Repair of foveal detachment of the triangular fibrocartilage complex: open and arthroscopic transosseous techniques

Because the radioulnar ligament attaches to the ulnar fovea and base of the ulnar styloid, foveal detachment of the triangular fibrocartilage complex (TFCC) induces severe distal radioulnar joint instability. This article describes both an arthroscopic and open repair technique to reattach the TFCC to the fovea. Both techniques reanchor the detached TFCC to the fovea. Both techniques are reliable and promising techniques in the repair of a foveal detachment of the TFCC.     

Sevoflurane stimulates MAP kinase signal transduction through the activation of PKC alpha and betaII in fetal rat cerebral cortex cultured neuron

Protein kinase C (PKC) is a key enzyme that participates in various neuronal functions. PKC has also been identified as a target molecule for general anesthetic actions. Raf, mitogen-activated protein kinase (MEK) and extracellular signal-regulated kinase (ERK1/2) have been thought to be target effectors of PKC. In the present study, we attempted to evaluate the effect of sevoflurane on PKC/MAPK cascade signaling in cultured fetal rat cerebral -cortex neurons, prepared from embryonic day 18 fetuses. The effects of sevoflurane on the translocation of 7 PKC isoforms (alpha, betaI, betaII, gamma, delta, varepsilon and zeta) were observed by immunoblotting using isoform-selective antibodies to PKCs. The treatment of neurons with sevoflurane induced the translocation of PKC alpha and PKC betaII species from the cytosol to the membrane fraction, which indicated the activation of these PKC isoforms. In contrast, there was no clear change in the distribution of other PKC isoforms. We next examined whether the specific activation of PKC alpha and betaII by sevoflurane could stimulate the MAP kinase signaling pathway in cultured neurons. Raf phosphorylation was increased by the administration of 0.25 mM sevoflurane. The phosphorylation of Raf proteins reached a maximum at 5-10 min. Subsequently, the phosphorylation of MEK proteins was increased at 10-15 min after sevoflurane treatments. That of ERK proteins was induced at 15-60 min. Moreover, the phosphorylation of ERK induced by sevoflurane was significantly decreased by the treatment of PKC inhibitor (staurosporine) and MEK inhibitor (PD98059). On the other hand, the contents of total Raf, MEK and ERK proteins were relatively constant at all times examined. To examine the -localization of phosphorylated-ERK protein, immunohistochemical staining of sevoflurane-treated cultured neurons was performed. The phosphorylated-ERK proteins were markedly accumulated in both the cytosol of the cell body and the neurites in the neuronal cells with time after 0.25 mM sevoflurane-treatment. These results demonstrated that sevoflurane induced the phosphorylation of the MAP kinase cascade through the activation of the PKC alpha and PKC betaII species.     

Identification and differentiation of methcathinone analogs by gas chromatography‐mass spectrometry

To overcome a number of challenges involved in analyzing methcathinone (MC) analogues, we performed gas chromatography‐mass spectrometry (GC‐MS) analysis, including sample preparation, of nine MC analogues ? 4‐methylmethcathinone, three positional isomers of fluoromethcathinones, 4‐methoxymethcathinone, N‐ethylcathinone, N,N‐dimethylcathinone, buphedrone, and pentedrone. The MC analogues underwent dehydrogenation when the free bases were analyzed using splitless injection. Most of this thermal degradation was prevented using split injection. This indicated that a shorter residence time in the hot injector prevented decomposition. Uniquely, 2‐fluoromethcathinone degraded to another product in a process that could not be prevented by the split injection. Replacing the liner with a new, clean one was also effective in preventing thermal degradation. Most of the analytes showed a substantial loss (>30%) when the free base solution in ethyl acetate was evaporated under a nitrogen stream. Adding a small amount of dimethylformamide as a solvent keeper had a noticeable effect, but it did not completely prevent the loss. Three positional isomers of fluoromethcathinones were separated with baseline resolution by heptafluorobutyrylation with a slow column heating rate (8 °C/min) using a non‐polar DB‐5 ms capillary column. These results will be useful for the forensic analysis of MC analogues in confiscated materials. Copyright © 2012 John Wiley & Sons, Ltd.     

Assessment of gastric emptying and duodenal motility upon ingestion of a liquid meal using rapid magnetic resonance imaging

Gastric emptying is achieved by co-operation between gastric and duodenal motor activity. Therefore, evaluation of gastric emptying and its associated mechanisms would benefit clinical therapy as well as medical research. Healthy volunteers underwent rapid magnetic resonance imaging (MRI) of the abdomen along the coronal plane after ingestion of a liquid meal. The gastric fundal and duodenal areas were quantified semi-automatically by self-developed segment software. The average gastric fundal area determined by the serosal end in 40 sequential images was reduced to ～81% 30 min after and to ～70% 60 min after ingestion of a liquid meal. The average duodenal area also decreased to ～86% after 30 min and to 83% after 60 min. In contrast, changes in the centre of gravity increased to about fivefold after 30 min and to about threefold after 60 min. The mean velocity of the duodenal wall mimicked changes in the centre of gravity. The application of metoclopramide, a dopamine D(2) receptor antagonist, accelerated gastric emptying, presumably due to facilitated duodenal activity even immediately after liquid meal ingestion. The ingestion of water caused fast gastric emptying in 30 min, accompanied by high duodenal motility, but it ceased after 60 min, presumably reflecting complete gastric emptying. A rapid MRI scan visualized the association between gastric emptying and duodenal motility that could be modified by calories and dopaminergic neurotransmission. Changes in the centre of gravity and mean velocity of the duodenal wall appear to quantify the motility obtained from cine MRI accurately.     

Laparoscopic resection of retroperitoneal schwannoma : report of three cases and review of 22 cases in Japanese literature

Retroperitoneal schwannoma is a rare tumor. Only 19 cases have been reported to be treated by laparoscopic surgery. We performed successful laparoscopic excision of retroperitoneal schwannoma using the four-trocar in three patients who had a left retroperitoneal mass. The patients were two women and one man. They were 62, 60 and 57 years old. The tumor was 70, 45 and 50 mm in greatest diameter and operative time was 204, 243 and 254 min. respectively. The pathological diagnosis of the tumor was schwannoma. There was no morbidity or mortality. Preoperative diagnosis of schwannoma is very difficult. However schwannoma is a benign tumor with a good prognosis. This laparoscopic excision for retroperitoneal schwannoma is effective and rather safe.     

Single chain variable fragment antibodies against Shiga toxins isolated from a human antibody phage display library

Shiga toxins (Stxs) are involved in the pathogenesis of hemolytic-uremic syndrome and other severe systemic complications following enterohemorrhagic Escherichia coli infection in humans. Passive immunotherapies using monoclonal antibodies have been shown to be effective for neutralizing the toxic effects of Stxs. However, animal-derived monoclonal antibodies are sometimes immunogenic and their production is both laborious and expensive. We here report the isolation of single-chain variable fragment antibodies against Stxs by screening a phage display library constructed from a naïve human repertoire. An antibody among the selected clones designated B22 bound to the binding subunits of both Stx-1 and Stx-2, and strongly neutralized the cytotoxicity of Stx-1. This is the first example of a monovalent antibody showing Stx-neutralizing activity. The B22 antibody is also completely naturally occurring in human, which reduces the possibility of adverse immunological effects, and can be easily produced using bacterial protein synthesis systems.     

Distribution of osteopontin and calprotectin as matrix protein in calcium-containing stone

We recently reported that osteopontin (OPN) and calprotectin (CPT) are present in the matrix of urinary calcium stones, and that OPN mRNA is expressed in the renal distal tubular cells. In the present study, we examined the immunohistochemical distributions of OPN and CPT in urinary stones. The stones used in this study were passed spontaneously from the upper urinary tract. One half of each of the stones was analyzed with an infrared spectrophotometer, and were shown to be comprised of calcium oxalate, calcium phosphate, uric acid and cystine. The other half of each stone was immersed in tetrasodium ethylenediamine-tetraacetate (EDTA) solution. The half-stones were embedded in paraffin and cut into 5-μm sections. The avidin-biotin-peroxidase complex technique was employed. A monoclonal antibody to human milk-derived OPN and a monoclonal antibody to human granulocyte-derived CPT were used as primary antibodies. The immunochemical study using the OPN and CPT antibodies showed positive staining of the matrix of the urinary calcium stones. The stones showed staining in two distinct zones: a core area was stained with randomly aggregated OPN and CPT, and peripheral layers were stained in concentric circles. On the basis of our observations, it is reasonable to presume that OPN and CPT play roles as the matrix in the structure of urinary calcium stones. Received: 24 February 1998 / Accepted: 28 January 1999     

Role of the Src homology 2 (SH2) domain and C-terminus tyrosine phosphorylation sites of SH2-containing inositol phosphatase (SHIP) in the regulation of insulin-induced mitogenesis.

To examine the role of SHIP in insulin-induced mitogenic signaling, we used a truncated SHIP lacking the SH2 domain (deltaSH2-SHIP) and a Y917/1020F-SHIP (2F-SHIP) in which two tyrosines contributing to Shc binding were mutated to phenylalanine. Wild-type (WT)-, deltaSH2-, and 2F-SHIP were transiently transfected into Rat1 fibroblasts overexpressing insulin receptors (HIRc). Insulin-stimulated tyrosine phosphorylation of WT-SHIP and deltaSH2-SHIP, whereas tyrosine phosphorylation of 2F-SHIP was not detectable, indicating that 917/1020-Tyr are key phosphorylation sites on SHIP. Although SHIP can bind via its 917/1020-Tyr residues and SH2 domain to Shc PTB domain and 317-Tyr residue, respectively, insulin-induced SHIP association with Shc was more greatly decreased in 2F-SHIP cells than that in deltaSH2-SHIP cells. Insulin stimulation of Shc association with Grb2, which is important for p21ras-MAP kinase activation, was decreased by overexpression of WT- and 2F-SHIP. Importantly, insulin-induced Shc x Grb2 association was not detectably reduced in deltaSH2-SHIP cells. In accordance with the extent of Shc association with Grb2, insulin-induced MAP kinase activation was relatively decreased in both WT-SHIP and 2F-SHIP cells, but not in deltaSH2-SHIP cells. To examine the functional role of SHIP in insulin's biological action, insulin-induced mitogenesis was compared among these transfected cells. Insulin stimulation of thymidine incorporation and bromodeoxyuridine incorporation was decreased in WT-SHIP cells compared with that of control HIRc cells. Expression of 2F-SHIP also significantly reduced insulin-induced mitogenesis, whereas it was only slightly affected by overexpression of deltaSH2-SHIP. Furthermore, the reduction of insulin-induced mitogenesis in WT-SHIP cells was partly compensated by coexpression of Shc. These results indicate that SHIP plays a negative regulatory role in insulin-induced mitogenesis and that the SH2 domain of SHIP is important for its negative regulatory function.