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Home energy management system is proposed to reduce the influences caused by the high ratio penetration of renewable energy generation, through managing and dispatching the residential power and energy consumption in the demand side. Being aware of how the electric energy is consumed is a key step of this system. Non-intrusive Load Monitoring is regarded as the most potential method to address this problem, which aims to separate individual appliances in households by decomposing the total power consumption. In recent years, NILM is framed as a multi-label classification problem and many researches has been investigated in this field. In this paper, a non-intrusive method which can identify appliances power usage information from the total power consumption is proposed and thoroughly investigated. Firstly, the random k-labelset multi-label classification algorithm is enhanced by introducing random forest algorithm as base classifier. Then, grid search method and cross validation method are integrated to determine the optimal paraments set. This algorithm is used to achieve the appliances identification. Finally, based on the identification result, the integer linear programming is employed for power estimation of each appliance, especially multi-state appliances. Experimental results on low voltage networks simulator demonstrate that the proposed method has a high identification accuracy compared with the traditional random k-labelset multi-label classification methods with other base classifiers, and it is capable of identifying the power usages of different appliances accurately. The desirable performance of power estimation has broadened the applications of machine learning based non-intrusive energy monitoring.

Previous studies suggest that gut microbiome disruption induced by chemotherapy, dietary deficiencies, and/or antibiotics are associated with increased incidence of acute graft-versus-host disease (aGVHD) following hematopoietic stem cell transplantation (HSCT). In a murine model of antibiotic-induced gut microbiome disruption, Holmes and colleagues show that oral administration of galactooligosaccharides (GOS) as a prebiotic attenuates lethal aGVHD, highlighting the crosstalk between diet and gut microbiota. Their data encourage clinical trials of GOS prebiotic diets during HSCT.

Quantities of advanced technologies have been utilized to realize the carbon neutrality, among which the smart implementations at energy user side are highlighted due to the extensive coverage. Supported by multiple energy management technologies, the integration of distributed renewable energy is prominent, but the compatibility problem of diverse technologies still exists especially considering the newly-developed features. In this paper, an interactive energy monitoring via non-intrusive way is allocated to analyze the roof-top photovoltaic generation and individual appliance consumption from integral energy measurements, and a complete solution is proposed to tackle the distributed generation intelligence with smart voltage maintenance. At first stage, aiming at the domestic reactive power management of photovoltaic inverters, the framework and strategy of coordination between smart meter and intelligent photovoltaic generation are proposed, and then the unified energy signature formulation of photovoltaic generation is presented. Afterwards, the energy disaggregation model is formularized by modified dictionary learning scheme with hybrid validation strategy. Lastly, a sparse coding and auxiliary optimization-based solution is proposed to solve the problem, achieving the robustness under real time architecture. Both the specific low voltage network simulator platform and the practical field measurement scenarios are utilized to verify the effectiveness of the proposed study, and results demonstrate that the proposed study provides an efficient monitoring solution to the intelligent photovoltaic generation, which helps to move toward the smart energy user implementation.

Mn-implanted Si with postannealing treatment at 873, 973, 1073, and 1173 K exhibited ferromagnetism at room temperature. Ferromagnetism was enhanced as the annealing temperature increased. The largest value of saturation magnetization was found in the sample annealed at 1173 K. X-ray absorption near-edge structure spectra showed no formation of substitutional–interstitial Mn–Mn dimmers in all samples. On the other hand, high-resolution transmission electron microscopy and glancing incidence X-ray diffraction revealed a variety of MnSi compounds. We propose that the ferromagnetism has the origin from the MnSi1.7 nanoparticles as well as the MnSi 1:1 phase, which possesses strong short-range spin correlation. The formation of antiferromagnetic Mn5Si3 compound in 873 and 973 K annealed samples substantially reduced the magnetism. This paper provides new insights into the understanding of ferromagnetism in Mn-implanted Si diluted magnetic semiconductors.

Si 1− x Mn x diluted magnetic semiconductor films were deposited on p-type Si(1 0 0) substrate by radio frequency magnetron sputtering method. Post thermal annealing was performed in an argon atmosphere at 1073 K for 300 s and at 1473 K for 120 s. The as-grown sample exhibits ferromagnetism at room temperature. Ferromagnetism is enhanced after annealing treatment. High resolution transmission electron microscopy shows that only Mn 4 Si 7 compound formed in all samples. X-ray diffraction patterns and Fast Fourier Transform image indicate Mn atoms incorporated into Si lattice upon annealing. X-ray absorption fine structure suggests the formation of substitutional–tetrahedral interstitial Mn–Mn and tetrahedral interstitial–substitutional–tetrahedral interstitial Mn–Mn–Mn complexes in the 1473 K annealed sample, which possesses the strongest ferromagnetism.

Si1−xCox magnetic semiconductors were prepared by implanting 200 keV Co ions into p-type Si(1 0 0) wafer at room temperature, followed by 600–900 °C annealing. Room temperature ferromagnetism was observed in all samples and saturation magnetization was enhanced after 900 °C annealing, for which nano-sized (several nm to 50 nm) CoSi2 precipitates were present. It was found that the formation of CoSi2 phase could play an important role in the enhancement of ferromagnetism.

Si 1− x Mn x diluted magnetic semiconductor films were deposited on the p-Si (100) single crystal wafer using magnetron sputtering method. Post-rapid thermal annealing treatments were performed at temperatures of 700 °C, 800 °C, and 900 °C in an argon atmosphere for approximately 5 min. Alternating gradient magnetometer, scanning electron microscope, atomic force microscope, X-ray diffraction and X-ray absorption near-edge structure spectra were employed to characterize magnetic properties and structure of the as-grown and annealed films. The films were about 2.8 μm thick and the RMS roughness of the surface was about 5–10 nm. All samples exhibit ferromagnetism at room temperature and the saturation magnetization reaches at the maximum value for the sample annealed at 700 °C. The silicide MnSi 1.7 was observed in the annealed samples. X-ray absorption near-edge structure spectra indicated that Mn atoms preferred to occupy substitutional or interstitial sites instead of precipitating to form silicide when annealing at 700 °C. It is inferred that the observed ferromagnetism is attributed to the interstitial and substitutional Mn dimers, which existed mostly in the sample annealed at 700 °C. The weaker ferromagnetism of the 900 °C annealed sample was closely related to the increased content of Mn 4 Si 7 compound.

a b s t r a c t Magnetic properties and microstructure of Cr-implanted Si have been investigated by alternating gradi- ent magnetometer (AGM), superconducting quantum interference device (SQUID) magnetometer, and transmission electron microscopy (TEM). p-Type (1 0 0) Si wafers were implanted at 200 keV at room temperature with a dosage of 1 × 10 16 cm −2

Two critical concerns in clinical cord blood transplantation are the initial time to engraftment and the subsequent restoration of immune function. These studies measured the impact of progenitor cell dose on both the pace and strength of hematopoietic reconstitution by transplanting nonobese diabetic/severe combined immunodeficiency/interleukin-2 receptor-gamma–null (NSγ) mice with lineage-depleted aldehyde dehydrogenase-bright CD34+ human cord blood progenitors. The progress of each transplant was monitored over an extended time course by repeatedly analyzing the peripheral blood for human hematopoietic cells. In vivo human hematopoietic development was complete. After long-term transplantation assays (≥ 19 weeks), human T-cell development was documented within multiple tissues in 16 of 32 NSγ mice. Human T-cell differentiation was active within NSγ thymuses, as documented by the presence of CD4+ CD8+ T-cell progenitors as well as T-cell receptor excision circles. It is important to note that although myeloid and B-cell engraftment was detected as early as 4 weeks after transplantation, human T-cell development was exclusively late onset. High progenitor cell doses were associated with a robust human hematopoietic chimerism that accelerated both initial time to engraftment and subsequent T-cell development. At lower progenitor cell doses, the chimerism was weak and the human hematopoietic lineage development was frequently incomplete.

Our purpose of this paper is to discuss who should take Precalculus Algebra, not the content of the course. Precalculus Algebra was originally intended for students who would progress to Calculus. However, many non-technical degree programs now require their majors to take it, even though it may be a terminal math course for these students. A review of the mathematics curriculum at various universities was conducted in order to identify similarities and differences regarding this particular course. In addition, a student survey was conducted at Alabama A&M University (AAMU) to determine students’ majors, their motivation for taking Precalculus Algebra, their attitude toward it, and the number of times they had taken it, reflecting their long-term success or failure with the course and its concepts. The curriculum reviews and the student surveys led us to question whether we, in the education community, are providing math skills that are relevant to the future careers of the students who are taking this as a terminal course. We propose alternative solutions and content for the different tracks of students taking Precalculus Algebra.

T-cell receptor variable β chain (TCRBV) repertoire spectratyping involves the estimation of CDR3 length distributions for monitoring T-cell receptor diversity and has proven useful for analyses of immune reconstitution and T-cell clonal expansions in graft-versus-host disease (GVHD) and graft-versus-leukemia after allogeneic stem cell transplantation. We performed a longitudinal spectratype analysis of 23 TCRBV families in 28 patients who underwent allogeneic T cell–depleted peripheral blood stem cell transplantation. Sixteen patients subsequently developed acute GVHD. We recently developed statistical methods that bring increased power and flexibility to spectratype analysis and allow us to analyze TCRBV repertoire development under appropriately complex statistical models. Applying these methods, we found that patients with acute GVHD demonstrated TCRBV repertoire development statistically distinct from that repertoire development in patients without GVHD. Specifically, GVHD patients showed spectratypes indicative of lower diversity and greater deviation from the spectratypes expected in healthy individuals at intermediate times. Most individual TCRBV subfamilies had spectratypes statistically distinguishable between GVHD and non-GVHD patients at 6 months after transplantation. These results suggest that the T-cell receptor repertoire perturbations associated with acute GVHD are widely spread throughout the TCRBV families.

The major challenge in allogeneic hematopoietic cell transplantation is how to transfer allogeneic T-cell immunity without causing graft-versus-host disease (GVHD). Here we report a novel strategy to selectively prevent GVHD by depleting CD62L+ T cells (naive and a subset of memory T cells). In unprimed mice, CD62L– T cells (a subset of memory T cells) failed to proliferate in response to alloantigens (which the mice have never previously encountered) and were unable to induce GVHD in allogeneic hosts. CD62L– T cells contributed to T-cell reconstitution by peripheral expansion as well as by promoting T-cell regeneration from bone marrow stem/progenitor cells. CD62L– T cells from the animals previously primed with a tumor cell line (BCL1) were able to inhibit the tumor growth in vivo but were unable to induce GVHD in the third-party recipients. This novel technology may allow transfer of allogeneic recall antitumor and antimicrobial immunity without causing GVHD.

Ion channels play an important role in cellular functions, and specific cellular activity can be produced by gating them. One important gating mechanism is produced by intra- or extracellular ligands. Although the ligand-mediated channel gating is an important cellular process, the relationship between ligand binding and channel gating is not well understood. It is possible that ligands are involved in the interactions of different protein domains of the channel leading to opening or closing. To test this hypothesis, we studied the gating of Kir2.3 (HIR) by intracellular protons. Our results showed that hypercapnia or intracellular acidification strongly inhibited these channels. This effect relied on both the N and C termini. The CO(2)/pH sensitivities were abolished or compromised when one of the intracellular termini was replaced. Using purified N- and C-terminal peptides, we found that the N and C termini bound to each other in vitro. Although their binding was weak at pH 7.4, stronger binding was seen at pH 6.6. Two short sequences in the N and C termini were found to be critical for the N/C-terminal interaction. Interestingly, there was no titratable residue in these motifs. To identify the potential protonation sites, we systematically mutated most histidine residues in the intracellular N and C termini. We found that mutations of several histidine residues in the C but not the N terminus had a major effect on channel sensitivities to CO(2) and pH(i). These results suggest that at acidic pH, protons appear to interact with the C-terminal histidine residues and present the C terminus to the N terminus. Consequentially, these two intracellular termini bound to each other through two short motifs and closed the channel. Thus, a novel mechanism for K(+) channel gating is demonstrated, which involves the N- and C-terminal interaction with protons as the mediator.

ROMK channels are inhibited by intracellular acidification. This pH sensitivity is related to several amino acid residues in the channel proteins such as Lys-61, Thr-51, and His-206 (in ROMK2). Unlike all other amino acids, histidine is titratable at pH 6-7 carrying a positive charge below pH 6. To test the hypothesis that certain histidine residues are engaged in CO(2) and pH sensing of ROMK1, we performed experiments by systematic mutations of all histidine residues in the channel using the site-directed mutagenesis. There are two histidine residues in the N terminus. Mutations of His-23, His-31, or both together did not affect channel sensitivity to CO(2). Six histidine residues are located in the C terminus. His-225, His-274, His-342, and His-354 were critical in CO(2) and pH sensing. Mutation of either of them reduced CO(2) and pH sensitivities by 20-50% and approximately 0.2 pH units, respectively. Simultaneous mutations of all of them eliminated the CO(2) sensitivity and caused this mutant channel to respond to only extremely acidic pH. Similar mutations of His-280 had no effect. The role of His-270 in CO(2) and pH sensing is unclear, because substitutions of this residue with either a neutral, negative, or positive amino acid did not produce any functional channel. These results therefore indicate that histidine residues contribute to the sensitivity of the ROMK1 channel to hypercapnia and intracellular acidosis.

The effect of interface roughness on exchange bias for NiFe/FeMn bilayers is investigated for polycrystalline films and epitaxial films. Three different systems were investigated: polycrystalline Ta (10 nm)/Ni80Fe20 (10nm)/Fe50Mn50 (20 nm) films on oxygen plasma-etched Si(100) or Cu/H–Si(100) and epitaxial Ni80Fe20 (10nm)/Fe60Mn40 (20 nm) films on Cu/H–Si(110). For films grown on plasma-etched substrates, as the etching time is increased, film roughness increases up to 12 nm. For the polycrystalline films grown on ultrathin Cu underlayers, x-ray diffraction shows the fcc (111) texture is greatly reduced as the thickness is increased. The epitaxial Cu/Si(110) buffer layer induces fcc (111) epitaxial growth and modifies the interface morphology. The dependence of exchange bias on roughness for each set of samples is explained in terms of a competition between the interfacial exchange coupling and the af uniaxial anisotropy.

A very thin Cu (/spl sim/1 nm) buffer layer on Si[110] is enough to induce Ni/sub 80/Fe/sub 20//Fe/sub 60/Mn/sub 40/ [111] epitaxial growth. The film surface roughness increases with increasing Cu thickness. The crystallinity improves as the Cu buffer thickness increases. The uniaxial anisotropy of the pinned Ni/sub 80/Fe/sub 20/ was greatly enhanced in the samples with thick Cu (>10 nm). This reflects the great effect of film crystallinity on exchange anisotropy.

Purpose Allogeneic transplantation is typically limited to younger patients having a matched donor. To allow a donor to be found for nearly all patients, we have used a nonmyeloablative conditioning regimen in conjunction with stem cells from a related donor with one fully mismatched HLA haplotype. Patients and Methods Fludarabine, cyclophosphamide, and alemtuzumab were used as the preparatory regimen. Additional graft-versus-host disease (GVHD) prophylaxis included mycophenolate with or without cyclosporine. Patients with persistence of disease had a donor lymphocyte boost planned. Toxicities, engraftment, response, survival, and immune recovery are reported. Results Forty-nine patients with hematologic malignancies or marrow failure and no other available donors were enrolled. Ninety-four percent of patients had successful engraftment, and 8% had secondary graft failure. The treatment-related mortality rate was 10.2%, and 8% of patients had severe GVHD. Encouraging evidence of quantitative lymphocyte recovery through expansion of transplanted T cells was noted by 3 to 6 months. Seventy-five percent of patients attained a complete remission, and 1-year survival rate was 31% (95% CI, 18% to 44%). A standard-risk group of 19 patients with aplasia or in remission at transplantation demonstrated a 63% 1-year survival rate (95% CI, 38% to 80%) and 2.9-year median overall survival time (95% CI, 6.2 to 48 months). Conclusion Nonmyeloablative therapy using haploidentical family member donors is feasible because the main obstacles of GVHD and graft rejection are manageable, allowing readily available stem-cell donors to be found for nearly all patients. Further qualitative and quantitative improvement in immune recovery is needed to address the high rate of relapse and risk of severe infections.

In this study, we investigated the possibility of selective depletion of donor alloantigen-specific T cells from C57BL/6 (H-2b) mice to prevent graft-versus-host disease (GVHD). These cells were first activated with irradiated BALB/c (H-2d) host spleen cells in a 5-day mixed lymphocyte culture. Following this activation, a photoactive rhodamine derivative called 4,5-dibromorhodamine 123 (TH9402), was added. This compound is selectively retained in the mitochondria of activated host-reactive cells but not tumor- or third-party–specific resting cells. The treated cells were subsequently exposed to visible light (514 nm) to deplete the TH9402-enriched activated host-reactive cells. Treatment with photodynamic cell purging process (PDP) inhibited antihost responses measured by cytotoxic T lymphocytes (CTL) by 93%, and interferon-γ production by 66%. By contrast, anti-BCL1 (BALB/c-origin leukemia/lymphoma) and anti–third-party C3H/HeJ (H-2k) responses were preserved. PDP-treated primed C57BL/6 cells were further tested in vivo. All lethally irradiated BALB/c mice inoculated with BCL1 cells and T-cell–depleted bone marrow cells developed leukemia by day +30, with 50% mortality by 100 days. All mice died of GVHD after addition of 5 × 106untreated primed C57BL/6 cells. However, addition of same numbers of PDP-treated cells allowed 90% of the recipients to survive more than 100 days without detectable BCL1 tumor cells and free of GVHD. Moreover, PDP-treated primed C57BL/6 cells retained the ability to induce GVHD in the third-party C3H/HeJ mice. These data suggest that PDP can selectively deplete host alloantigen-specific T cells for GVHD prevention and immune and antileukemia function preserve.

Umbilical cord blood has been increasingly used as a source of hematopoietic stem cells. A major area of concern for the use of cord blood transplantation is the delay in myeloid and lymphoid recovery. To directly compare myeloid and lymphoid recovery using an animal model of bone marrow and cord blood as sources of stem cells, hematopoietic engraftment and immune recovery were studied following infusion of T-cell–depleted adult bone marrow or full-term fetal blood cells, as a model of cord blood in a murine allogeneic transplantation model (C57BL/6 [H-2b] → BALB/c [H-2d]). Allogeneic full-term fetal blood has poorer radioprotective capacity but greater long-term engraftment potential on a cell-to-cell basis compared with T-cell–depleted bone marrow. Allogeneic full-term fetal blood recipients had decreased absolute numbers of T, B, and dendritic cells compared with bone marrow recipients. Splenic T cells in allogeneic full-term fetal blood recipients proliferated poorly, were unable to generate cytotoxic effectors against third-party alloantigens in vitro, and failed to generate alloantigen-specific cytotoxic antibodies in vivo. In addition, reconstituting T cells in fetal blood recipients had decreased mouse T-cell receptorδ single-joint excision circles compared with bone marrow recipients. At a per-cell level, B cells from fetal blood recipients did not proliferate as well as those found in bone marrow recipients. These results suggest that full-term fetal blood can engraft allogeneic hosts across the major histocompatibility barrier with slower hematopoietic engraftment and impaired immune reconstitution.

Abstract 2433 Poster Board II-410 We previously developed robust methods to purify human hematopoietic progenitors based on their high expression of aldehyde dehydrogenase (ALDHbr cells). These cells are enriched with both short- and long-term NOD/SCID repopulating cells. One early clinical trial suggested that augmenting a conventional cord blood transplant (CBT) with ALDHbr cells accelerated both neutrophil and platelet engraftment. We now describe experimental models for these clinical transplants, performed in two immunologically disparate strains of NOD/SCID mice. In the clinical study, pediatric patients first received 80% of an unmanipulated cord blood (CB) graft. 4 hours later they received the ALDHbr cells purified from the remaining 20% of the graft. In the experimental model, the mice were divided among three cohorts. Some mice were transplanted with 4,000 purified ALDHbr cells, alone. Other mice were transplanted with total CB using a cell dose that contained 4,000 ALDHbr cells. In the final group, mice first received the same dose of unmanipulated CB and, after 4 hours, 4,000 purified ALDHbr cells were also administered. After 4 weeks, the mice were sacrificed to determine their levels of human hematopoietic chimerism. When these transplants were performed using NOD/SCID-IL2Rγnull (NSγ) mice, the ALDHbr cells demonstrated strong short-term engraftment to the bone marrow (12 ± 4.9%; n = 5) that was characterized by human CD19+ B cells and CD33+ myeloid cells. The latter included CD15+ cells that indicate neutrophil engraftment. In addition, the peripheral blood of these mice contained low levels of human CD41+ CD61+ platelets. Unmanipulated CB also engrafted the bone marrow of NSγ mice (7.4 ± 4.7%; n = 8); however, >95% of the human cells appeared to be mature CD3+ T cells. Engraftment by either B cells or myeloid cells was consistently low to undetectable. Similarly, human platelets were not detected in the peripheral blood. When NSγ mice were transplanted first with total CB and subsequently with purified ALDHbr cells, the level of engraftment to the bone marrow increased >2-fold over what had been observed in mice transplanted with CB alone (18.9 ± 9.3%; n = 10; P = 0.006). However, nearly all of the human cells present within the bone marrow were T cells, as had been observed in animals that received only unmanipulated CB. In addition, human platelets were not observed in the peripheral blood of NSγ mice that had received both CB and ALDHbr cells. When similar transplants were performed using NOD/SCID-β2-microglobulinnull (NSβ) mice, the ALDHbr cells again demonstrated strong short-term engraftment to the bone marrow (5.6 ± 4.7%; n = 5) that was characterized by human CD19+ B cells and CD33+ myeloid cells. The peripheral blood of these mice also contained low levels of human platelets. In contrast, total CB achieved only very low engraftment to the bone marrow of NSβ mice (0.32 ± 0.19%; n = 4) and human platelets were not detected in the peripheral blood. However, when NSβ mice first received total CB which was augmented 4 hours later with purified ALDHbr progenitors, the level of human hematopoietic chimerism in the bone marrow increased >10-fold (4.3 ± 1.9%; n = 5), with engraftment of human B cells and myeloid cells. The co-transplanted NSβ mice also demonstrated low-level engraftment of human platelets in the peripheral blood. Continuing studies will resolve the relative contributions of the ALDHbr cells and the unmanipulated CB by using two HLA-matched (6/6), but sex-mismatched, CBs. In total, these studies confirmed that ALDHbr progenitors by themselves provided efficient short-term myeloid engraftment in both NOD/SCID strains. This was in contrast to what was observed after transplantation of bulk CB, which by itself did not provide efficient myeloid engraftment in either strain. Finally, in both mouse strains, ALDHbr cells altered the outcome of CB transplants. In NSγ mice, ALDHbr progenitors appeared to facilitate either the engraftment or proliferation of mature CB T cells. Most importantly, the studies in NSβ mice strongly suggested that ALDHbr progenitors directly augment short-term myeloid and platelet engraftment by total CB. The latter studies in particular mirror the experience of early clinical CBT studies that use the same strategy. Disclosures: Storms: Aldagen, Inc: Equity Ownership, Patents & Royalties. Gentry:Aldagen, Inc: Employment. Balber:Aldagen, Inc: Employment, Equity Ownership. Kurtzberg:Aldagen, Inc: Research Funding.

Background. PG490-88 is a water soluble, semisynthetic derivative of a novel compound PG490 (triptolide) purified from the Chinese herb Tripterygium Wilfordii Hook F. Methods. PG490-88 was administrated into recipient mice in a model (B10.D2→BALB/c) of lethal graft-versus-host disease (GVHD) to study the effects of PG490-88 on GVHD and on the various steps involved in the pathological course of GVHD. Results. Injection of PG490-88 i.p. at a dose of 0.535 mg/kg/day for the first 3 weeks after transplantation protected all the recipients from developing GVHD up to 100 days after transplantation. PG490-88 inhibited in vivo both CD4 + Vβ3 + and CD8 + Vβ3 + T cell (alloreactive T cells in this model) expansion in the spleen by 64.09 and 34.02%, respectively, at the time when Vβ3 + cell expansion was in the logarithmic phase (day 3 after transplantation). Intracellular cytokine staining without further in vitro activation demonstrated 47.42% inhibition of IL-2 production among CD4 + spleen cells in PG490-88-treated mice as compared to GVHD control on day 3 after transplantation. In contrast, CD25 (a chain of interleukin-2 receptor) expression did not differ. Conclusions. PG490-88 is highly effective in prevention of murine GVHD. The immunosuppressive effect of PG490-88 is mediated by inhibition of alloreactive T cell expansion through interleukin-2 production.

Hypercapnia has been shown to affect cellular excitability by modulating K+ channels. To understand the mechanisms for this modulation, four cloned K+ channels were studied by expressing them in Xenopus oocytes. Exposures of the oocytes to CO2 for 4–6 min produced reversible and concentration-dependent inhibitions of Kir1.1 and Kir2.3 currents, but had no effect on Kir2.1 and Kir6.1 currents. Intra- and extracellular pH (pHi, pHo) dropped during CO2 exposures. The inhibition of Kir2.3 currents was mediated by reductions in both intra- and extracellular pH, whereas the suppression of Kir1.1 resulted from intracellular acidification. In cell-free excised inside-out patches with cytosolic-soluble factors washed out, a decrease in pHi produced a fast and reversible inhibition of macroscopic Kir2.3 currents. The degree of this inhibition was similar to that produced by hypercapnia when compared at the same pHi level. Exposure of cytosolic surface of patch membranes to a perfusate bubbled with 15% CO2 without changing pH failed to inhibit the Kir2.3 currents. These results therefore indicate that (1) hypercapnia inhibits specific K+ channels, (2) these inhibitions are caused by intra- and extracellular protons rather than molecular CO2, and (3) these effects are independent of cytosol-soluble factors. J. Cell. Physiol. 183:53–64, 2000. © 2000 Wiley-Liss, Inc.

Room temperature ferromagnetism in Mn-implanted p-Si was enhanced dramatically by implantation of He. A 75 nm end-of-range region was found in the sample, with large scale and inhomogeneous damaging but preserved Si lattice periodicity. The end-of-range region shows an intrinsic magnetization of ∼100 emu/cm3. High resolution transmission electron microscopy and x-ray photoelectron spectroscopy measurements indicate that the spin polarization of Si dangling bonds rather than Mn impurity was the major source for the enhanced magnetism.

Graft-versus-host disease (GVHD) is a major complication following hematopoietic cell transplantation. While prophylaxis of GVHD has improved, treatment for GVHD remains unsatisfactory. PG490–88, a semi-synthetic derivative of a novel compound purified from a Chinese herb, is very effective in prevention of both acute and chronic GVHD. In this study, we tested whether PG490–88 is effective in treating established GVHD. The study was performed in a clinically relevant MHC-matched and minor mismatched model (B10.D2 to BALB/c). BALB/c (H2d, Mls-2a, Mls-3a) mice were lethally irradiated (8.5 Gy) and transplanted with 1x107 bone marrow cells and 1x108 spleen cells obtained from B10D.2 (H2d, Mls-2b, Mls-3b) mice. PG490–88 was administered intraperitoneally (i.p.) daily at a dose of 0.0535 mg/kg/day starting on day +15 post transplantation when the clinical signs of GVHD were first observed. Therefore, all animals in both vehicle control and PG490–88-treated groups developed GVHD before the treatment was started. After treatment, there was no difference in the severity of clinical GVHD between the treated and the control groups. However, PG490–88-treated mice survived significantly longer than the mice in the vehicle control group (Figure, median survival time: 50 vs. 65 days, P Figure Figure

Complementary nature of coercivity enhancement and exchange bias is generalized from the layered systems to ferro-antiferromagnet (F-AF) exchange coupled systems with arbitrary configurations and is proved based on the coherent rotation of the F magnetization. In the proof, the effect of F-AF coupling is absorbed into the anisotropy of the F part, resulting in an arbitrary anisotropy for the F part. The proof starts from a general discussion on the initial susceptibility of a single domain particle. Then the fundamental correlation between the maximal initial susceptibility and the critical field along an arbitrary easy direction of a single domain particle, at which the magnetization becomes unstable, is discussed. Finally, the difference of the initial switching field and the actual switching field along the arbitrarily chosen easy direction is discussed.

A circuit with two long parallel micron size wires was fabricated by photolithography to calibrate magnetic force microscopy (MFM) tips. The tip phase shift increased as the tip scan height decreased. With the tip scan height kept constant, a linear relationship was found between the current amplitude and the phase shift of the tip at the center position of the two wires separation. The estimated magnetic moment of the tip was one order larger than its nominal value. The results imply that with better control over the fabrication process, the micron size straight wires can be used to calibrate MFM tips.

T-cell reconstitution following allogeneic stem cell transplantation may involve thymic education of donor-derived precursors or peripheral expansion of mature T cells transferred in the graft. T cell-receptor excision circles (sjTRECs) are generated within the thymus and identify new thymic emigrants and those that have not divided. We measured quantitative and qualitative immunologic reconstitution and sjTREC levels in adult and pediatric recipients of umbilical cord blood transplants (UCBTs). sjTRECs were detected at normal levels in all children, starting 12 months after transplantation. sjTRECs were not detected until 18 months after transplantation in adults, and then only at a 3-fold lower level than expected for age. We used complementarity-determining region 3 (CDR3) spectratyping to measure changes in T cell-receptor diversity occurring with restoration of thymic function. T-cell repertoires were skewed in adults and children at 12 to 18 months after transplantation but recovered to nearnormal diversity at 2 to 3 years post-UCBT. T-cell repertoires appeared more diverse earlier in children (at 1 to 2 years post-UCBT) than in adults (at 3 to 4 years post-UCBT). We conclude that early T-cell recovery after UCBT occurs primarily through peripheral expansion of adoptively transferred donor T cells and results in skewing of the T-cell repertoire. The reappearance of sjTREC-containing cells after UCBT is associated with increasing numbers of phenotypically naive T cells, improved mitogen and recall antigen responses, and diversification of the T-cell repertoire. The delay in central T-cell recovery in adults relative to children may be due to differences in thymic function resulting from age-related atrophy, graft-versus-host disease, or the pharmacologic effects of prophylaxis and treatment of graft-versus-host disease.