Usefulness and complications associated with thenar and standard portals during arthroscopic surgery of thumb carpometacarpal joint.

PURPOSE: Advances in small arthroscopy have enabled a minimally invasive surgery for thumb carpometacarpal joints. However, surgery is often difficult using standard CM-radial (CM-R) and CM-ulnar portals (CM-U). Here, we describe the clinical applications and complications associated with using thenar portal (TP) and standard portals. METHODS: Arthroscopic surgeries of thumb carpometacarpal joint were performed in 21 patients including 15 patients with osteoarthritis and six Bennett's fracture-dislocations. Complications and the frequency of use associated with each portal were evaluated. RESULTS: Complications associated with the CM-R portal comprised paresthesia due to damage of the radial nerve branches in two patients. No nerves were damaged but the operation scar became tender at the TP in three patients. The CM-R was used at a lower frequency when the TP was utilized. CONCLUSION: The clinical use of TP may decrease the risk of radial sensory nerve damage through decreasing frequency of use of the CM-R that is located near the nerve. LEVEL OF STUDY: IV.

Serum levels of P-selectin in men with high-functioning autism.

Immune dysfunction has been proposed as a mechanism for the pathophysiology of autistic-spectrum disorders. The selectin family of adhesion molecules plays a prominent role in immune/inflammatory responses. We determined the serum levels of three types of soluble-form selectin (sP, sL and sE) in 15 men with high-functioning autism and 22 age-matched healthy controls by enzyme-linked immunosorbent assay. Levels of sP-selectin and sL-selectin were significantly lower in patients than in controls. Furthermore, sP-selectin levels were negatively correlated with impaired social development during early childhood.

Changes in biochemical markers and prediction of effectiveness of intra-articular hyaluronan in patients with knee osteoarthritis.

OBJECTIVE: Intra-articular injection of hyaluronan (HA) is frequently used to treat knee osteoarthritis (OA). We studied whether HA injections induced significant changes in levels of biochemical markers in synovial fluid (SF). In addition, we investigated the possibility of predicting the effectiveness of HA based on these biochemical markers. METHODS: Twenty-eight patients with knee OA underwent five weekly intra-articular injections of HA. Knee pain was measured on visual analog scale (VAS) before and after the five injections. Levels of biochemical markers, including chondroitin 6-sulfate (C6S), chondroitin 4-sulfate (C4S), keratan sulfate (KS), and tenascin-C (TN-C), were determined before and after the five injections. Correlations between the biochemical markers before HA injection and the improvement of VAS after the five injections were evaluated. RESULTS: After HA injections, levels of C6S, C4S, and KS decreased significantly. Inverse correlations were observed between the levels of TN-C and C4S before HA injection and improvement of VAS after the five injections. In contrast, no significant correlation was seen between levels of C6S and KS before injections and improvement of VAS after the five injections. CONCLUSION: The reduction in C6S, C4S, and KS levels after HA injections reflects that HA could help maintain normal cartilage metabolism. Our findings suggest that HA injections are effective in patients whose knees contain low levels of TN-C and C4S, reflecting an early stage of OA and limited synovitis.

Caldesmon suppresses cancer cell invasion by regulating podosome/invadopodium formation.

The podosome and invadopodium are dynamic cell-adhesion structures that degrade the extracellular matrix (ECM) and promote cell invasion. We recently reported that the actin-binding protein caldesmon is a pivotal regulator of podosome formation. Here, we analyzed the caldesmon's involvement in podosome/invadopodium-mediated invasion by transformed and cancer cells. The ectopic expression of caldesmon reduced the number of podosomes/invadopodia and decreased the ECM degradation activity, resulting in the suppression of cell invasion. Conversely, the depletion of caldesmon facilitated the formation of podosomes/invadopodia and cell invasion. Taken together, our results indicate that caldesmon acts as a potent repressor of cancer cell invasion.

Intra-osseous ganglion of the proximal humerus: a case report.

We report a 72-year-old woman with a type-1 intra-osseous ganglion in the proximal humerus, extending to the bone surface. We conducted a systemic review of intra-osseous ganglion cases in Japan to identify clinical features and pathogenesis of this condition. The anatomical distribution between intra-osseous ganglia without a communicating soft tissue ganglion (type 1) and those with (type 2) is different. The origins of intra-osseous ganglia vary and depend on their anatomical location. They can arise from within the bone or in the adjacent soft tissue, and can progress to a type-2 lesion in either an outside-in or inside-out fashion.

Locking of the metacarpophalangeal joint of the thumb caused by a fracture fragment of the radial condyle of the metacarpal head after dorsal dislocation.

We report a case of a locked thumb metacarpophalangeal joint secondary to metacarpal head fracture. As fractures of the radial condyle are not readily seen in routine X-rays, other imaging modalities, including CT, should be considered if the patient complains of limited extension after hyperextension injury of the thumb.

Involvement of tenascin-C and PG-M/versican in flexor tenosynovial pathology of idiopathic carpal tunnel syndrome.

Increased intra-carpal-tunnel pressure due to swelling of the flexor tenosynovium is the most probable pathological mechanism of idiopathic carpal tunnel syndrome (CTS). To clarify the role of tenascin-C and PG-M/versican, which have often been found to be involved in tissue remodeling and vascular stenosis in the pathogenesis of CTS, we histologically and biochemically examined the production of extracellular matrix in the flexor tenosynovium from 40 idiopathic CTS patients. Tenascin-C was temporarily expressed in the vessel wall, synovial lining and fibrous tissue, with expression regulated differently in each tissue. Tenascin-C expression by vessels correlated with disease duration and appeared to be involved in vascular lesion pathology. Morphometric analysis showed that tenascin-C expression by small arteries is correlated with PG-M/versican expression in surrounding connective tissue. PG-M/versican was also present at the neointima of severely narrowed vessels. Although tenascin-C expression by synovial lining and connective tissue shows marked regional variation and seems inconsistent, in vitro examination suggested that tenascin-C production by these tissues is regulated in response to mechanical strain on the flexor tenosynovium.

Injuries in elite motorcycle racing in Japan.

OBJECTIVES: To investigate the incidence and pattern of injuries, relative risks, and factors affecting incidence among elite motorcycle competitors in Japan. METHODS: A total of 117 elite motorcycle competitors including 36 road racers, 60 motocross racers, and 21 trial bike riders completed a questionnaire about injuries. RESULTS: Sixty major injuries (25 in road racing, 32 in motocross, and three in trial bike riding) were reported. The most common injuries were fractures (45), followed by ligament injuries (8), dislocations (5), and soft tissue injuries (2). The overall injury rate was 22.4 per 1000 hours, and the death rate was zero. There was no significant correlation between risk of injury and age, experience, or accumulated competition points. CONCLUSIONS: Injury rates in competitions such as road racing and motocross are high, and therefore additional safety measures are needed to protect competitors from injury.

Helicobacter bilis infection in biliary tract cancer.

BACKGROUND: Biliary tract cancer is a highly fatal disease with poor prognosis, but the aetiology is poorly understood. AIM: We aimed to identify Helicobacter bilis infection in the gallbladder in patients with biliary tract disease. METHODS: Archival gallbladder specimens from 34 patients (14 males and 20 females) with an average age of 61.4 +/- 12.2 years (mean +/- SE) were retrieved, consisting of 11 cases of gallbladder cancer, three of bile duct cancer, 16 of cholecystolithiasis and four of pancreatic cancer. DNA was extracted and nested PCR using primers specific for 16S rRNA of H. bilis was performed. RESULTS: Amplification was observed in 3 of 11 gallbladder cancer cases (27.2%) and one of three cases with biliary duct cancer (33.3%). In total, four of 14 cases with biliary tract cancer were positive for H. bilis (28.6%). In addition, the presence of H. bilis was shown in two of 16 cases (12.5%) with cholecystolithiasis. Notably, although the number of cases examined was small, none of the four cases with pancreatic cancer showed the presence of H. bilis infection in the gallbladder without apparent abnormalities. CONCLUSION: H. bilis infection may play a role in biliary tract disease, particularly in biliary tract cancer.

Review article: inflammation-related promotion of gastrointestinal carcinogenesis--a perigenetic pathway.

Chronic inflammation has been reported to accelerate neoplasmas in gastrointestinal tract. Certain bacteria including Helicobacter pylori directly interact with host cells, induce proinflammatory cytokines and stimulate production of free radicals. Free radicals cause mutations in target cells so that neoplastic clones are established. Accumulation of such genetic alterations may cause malignant transformation of some established clones. In addition, inflammatory alterations may promote growth, expansion and invasion of gastrointestinal epithelial cells. The latter changes caused by inflammation may occur even without further genetic mutations or epigenetic alterations, and therefore may be categorized as 'perigenetic alterations' of neoplastic cells. For an example, tumour necrosis factor alpha (TNF-alpha) plays pivotal roles not only in the reduction but also in the growth, invasion and metastases of certain neoplasmas. Our studies show that TNF-alpha increases intracellular radical production, degradates E-cadherin / beta-catenin complex and promotes dispersion and migration in epithelial cells transformed with an activated src oncogene (v-src). These data indicate that an inflammatory cytokine induces the malignant potential of src-activated neoplastic cells. Interestingly, TNF-alpha also induced these phenotypic changes in nonmutated cells whose c-Src was activated by TGF-alpha, suggesting that the invasive properties of the cell were not necessarily related to gene mutation. Furthermore, certain radical scavengers suppressed the invasive phenotype of the cells. These results indicate that perigenetic alterations are an important target of pharmacological intervention of carcinogenesis.

[COX-2 inhibitor and colon cancer].

It is suggested that nonsteroidal antiinflammatory inhibitors alter the biology of colorectal carcinogenesis. Cyclooxygenase-2, one of target molecules of these drugs, is reported to be upregulated in cancer tissues. Cultured cells which were derived from intestinal epithelium and programmed to express COX-2 showed several phenotypic changes in favor of carcinogenesis, including resistance to apoptosis and enhancement of cell proliferation, angiogenesis, and invasion. Tumor growth implanted in COX-2 null mice was significantly attenuated, but not in COX-1 null or wild type mice, suggesting that COX-2 in stroma also has an important role in tumor growth. Moreover, PGE2, one of COX-2 metabolites, reversed these antitumor effects, indicating that inhibition of PGE2 production has a pivotal role in tumor suppression. However, NSAIDs show antitumor effects in cancer cells lacking COX-1 or COX-2 expression, and some derivatives lacking the ability to suppress COX activity show antitumor effects. These results suggest that COX independent pathway might be involved in antitumor effects of NSAIDs. For the development of novel and effective therapies, it is required to elucidate mechanisms underlying antitumor effects of NSAIDs.

Cyclooxygenase-2 downregulates inducible nitric oxide synthase in rat intestinal epithelial cells.

Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression has been demonstrated in inflamed intestinal mucosa. Although regulation of COX-2 and iNOS expression has been studied extensively, the interplay between these two enzymes remains unclear. Because they play crucial roles in inflammation and/or carcinogenesis, we investigated whether COX-2 regulates iNOS expression and evaluated the effects of COX-2 inhibitor and arachidonic acid (AA) on iNOS induction. The COX-2 gene coding region was stably transfected into rat intestinal epithelial cells (RIE sense cells). After interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) administration, iNOS and COX-2 expression was evaluated by Western blotting. PGE(2) was measured by the enzyme immunoassay (EIA) method. Expression of IFN response factor-1, phosphorylated extracellular signal-related kinase-1 and -2, and Ikappa-Balpha was evaluated. Activator protein-1 and nuclear factor-kappaB (NF-kappaB) were examined by gel mobility shift assay; a supershift assay was performed to identify the NF-kappaB complex components. JTE-522 or AA was added before IFN-gamma and LPS administration, and effects on iNOS and PGE(2) induction were evaluated by Western blotting or EIA. iNOS protein and mRNA expression was inhibited in RIE sense cells. Although NF-kappaB activation was suppressed and Ikappa-Balpha protein was more stable, respectively, in RIE sense cells, no difference was noted in other transcription factors. JTE-522 increased iNOS protein expression in RIE cells. We conclude that COX-2 suppressed iNOS expression in RIE cells through suppression of NF-kappaB by stabilizing Ikappa-Balpha.