[A Problem with Flow Indicators of Anesthesia Machine].

Some anesthesia machines indicate both analog and digital flow volumes of oxygen, air and nitrous oxide. We have noticed that there are discrepancies in the flows between analog and digital flow indicators of two anesthesia machine models (Dräger ; Fabius GS premium and Fabius Tiro). When oxygen or air flow is low, the analog indicator shows higher flows than the digital indicator. In contrast, when oxygen or air flow is high, the analog indicator shows lower flows than the digital indicator. This discrepancy is comparatively small when total gas flow is within the range of 2-5 l x min(-1). We contacted the manufacturer, which replied that the digital indicator is correct and the analog indicator should be regarded as an adjunctive, in case of a power failure when the digital indicator does not function. But this discrepancy may cause practical problems. When we cannot use a digital indicator and have to perform ventilation using a supporting gas cylinder, we may misjudge the available time for oxygen. In addition, when we use only analog indicator, insufficient volume of oxygen may be delivered, leading to the grave hypoxia.

[Problems with the Structure of a New Pentax-Airwayscope S200].

BACKGROUND: Pentax-Airwayscope (AWS-S100) is useful for tracheal intubation, and a new version S200 has recently been introduced to clinical practice. We felt that S200 was more difficult than the S100 in attaching and detaching a single-use Introck blade. METHODS: In a randomized cross-over design, we compared S100 and S200, for the ease of attaching to and detaching from the Introck, fixation of the Introck using the fixation ring of the main body, and insertion time. RESULTS: Compared with S100, it was easier for S200 to fix the Introck using the fixation ring (78% vs 72%) (P < 0.05), but it was more difficult for S200 to attach (the incidence 43% vs 2%) and detach (53% vs 11%) the Introck (both P < 0.001). Insertion time was also significantly longer for S200 than S100 (median 9 [IQR : 6-19] s vs 4 [IQR : 3-6] s) (P < 0.001). The flexible scope of one of two S200s kinked and was broken during attachment. CONCLUSIONS: It is necessary to apply lubricant to the distal part of the scope to prevent damage to the scope.

[Anesthetic management of a patient with aortocaval fistula caused by rupture of a huge abdominal aortic aneurysm into the inferior vena cava].

Aortocaval fistula is a rare complication of ruptured abdominal aortic aneurysm. We report anesthetic management of a patient with aortocaval fistula caused by rupture of a huge abdominal aortic aneurysm into the inferior vena cava. A 51-year-old man who had complained of low back pain and general fatigue was referred to our hospital because of his liver damage. Aortocaval fistula due to rupture of a huge abdominal aortic aneurysm was diagnosed from physical examination, enhanced computed tomography and color Doppler ultrasonography. Anesthesia was induced with propofol and rocuronium, and was maintained with sevoflurane and remifentanil. After induction of anesthesia, the central venous pressure and cardiac index showed remarkably high values because of arteriovenous shunt. When the aneurysm was incised after the clamping of the abdominal aorta, massive venous bleeding occurred from the fistula and caused severe hypotension. Blood pressure recovered by digital compression of the bleeding point and the use of an autotransfusion device. After the repair of the aortocaval fistula, the hemodynamics became stable. The patient had a high output but a good cardiac function in preoperative examination. Therefore anesthesia was managed successfully without worsening high-output heart failure.

A case of necrotizing fasciitis following intra-articular injections - Iatrogenic or spontaneous?

Here, we report a case of necrotizing fasciitis following intra-articular injection of hyaluronic acid. A 73-year-old female received intra-articular injections of hyaluronic acid due to arthralgia at the left shoulder and knee, and was found dead in her living room at one day. At the forensic autopsy, injection marks with bullae and erythema were found at the left shoulder and knee and liquefactive necrosis of muscle tissues was observed in the left but not right extremities. Histopathological examinations of the left upper arm and thigh revealed severe rhabdomyolysis with lots of bacterial clusters. Bacteriological examinations detected group A Streptococcus from intracardiac blood and affected muscle tissues. Postmortem biochemical analysis of blood showed escalated blood urea nitrogen (133.8 mg/dL), creatinine (4.57 mg/dL) and C-reactive protein (45.0 mg/dL). The cause of her death was diagnosed as streptococcal toxic shock syndrome (STSS). Moreover, it was suggested that the injection was inappropriately conducted and served as a portal of bacterial entry.

Overexpression of ADAM9 enhances growth factor-mediated recycling of E-cadherin in human colon cancer cell line HT29 cells.

Growth factor-mediated stimulation of epithelial cells induces the disassembly of E-cadherin-mediated cell-cell adhesion. We found that overexpression of a disintegrin and metalloprotease 9 (ADAM9) enhanced growth factor-mediated induction of endocytosis and dynamic recycling of E-cadherin in HT29 human colon cancer cells. In addition, ubiquitination and degradation of E-cadherin were reduced in these cells. ADAM9 constitutively interacted with E-cadherin, and the two proteins co-localized at the plasma membrane of HT29 cells. Administration of a metalloprotease inhibitor or overexpression of an ADAM9 mutant lacking metalloprotease activity attenuated growth factor-dependent endocytosis and recycling of E-cadherin as well as scattering of HT29 cells. These results suggest that the metalloprotease activity of ADAM9 mediates growth factor-induced endocytosis and dynamic recycling of E-cadherin and prevents E-cadherin degradation.

Premature failure of the polyethylene tibial bearing surface of the Interax knee arthroplasty.

Thirty-four patients (37 knees) were treated with the Interax knee arthroplasty. There were 31 female and 3 male patients with a mean age at surgery of 70 years (range, 53-84 years). Premature failure of the polyethylene tibial bearing surface occurred in 9 patients (9 knees). Eight patients of these required a revision operation because of early wearing out of the tibial surface 20 to 38 months after the operation. The failure was due to inadequate implant design in small component and polyethylene gamma irradiated in the air.

Structural determinants for membrane trafficking and G protein selectivity of a mouse olfactory receptor.

The G protein-coupled olfactory receptor (OR) superfamily plays a critical role in recognizing a broad range of odorants. Each OR appears to recognize odorants based on similarities in molecular structures such that mOR-EG, a mouse OR, binds eugenol, vanillin, and some other structurally related odorants. Only a few ORs, however, have been characterized functionally due to the difficulties in expressing ORs in heterologous cells. In this report, we demonstrate roles of the N- and C-terminal domains as key elements in the functional expression and signal transducing activity of an OR. Disruption of the N-terminal glycosylation site of the mOR-EG completely impaired its membrane trafficking to the cell surface. Functional expression of the mOR-EG was greatly enhanced by addition of extra N-terminal glycosylation sequences. Addition of a C-terminal epitope-tag or C-terminal truncation significantly reduced the odorant-response activity, although the receptors were properly targeted to the plasma membrane. Analysis of a series of truncated ORs revealed a region in the C-terminus that was crucial for the receptor activity. Replacement of the C-terminal portion of the mOR-EG with that of rhodopsin disrupted the coupling to G(alphas) but not to G(alpha15), demonstrating that the C-terminus is involved in regulating G protein specificity. These results suggest that glycosylation of the N-terminal portion is critical for OR expression and membrane trafficking, while the C-terminal portion plays a role in defining proper conformation, which, in turn, specifies the G protein selectivity of the OR. This information helps clarify the mechanisms that regulate membrane trafficking and G protein interaction of the OR superfamily.

Intra-articular synovial hemangioma; a rare cause of knee pain and swelling.

INTRODUCTION: Synovial hemangioma is a rare intra-articular benign tumor that is difficult to diagnose because of its nonspecific symptoms. Patients are generally children or young adults with a nontraumatic recurrent swollen painful knee. CASE PRESENTATION: A 24-year-old woman presented with a 20-year history of recurrent pain and swelling in the right knee. Physical examination revealed a small painful point adjacent to the medial side of the patella. Magnetic resonance imaging revealed an intra-articular tumor. After arthroscopic examination, surgical excision was performed. The histology was characteristic of synovial hemangioma. RESULTS: Open complete synovectomy of the circumscribed capillary hemangioma was successful, and the patient remains asymptomatic 2 years after surgery.

PACSIN3 binds ADAM12/meltrin alpha and up-regulates ectodomain shedding of heparin-binding epidermal growth factor-like growth factor.

A disintegrin and metalloprotease 12 (ADAM12/meltrin alpha) is a key enzyme implicated in the ectodomain shedding of membrane-anchored heparin-binding epidermal growth factor (EGF)-like growth factor (proHB-EGF)-dependent epidermal growth factor receptor (EGFR) transactivation. However, the activation mechanisms of ADAM12 are obscure. To determine how ADAM12 is activated, we screened proteins that bind to the cytoplasmic domain of ADAM12 using a yeast two-hybrid system and identified a protein called PACSIN3 that contains a Src homology 3 domain. An analysis of interactions between ADAM12 and PACSIN3 using glutathione S-transferase fusion protein revealed that a proline-rich region (amino acid residues 829-840) of ADAM12 was required to bind PACSIN3. Furthermore, co-immunoprecipitation and co-localization analyses of ADAM12 and PACSIN3 proteins also revealed their interaction in mammalian cells expressing both of them. The overexpression of PACSIN3 in HT1080 cells enhanced 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced proHB-EGF shedding. Furthermore, knockdown of endogenous PACSIN3 by small interfering RNA in HT1080 cells significantly attenuated the shedding of proHB-EGF induced by TPA and angiotensin II. Our data indicate that PACSIN3 has a novel function as an up-regulator in the signaling of proHB-EGF shedding induced by TPA and angiotensin II.

ADAM binding protein Eve-1 is required for ectodomain shedding of epidermal growth factor receptor ligands.

A disintegrin and metalloproteases (ADAMs) are implicated in the ectodomain shedding of epidermal growth factor receptor (EGFR) ligands in EGFR transactivation. However, the activation mechanisms of ADAMs remain elusive. To analyze the regulatory mechanisms of ADAM activation, we performed yeast two-hybrid screening using the cytoplasmic domain of ADAM12 as bait, and identified a protein that we designated Eve-1. Two cDNAs were cloned and characterized. They encode alternatively spliced isoforms of Eve-1, called Eve-1a and Eve-1b, that have four and five tandem Src homology 3 (SH3) domains in the carboxyl-terminal region, respectively, and seven proline-rich SH3 domain binding motifs in the amino-terminal region. The short forms of Eve-1, Eve-1c and Eve-1d, translated at Met-371 are human counterparts of mouse Sh3d19. Northern blot analysis demonstrated that Eve-1 is abundantly expressed in skeletal muscle and heart. Western blot analysis revealed the dominant production of Eve-1c in human cancer cell lines. Knockdown of Eve-1 by small interfering RNA in HT1080 cells reduced the shedding of proHB-EGF induced by angiotensin II and 12-O-tetradecanoylphorbol-13-acetate, as well as the shedding of pro-transforming growth factor-alpha, promphiregulin, and proepiregulin by 12-O-tetradecanoylphorbol-13-acetate, suggesting that Eve-1 plays a role in positively regulating the activity of ADAMs in the signaling of EGFR-ligand shedding.