All-optical flip-flop operation based on asymmetric active-multimode interferometer bi-stable laser diodes.

We demonstrate fast and low energy all optical flip-flop devices based on asymmetric active-multimode interferometer using high-mesa waveguide structure. The implemented devices showed high speed all-optical flip-flop operation with 25 ps long pulses. The rising and falling times of the output signal were 121 ps and 25 ps, respectively. The required set and reset pulse energies were only 7.1 fJ and 3.4 fJ, respectively.

Estimation of visceral fat in 9- to 13-year-old girls using dual-energy X-ray absorptiometry (DXA) and anthropometry.

OBJECTIVES: Accumulation of visceral fat (VF) in children increases the risk of cardiovascular disease and type 2 diabetes, and measurement of VF in children using computed tomography and magnetic resonance imaging (MRI) is expensive. Dual-energy X-ray absorptiometry (DXA) may provide a low-cost alternative. This study aims to determine if DXA VF estimates can accurately estimate VF in young girls, determine if adding anthropometry would improve the estimate and determine if other DXA fat measures, with and without anthropometry, could be used to estimate VF in young girls. METHODS: Visceral fat was measured at lumbar intervertebral sites (L1-L2, L2-L3, L3-L4 and L4-L5) using 3.0T MRI on 32 young girls (mean age 11.3 ± 1.3 years). VF was estimated using the GE CoreScan application. Measurement of DXA android and total body fat was performed. Weight, height and waist circumference (WC) measurements were also obtained. RESULTS: Waist circumference and body mass index were both strongly correlated with MRI, although WC was the best anthropometric covariate. Per cent fat (%fat) variables had the strongest correlation and did best in regression models. DXA %VF (GE CoreScan) and DXA android %fat and total body %fat accounted for 65% to 74% of the variation in MRI VF. CONCLUSION: Waist circumference predicted MRI VF almost as well as DXA estimates in this population, and a combination of WC and DXA fat improves the predictability of VF. DXA VF estimate was improved by the addition of WC; however, DXA android %fat with WC was better at predicting MRI VF.

Do labral tears influence poor outcomes after periacetabular osteotomy for acetabular dysplasia?

AIMS: Acetabular dysplasia is frequently associated with intra-articular pathology such as labral tears, but whether labral tears should be treated at the time of periacetabular osteotomy (PAO) remains controversial. The purpose of this study was to compare the clinical outcomes and radiographic corrections of PAO for acetabular dysplasia between patients with and without labral tears pre-operatively. PATIENTS AND METHODS: We retrospectively reviewed 70 hips in 67 patients with acetabular dysplasia who underwent PAO. Of 47 hips (45 patients) with labral tears pre-operatively, 27 (25 patients) underwent PAO alone, and were classified as the labral tear alone (LT) group, and 20 (20 patients) underwent combined PAO and osteochondroplasty, and were classified as the labral tear osteochondroplasty (LTO) group. The non-labral tear (NLT) group included 23 hips in 22 patients. RESULTS: There were no significant differences between groups for post-operative Harris hip scores, degree of progression of osteoarthritis or rate of reoperation. The pre-operative alpha angle was significantly larger in the LTO group compared with the other groups (p < 0.0001). CONCLUSION: PAO provides equivalent short-term relief of pain and functional outcome in patients with or without labral tears. The rate of progression of osteoarthritis and reoperation was not significantly increased in patients with labral tears. TAKE HOME MESSAGE: PAO provides equivalent short-term pain relief and functional outcomes in patients with acetabular dysplasia with and without labral tears. We did not find significantly increased risks of progression of osteoarthritis or re-operation in those with labral tears. Cite this article: Bone Joint J 2016;98-B:741-6.

Distribution of neurokinin A-like and neurokinin B-like immunoreactivity in human peripheral tissues.

Using specific radioimmunoassay and immunocytochemistry for neurokinin A (NKA) and neurokinin B (NKB), distribution and localization of the two peptides in human peripheral tissues were studied. Both NKA-like immunoreactivity (NKA-LI) and NKB-like immunoreactivity (NKB-LI) were present in the walls of the gut and gall bladder and in the pancreas. In the gut, the values for NKA-LI were 0.56-35.73 pmol/g wet weight, while those in pancreas and gall bladder were 0.64-0.68 and 0.36 pmol/g wet weight, respectively. The values of NKB-LI were 0.45-2.66 pmol/g wet weight in the gut, 0.93-1.65 pmol/g wet weight in the pancreas, and 0.30 pmol/g wet weight in the gall bladder. The immunocytochemical reactivity to both peptides was localized to ganglia of the submucosal and myenteric nerve plexuses in the gut wall, and to neurons in the muscle layer and mucosa of the gut wall. Weak but positive NKA-LI appeared in nerve cells of the pancreas, while NKB-LI was not detectable in the pancreas. Conversely, in the gall bladder wall, NKA-LI was undetectable while a very faint NKB-LI was found in the muscle layer. The localization of NKA corresponded closely to that of NKB in the tissues although the relative concentrations of the peptides varied from organ to organ.

Role of central tachykinin peptides in cardiovascular regulation in rats.

The mechanisms of action of tachykinin peptides thought to be involved in central cardiovascular regulation were examined. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dose-dependent increases in blood pressure and heart rate. The pressor responses to substance P (SP) (10 micrograms, i.c.v.) and neurokinin A (NKA) (10 micrograms, i.c.v.) were blocked by peripheral administration of pentolinium or phentolamine, and partially attenuated by adrenalectomy. In contrast, the only initial pressor response to the neurokinin B (NKB) analogue senktide (10 micrograms, i.c.v.) was blocked by pentolinium or phentolamine. The pressor response to senktide was inhibited by pretreatment with a vasopressin V1 receptor antagonist (d(CH2)5OMe(Tyr)AVP) (10 micrograms/kg, i.v.), and senktide (10 micrograms, i.c.v.) caused an increase in plasma vasopressin level. However, the vasopressin antagonist did not influence the SP- and NKA-induced pressor responses. These results suggest that central SP and NKA increase the blood pressure and heart rate via sympathetic nerve activity, whereas central NKB increases the blood pressure mainly via release of vasopressin from the hypothalamus.

The central pressor actions of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide.

Intracerebroventricular (i.c.v.) injections of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide (neuropeptide gamma, NP gamma), caused dose-dependent increases in blood pressure. The NP gamma-induced pressor responses (1 microgram i.c.v.) were blocked by peripheral administration of pentolinium (10 mg/kg i.v.) and phentolamine (10 mg/kg i.v.), but were not inhibited by a vasopressin antagonist. These results suggest that central NP gamma increases the blood pressure via sympathetic nerve activity.

Inhibition of neutrophil elastase activity attenuates complement-mediated lung injury in the hamster.

The role of neutrophil elastase in complement-mediated lung injury was examined in hamsters using a specific neutrophil elastase inhibitor, sodium N-[2-[4-(2,2 dimethylpropionyloxy)phenylsulfonylamino]benzoyl]aminoacetate tetrahydrate (sivelestat). Intravenous injection with cobra venom factor (CVF) into hamsters transiently increased plasma neutrophil elastase activity by about 10-fold. This increase was followed by a sustained increase in lung vascular [125I]bovine serum albumin permeability peaking 30 min after CVF injection. The increase in lung vascular permeability was associated with neutrophil accumulation in lung tissue and an increase in protein concentration in the bronchoalveolar lavage fluid. Inhibition of the elevated plasma neutrophil elastase activity (36.5%, 66.9% and 104.3%) by continuous i.v. infusion with sivelestat (0.1, 0.3 and 1 mg/kg/h), dose-dependently attenuated the increase in lung vascular permeability 30 min after CVF injection. Furthermore, sivelestat at 1 mg/kg/h almost totally prevented the increase in protein concentration in the bronchoalveolar lavage fluid without affecting lung neutrophil accumulation. These results suggest that neutrophil elastase is an important mediator in complement-mediated acute lung injury.

Sivelestat, a specific neutrophil elastase inhibitor, prevented phorbol myristate acetate-induced acute lung injury in conscious rabbits.

The in vivo contribution of neutrophil elastase (NE) in phorbol myristate acetate (PMA)-induced acute lung injury has so far been unclear. This study examined the role of NE in PMA-induced acute lung injury in conscious rabbits, using a specific NE inhibitor, sivelestat sodium hydrate (Sivelestat). A single bolus injection of PMA (40 microg/kg) caused acute lung injury as indicated by an increase in protein concentration and hemorrhage in bronchoalveolar lavage fluid (BALF) 4h after PMA injection. These changes were associated with mild decrease in arterial oxygen pressure and peripheral white blood cell and platelet. When continuously infused starting 1h before and ending 4h post-PMA injection, Sivelestat at 3-30 mg/kg/h that are able to inhibit rabbit NE activity by 60-90%, dose-dependently attenuated both PMA-induced hemorrhagic pneumonitis and the increase in protein concentration in BALF without affecting myeloperoxidase activity in the lung. Histopathological study indicated that sivelestat (30 mg/kg/h) markedly attenuated lung histopathological changes, alveolar hemorrhage and white blood cells migration with evidence of inhibition of NE activity in BALF. These results suggest that NE plays a significant role in PMA-induced acute lung injury and further supports the importance of this enzyme in acute lung injury.

Stable transformation of sorghum cell cultures after bombardment with DNA-coated microprojectiles.

Cells from a suspension culture of Sorghum vulgare (sorghum) have been transformed to either hygromycin or kanamycin resistance following uptake of pBC1 or pNGI plasmids, respectively, introduced on DNA-coated high velocity microprojectiles. Hygromycin- and kanamycin-resistant transformants contained hygromycin B phosphotransferase- and neomycin phosphotransferasehybridizing restriction fragments of the expected size, respectively. A second introduced, but unselected for, reporter uidA gene which encodes ß-glucuronidase activity was also detected by DNA gel blot analysis in these transformants and shown to be expressed at low levels in two of the ten transformants analyzed. Transcripts from the introduced foreign genes accumulated to detectable levels in only these two transformants, both of which had a high copy number of genes integrated into their genome. This report further establishes the biolistic method as a useful route for delivery of DNA into the difficult-to-transform monocotyledonous plant species and represents the first stable transformation of this agronomically-important cereal grain.

Production of fertile transgenic barley (Hordeum vulgare L.) plant using the hygromycin-resistance marker.

Fertile transgenic barley (Hordeum vulgare L.) plants were obtained by high velocity particle bombardment. The plasmid pBCl was used to deliver the selectable hph gene and reporter Gus gene into immature embryo. After the selection culture 18 hygromycin resistant plants were obtained. Samples for Southern hybridization and enzymatic Gus assay were obtained from 11 plants. Southern hybridization confirmed the presence of the hph gene in the 11 hygromycin resistant plants(T0). Enzymatic assay indicated that all the t0 plants that showed hph positive in Southern analysis possessed detectable amount of Gus activity. To date all the 11 t0 plants reached maturity and mature seeds were obtained Transmission of the hph gene to progeny(T1) of two independent t0 plants was confirmed by Southern hybridization.

Purification and characterization of a dipeptidyl carboxypeptidase from Pseudomonas sp. WO24.

A dipeptidyl carboxypeptidase (DCP) activity was detected in cell-free extracts of Pseudomonas sp. WO24. After purification and characterization the enzyme was found to be homogeneous by SDS-PAGE, and had a molecular mass of 74,000 Da by SDS-PAGE and 72,000 Da by gel filtration, indicating that it is monomeric. The isoelectric point was 5.2 and optimum pH was 6.5-7.0. It showed a specific activity of 780 mumol/min/mg, which is the highest of the values shown by known enzymes. The enzyme hydrolyzed angiotensin I to angiotensin II and sequentially released Phe-Arg and Ser-Pro from the C-terminus bradykinin. The DCP could not cleave imido-bonds, Gly-Gly bonds, or tripeptides. The enzymatic activity was completely inhibited by 0.001 mM EDTA and 0.1 mM O-phenanthroline, but it was not affected by general serine and cysteine protease inhibitors. Addition of Zn2+ completely restored the original activity of the inactivated DCP treated with EDTA. These results suggest that this enzyme is a zinc metalloprotease. The characteristics of the purified enzyme are slightly different from those of the DCPs from Escherichia coli, Pseudomonas maltophilia, and Corynebacterium equi, and considerably from those of the DCP from Bacillus pumilus.

Delayed neutrophil elastase inhibition prevents subsequent progression of acute lung injury induced by endotoxin inhalation in hamsters.

To define the role of neutrophil elastase (NE) in the progression of acute lung injury (ALI), we examined the effects of post-treatment with a specific NE inhibitor, sivelestat sodium hydrate (sivelestat), on ALI induced by endotoxin (ET) inhalation in hamsters. Inhalation of ET (300 microg/ml, 30 min) in conscious hamsters increased inflammatory cell count, protein concentration, and hemorrhage in bronchoalveolar lavage fluid (BALF) that peaked 24 h after ET inhalation. These changes were significant 2 h after ET inhalation and paralleled the increase in NE activity in BALF. When intravenously infused from 2 to 24 h post-ET inhalation, sivelestat (0.03 to 3 mg/kg/h) dose-dependently attenuated changes in these BALF parameters at 24 h post-ET inhalation in a manner dependent on the inhibition of NE activity in BALF. Histopathological analysis also indicated that sivelestat prevented the progression of lung inflammation such as alveolar neutrophil infiltration and hemorrhage. In contrast, dexamethasone (3 mg/kg, intravenously) was not effective in this model when administered 2 h after ET inhalation, although it was highly effective when applied before ET. We conclude that delayed inhibition of NE activity with sivelestat prevents subsequent progression of ALI in hamsters after ET inhalation. Thus NE may play an important role in the progression of ALI.