time- and dose-dependent manner in AsPC-1 and BxPC-3 cells (p16-negative and pRb-positive), whereas Saos-2 cells (p16-positive and pRb-negative) showed no inhibitory effect. In AsPC-1 and BxPC-3 cells, the proportion of cells in the G(1) phase markedly increased 48 h after treatment with 20 microM p16-derived peptide. Cell-cycle analysis of Saos-2 cells showed little change during the entire period of treatment. Immunoblot analysis showed inhibition of pRb phosphorylation after treatment of BxPC-3 with 10 microM p16 peptide. Furthermore, the p16 peptide caused a decrease in cyclin A at later times of treatment. These results demonstrate that the p16-derived peptide can inhibit the growth of p16-negative and pRb-positive pancreatic cancer cells by means of G(1) phase cell cycle arrest resulting from the inhibition of pRb phosphorylation. Restoration of p16/pRb tumor-suppressive pathway by re-expression of p16(INK4A) may play a therapeutic role in the treatment of pancreatic cancer.     

Deposition of extracellular matrix on silicone intraocular lens implants in rabbits

Purpose: To examine the deposition of extracellullar matrix on silicone intraocular lenses (IOLs) implanted experimentally into rabbit eyes by electron microscopy and to determine the immunolocalization of extracellular matrix components, including collagen types and cellular fibronectin, on these IOLs. Methods: We performed phacoemulsification and aspiration of the crystalline lens and implanted a foldable silicone IOL in the capsular bag of one eye of each of 26 adult albino rabbits under general anesthesia. After 8 weeks the animals were killed and the eyes were enucleated. The silicone IOLs were processed for electron microscopy and for immunohistochemical detection of collagen types I, III, and IV and cellular fibronectin. Results: Electron microscopy revealed deposition of a presumed cell matrix complex on the optic portion of all silicone IOLs, as well as the adhesion of presumed macrophages and foreign-body giant cells. Cellular deposits showed immunoreactivity for cellular fibronectin. Fibrous or membranous deposits exhibited immunoreactivity for cellular fibronectin and collagen types I and III. A few type IV collagen-immunoreactive deposits were also seen. Conclusion: Deposits of extracellular matrix components were observed on silicone IOLs. These deposits may form the scaffolding for the adhesion and proliferation of cells. These matrix components appeared to be the products of cells adhering to the surfaces of IOLs, including lens epithelial cells, macrophages and foreign-body giant cells, indicating that the process of granulation was incomplete.     

Erratum to: Short-Segment Coil Embolization Using a Double-Balloon Technique in an Experimental Vascular Model

CardioVascular and Interventional Radiology -     

Short-Segment Coil Embolization Using a Double-Balloon Technique in an Experimental Vascular Model

CardioVascular and Interventional Radiology - To evaluate the feasibility of short-segment coil embolization between 2 balloons for tight packing in an experimental vascular model. Three coil...