Body odour aldehyde reduction by acetic acid bacterial extract including enzymes: alcohol dehydrogenase and aldehyde dehydrogenase.

OBJECTIVE: The major causes of unpleasant human body odour are aldehydes produced by axillary-resident bacteria. There are many methods of body odour prevention; however, they all carry risks of destroying indigenous dermal bacteria that are necessary for the maintenance of the normal physical function of the skin. Furthermore, some methods cannot directly reduce the concentrations of substances that cause body odour. Therefore, a novel method of reducing body odour more safely and effectively is required. We focused on acetic acid bacterial enzymes, which can convert aldehydes into carboxylic acids, and investigated their effect on aldehydes and body odour. METHODS: Subjects with strong body odour were recruited using screening questionnaires. Acetic acid bacterial extract including enzymes was applied to subjects' skin, and their effects were evaluated by trained panellists and by quantitative aldehyde analysis using thermal detector gas chromatography/mass spectrometry. RESULTS: Acetic acid bacterial extract including enzymes decreased the ratio of dilution to threshold and the concentration of body odour-producing aldehydes dropped by up to 98.7%. CONCLUSION: These results indicate that simply applying acetic acid bacterial enzymes on the skin can reduce the concentration of aldehydes that cause unpleasant body odour by directly converting them into carboxylic acids. Therefore, acetic acid bacterial enzymes can potentially be developed into new products that do not destroy indigenous bacteria and yet can effectively reduce unpleasant body odour.

Navigation-guided fence-post tube technique for resection of a brain tumor: technical note.

INTRODUCTION: A new technique using a navigation system to minimize the influence of brain shift and to perform precise resection of brain tumors is demonstrated. To determine the resection plane, one to six tubes were inserted around the tumor under the guidance of a navigation system before dural incision. RESULTS: This technique termed the "navigation-guided fence-post tube" (NGFP) procedure was used to treat 34 patients with intraaxial brain tumors including gliomas (23 cases), malignant lymphomas (4 cases) and metastatic tumors (7 cases). Tumors were removed totally in 23 cases (67.6%), subtotally (95% or more removal) in 6 cases (17.6%) and partially (less than 95% removal) in 5 cases (14.7%). The cases with subtotal or partial resection contained tumors that were close to or involved the eloquent area, or disseminated lesions. No complications due to tube insertion occurred. CONCLUSION: NGFP is a useful and safe technique for brain tumor surgery with no influence of brain shift during tumor resection.

Does eicosapentaenoic acid (EPA) inhibit cerebral vasospasm in patients after aneurysmal subarachnoid hemorrhage?

BACKGROUND: Cerebral vasospasm following subarachnoid hemorrhage (SAH) is a significant cause of morbidity and mortality and recent studies indicate that Rho-kinase plays an important role in the occurrence of such cerebral vasospasm. Eicosapentaenoic acid (EPA), an n-3 polyunsaturated fatty acid, inhibits sphingosylphosphorylcholine (SPC)-induced Rho-kinase activation in vitro, so this study examined whether EPA prevented cerebral vasospasm occurrence after SAH in patients. METHODS: The trial population was 101 patients with SAH subjected to craniotomy and clip application. EPA was orally administered at a daily dose of 1800 mg EPA from day 4 to day 14 to 73 patients; the other 28 constituted the control group, receiving no EPA. RESULTS: EPA significantly curtailed both the occurrence of symptomatic vasospasm (14% EPA group, 36% control, P = 0.019) and of cerebral infarction because of cerebral vasospasm (4% EPA group, 29% control, P = 0.001). Moreover, the percentage of patients with a clinically good outcome was significantly higher in the EPA group (85%, P = 0.022) than in control (64%); there were no deaths in the EPA group but three (11%) in control (P = 0.020). CONCLUSION: These findings suggest EPA inhibits symptomatic cerebral vasospasm and cerebral infarction after SAH and also improves clinical prognosis.

Side selection of pterional approach for anterior communicating artery aneurysms--surgical anatomy and strategy.

BACKGROUND: To evaluate our decision policy based on vertical aneurysm projection for selecting the side of the pterional approach for the surgical treatment of anterior communicating artery aneurysms. METHODS: Inferiorly projecting aneurysms were treated through the dominant A1 side, and superiorly projecting aneurysms were treated through the side of aneurysm fundus projection. We analysed postoperative outcome and surgical complications, and the correlations between the anatomical factors such as position (high or low), projection (dorsal or anterior), and the plane containing both A2 vessels (open A2 plane defined as the A2 of the approach side located more posteriorly than the contralateral A2; closed A2 plane as the ipsilateral A2 located more anteriorly than the contralateral A2), to assess the surgical requirements of approaches in patients with superiorly projecting aneurysms. FINDINGS: A favorable outcome was achieved in 95.1% of patients with inferior type aneurysms and 85.2% of patients with superior type aneurysms (P = 0.088). Surgical complications occurred in 8.9% of patients with inferior type aneurysms and 17.9% with superior type aneurysms. However, there was a distinct group of patients with superior type aneurysms characterised by a closed A2 plane, in which the ipsilateral A2 was located anterior to the contralateral A2, in whom the approach toward the neck was significantly more difficult, requiring A2 displacement or gyrus aspiration, and resulting in a neck remnant and more surgical complications such as vascular injury or cerebral contusion. This group also had a significantly high correlation with high position and dorsal projection of aneurysms causing more difficult dissection. CONCLUSIONS: This policy provided good postoperative outcomes. However, use of skull base techniques or the interhemispheric approach, instead of the normal pterional approach, may further improve the postoperative outcome for closed A2 plane aneurysms.

A surgical case of pulmonary adenocarcinoma complicated with pulmonary infarction presenting as an intrapulmonary metastasis.

Pulmonary adenocarcinoma complicated with a pulmonary infarction presenting as an intrapulmonary metastasis is relatively rare. We present a case of pulmonary infarction manifesting as intrapulmonary metastases of lung cancer. A previously healthy 59-year-old woman was admitted to our hospital on May 16, 2002 for evaluation of multiple abnormal radiographic shadows in the right lower lung field. Laboratory tests showed no abnormalities except for a slight elevation of carcinoembryonic antigens. Computed tomography of the chest revealed a hilar mass lesion with parenchymal lesions in the periphery of the right lower lobe, highly suspected to be a pulmonary adenocarcinoma with intrapulmonary metastases. A diagnosis of pulmonary adenocarcinoma was confirmed by a transbronchial brushing examination. A right middle and lower bilobectomy with mediastinal lymph node dissection was needed by hilum lymphadenopathy and a lower lobe invasion of the main tumor. Histopathological findings of the resected specimens revealed poorly differentiated adenocarcinoma of the lung with N1 (#11i) disease and multiple pulmonary infarctions with coagulation necrosis and recanalization. Pulmonary infarctions are demonstrated on chest x-rays as round or polygonal in shape, and located at the periphery of the same lobe as the primary tumor. Computed tomography is more sensitive than conventional radiography in the detection of pulmonary infarction. Our case suggests that pulmonary infarction associated with lung cancer should be considered as one important cause of peripheral pulmonary nodules.

Effects of different regions of the developing gut on the migration of enteric neural crest-derived cells: a role for Sema3A, but not Sema3F.

The enteric nervous system arises from vagal (caudal hindbrain) and sacral level neural crest-derived cells that migrate into and along the developing gut. Data from previous studies have suggested that (i) there may be gradients along the gut that induce the caudally directed migration of vagal enteric neural precursors (ENPs), (ii) exposure to the caecum might alter the migratory ability of vagal ENPs and (iii) Sema3A might regulate the entry into the hindgut of ENPs derived from sacral neural crest. Using co-cultures we show that there is no detectable gradient of chemoattractive molecules along the pre-caecal gut that specifically promotes the caudally directed migration of vagal ENPs, although vagal ENPs migrate faster caudally than rostrally along explants of hindgut. Exposure to the caecum did not alter the rate at which ENPs colonized explants of hindgut, but it did alter the ability of ENPs to colonize the midgut. The co-cultures also revealed that there is localized expression of a repulsive cue in the distal hindgut, which might delay the entry of sacral ENPs. We show that Sema3A is expressed by the hindgut mesenchyme and its receptor, neuropilin-1, is expressed by migrating ENPs. Furthermore, there is premature entry of sacral ENPs and extrinsic axons into the distal hindgut of fetal mice lacking Sema3A. These data show that Sema3A expressed by the distal hindgut regulates the entry of sacral ENPs and extrinsic axons into the hindgut. ENPs did not express neuropilin-2 and there was no detectable change in the timetable by which ENPs colonize the gut in mice lacking neuropilin-2.

Transvenous embolization for dural arteriovenous shunt of the cavernous sinus. Comparison of multi-staged transvenous embolization and transvenous embolization with sinus packing.

SUMMARY: We describe the treatment and follow-up clinical symptoms and angiographic results in patients with dural arteriovenous fistula of the cavernous sinus treated by transvenous embolization (TVE). We have treated eight cases of dural arteriovenous fistula of the cavernous sinus by multi-staged TVE in two cases and TVE with sinus packing in six and three of six cases were treated with a combination of transarterial embolization. Multi-staged TVE was performed by occlusion from dangerous drainage veins to the cavernous sinus on several occasions. Angiographical results showed disappearance or reduction of the arteriovenous shunt in all cases. Six patients presented with ophthalmic symptoms and two had tinnitus. Six cases had complete disappearance of clinical symptoms after treatment. There was a deterioration of ocular movement in one patient treated by TVE with sinus packing. Multi-staged TVE was performed to reduce the coil volume for the packing of the cavernous sinus in two cases without cranial nerve palsy. Embolization, especially multi-staged TVE, was considered a good treatment to occlude arteriovenous shunts at the cavernous sinus without cranial nerve complications.

Surgical pathology of spinal schwannoma: has the nerve of its origin been preserved or already degenerated during tumor growth?

OBJECTIVE: This study was aimed to understand ultrastructural pathology of nerves of tumor origin of spinal schwannomas, which has not been reported so far, in order to understand the mechanism of the postoperative functional restoration after the nerve transection. METHODS: From 13 patients who underwent sacrifice of an affected nerve root at total removal of spinal schwannomas (C2 conus), the proximal (spinal cord side, n = 12) and distal (dorsal root ganglion side, n = 10) stumps of the nerves of the tumor origin were collected and examined by light and electron microscope, followed by morphometric analysis (n = 9). RESULTS: Almost all of affected nerves at both proximal and distal to the lesion were composed of well-preserved myelin sheath and axons with mild disturbance of endo- and perineurial structures at light microscopic level except one case, which showed severe fibrosis. Electron-microscopically, regenerated axons with thin myelin were found in part in the proximal and distal nerves with few macrophages in three cases. The area of nerves (mm2), density of myelinated axons (axons/mm2) and total number of myelinated axons in the proximal stump (0.552 +/- 0.430, 10,400 +/- 5,240 and 5,480 +/- 4,790) was approximately 70%, 80% and 60%, respectively, of those in the distal stump (0.765 +/- 0.333, 12,400 +/- 5,180 and 9,970 +/- 8,630). CONCLUSIONS: This data combined with no permanent deficits after nerve transection suggest that the nerves of tumor origin are in the processes of slowly progressed deterioration with repeated degeneration and regeneration/remyelination, and the postoperative rapid recovery from the transient neurological deficit may be explained by functional compensation by the adjacent non-affected nerves with slow tumor growth.

Development of the amygdalohypothalamic projection in the mouse embryonic forebrain.

The amygdalohypothalamic projection, a major component of the stria terminalis, is involved in the conduction of emotional and olfactory information integrated in the amygdala to the hypothalamus to elicit emotional reactions. Despite the extensive studies on functional aspects of the amygdaloid complex, developmental mechanisms of the amygdala and related structures are still poorly understood. To investigate the development of the amygdalohypothalamic projection in the mouse embryonic brain, carbocyanine dye was applied to the amygdala to label the growing axons anterogradely and to the hypothalamus to label the amygdaloid neurons retrogradely. The initial outgrowth of the stria terminalis was found to be as early as E11.5. The pathway crossed in a saddle over the internal capsule, another prominent connection in the developing forebrain of the mammalian embryo. Bipolar immature neurons were distributed along the stria terminalis at the telencephalo-diencephalic boundary, and the internal capsule was also surrounded by these cells. These cells expressed immunoreactivities to calretinin and the lot-1 antigen which has been shown to be involved in guidance of the developing lateral olfactory tract. Ultrastructural analysis revealed an adherens-like junction between the stria terminalis and the apposed cells, implying contact-mediated guidance. These results suggest that, in the development of the stria terminalis, the axonal outgrowth is guided by a mechanism similar to that of the developing lateral olfactory tract, a major amygdalopetal connection.

Genotyping of single nucleotide polymorphism using model-based clustering.

MOTIVATION: Single nucleotide polymorphisms have been investigated as biological markers and the representative high-throughput genotyping method is a combination of the Invader assay and a statistical clustering method. A typical statistical clustering method is the k-means method, but it often fails because of the lack of flexibility. An alternative fast and reliable method is therefore desirable. RESULTS: This paper proposes a model-based clustering method using a normal mixture model and a well-conceived penalized likelihood. The proposed method can judge unclear genotypings to be re-examined and also work well even when the number of clusters is unknown. Some results are illustrated and then satisfactory genotypings are shown. Even when the conventional maximum likelihood method and the typical k-means clustering method failed, the proposed method succeeded.

Expression of basic fibroblast growth factor and its receptor-1 in cardiac myxoma.

BACKGROUND: To clarify the significance of basic fibroblast growth factor (bFGF) in angiogenesis or proliferative activity in cardiac myxoma, the expression of bFGF and its receptor (FGFR-1) were immunohistochemically examined. METHODS: Formalin-embedded tissues of cardiac myxomas were obtained by surgical resection from 15 patients and analyzed by immunostaining of bFGF and FGFR-1. The microvessel density was measured in the 15 myxomas using platelet derived endothelial cell adhesion molecule-1. For evaluation of proliferative activity of the cardiac myxomas, proliferating cell nuclear antigen (PCNA) immunostaining was performed, and the PCNA labeling index was measured in each section. RESULTS: bFGF and FGFR-1 were observed in 73.3% and 67.7% of the myxomas, respectively. There was a close correlation between the expression of bFGF and FGFR-1. This co-expression was frequently observed in the myxoma cells around the microvessels appearing as a ring structure. Regarding possible relationships between the expression of bFGF or FGFR-1 and the clinicopathologic features, there were no parameters excluding the macroscopic type of myxoma. The microvessel density in the myxomas with bFGF or FGFR-1 expression was higher than that in myxomas without it. The PCNA labeling index in myxomas with bFGF expression was higher than that in myxomas without it, and the PCNA labeling index tended to be higher in myxomas with FGFR-1 expression than that in myxomas without it. CONCLUSIONS: bFGF and/or FGFR-1 was expressed in some of cardiac myxoma, and may be an important role for tumor angiogenesis and proliferative activity.

Murine leukemia virus in organs of senescence-prone and -resistant mouse strains.

A series of inbred strains of mice have been developed that are either prone (SAMP) or resistant (SAMR) to accelerated senescence. All of these strains originated from an inadvertent cross or crosses between the AKR/J mouse strain and an unknown strain(s). The characteristics of the nine senescence-prone lines differ, with all strains showing generalized aspects of accelerated aging but with each line having a specific aging-related change that is emphasized, e.g. learning and memory deficits, osteoporosis and senile amyloidosis. The senescence-resistant strains have normal patterns of aging and do not show the specific aging-related changes seen in SAMP strains. The fact that AKR mice have high levels of endogenous, ecotropic murine leukemia virus (MuLV) prompted an examination of the expression levels of MuLV in SAM strains. Analysis of brain, spleen and thymus samples revealed that seven of nine SAMP strains had high levels of MuLV and contained the Emv11 provirus (previously termed Akv1) that encodes the predominant MuLV found in AKR mice. In contrast, none of the SAMR strains had Emv11 or significant amounts of virus. The current findings represent an initial step in determining the role of MuLV in the accelerated senescence seen in SAMP strains.

Expression of E-cadherin-catenin complex in human benign schwannomas.

The Ca2+-dependent cell adhesion molecule E-cadherin has been known to express in normal and reactive Schwann cells in rodents, and to play an important role in Schwann cell-Schwann cell adhesion and maintenance of peripheral nervous tissue architecture. However, little is known about expression of E-cadherin in schwannomas. The aim of the present study was to investigate the cellular expression and localization of E-cadherin, and its associated protein, alpha E-, alpha N- and beta-catenins in human schwannomas, which are supposed to derive from Schwann cells. We tested the hypothesis that these proteins might show an altered expression/distribution in schwannoma cells which correlates with their neoplastic behavior, including sparse cell-cell contact, as seen those in meningiomas and various carcinomas. In human schwannomas, however, E-cadherin, alpha E-catenin, and beta-catenin were detected by western blotting and immunohistochemistry, whereas alpha N-catenin was not. Immunoprecipitation using anti-E-cadherin antibody resulted in alpha E-catenin forming a complex with E-cadherin. SSCP analysis revealed no mutations in the transmembrane domain or in intracellular catenin-binding site of E-cadherin. These data suggest that the E-cadherin-alpha E-catenin complex is well preserved in human schwannoma cells, which is compatible with its benign behavior, and these molecules might be used as additional cell markers of Schwann cell-derived tumors.

Identification and characterization of CaMKP-N, nuclear calmodulin-dependent protein kinase phosphatase.

Calmodulin-dependent protein kinase phosphatase (CaMKP) dephosphorylates and concomitantly deactivates multifunctional Ca(2+)/calmodulin-dependent protein kinases (CaMKs), such as CaMKI, CaMKII, and CaMKIV. In the present study, a nuclear CaMKP-related protein, CaMKP-N, was identified. This protein consisted of 757 amino acid residues with a calculated molecular weight of 84,176. Recombinant CaMKP-N dephosphorylated CaMKIV. The activity of CaMKP-N requires Mn(2+) ions and is stimulated by polycations. Transiently expressed CaMKP-N in COS-7 cells was localized in the nucleus. This finding together with previous reports regarding localization of CaMKs indicates that CaMKP-N dephosphorylates CaMKIV and nuclear CaMKII, whereas CaMKP dephosphorylates CaMKI and cytosolic CaMKII.

Regulation of Ca(2+)/calmodulin-dependent protein kinase kinase alpha by cAMP-dependent protein kinase: I. Biochemical analysis.

Ca(2+)/calmodulin-dependent protein kinases (CaM-kinases) I and IV are activated upon phosphorylation of their Thr(177) and Thr(196), respectively, by the upstream Ca(2+)/calmodulin-dependent protein kinases CaM-kinase kinase alpha and beta, and deactivated upon dephosphorylation by protein phosphatases such as CaM-kinase phosphatase. Recent studies demonstrated that the activity of CaM-kinase kinase alpha is decreased upon phosphorylation by cAMP-dependent protein kinase (PKA), and the relationship between the inhibition and phosphorylation of CaM-kinase kinase alpha by PKA has been studied. In the present study, we demonstrate that the activity of CaM-kinase kinase alpha toward PKIV peptide, which contains the sequence surrounding Thr(196) of CaM-kinase IV, is increased by incubation with PKA in the presence of Ca(2+)/calmodulin but decreased in its absence, while the activity toward CaM-kinase IV is decreased by incubation with PKA in both the presence and absence of Ca(2+)/calmodulin. Six phosphorylation sites on CaM-kinase kinase alpha, Ser(24) for autophosphorylation, and Ser(52), Ser(74), Thr(108), Ser(458), and Ser(475) for phosphorylation by PKA, were identified by amino acid sequence analysis of the phosphopeptides purified from the tryptic digest of the phosphorylated enzymes. The presence of Ca(2+)/calmodulin suppresses phosphorylation on Ser(52), Ser(74), Thr(108), and Ser(458) by PKA, but accelerates phosphorylation on Ser(475). The changes in the activity of the enzyme upon phosphorylation appear to occur as a result of conformational changes induced by phosphorylation on several sites.

Regulation of Ca(2+)/calmodulin-dependent protein kinase kinase alpha by cAMP-dependent protein kinase: II. Mutational analysis.

We previously reported that rat brain Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) IV is inactivated by cAMP-dependent protein kinase (PKA) [Kameshita, I. and Fujisawa, H. (1991) Biochem. Biophys. Res. Commun. 180, 191-196]. In the preceding paper, we demonstrated that changes in the activity of CaM-kinase IV by PKA results from the phosphorylation of CaM-kinase kinase alpha by PKA and identified six phosphorylation sites, Ser(24) for autophosphorylation, and Ser(52), Ser(74), Thr(108), Ser(458), and Ser(475) for phosphorylation by PKA. In the present study, a causal relationship between the phosphorylation and change in the activity toward PKIV peptide has been studied using mutant enzymes with amino acid substitutions at the six phosphorylation sites. The following conclusions can be drawn from the experimental results: (i) Phosphorylation of Ser74 and/or unidentified sites causes an increase in activity; (ii) phosphorylation of Thr(108) or Ser(458) causes a decrease in the activity; (iii) the inhibitory effect of the phosphorylation of Thr(108) is canceled by the stimulatory effect of the phosphorylation, but that of Ser(458) is not; and (iv) the inhibitory effects of Thr(108) and Ser(458) are synergistic. In contrast to the activity toward PKIV peptide, the activity toward CaM-kinase IV appears to be decreased by the phosphorylation of Thr(108), but not significantly affected by the phosphorylation of Ser(458).

Reduced expression of the Aalpha subunit of protein phosphatase 2A in human gliomas in the absence of mutations in the Aalpha and Abeta subunit genes.

Protein phosphatase 2A (PP2A) consists of 3 subunits: the catalytic subunit, C, and the regulatory subunits, A and B. The A and C subunits both exist as 2 isoforms (alpha and beta) and the B subunit as multiple forms subdivided into 3 families, B, B' and B". It has been reported that the genes encoding the Aalpha and Abeta subunits are mutated in various human cancers, suggesting that they may function as tumor suppressors. We investigated whether Aalpha and Abeta mutations occur in human gliomas. Using single strand conformational polymorphism analysis and DNA sequencing, 58 brain tumors were investigated, including 23 glioblastomas, 19 oligodendrogliomas and 16 anaplastic oligodendrogliomas. Only silent mutations were detected in the Aalpha gene and no mutations in the Abeta gene. However, in 43% of the tumors, the level of Aalpha was reduced at least 10-fold. By comparison, the levels of the Balpha and Calpha subunits were mostly normal. Our data indicate that these tumors contain very low levels of core and holoenzyme and high amounts of unregulated catalytic C subunit.

[Bowel perforation after extracorporeal shock wave lithotripsy: a case report].

A case of intestinal perforation caused by ESWL for left ureteral calculus is reported. A 69-year-old male underwent the graft replacement for bilateral iliac aneurysm in March, 1996. In February, 1999, there appeared left flank pain, and a diagnosis of left ureterolithiasis was made by radiological examination. On March 29 he was admitted to our department for ESWL. On March 30, ESWL for calculus in the pelvic region was performed with the patient in the prone position. The patient complained of the left lower abdominal pain immediately after ESWL, but no muscular defense was observed. Since the pain was not relieved, CT was performed on March 31, but no evident abnormal finding was found. Thereafter the pain continued and on April 2 muscular defense was also noted. On CT performed a second time, free air and evidence of ileus were found, so emergency operation was performed. Two perforations about 2 mm in size were found in the jejunum 130 cm from the Treitz' ligament, which led to diagnosis of intestinal perforation due to ESWL. The patient followed a satisfactory postoperative course and was discharged on April 23. There has been only one reported case of intestinal perforation due to ESWL. It is a very rare complication. However, this complication should be taken into consideration where the patient has the history of abdominal surgery and where ESWL was performed with the patient in the prone position.