The effect of lengthening the gastrocnemius muscle in chronic therapy resistant plantar fasciitis

BackgroundThe aetiology of chronic therapy resistant plantar fasciitis (CTRPF) is multifactorial with more focus in recent times on the gastroc-soleus complex. This study evaluates the effect of lengthening the gastrocnemius muscle in CTRPF.MethodsAll patients with CRTPF complaints for at least one year underwent the same standard conservative treatment prior to surgery. 32 patients failed this treatment and underwent gastrocnemius recession. Silfverskiöld test, questionnaires and plantar pressure measurements were obtained at 5 visits.ResultsOne year follow up showed a significantly increase in dorsiflexion of the ankle (16 degrees), a decrease in VAS; 78 (SD: 19) to 20 (SD: 24) and significant improved functional scores. Plantar pressure measurements showed an increase of pressure under the medial proximal part of the midfoot and the 1 st metatarsal and a decrease under the hallux.ConclusionsA gastrocnemius recession results in a significant gain in dorsiflexion, altered loading of the foot and good clinical outcome in patients with CTRPF.Level of EvidenceLevel 2     

Non-polarized expression of Basal-cell adhesion molecule B-cam in epithelial ovarian cancers

The basal cell adhesion molecule (B-CAM) is a M(r) 90,000 cell surface glycoprotein identified by two monoclonal antibodies (mAbs), F8 and G253, raised against human tumor cells. Cloning and sequence analysis of a B-CAM cDNA has revealed a characteristic immunoglobulin domain structure of the B-CAM polypeptide, most closely related to MUC18, a cell surface protein of invasive human melanomas. The pattern of B-CAM expression in cultured cells suggests that the molecule is associated with a substrate-adherent growth pattern in some lineages. Moreover, B-CAM expression is upregulated following malignant transformation in some cell types. In the present study, we have used immunohistochemical methods to examine S-CAM expression in normal and neoplastic tissues, including over 200 tumors of diverse histological type. B-CAM was detected in several normal tissues, including polarized expression in several epithelia and expression in vascular endothelium and smooth muscle. Among the tumors tested, B-CAM was found most uniformly and with a non-polarized pattern in epithelial cancers of the ovary (27 of 31 tumors B-CAM-positive), By contrast, only small subsets of epithelial cancers of other organs, including some neuroendocrine, breast, and lung carcinomas, showed uniform or polarized B-CAM expression. Most non-ovarian carcinomas, lymphomas, sarcomas, and neuroectodermal tumors tested were B-CAM-negative. Immunoprecipitation studies with ovarian carcinoma cell lines showed that B-CAM in these cells is a M, 90,000 glycoprotein, composed of M(r) 65,000-75,000 polypeptides with abundant, N-linked carbohydrate side chains. These findings identify B-CAM as a characteristic cell surface protein of epithelial ovarian cancers. The availability of B-CAM-specific mAbs and cDNAs may help identify the role of B-CAM in normal endothelial and epithelial cells and ovarian cancers.     

Inflamed fibronectin: an altered fibronectin enhances neutrophil adhesion

Recent investigations have emphasized the role of activated granulocytes in mediating vascular endothelial injury in the pathogenesis of shock lung. In vitro studies have indicated that tight adherence of the neutrophil to the endothelium is crucial for the development of cellular injury. Fibronectin is critical to cell-to- substratum and cell-to-cell interactions. Since fibronectin resides in plasma, on endothelial cell surfaces and is secreted into cell matrices, the adhesive properties of fibronectin must be modulated, lest universal cell agglomeration occur, yet be enhanced when cell attachment is appropriate. In these studies, treatment of fibronectin- coated surfaces with neutrophil release products increased the adhesion of activated neutrophils. Similarly, endothelial cells treated with neutrophil release products become a more adherent substrate for neutrophils. This enhanced adherence generated by treatment of fibronectin with neutrophil supernatants is inhibitable by heat and the lysosomal proteinase inhibitor, pepstatin-A. Neutrophil release products cause proteolytic fragmentation of fibronectin and enhanced fibronectin immunofluorescence on endothelial cells. In addition, neutrophils are more injurious to endothelial cells that have been pretreated with neutrophil release products. Neutrophils may enhance their own adherence to endothelial cells by altering fibronectin, and this altered, or "inflamed," fibronectin may serve as an amplifier of inflammation.     

Antitumor effects of bortezomib (PS-341) on primary effusion lymphomas.

Primary effusion lymphomas (PELs) are a rare type of non-Hodgkin's lymphoma that are resistant to cytotoxic chemotherapy. PELs manifest constitutive activation of nuclear factor kappa B (NF-kappaB), and inhibition of NF-kappaB induces apoptosis of PELs and sensitizes to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced death. Bortezomib (PS-341), a peptidyl boronic acid inhibitor of the proteasome, is a potent agent against a wide range of hematologic malignancies and has been shown to inhibit NF-kappaB. Thus, we examined the cytotoxic effects of bortezomib alone and in combination with various drugs. Bortezomib potently inhibited NF-kappaB in PEL cells in a dose-dependent manner. In addition, bortezomib inhibited growth and induced apoptosis of PEL cell lines (IC(50) values of 3.4-5.0 nM). Results of drug interactions between bortezomib and chemotherapy (doxorubicin and Taxol) were schedule-dependent: synergistic interactions were generally observed when PEL cells were pretreated with bortezomib prior to chemotherapy, whereas additive or even antagonistic interactions occurred with chemotherapy pretreatment or simultaneous treatment with bortezomib and chemotherapy. Most schedules of bortezomib and dexamethasone were synergistic, although pretreatment with dexamethasone resulted in additive interactions. Effects of combinations of bortezomib and TRAIL were generally additive. Thus, bortezomib represents a promising potential therapy for the treatment of PEL.     

Acute fractures of the distal radius

Distal radius fractures commonly are sustained by athletes during competition. Typically, these are high energy injuries with severe displacement, metaphyseal comminution, and articular surface disruption. Each fracture is distinguished by its degree of articular displacement, stability, and reducibility. Management is contingent on recognition of the variable magnitude of articular disruption and skillful treatment based on specific fracture configuration.     

Management of acute scaphoid fractures

Scaphoid fractures in the athlete present a dilemma to the treating clinician. Diagnosis of scaphoid fractures should be suspected in any athlete, especially those participating in contact sports, presenting with radial wrist pain. Appropriate imaging studies should be obtained to make a timely and complete diagnosis. Treatment alternatives for acute scaphoid fractures in the athlete include casting and staying out of sports, casting with use of a playing cast, and internal fixation. Displaced unstable fractures and proximal pole fractures should be treated by open reduction and internal fixation. Nondisplaced mid-third fractures are the most common type seen in the athlete. Alternatives of treatment should be carefully explained to the patients and family and the most appropriate treatment employed.     

5-Fluorouracil plus leucovorin is an effective adjuvant chemotherapy in curatively resected stage III colon cancer: long-term follow-up results of the adjCCA-01 trial.

BACKGROUND: Adjuvant postoperative treatment with 5-fluorouracil (5-FU) and leucovorin in curatively resected stage III colon cancer significantly reduces the risk of cancer recurrences and improves survival. The impact of 5-FU plus leucovorin on survival and tumor recurrence was analyzed in a long-term follow-up study in comparison with the effects of 5-FU plus levamisole in the prospective multicenter trial adjCCA-01. PATIENTS AND METHODS: Patients with a curatively resected stage III (International Union Against Cancer) colon cancer were stratified according to tumor, node and grading category and randomly assigned to receive one of the two adjuvant treatment schemes: 5-FU 400 mg/m2 body surface area intravenously in the first chemotherapy course, then 450 mg/m2 x 5 days, plus leucovorin 100 mg/m2, 12 cycles (arm A), or 5-FU plus levamisole (Moertel scheme; arm B). RESULTS: Six hundred and eighty (96.9%) of 702 patients enrolled into this study were eligible. To date, 261 patients have died, 117 on arm A and 144 on arm B (P = 0.007). After a median follow-up time of 82 months, the 5-FU plus leucovorin combination significantly improved disease-free survival [79.8 months in arm A versus 69.3 months in arm B (P = 0.012)] and significantly increased median overall survival (88.9 months in arm A versus 78.6 months in arm B; P = 0.003). Adjuvant treatment with 5-FU plus levamisole as well as 5-FU plus leucovorin was generally well tolerated; only a minority of patients experienced grade 3 and 4 toxicities. CONCLUSIONS: After curative resection of a stage III colon cancer, adjuvant treatment with 5-FU plus leucovorin is generally well tolerated. This long-term follow-up study demonstrates that adjuvant treatment with 5-FU plus leucovorin given for 12 cycles is significantly more effective than 5-FU plus levamisole (Moertel scheme) in reducing tumor relapse and improving survival.     

Effects of dietary fat and a vegetable-fruit mixture on the development of intestinal neoplasia in the ApcMin mouse

The variation in colorectal cancer (CRC) incidence worldwide strongly suggests a role for dietary influences. Based on epidemiological data, protective effects of vegetables and fruit intake on CRC are widely claimed, while other data indicate a possible increased CRC risk from (higher) dietary fat intake. Therefore, we have investigated single and interactive effects of dietary fat and a vegetable-fruit mixture (VFM) in the ApcMin mouse, a mouse model for multiple intestinal neoplasia. In this study, four different diets (A-D) were compared, which were either low in fat (20% energy diets A/B) or high in fat (40% energy diets C/D). In addition, 19.5% (wt/wt) of the carbohydrates in diets B and D were replaced by a freeze-dried VFM. The diets were balanced so that they only differed among each other in fat/carbohydrate content and the presence of specific plant-constituents. Because the initiation of intestinal tumors in ApcMin mice occurs relatively early in life, exposure to the diets was started in utero. Without the addition of VFM, mice maintained at a high-fat diet did not develop significantly higher numbers of small or large intestinal adenomas than mice maintained at a low-fat diet. VFM added to a low-fat diet significantly lowered multiplicity of small intestinal polyps (from 16.2 to 10.2/mouse, 15 animals/group), but not of colon tumors in male ApcMin mice only. Strikingly, addition of VFM to female mice maintained on a low-fat diet and to both sexes maintained on a high-fat diet significantly enhanced intestinal polyp multiplicity (from 16.5 to 26.7 polyps/mouse). In conclusion, our results indicate that neither a lower fat intake nor consumption of VFM included in a high-fat diet decreases the development of polyps in mice genetically predisposed to intestinal tumor development.