Gallium Phosphide photoanode coated with TiO2 and CoOx for stable photoelectrochemical water oxidation.

Gallium Phosphide (GaP) has a band gap of 2.26 eV and a valance band edge that is more negative than the water oxidation level. Hence, it may be a promising material for photoelectrochemical water splitting. However, one thing GaP has in common with other III-V semiconductors is that it corrodes in photoelectrochemical reactions. Cobalt oxide (CoOx) is a chemically stable and highly active oxygen evolution reaction co-catalyst. In this study, we protected a GaP photoanode by using a 20 nm TiO2 as a protection layer and a 2 nm cobalt oxide co-catalyst layer, which were both deposited via atomic layer deposition (ALD). A GaP photoanode that was modified by CoOx exhibited much higher photocurrent, potential, and photon-to-current efficiency than a bare GaP photoanode under AM1.5G illumination. A photoanode that was coated with both TiO2 and CoOx layers was stable for over 24 h during constant reaction in 1 M NaOH (pH 13.7) solution under one sun illumination.

Optimization of polyvinylidene fluoride (PVDF) membrane fabrication for protein binding using statistical experimental design.

Statistical experimental design was employed to optimize the preparation conditions of polyvinylidenefluoride (PVDF) membranes. Three variables considered were polymer concentration, dissolving temperature, and casting thickness, whereby the response variable was membrane-protein binding. The optimum preparation for the PVDF membrane was a polymer concentration of 16.55 wt%, a dissolving temperature of 27.5°C, and a casting thickness of 450 µm. The statistical model exhibits a deviation between the predicted and actual responses of less than 5%. Further characterization of the formed PVDF membrane showed that the morphology of the membrane was in line with the membrane-protein binding performance.

Simultaneous quantum dash-well emission in a chirped dash-in-well superluminescent diode with spectral bandwidth >700 nm.

We report on the quantitative evidence of simultaneous amplified spontaneous emission from the AlGaInAs/InAs/InP-based quantum-well (Qwell) and quantum-dashes (Qdash) in a multistack dash-in-an-asymmetric-well superluminescent diode heterostructure. As a result, an emission bandwidth (full width at half-maximum) of >700 nm is achieved, covering entire O-E-S-C-L-U communication bands, and a maximum continuous wave output power of 1.3 mW, from this device structure. This demonstration paves a way to bridge entire telecommunication bands through proper optimization of device gain region, bringing significant advances and impact to a variety of cross-disciplinary field applications.

Effect of the number of stacking layers on the characteristics of quantum-dash lasers.

A theoretical model is evaluated to investigate the characteristics of InAs/InP quantum dash (Qdash) lasers as a function of the stack number. The model is based on multimode carrier-photon rate equations and accounts for both inhomogeneous and homogeneous broadenings of the optical gain. The numerical results show a non monotonic increase in the threshold current density and a red shift in the lasing wavelength on increasing the stack number, which agrees well with reported experimental results. This observation may partly be attributed to an increase of inhomogeneity in the active region.

Optical injection modulation of quantum-dash semiconductor lasers by intra-cavity stimulated Raman scattering.

We report the optical injection modulation of semiconductor lasers by intra-cavity stimulated Raman scattering. This mechanism manifests itself as sharply enhanced modulation bandwidth in InAs/InGaAlAs/InP quantum-dash lasers when the injected photons are 33 +/- 3 meV more energetic than the lasing photons. Raman scattering measurements on the quantum-dash structure and rate equation models strongly support direct gain modulation by stimulated Raman scattering. We believe this new bandwidth enhancement mechanism may have important applications in optical communication and signal processing.

Laparoscopic high anterior resection with natural orifice specimen extraction (NOSE) for early rectal cancer.

Laparoscopic surgery for colorectal cancer requires an abdominal incision to extract the resected specimen. We describe a technique for laparoscopic resection of an early-stage upper rectal cancer in a 51-year-old man followed by transanal specimen delivery, hence avoiding the need for making any additional abdominal incisions for retrieval of the specimen. Pneumoperitoneum was created, followed by medial-tolateral mobilization of the sigmoid colon, and take down of the splenic flexure and division of the inferior mesenteric vessels laparoscopically. The upper rectum distal to the tumour and proximal colon was transected with a laparoscopic stapler. The specimen was retrieved transanally via an opening in the rectal stump. The proximal colon was then delivered transanally and the anvil of the circular stapler inserted before returning it to the pelvic cavity. The rectal stump was transected again just below the opening to close off the stump, and the colorectal anastomosis was then completed intracorporeally. The patient, a 51-year-old male (BMI 18.6 kg/m(2)) with a 2.5-cm, early-stage posterior rectal cancer 12 cm from the anal verge, underwent the above-described procedure. Postoperative recovery was uneventful. He resumed normal daily activities 1 week after surgery. Histology confirmed a T1N0 upper rectal cancer. In the effort to minimize surgical trauma and postoperative pain, natural orifice specimen extraction techniques have been attempted. This procedure may be applicable to benign tumours and early colorectal cancer, and serves as an intermediate step between laparoscopic and natural orifice surgery.

A prospective study assessing anal plug for containment of faecal soilage and incontinence.

OBJECTIVE: Faecal incontinence is a common and embarrassing problem for many individuals. Some patients remained symptomatic despite the availability of different treatments. There is a limited range of commercially available products designed to cope with faecal incontinence. The anal plug has been developed to contain the loss of stool. This study aimed to evaluate the use of anal plug in Asian patients with intractable faecal soilage and incontinence judged by clinical and functional outcomes. METHOD: A prospective study of consecutive patients with intractable faecal incontinence was carried out. Suitable patients tested the anal plug for 3 weeks. They completed a structured questionnaire on its use including the ASCRS quality of life questionnaire for faecal incontinence. RESULTS: Thirty patients, median age 63 (interquartile range 52-70) years, participated in the trial. Nineteen of 30 patients were comfortable wearing the plug, seven patients withdrew from the study because of discomfort, and four had tolerable discomfort and managed to complete the trial protocol. Patients who tolerated the plug found that it was highly successful in controlling faecal incontinence. Twenty-one of 30 patients wished to continue to use the plug regularly after the study. There was a trend toward improvement in quality of life scores during the study. CONCLUSION: The anal plug was effective in containing faecal incontinence and was well tolerated in the majority of patients selected for this treatment.

A 6-year review of surgical morbidity and oncological outcome after high anterior resection for colorectal malignancy with and without splenic flexure mobilization.

OBJECTIVE: High anterior resection (HAR) for colorectal cancer is traditionally performed with routine mobilization of the splenic flexure. This is a retrospective review of mortality and morbidity following HAR in which the splenic flexure has been preserved. METHOD: From a prospective database, all patients who had undergone elective HAR for colorectal cancer between 1999 and 2005 were identified. Morbidity, mortality, pathology and survival data for patients having HAR with and without splenic flexure mobilization were analysed. RESULTS: A total of 707 patients were identified. Five hundred and thirty-one had HAR with preservation of the splenic flexure. In these patients outcome was: anastomotic leak (0.4%), wound infection (3.6%), anastomotic stricture (0.4%) and 30-day mortality (0.9%). No statistical significant difference was found for postoperative morbidity (P = 0.1926), 30-day mortality (P =0.3285), lymph node harvest (P = 0.2127) or survival (P = 0.1457) compared with patients in whom the splenic flexure was mobilized. Longitudinal resection margins were greater following HAR with splenic flexure mobilization (P < 0.0001). CONCLUSION: No morbidity, oncological or survival disadvantage in performing splenic flexure preserving HAR was found.

Evidence for a mouse mesangial cell-derived factor that stimulates lymphocyte proliferation.

The functions of the glomerular mesangium are served by at least two populations of cells--a cell bearing microfilaments that regulates blood flow, and a phagocytic cell bearing Ia determinants and Fc receptors. We provide evidence that mouse mesangial cells (bearing microfilaments) produce a factor(s) that stimulates spleen cell proliferation. The factor(s) appears to act via monocytes/macrophages, since its stimulatory activity is abrogated by prior depletion of the responding mononuclear cell population of monocytes/macrophages. Confirmation of its action on macrophages was documented by experiments that showed that medium from macrophages incubated with mesangial cell supernatant contained greater amounts of a factor that stimulated [3H]thymidine uptake by macrophage-depleted spleen cell populations. By the cothymocyte proliferation assay, it could be shown that mesangial cell supernatant induced splenic macrophage production of interleukin-1-like activity. Preliminary characterization reveals the factor to have a molecular weight greater than 100,000. Thus, a novel function is delineated for this mesangial cell type that appears capable of modulating the local immune response by providing an amplification signal.

Diminished synthesis of immunoglobulin by peripheral lymphocytes of patients with idiopathic membranous glomerulonephropathy.

Some studies of animal models of serum-sickness nephritis have shown that the lesions of membranous nephropathy develop in animals exhibiting a poor antibody response to the administered antigen (if given in constant amounts). It is postulated that patients with idiopathic membranous nephropathy may share a similar characteristic, namely, a diminished capacity to produce sufficient amounts of antibody. To test this hypothesis, we examined the ability of lymphocytes isolated from 11 patients with this disorder to produce immunoglobulin (Ig)G and IgM on stimulation with a polyclonal B-cell activator, pokeweed mitogen. The peripheral blood lymphocytes (2 x 10(6) cells) from 24 normal individuals had geometric mean production rates of 1,779 ng for IgG, and 2,940 ng for IgM after 7 d of culture in the presence of pokeweed mitogen. By contrast, under identical conditions, lymphocytes from the 11 patients with membranous nephropathy produced significantly lower quantities of both immunoglobulins, with geometric mean concentrations of 511 ng for IgG and 439 ng for IgM. When lymphocytes from patients with membranous nephropathy were co-cultured with normal lymphocytes, the production of immunoglobulin by normal lymphocytes was depressed by 22-82%, suggesting that a population of suppressor cells was responsible for this disturbance in B-cell function. By co-culturing normal lymphocytes with patient lymphocytes depleted of either T cells or monocytes, the suppressor cell was identified as a monocyte.

Modification of glomerular immune complex deposition in mice by activation of the reticuloendothelial system.

To determine the effect of activation of the reticuloendothelial system on the localization of immune complexes in the kidney, a model of passive serum sickness nephritis in the mouse was used, with activation of the reticuloendothelial system with Corynebacterium parvum. Groups of mice, control and C. parvum-treated animals, were injected with BSA-125I-anti-BSA complexes containing 3 mg 125I-anti-BSA. Blood was obtained at 5 min, at 3 h, and at 12 h, when the animals were killed. Blood concentrations of BSA-125I-anti-BSA complexes were reduced in C. parvum-treated animals compared with controls. This appeared to be mediated by two effects, increased uptake of complexes in the liver and spleen, and enhanced degradation of immune complexes as measured by TCA-soluble radioactivity. In vitro studies using cultures of peritoneal macrophages also showed enhanced uptake of immune complexes. The amount of immune complexes deposited in the glomeruli of C. parvum-treated animals was reduced as determined by quantitation of radiolabeled material bound to isolated gomeruli and by immunofluorescence techniques. The results of the study emphasize the role of the reticuloendothelial system in the modulation of immune complex localization in the kidney and suggest a potential use of stimulants of the reticuloendothelial system in the therapy of immune complex nephritis.

Circulating immune complexes after renal transplantation. Correlation of increased 125I-Clq binding activity with acute rejection characterized by fibrin deposition in the kidney.

To assess the role of circulating immune complexes in the pathogenesis of acute rejection, sera were measured for such complexes by the (125)I-C1(q) binding assay in 45 normal subjects, 24 allografted patients undergoing acute rejection, and in 11 allografted patients in a quiescent phase. Increased C1(q)-binding activity (C1(q)-BA) was detected in 14 patients with acute rejection, 9 of whom had renal biopsies showing fibrin deposition in the vasculature together with cellular infiltrates in the tubulo-interstitial structures; renal histology was not available in the other 5 patients. The other 10 patients with acute rejection, whose biopsies showed only cellular infiltrates, and the 11 patients in a quiescent phase posttransplantation did not have increased levels of serum C1(q)-BA. Of the group with increased serum C1(q)-BA, serial studies in eight patients showed a correlation between increased serum C1(q)-BA and the occurrence of rejection; with reversal by therapy, serum C1(q)-BA returned to within normal levels. Complexes from six patients were analyzed by sucrose density gradient ultracentrifugation to have sedimentation coefficients ranging from 15S to 18.4S. After acid dissociation and analysis by double-diffusion techniques, C1(q)-reactive complexes were shown to contain IgG. Immunofluorescent studies done in five renal biopsies from this group revealed granular deposits of immunoglobulin, and (or) less frequently, of complement in the glomeruli or the tubular basement membranes. The findings suggest that circulating immune complexes may mediate the type of acute rejection characterized by fibrin deposition in the kidney. The role of circulating immune complexes arising from the recipient's original kidney disease could be excluded in 10 patients with humoral rejection, inasmuch as the underlying renal pathology was of a "nonimmunologic" nature; this was corroborated by sequential studies in six patients in whom circulating immune complexes could not be demonstrated before rejection. The participation of administered antilymphocyte globulin (ALG) as an antigen also appears to be excluded in four patients, two who were not given ALG, and in two of whom episodes of rejection occurred unrelated temporally to ALG administration.

Self-planarized quantum-disks-in-nanowires ultraviolet-B emitters utilizing pendeo-epitaxy.

The growth of self-assembled, vertically oriented and uniform nanowires (NWs) has remained a challenge for efficient light-emitting devices. Here, we demonstrate dislocation-free AlGaN NWs with spontaneous coalescence, which are grown by plasma-assisted molecular beam epitaxy on an n-type doped silicon (100) substrate. A high density of NWs (filling factor >95%) was achieved under optimized growth conditions, enabling device fabrication without planarization using ultraviolet (UV)-absorbing polymer materials. UV-B (280-320 nm) light-emitting diodes (LEDs), which emit at ∼303 nm with a narrow full width at half maximum (FWHM) (∼20 nm) of the emission spectrum, are demonstrated using a large active region ("active region/NW length-ratio" ∼50%) embedded with 15 stacks of AlxGa1-xN/AlyGa1-yN quantum-disks (Qdisks). To improve the carrier injection, a graded layer is introduced at the AlGaN/GaN interfaces on both p- and n-type regions. This work demonstrates a viable approach to easily fabricate ultra-thin, efficient UV optoelectronic devices on low-cost and scalable silicon substrates.

1,25-Dihydroxyvitamin D3 and rat vascular smooth muscle cell growth.

Recent studies from several laboratories have shown perturbations of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] metabolism in hypertension. While these perturbations may exert their effect on blood pressure via their actions on calcium metabolism, it is possible that this vitamin D metabolite may have direct effects on vascular smooth muscle cell (VSMC) physiology. To examine this, we studied the effect of 1,25(OH)2D3 on VSMC growth and found that this substance suppressed VSMC [3H]thymidine uptake; furthermore, this vitamin D metabolite also suppressed the stimulatory effect of epidermal growth factor (EGF) on VSMC proliferation. The concomitant presence of this substance appeared to be required for its action on VSMC growth since cells pretreated with the vitamin D metabolite for up to 72 hours and then washed of the substance grew normally and responded to EGF. Studies were also done to determine if 1,25(OH)2D3 had any effect on the function of EGF receptors on VSMC. Experiments using Iodine-125-labeled EGF showed no differences in the binding of this ligand to VSMC, either untreated or treated with 1,25(OH)2D3, which indicates the effect of the vitamin D metabolite on VSMC growth (when exposed to EGF) was not mediated by an alteration of EGF receptor function. The results of these studies have implications for the pathogenesis of vascular diseases such as hypertension and atherosclerosis.

Acute interstitial nephritis. A clinical and pathologic study based on renal biopsies.

To define interstitial nephritis without preselection bias, 25 consecutive renal biopsy specimens from patients with tubular damage, interstitial damage and interstitial inflammation were analyzed in detail. In four patients (all with acute renal failure), tubulitis, and interstitial eosinophil and lymphocyte infiltration were found, but no glomerular abnormalities. In four others, the findings were similar but some glomerular abnormalities were noted. Two patients had probable healed interstitial nephritis. The clinical presentation varied from transient renal insufficincy to oliguric renal failure. Three of the patients with glomerular abnormalities had significant proteinuria. When the 10 patients with interstitial nephritis were compared with the other 15 serving as controls, striking features in the former group were skin rash, eosinophilia, the absence of hypertension and the frequency of administration of penicillin and its analogs. Serum immunoglobulin E (IgE) levels were elevated in three of the patients. The striking eosinophilia, interstitial eosinophil infiltration and increased IgE levels suggest that allergen-reaginic complexes may be involved in the pathogenesis of the lesion.

Differential effects of costimulator signals and interleukin-2 on T cell receptor-mediated cell death of resting and activated CD4+ murine splenic T cells.

Postthymic T cell receptor (TCR)-mediated cell death offers the potential for creating antigen-specific transplant tolerance analogous to thymic clonal deletion. Murine specific CD4+ cell were rigorously purified by: (a) adherent cell depletion and (b) magnetic bead/monoclonal antibody (mAb) depletion of macrophages, Ia+ cells, mu-chain+ cells, NK cells, and CD8+ T cells. CD4+s were typically > 95% pure by flow cytometry. Resting CD4+s stimulated by plastic-immobilized anti-TCR/CD3 mAb wee shown to die in the absence of exogenous interleukin (IL)-2. Blasting CD4+s showed dose-dependent cell death upon religation of TCR/CD3 in the presence of IL-2; however, withdrawal of IL-2 from blasting CD4+s also resulted in cell death. Cell death was shown to be apoptotic by flow cytometry DNA content analysis. Anti-CD28 mAb, co-immobilized with anti-TCR/CD3 mAb, inhibited cell death of resting CD4+s in the absence of exogenous IL-2; however, anti-CD28 mAb showed minimal cell death inhibition of CD4+ blasts when TCR/CD3 was religated. In contrast, splenic adherent cells effectively inhibited cell death of blasting CD4+s induced by TCR/CD3 mAb religation. We conclude that TCR-mediated programmed cell death of highly purified splenic CD4+s is dependent upon activation state, availability of IL-2, and accessory cell or CD28 costimulator signals. Furthermore, IL-2 acts to protect against cell death in both resting and activated CD4+ T cells. IL-2 protection could be overcome by high concentrations of anti-TCR/CD3 mAb, which results in cell death of CD4+ blasts. In the effort to understand potential mechanisms of peripheral tolerance induction, these findings assist to distinguish and define conditions for antigen receptor-mediated programmed cell death of mature CD4+ T cells.

Immunofluorescent localization of beta2-microglobulin in the human kidney.

Using antisera to human beta2-microglobulin and an immunofluorescent technique, beta2-microglobulin was found to be localized along tubular and glomerular basement membranes of renal bipsies studied. Since beta2-microglobulin is a subunit of HLA preparations, it may also serve as an indirect marker for the presence of HLA antigens in these structures.

Modulation of macrophage proliferation by hyperglycemia.

Macrophages have been show to be of importance in three areas of pathology in the diabetic state: (a) in the destruction of the beta cells of the pancreas; (b) in the pathogenesis of the microvascular lesions; and (c) in the atherosclerotic lesion which is a common complication of diabetes. However, there is only scanty information on the behavior of the macrophage in the hyperglycemic environment. The present study investigates the growth of WEHI-3 monocytes/macrophages and the proliferative response of splenic macrophages to colony stimulating factor-1 when cultured in media containing high glucose concentrations. The results of the study show that hyperglycemia increases the proliferation of these macrophages; this effect is not mediated by the effect of osmolality since mannitol and L-glucose failed to produce a similar result. These findings suggest that alterations of macrophage physiology may be an important component of the diabetic state; such alterations may have a role in the production of some of the lesions found in diabetes mellitus.

Demonstration of endothelial-activating properties of hypertensive sera.

Sera from patients with hypertension were examined for their ability to influence endothelial cell function. Sera from 10 patients with hypertension and from 11 age-matched controls were incubated with endothelial cells and their effect on cell growth assessed by endothelial cell 3H-thymidine uptake. Sera from patients with hypertension had a more pronounced stimulatory effect on endothelial cell proliferation than control sera. In addition, hypertensive sera were also examined for their capacity to stimulate endothelial cell production of the vasoactive peptide endothelin. Confluent monolayers of endothelial cells were incubated with sera and the amount of endothelin generated in the supernatant measured by an immunoassay. Amounts of endothelin produced by the endothelial cells in response to hypertensive sera were significantly higher compared with the amounts produced in response to normal sera. The results of the studies suggest that a serum factor(s) in hypertensive patients may be of importance in modulating endothelial cell function. Such a factor(s) may have a significant role in the pathogenesis of hypertension.