Discrimination of Frailty Phenotype by KinectTM-Based Stepping Parameters.

Background: Frailty increases the risk of falling, hospitalization, and premature death, necessitating practical early-detection tools. Objectives: To examine the discriminative ability of KinectTM-based stepping parameters for identifying frailty phenotype. Design: Population-based cross-sectional study. Setting: Eighteen neighborhoods near Tokyo Metropolitan Institute for Geriatrics and Gerontology, Itabashi, Tokyo, Japan. Participants: In total, 563 community-dwelling older adults aged ≥75 years without mobility limitations, neurological disease, or dementia were included. Measurements: Step number (SN) and knee total movement distance (KMD) during a 20-s stepping test were evaluated using the KinectTM infrared depth sensor. Results: The number (%) of participants with frailty were 51 (9.1). The area under the receiver operating characteristic curves (95% confidence interval) of a parameter consisting of SN and KMD for frailty was 0.72 (0.64, 0.79). Conclusions: Stepping parameters evaluated using KinectTM provided acceptable ability in identifying frailty phenotype, making it a practical screening tool in primary care and home settings.

Impact of Fat-Free Adipose Tissue on the Prevalence of Low Muscle Mass Estimated Using Calf Circumference in Middle-Aged and Older Adults.

Previous studies proposed calf circumference cutoff values for predicting dual-energy X-ray absorptiometry (DXA)-derived low muscle mass. However, DXA-derived appendicular lean mass (aLM) includes non-skeletal muscle components such as the appendicular fat-free component of adipose tissue fat cells (aFFAT). The purpose of this study was to compare the calf circumference method of classification before (Model #1) and after (Model #2) eliminating the influence of FFAT in healthy Japanese adults (50 to 79 years; mean age 70 (SD 7) years). Model 1, and Model 2 for classifying low muscle mass had a sensitivity of 78% and 64%, specificity of 76% and 75%, positive predictive value of 31% and 28%, and negative predictive value of 96% and 93%, respectively. Appendicular fat-free component of adipose tissue has the potential to influence the ability of calf circumference to accurately classify individuals with low muscle mass. Consideration should be made when using this as a screening tool for low muscle mass.

Development of Simple, Objective Chair-Standing Assessment of Physical Function in Older Individuals Using a KinectTM Sensor.

BACKGROUND: With increasing interest in addressing quality of life of older individuals, tests such as the Functional Independence Measure (FIM) are widely used measures of infirmity and burden of care. However, these scales are largely qualitative and especially problematic when assessing movement-based tasks. While effective, reliable analysis of human movement is technically complicated and expensive; an infrared depth sensor is potentially a low-cost, portable devise which may provide a quantitative aspect to clinical testing. OBJECTIVE: to assess the utility of the KinectTM sensor in providing an objective evaluation of human movement using an oft measured ADL (chair stand). DESIGN: Cross-sectional study. SETTING: Community, geriatric day-care center in Japan. PARTICIPANTS: Men (n=136) and women (n=266) between 50 and 93 years of age, consisting of healthy (HE; n=312) and physically frail (FR; n= 90) individuals. MEASUREMENTS: Subjects completed two trials of the chair stand, conducted without assistance. Trials were timed and recorded with KinectTM v2. Coronal plane angle (CPA) was determined by a line transecting the shoulder-center and waist relative to the vertical axis and was used to assess quality of the chair stand movement pattern. RESULTS: Age, height, and body mass were not different between groups. CPA was significantly greater in FR (29.3 ± 8.3°) than HE (19.5 ± 6.5°). CPA and age were significantly related (r=0.148, p<0.01). An optimal threshold for CPA identifying frailty was determined by a receiver-operator characteristic curve with a CPA of 23.1° providing the greatest combination of sensitivity (79%) and specificity (73%). CONCLUSION: During the chair stand, frail older adults adopted a forward lean position (increased CPA) compared to healthy older adults. This compensatory posture appears to facilitate torso rotation while reducing lower-limb muscular effort during standing. As such, CPA serves as an indicator of reduced lower-body function in older, frail adults.

DXA-Rectified Appendicular Lean Mass: Development of Ultrasound Prediction Models in Older Adults.

OBJECTIVE: Dual-energy X-ray absorptiometry (DXA)-derived appendicular lean soft tissue mass (aLM) is used to diagnose sarcopenia. However, DXA-derived aLM includes non-skeletal muscle components, such as fat-free component of adipose tissue fat cell. These components, if not accounted for, could falsely inflate the aLM in individuals with a high amount of adipose tissue mass. B-mode ultrasound accurately measures muscle size in older adults. We sought to develop regression-based prediction equations for estimating DXA-rectified appendicular lean tissue mass (i.e. DXA-derived aLM minus appendicular fat-free adipose tissue (aFFAT); abbreviated as aLM minus aFFAT) using B-mode ultrasound. DESIGN: Cross-sectional study. MEASUREMENTS: Three hundred and eighty-nine Japanese older adults (aged 60 to 79 years) volunteered in the study. aLM was measured using a DXA, and muscle thickness (MT) was measured using ultrasound at nine sites. An ordinary least-squares multiple linear regression model was used to predict aLM minus aFFAT from sex, age and varying muscle thicknesses multiplied by height. Based on previous studies, we chose to use 4 MT sites at the upper and lower extremities (4-site MT model) and a single site (1-site MT model) at the upper extremity to develop prediction models. RESULTS: The linear prediction models (4 site MT model; R2 = 0.902, adjusted R2 = 0.899, and 1-site MT model; R2 = 0.868, adjusted R2 = 0.866) were found to be stable and accurate for estimating aLM minus aFFAT. Bootstrapping (n=1000) resulted in optimism values of 0.0062 (4-site MT model) and 0.0036 (1-site MT model). CONCLUSION: The results indicated that ultrasound MT combined with height, age and sex can be used to accurately estimate aLM minus aFFAT in older Japanese adults. Newly developed ultrasound prediction equations to estimate aLM minus aFFAT may be a valuable tool in population-based studies to assess age-related rectified lean tissue mass loss.

Quantification of personal exposure concentrations to gasoline vehicle emissions in high-end exposure microenvironments: effects of fuel and season.

Mobile-source air toxic (MSAT) levels increase in confining microenvironments (MEs) with numerous emission sources of vehicle exhaust or evaporative emissions or during high-load and cold-start conditions. Reformulated fuels are expected to reduce MSAT and ozone precursor emissions. This study, required under the Clean Air Act Section 211b, evaluated high-end exposures in cities using reformulated (methyl tertiary-butyl ether [MTBE] or ethanol [EtOH]) fuels and conventional gasoline blends. The study investigates 13 high-end MEs, sampling under enhanced exposure conditions expected to result in maximal fuel and exhaust component exposures to carbon monoxide (CO), carbon dioxide (CO2), BTEX (benzene, toluene, ethylbenzene, xylenes), MTBE, 1,3-butadiene (1,3-BD), EtOH,formaldehyde (HCHO), and acetaldehyde (CH3CHO). The authors found that day-to-day ME variations in high-end benzene, 1,3-BD, HCHO, and CO concentrations are substantial, but independent of gasoline composition and season, and related to the activity and emission rates of ME sources, which differ from day to day.

Muscle oxygenation and fascicle length during passive muscle stretching in ballet-trained subjects.

Muscle stretching transiently decreases muscle-blood flow corresponding to a muscle extension. It may disturb a balance between muscular oxygen demand and oxygen supply to muscles and reduce muscle oxygenation. However, muscle-stretching training may improve blood circulatory condition, resulting in the maintained muscle oxygenation during muscle stretching. The aim of this study was to investigate changes in muscle-blood volume (tHb) and tissue oxygenation index (TOI) during muscle stretching determined by using near-infrared spectroscopy (NIRS) in ballet-trained (BT) and untrained (C) subjects. 11 BT women who regularly perform muscle stretching and 11 C women participated in this study. Fascicle lengths, tHb and TOI in the tibialis anterior muscle were measured during passive plantar flexion from ankle joint angles of 120° (baseline) to 140°, 160°, the maximal comfortable position without pain (CP), and the maximal position (MP). At 160°, the % fascicle-length change from baseline was significantly lower in the BT than the C group, however, for the changes in tHb and TOI the significant interaction effect between the 2 groups was not detected. On the other hand, although the increases in the fascicle length from baseline to CP and MP were greater in BT than C, the tHb and TOI reductions were comparable between groups. We concluded that it appears that BT can extend their muscles without excessive reduction in muscle-blood volume and muscle oxygenation at relatively same but absolutely greater muscle-stretching levels than C. The attenuation in these indices during high-level muscle stretching may be associated with the repetitive muscle stretching of long-term ballet training.

Localisation of RA175 (Cadm1), a cell adhesion molecule of the immunoglobulin superfamily, in the mouse testis, and analysis of male infertility in the RA175-deficient mouse.

RA175, a member of the immunoglobulin superfamily, plays an important role in cell adhesion, and RA175 gene-deficient mice (RA175(-/-) ) show oligoastheno-teratozoospermia. To understand the function of RA175, location in the testis and the morphological features of its spermatogenic cells in RA175(-/-) mice were investigated. Immunohistochemical studies revealed that RA175 immunoreactivity was observed on the cell surface of the spermatogenic cells at specific stages. A strong reaction was detected from type A spermatogonia to pachytene spermatocytes at stage IV and from step 6 to step 16 spermatids during spermatogenesis. From pachytene spermatocytes at stage VI to step 4 spermatids, the reaction was not detected by the enzyme-labelled antibody method and was faintly detected by the indirect immunofluorescence method. Abnormal vacuoles in the seminiferous epithelium, showing exfoliation of germ cells, and ultrastructural abnormality of the elongate spermatids were revealed in the RA175(-/-) testes. Other members of the immunoglobulin superfamily such as basigin, nectin-2 and nectin-3, which have an important role in spermatogenesis, were immunohistochemically detected in the RA175(-/-) testis. These observations indicate a unique expression pattern of RA175 in the testis and provide clues regarding the mechanism of male infertility in the testis.

Autism spectrum disorder is related to endoplasmic reticulum stress induced by mutations in the synaptic cell adhesion molecule, CADM1.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with an unknown molecular pathogenesis. A recent molecular focus has been the mutated neuroligin 3, neuroligin 3(R451C), in gain-of-function studies and for its role in induced impairment of synaptic function, but endoplasmic reticulum (ER) stress induced by mutated molecules also deserves investigation. We previously found two missense mutations, H246N and Y251S, in the gene-encoding synaptic cell adhesion molecule-1 (CADM1) in ASD patients, including cleavage of the mutated CADM1 and its intracellular accumulation. In this study, we found that the mutated CADM1 showed slightly reduced homophilic interactions in vitro but that most of its interactions persist. The mutated CADM1 also showed morphological abnormalities, including shorter dendrites, and impaired synaptogenesis in neurons. Wild-type CADM1 was partly localized to the ER of C2C5 cells, whereas mutated CADM1 mainly accumulated in the ER despite different sensitivities toward 4-phenyl butyric acid with chemical chaperone activity and rapamycin with promotion activity for degradation of the aggregated protein. Modeling analysis suggested a direct relationship between the mutations and the conformation alteration. Both mutated CADM1 and neuroligin 3(R451C) induced upregulation of C/EBP-homologous protein (CHOP), an ER stress marker, suggesting that in addition to the trafficking impairment, this CHOP upregulation may also be involved in ASD pathogenesis.

Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells.

Previously, we analyzed mice lacking either caspase-2 or caspase-3 and documented a role for caspase-2 in developmental and chemotherapy-induced apoptosis of oocytes. Those data also revealed dispensability of caspase-3, although we found this caspase critical for ovarian granulosa cell death. Because of the mutual interdependence of germ cells and granulosa cells, herein we generated caspase-2 and -3 double-mutant (DKO) mice to evaluate how these two caspases functionally relate to each other in orchestrating oocyte apoptosis. No difference was observed in the rate of spontaneous oocyte apoptosis between DKO and wildtype (WT) females. In contrast, the oocytes from DKO females were more susceptible to apoptosis induced by DNA damaging agents, compared with oocytes from WT females. This increased sensitivity to death of DKO oocytes appears to be a specific response to DNA damage, and it was associated with a compensatory upregulation of caspase-12. Interestingly, DKO oocytes were more resistant to apoptosis induced by methotrexate (MTX) than WT oocytes. These results revealed that in female germ cells, insults that directly interfere with their metabolic status (e.g. MTX) require caspase-2 and caspase-3 as obligatory executioners of the ensuing cell death cascade. However, when DNA damage is involved, and in the absence of caspase-2 and -3, caspase-12 becomes upregulated and mediates apoptosis in oocytes.

ER stress (PERK/eIF2alpha phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation.

Expanded polyglutamine 72 repeat (polyQ72) aggregates induce endoplasmic reticulum (ER) stress-mediated cell death with caspase-12 activation and vesicular formation (autophagy). We examined this relationship and the molecular mechanism of autophagy formation. Rapamycin, a stimulator of autophagy, inhibited the polyQ72-induced cell death with caspase-12 activation. PolyQ72, but not polyQ11, stimulated Atg5-Atg12-Atg16 complex-dependent microtubule-associated protein 1 (MAP1) light chain 3 (LC3) conversion from LC3-I to -II, which plays a key role in autophagy. The eucaryotic translation initiation factor 2 alpha (eIF2alpha) A/A mutation, a knock-in to replace a phosphorylatable Ser51 with Ala51, and dominant-negative PERK inhibited polyQ72-induced LC3 conversion. PolyQ72 as well as ER stress stimulators upregulated Atg12 mRNA and proteins via eIF2alpha phosphorylation. Furthermore, Atg5 deficiency as well as the eIF2alpha A/A mutation increased the number of cells showing polyQ72 aggregates and polyQ72-induced caspase-12 activation. Thus, autophagy formation is a cellular defense mechanism against polyQ72-induced ER-stress-mediated cell death by degrading polyQ72 aggregates, with PERK/eIF2alpha phosphorylation being involved in polyQ72-induced LC3 conversion.

N doping of TiO2(110): photoemission and density-functional studies.

The electronic properties of N-doped rutile TiO2(110) have been investigated using synchrotron-based photoemission and density-functional calculations. The doping via N2+ ion bombardment leads to the implantation of N atoms (approximately 5% saturation concentration) that coexist with O vacancies. Ti 2p core level spectra show the formation of Ti3+ and a second partially reduced Ti species with oxidation states between +4 and +3. The valence region of the TiO(2-x)N(y)(110) systems exhibits a broad peak for Ti3+ near the Fermi level and N-induced features above the O 2p valence band that shift the edge up by approximately 0.5 eV. The magnitude of this shift is consistent with the "redshift" observed in the ultraviolet spectrum of N-doped TiO2. The experimental and theoretical results show the existence of attractive interactions between the dopant and O vacancies. First, the presence of N embedded in the surface layer reduces the formation energy of O vacancies. Second, the existence of O vacancies stabilizes the N impurities with respect to N2(g) formation. When oxygen vacancies and N impurities are together there is an electron transfer from the higher energy 3d band of Ti3+ to the lower energy 2p band of the N(2-) impurities.

ER stress induces caspase-8 activation, stimulating cytochrome c release and caspase-9 activation.

Excess ER stress induces caspase-12 activation and/or cytochrome c release, causing caspase-9 activation. Little is known about their relationship during ER stress-mediated cell death. Upon ER stress, P19 embryonal carcinoma (EC) cells showed activation of various caspases, including caspase-3, caspase-8, caspase-9, and caspase-12, and extensive DNA fragmentation. We examined the relationship between ER stress-mediated cytochrome c/caspase-9 and caspase-12 activation by using caspase-9- and caspase-8-deficient mouse embryonic fibroblasts and a P19 EC cell clone [P19-36/12 (-) cells] lacking expression of caspase-12. Caspase-9 and caspase-8 deficiency inhibited and delayed the onset of DNA fragmentation but did not inhibit caspase-12 processing induced by ER stress. P19-36/12 (-) cells underwent apoptosis upon ER stress, with cytochrome c release and caspase-8 and caspase-9 activation. The dominant negative form of FADD and z-VAD-fmk inhibited caspase-8, caspase-9, Bid processing, cytochrome c release, and DNA fragmentation induced by ER stress, suggesting that caspase-8 and caspase-9 are the main caspases involved in ER stress-mediated apoptosis of P19-36/12 (-) cells. Caspase-8 deficiency also inhibited the cytochrome c release induced by ER stress. Thus, in parallel with the caspase-12 activation, ER stress triggers caspase-8 activation, resulting in cytochrome c/caspase-9 activation via Bid processing.

Caspase-12 processing and fragment translocation into nuclei of tunicamycin-treated cells.

Excess endoplasmic reticulum (ER) stress induces processing of caspase-12, which is located in the ER, and cell death. However, little is known about the relationship between caspase-12 processing and cell death. We prepared antisera against putative caspase-12 cleavage sites (anti-m12D318 and anti-m12D341) and showed that overexpression of caspase-12 induced autoprocessing at D(318) but did not induce cell death. Mutation analysis confirmed that D(318) was a unique autoprocessing site. In contrast, tunicamycin, one of the ER stress stimuli, induced caspase-12 processing at the N-terminal region and the C-terminal region (both at D(318) and D(341)) and cell death. Anti-m12D318 and anti-m12D341 immunoreactivities were located in the ER of the tunicamycin-treated cells, and some immunoreactivities were located around and in the nuclei of the apoptotic cells. Thus, processing at the N-terminal region may be necessary for the translocation of processed caspase-12 into nuclei and cell death induced by ER stress. Some of the caspase-12 processed at the N-terminal and C-terminal regions may directly participate in the apoptotic events in nuclei.

Vascular regulation of type II cell exocytosis.

To determine whether lung capillary pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca(2+) concentration ([Ca(2+)](i)) and type II cell exocytosis. Increasing left atrial pressure (Pla) from 5 to 10 cmH(2)O increased septal capillary diameter by 26% and induced marked alveolar [Ca(2+)](i) oscillations that abated on relief of pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the pressure elevation and continued at the same rate even after pressure and [Ca(2+)](i) oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, the intracellular Ca(2+) chelator, or heptanol, the gap junctional blocker, the pressure-induced exocytosis was completely inhibited. We conclude that capillary pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca(2+)-dependent manner but is sustained by Ca(2+)-independent mechanisms.

Catalysis research of relevance to carbon management: progress, challenges, and opportunities.

The goal of the "Opportunities for Catalysis Research in Carbon Management" workshop was to review within the context of greenhouse gas/carbon issues the current state of knowledge, barriers to further scientific and technological progress, and basic scientific research needs in the areas of H2 generation and utilization, light hydrocarbon activation and utilization, carbon dioxide activation, utilization, and sequestration, emerging techniques and research directions in relevant catalysis research, and in catalysis for more efficient transportation engines. Several overarching themes emerge from this review. First and foremost, there is a pressing need to better understand in detail the catalytic mechanisms involved in almost every process area mentioned above. This includes the structures, energetics, lifetimes, and reactivities of the species thought to be important in the key catalytic cycles. As much of this type of information as is possible to acquire would also greatly aid in better understanding perplexing, incomplete/inefficient catalytic cycles and in inventing new, efficient ones. The most productive way to attack such problems must include long-term, in-depth fundamental studies of both commercial and model processes, by conventional research techniques and, importantly, by applying various promising new physicochemical and computational approaches which would allow incisive, in situ elucidation of reaction pathways. There is also a consensus that more exploratory experiments, especially high-risk, unconventional catalytic and model studies, should be undertaken. Such an effort will likely require specialized equipment, instrumentation, and computational facilities. The most expeditious and cost-effective means to carry out this research would be by close coupling of academic, industrial, and national laboratory catalysis efforts worldwide. Completely new research approaches should be vigorously explored, ranging from novel compositions, fabrication techniques, reactors, and reaction conditions for heterogeneous catalysts, to novel ligands and ligation geometries (e.g., biomimetic), reaction media, and activation methods for homogeneous ones. The interplay between these two areas involving various hybrid and single-site supported catalyst systems should also be productive. Finally, new combinatorial and semicombinatorial means to rapidly create and screen catalyst systems are now available. As a complement to the approaches noted above, these techniques promise to greatly accelerate catalyst discovery, evaluation, and understanding. They should be incorporated in the vigorous international research effort needed in this field.

Expression of RA175 mRNA, a new member of the immunoglobulin superfamily, in developing mouse brain.

RA175, a new member of the immunoglobulin superfamily, is highly expressed during neuronal differentiation of P19 embryonal carcinoma cells. In situ hybridization showed that RA175 mRNA was detected in the developing nervous system, as well as the epithelium of the various non-neuronal tissues of mouse embryo. In contrast with the epithelia of the non-neuronal tissues, RA175 mRNA was not co-expressed with Sonic hedgehog mRNA and Patched mRNA during brain morphogenesis. RA175 mRNA was highly expressed in the anterior horn cells and the peripheral nervous system at embryonic day (E) 11.5 and in the central nervous system at E14.5-E18.5, but its expression decreased after birth and was undetectable in the adult mouse brain.

Keratin attenuates tumor necrosis factor-induced cytotoxicity through association with TRADD.

Keratin 8 and 18 (K8/18) are the major components of intermediate filament (IF) proteins of simple or single-layered epithelia. Recent data show that normal and malignant epithelial cells deficient in K8/18 are nearly 100 times more sensitive to tumor necrosis factor (TNF)-induced cell death. We have now identified human TNF receptor type 1 (TNFR1)-associated death domain protein (TRADD) to be the K18-interacting protein. Among IF proteins tested in two-hybrid systems, TRADD specifically bound K18 and K14, type I (acidic) keratins. The COOH-terminal region of TRADD interacted with the coil Ia of the rod domain of K18. Endogenous TRADD coimmunoprecipitated with K18, and colocalized with K8/18 filaments in human mammary epithelial cells. Overexpression of the NH2 terminus (amino acids 1-270) of K18 containing the TRADD-binding domain as well as overexpression of K8/18 in SW13 cells, which are devoid of keratins, rendered the cells more resistant to killing by TNF. We also showed that overexpressed NH2 termini of K18 and K8/18 were associated with endogenous TRADD in SW13 cells, resulting in the inhibition of caspase-8 activation. These results indicate that K18 may sequester TRADD to attenuate interactions between TRADD and activated TNFR1 and moderate TNF-induced apoptosis in simple epithelial cells.

Caspase-9 processing by caspase-3 via a feedback amplification loop in vivo.

In contrast to the autoprocessing of caspase-9, little is known about the biological significance of caspase-9 processing by caspase-3 via a feedback loop in vivo. We prepared antisera against mouse caspase-9 cleavage sites so that only the activated form of mouse caspase-9 was recognized. Using these antisera and caspase-9- and caspase-3-deficient mouse embryonic fibroblasts, we demonstrated that mouse caspase-9 is initially autoprocessed at D(353) and D(368) at low levels during staurosporine-induced apoptosis, whereupon the D(368) and D(168) sites are preferentially processed over D(353) by activated caspase-3 as part of a feedback amplification loop. Ac-DEVD-MCA (caspase-3-like) and Ac-LEHD-MCA (caspase-9-like) cleavage activities clearly showed that caspase-9 autoprocessing was necessary for the activation of caspase-3, whereas full activation of caspase-3 and caspase-9 was achieved only through the feedback amplification loop. This feedback amplification loop also played a predominant role during programmed cell death of dorsal root ganglia neurons at mouse embryonic day 11.5.

Hydrocarbon source apportionment for the 1996 Paso del Norte Ozone Study.

The 1996 Paso del Norte (PdN) ozone study was conducted to improve current understanding of the significant meteorological and air quality processes that lead to high concentrations of ozone in El Paso, Texas (USA) and Ciudad Juárez, Chihuahua (Mexico). Two-hour canister samples were collected five times daily at 05.00-07.00 h, 07.00-09.00 h, 09.00-11.00 h, 11.00-13.00 h, and 15.00-17.00 h MST during intensive study periods at one urban and one rural site on each side of the border. An automated gas chromatograph was operated at one site in central El Paso. Source profiles (the fractional chemical composition of emissions) from motor vehicles, gasoline, liquefied petroleum gas, and commercial natural gas were combined with source profiles from other studies for input to the Chemical Mass Balance (CMB) receptor model to apportion the measured non-methane hydrocarbons (NMHC) to sources. On-road vehicle emissions accounted for one-half to two-thirds of the NMHC in Ciudad Juárez and El Paso with the highest contributions occurring during the morning and afternoon commute periods. Emissions from diesel exhaust contributed approximately 2-3% of NMHC in Ciudad Juárez and less than 2% in El Paso. The average sum of liquid gasoline and gasoline vapor increased during the day in Ciudad Juárez from 2% at 06.00 h to approximately 12% at 16.00 h. Diurnal and day-of-the-week patterns in the liquid gasoline contributions are essentially identical to the corresponding patterns for motor vehicle exhaust, which suggest that a large fraction of the liquid gasoline contribution may be associated with tailpipe emissions rather than evaporative emissions from motor vehicles or industrial sources. Including the sum of the two sources put the upper limit for tailpipe contributions at 60-70% of NMHC.

A case of persistent acute allograft glomerulopathy with long-standing stable renal function.

Acute allograft glomerulopathy (AAG) characterized by hypercellularity, enlargement of endothelial cells, infiltration of glomeruli by mononuclear cells and webs of PAS-positive material has been reported as an unusual but distinct form of acute rejection in kidney transplant recipients. We present a case of persistent AAG proven by serial biopsies. The patient was 53 years old when she received kidney transplantation from her mother. The immunosuppressants were methylprednisolone, azathioprine and FK506. She developed several acute rejections and received antirejection therapy. The patient transferred to our hospital 15 months after transplantation. Serum creatinine was 2.11 mg/dL. The level of serum creatinine was gradually elevated from 2.11 mg/dL to 3.09 mg/dL. Graft biopsy, performed 16.5 months after transplantation, represented prominent intraglomerular infiltration of mononuclear cells, segmental thickening of glomerular basement membrane (GBM) with double contour, grade 1 tubulitis, marked accumulation of mononuclear cells in peritubular capillaries and margination of mononuclear cells in a small artery. It was diagnosed as acute allograft glomerulopathy (AAG). Intravenous methylprednisolone pulse therapy, discontinuation of FK506 and administration of cyclosporin (CYA) resulted in decrease of serum creatinine. To evaluate histological evolution of AAG we performed two subsequent biopsies over 3 yr. Severe glomerulitis persisted as a prominent feature 8 months later and still existed 53.4 months after transplantation with decreased severity. The extent of GBM reduplication also decreased, but the percentage of glomerular sclerosis increased gradually. Multi-layering of basement membrane of peritubular capillary and interstitial fibrosis also increased. The prominence of infiltration of mononuclear cells in peritubular capillary was unchanged. At the last follow-up, i.e. 71 months after transplantation, her serum creatinine was 1.34 mg/dL. Neither proteinuria nor haematuria was observed. We consider that our immunosuppressive treatment has been successful so far, because the patient is still maintaining stable graft function since the transplantation over 6 yr ago. It is thus suggested that AAG per se probably has no influence on acute aggravation of graft function, but AAG and capillaritis in peritubular capillaries may cause an evolution of chronic allograft nephropathy, resulting in a slowly progressive deterioration of graft function.