bcl-2 and c-erbB-2 proteins are involved in the regulation of VEGF and of thymidine phosphorylase angiogenic activity in non-small-cell lung cancer

Tumour angiogenesis has been recently recognised as one of the most important prognostic factors in lung cancer. Although a variety of angiogenic factors have been identified, the angiogenesis process remains poorly understood. Bcl-2, c-erbB-2 and p53 are well-known oncogenes involved in non- small-cell lung cancer pathogenesis. A direct correlation of thymidine phosphorylase (TP) and of vascular endothelial growth factor (VEGF) with intratumoural angiogenesis has been reported. In the present study we investigated the possible regulatory role if bcl-2, c-erB-2 proteins in angiogenesis and in VEGF and TP expression in non-small-cell lung cancer. Two hundred sixteen specimens from T1,2-NO, 1 staged patients treated with surgery alone were immunohistochemically examined. Bcl-2 and c-erbB-2 were significantly inversely related to each other (P = 0.04) and both were inversely associated with microvessel density (P < 0.02). High TP and VEGF reactivity was statistically related to loss of bcl-2 expression (P < 0.01). A significant co-expression of c-erbB-2 with TP was noted (P = 0.01). However, TP expression was related to high angiogenesis only in cases with absence of c-erB-2 expression (P < 0.0001). c-erbB-2 expression in poorly vascularised tumours was linked with poor outcome (P = 0.03). The present study provides strong evidence that the bcl-2 gene has a suppressive function over genes involved in both angiogenesis (VEGF and TP) and cell migration (c- erbB-2) in NSCLC. TP and c-erbB-2 proteins are significantly, and often simultaneously, expressed in bcl-2 negative cases. However, expression of the c-erbB-2 abolishes the TP-related angiogenic activity. Whether this is a result of a direct activity of the c-erbB-2 protein or a consequence of a c- erbB-2-related immune response remains to be further investigated.

Cyclooxygenase-2 protein levels are independent of epidermal growth factor receptor expression or activation in operable non-small cell lung cancer

Both cyclooxygenase (COX)-2 and epidermal growth factor receptor (EGFR) are thought to play important roles in the pathogenesis of non-small cell lung cancer (NSCLC). A number of in vitro studies have postulated a link between EGFR activation and subsequent COX-2 upregulation. The relationship between these factors has not been established in patients with NSCLC. COX-2 and EGFR expression were studied in 172 NSCLC specimens using standard immunohistochemical techniques. Western blotting was used to determine COX-2 and EGFR levels in five NSCLC cell lines. The effect of treatment with EGF on COX-2 expression in A549 cells was assessed. Results: Both EGFR and COX-2 are overexpressed in NSCLC. The predominant pattern of COX-2 and EGFR staining was cytoplasmic. Membranous EGFR staining was seen in 23.3% of cases. There was no relationship between COX-2 and EGFR expression and survival or any clinicopathological features. No correlation was seen between EGFR expression and COX-2 expression in the immunohistochemical series or in the cell lines. Treatment with EGF did not upregulate COX-2 levels in A549 cells, either in serum free or serum-supplemented conditions. Conclusions: Although COX-2 and EGFR are over-expressed in NSCLC neither was of prognostic significance in this series of cases. There is no correlation between these two factors in either tumour samples or cell lines. Although these factors show no correlation in NSCLC, they remain potential, though independent targets for treatment. © 2004 Elsevier Ireland Ltd. All rights reserved.

Matrix metalloproteinase 13-deficient mice are resistant to osteoarthritic cartilage erosion but not chondrocyte hypertrophy or osteophyte development

Objective To investigate the role of matrix metalloproteinase 13 (MMP-13; collagenase 3) in osteoarthritis (OA). Methods OA was surgically induced in the knees of MMP-13-knockout mice and wild-type mice, and mice were compared. Histologic scoring of femoral and tibial cartilage aggrecan loss (0-3 scale), erosion (0-7 scale), and chondrocyte hypertrophy (0-1 scale), as well as osteophyte size (0-3 scale) and maturity (0-3 scale) was performed. Serial sections were stained for type X collagen and the MMP-generated aggrecan neoepitope DIPEN. Results Following surgery, aggrecan loss and cartilage erosion were more severe in the tibia than femur (P < 0.01) and tibial cartilage erosion increased with time (P < 0.05) in wild-type mice. Cartilaginous osteophytes were present at 4 weeks and underwent ossification, with size and maturity increasing by 8 weeks (P < 0.01). There was no difference between genotypes in aggrecan loss or cartilage erosion at 4 weeks. There was less tibial cartilage erosion in knockout mice than in wild-type mice at 8 weeks (P < 0.02). Cartilaginous osteophytes were larger in knockout mice at 4 weeks (P < 0.01), but by 8 weeks osteophyte maturity and size were no different from those in wild-type mice. Articular chondrocyte hypertrophy with positive type X collagen and DIPEN staining occurred in both wild-type and knockout mouse joints. Conclusion Our findings indicate that structural cartilage damage in a mouse model of OA is dependent on MMP-13 activity. Chondrocyte hypertrophy is not regulated by MMP-13 activity in this model and does not in itself lead to cartilage erosion. MMP-13 deficiency can inhibit cartilage erosion in the presence of aggrecan depletion, supporting the potential for therapeutic intervention in established OA with MMP-13 inhibitors.

Health consequences of exposure to e-waste : a systematic review

Background The population exposed to potentially hazardous substances through inappropriate and unsafe management practices related to disposal and recycling of end-of-life electrical and electronic equipment, collectively known as e-waste, is increasing. We aimed to summarise the evidence for the association between such exposures and adverse health outcomes. Methods We systematically searched five electronic databases (PubMed, Embase, Web of Science, PsycNET, and CINAHL) for studies assessing the association between exposure to e-waste and outcomes related to mental health and neurodevelopment, physical health, education, and violence and criminal behaviour, from Jan 1, 1965, to Dec 17, 2012, and yielded 2274 records. Of the 165 full-text articles assessed for eligibility, we excluded a further 142, resulting in the inclusion of 23 published epidemiological studies that met the predetermined criteria. All studies were from southeast China. We assessed evidence of a causal association between exposure to e-waste and health outcomes within the Bradford Hill framework. Findings We recorded plausible outcomes associated with exposure to e-waste including change in thyroid function, changes in cellular expression and function, adverse neonatal outcomes, changes in temperament and behaviour, and decreased lung function. Boys aged 8–9 years living in an e-waste recycling town had a lower forced vital capacity than did those living in a control town. Significant negative correlations between blood chromium concentrations and forced vital capacity in children aged 11 and 13 years were also reported. Findings from most studies showed increases in spontaneous abortions, stillbirths, and premature births, and reduced birthweights and birth lengths associated with exposure to e-waste. People living in e-waste recycling towns or working in e-waste recycling had evidence of greater DNA damage than did those living in control towns. Studies of the effects of exposure to e-waste on thyroid function were not consistent. One study related exposure to e-waste and waste electrical and electronic equipment to educational outcomes. Interpretation Although data suggest that exposure to e-waste is harmful to health, more well designed epidemiological investigations in vulnerable populations, especially pregnant women and children, are needed to confirm these associations. Funding Children's Health and Environment Program, Queensland Children's Medical Research Institute, The University of Queensland, Australia.

Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010

BACKGROUND Measuring disease and injury burden in populations requires a composite metric that captures both premature mortality and the prevalence and severity of ill-health. The 1990 Global Burden of Disease study proposed disability-adjusted life years (DALYs) to measure disease burden. No comprehensive update of disease burden worldwide incorporating a systematic reassessment of disease and injury-specific epidemiology has been done since the 1990 study. We aimed to calculate disease burden worldwide and for 21 regions for 1990, 2005, and 2010 with methods to enable meaningful comparisons over time. METHODS We calculated DALYs as the sum of years of life lost (YLLs) and years lived with disability (YLDs). DALYs were calculated for 291 causes, 20 age groups, both sexes, and for 187 countries, and aggregated to regional and global estimates of disease burden for three points in time with strictly comparable definitions and methods. YLLs were calculated from age-sex-country-time-specific estimates of mortality by cause, with death by standardised lost life expectancy at each age. YLDs were calculated as prevalence of 1160 disabling sequelae, by age, sex, and cause, and weighted by new disability weights for each health state. Neither YLLs nor YLDs were age-weighted or discounted. Uncertainty around cause-specific DALYs was calculated incorporating uncertainty in levels of all-cause mortality, cause-specific mortality, prevalence, and disability weights. FINDINGS Global DALYs remained stable from 1990 (2·503 billion) to 2010 (2·490 billion). Crude DALYs per 1000 decreased by 23% (472 per 1000 to 361 per 1000). An important shift has occurred in DALY composition with the contribution of deaths and disability among children (younger than 5 years of age) declining from 41% of global DALYs in 1990 to 25% in 2010. YLLs typically account for about half of disease burden in more developed regions (high-income Asia Pacific, western Europe, high-income North America, and Australasia), rising to over 80% of DALYs in sub-Saharan Africa. In 1990, 47% of DALYs worldwide were from communicable, maternal, neonatal, and nutritional disorders, 43% from non-communicable diseases, and 10% from injuries. By 2010, this had shifted to 35%, 54%, and 11%, respectively. Ischaemic heart disease was the leading cause of DALYs worldwide in 2010 (up from fourth rank in 1990, increasing by 29%), followed by lower respiratory infections (top rank in 1990; 44% decline in DALYs), stroke (fifth in 1990; 19% increase), diarrhoeal diseases (second in 1990; 51% decrease), and HIV/AIDS (33rd in 1990; 351% increase). Major depressive disorder increased from 15th to 11th rank (37% increase) and road injury from 12th to 10th rank (34% increase). Substantial heterogeneity exists in rankings of leading causes of disease burden among regions. INTERPRETATION Global disease burden has continued to shift away from communicable to non-communicable diseases and from premature death to years lived with disability. In sub-Saharan Africa, however, many communicable, maternal, neonatal, and nutritional disorders remain the dominant causes of disease burden. The rising burden from mental and behavioural disorders, musculoskeletal disorders, and diabetes will impose new challenges on health systems. Regional heterogeneity highlights the importance of understanding local burden of disease and setting goals and targets for the post-2015 agenda taking such patterns into account. Because of improved definitions, methods, and data, these results for 1990 and 2010 supersede all previously published Global Burden of Disease results.

Effect of the puroindoline locus and environment on Chinese fresh noodle texture

Grain produced from doubled-haploid (DH) wheat lines, developed from a hard- and a soft-grained wheat cultivar, were bulked according to Pinb (puroindoline b) genotypes for an assessment of Chinese fresh noodle texture by a trained taste panel. Each DH line was designated as 'soft' or 'hard' grained, based on a PCR amplification of the wildtype, soft allele, or the mutant, hard allele. Theoretically, the soft and hard grain bulks represented respective Pinb alleles and an independent assortment of unlinked alleles from the parents, Sunco and Chuanyu 12. Grains from the parents and DH lines were grown at 2 locations in Queensland, Australia, and one in Sichuan, China. The grains were milled and processed for a taste panel evaluation in Chengdu, Sichuan. Results suggest the Pinb alleles had a significant effect on noodle softness and explained 30% of the variation; the 'soft' Pinb allele conferred a softer noodle texture. Location had a significant effect on noodle smoothness; wheat grain grown at Biloela, Queensland, produced a smoother noodle texture than grain grown in Sichuan. The effect of location confirms the importance of environment as a variable for this quality character. This investigation exemplifies the utility of Pinb markers for specifically altering Chinese Fresh Noodle texture.

A contemporary assessment of land condition in the Northern Gulf region of Queensland

A framework using assessments of soil condition, pasture composition and woodland density was applied to describe 14 grazing land types as being in A (100% of original carrying capacity), B (75%), C (45%) or D (20%) condition. We assessed the condition of 260 sites, principally along public and some station roads, to provide a benchmark for current land condition. Land types were also assigned relative grazing values between 10 (best) and 0, reflecting soil fertility and potential biomass production. The method identifies particular, 'at-risk' land types for priority investment of resources, while the rationale behind assessments might point to management interventions to improve the condition of those land types. Across all land types, 47% of sites were in A condition, 34% in B condition, 17% in C condition and only 2% in D condition. Seventy-five percent of land types with grazing values >5 were in A or B condition, compared with 88% for those with grazing values ?5. For Georgetown granites, only 27% of sites were in A or B condition, with values for other land types being: alluvials 59%, black soils 64% and red duplex soils 57%, suggesting that improving management of these land types is a priority issue. On land types with high grazing value, the major discounting factor was pasture composition (72% of sites discounted), while increasing woodland density was the main discount (73% of sites discounted) on low grazing value land types.

Genome-wide association study of major depressive disorder: New results, meta-analysis, and lessons learned

Major depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1 M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were: (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P=0.020, odds ratio=1.10), and; (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P=0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD.

G-protein beta3 subunit gene (GNB3) variant in causation of essential hypertension

-Essential hypertensives display enhanced signal transduction through pertussis toxin-sensitive G proteins. The T allele of a C825T variant in exon 10 of the G protein beta3 subunit gene (GNB3) induces formation of a splice variant (Gbeta3-s) with enhanced activity. The T allele of GNB3 was shown recently to be associated with hypertension in unselected German patients (frequency=0.31 versus 0.25 in control). To confirm and extend this finding in a different setting, we performed an association study in Australian white hypertensives. This involved an extensively examined cohort of 110 hypertensives, each of whom were the offspring of 2 hypertensive parents, and 189 normotensives whose parents were both normotensive beyond age 50 years. Genotyping was performed by polymerase chain reaction and digestion with BseDI, which either cut (C allele) or did not cut (T allele) the 268-bp polymerase chain reaction product. T allele frequency in the hypertensive group was 0.43 compared with 0.25 in the normotensive group (chi2=22; P=0.00002; odds ratio=2.3; 95% CI=1.7 to 3.3). The T allele tracked with higher pretreatment blood pressure: diastolic=105+/-7, 109+/-16, and 128+/-28 mm Hg (mean+/-SD) for CC, CT, and TT, respectively (P=0.001 by 1-way ANOVA). Blood pressures were higher in female hypertensives with a T allele (P=0.006 for systolic and 0.0003 for diastolic by ANOVA) than they were in male hypertensives. In conclusion, the present study of a group with strong family history supports a role for a genetically determined, physiologically active splice variant of the G protein beta3 subunit gene in the causation of essential hypertension.

ERAP2 functional knockout in humans does not alter surface heavy chains or HLA-B27, inflammatory cytokines or endoplasmic reticulum stress markers

Introduction Single nucleotide polymorphisms in ERAP2 are strongly associated with ankylosing spondylitis (AS). One AS-associated single nucleotide polymorphism, rs2248374, causes a truncated ERAP2 protein that is degraded by nonsense-mediated decay. Approximately 25% of the populations of European ancestry are therefore natural ERAP2 knockouts. We investigated the effect of this associated variant on HLA class I allele presentation, surface heavy chains, endoplasmic reticulum (ER) stress markers and cytokine gene transcription in AS. Methods Patients with AS and healthy controls with either AA or GG homozygous status for rs2248374 were studied. Antibodies to CD14, CD19-ECD, HLA-A-B-C, Valpha7.2, CD161, anti-HC10 and anti-HLA-B27 were used to analyse peripheral blood mononuclear cells. Expression levels of ER stress markers (GRP78 and CHOP) and proinflammatory genes (tumour necrosis factor (TNF), IL6, IL17 and IL22) were assessed by qPCR. Results There was no significant difference in HLAclass I allele presentation or major histocompatibility class I heavy chains or ER stress markers GRP78 and CHOP or proinflammatory gene expression between genotypes for rs2248374 either between cases, between cases and controls, and between controls. Discussion Large differences were not seen in HLAB27 expression or cytokine levels between subjects with and without ERAP2 in AS cases and controls. This suggests that ERAP2 is more likely to influence AS risk through other mechanisms.

Observation of the Ωb- baryon and measurement of the properties of the Ξb- and Ωb- baryons

We report the observation of the bottom, doubly-strange baryon Omega^-_b through the decay chain Omega^-_b -> J/psi Omega^-, where J/psi -> mu^+ mu^-, Omega^- -> Lambda K^-, and Lambda -> p pi^-, using 4.2 fb^{-1} of data from p\bar p collisions at sqrt{s}=1.96 TeV, and recorded with the Collider Detector at Fermilab. A signal is observed whose probability of arising from a background fluctuation is 4.0 * 10^{-8}, or 5.5 Gaussian standard deviations. The Omega^-_b mass is measured to be 6054.4 +/- 6.8 (stat.) +/- 0.9 (syst.) MeV/c^2. The lifetime of the Omega^-_b baryon is measured to be 1.13^{+0.53}_{-0.40}(stat.) +/- 0.02(syst.)$ ps. In addition, for the \Xi^-_b baryon we measure a mass of 5790.9 +/- 2.6(stat.) +/- 0.8(syst.) MeV/c^2 and a lifetime of 1.56^{+0.27}_{-0.25}(stat.) +/-0.02(syst.) ps. Under the assumption that the \Xi_b^- and \Omega_b^- are produced with similar kinematic distributions to the \Lambda^0_b baryon, we find sigma(Xi_b^-) B(Xi_b^- -> J/psi Xi^-)}/ sigma(Lambda^0_b) B(Lambda^0_b -> J/psi Lambda)} = 0.167^{+0.037}_{-0.025}(stat.) +/-0.012(syst.) and sigma(Omega_b^-) B(Omega_b^- -> J/psi Omega^-)/ sigma(Lambda^0_b) B(Lambda^0_b -> J/psi Lambda)} = 0.045^{+0.017}_{-0.012}(stat.) +/- 0.004(syst.) for baryons produced with transverse momentum in the range of 6-20 GeV/c.

Structure of N-tert-butyloxycarbonyl-[alpha]-aminoisobutyryl-DL-pipecolyl-[alpha]-aminoisobutyric acid methyl ester

C20H35N3O6 (Boc-Aib-DL-Pip-Aib-OMe, Boc = tert-butyloxycarbonyl, Aib = alpha-aminoisobutyric acid, Pip = pipecolic acid, OMe = methoxy), M(r) = 413.5, monoclinic, P2(1)/c, a = 18.055 (3), b = 15.048 (3), c = 17.173 (3) angstrom, beta = 91.7 (1)-degrees, V = 4663.8 (9) angstrom3, Z = 8, D(m) = 1.16, D(x) = 1.178 Mg m-3, lambda(Mo Kalpha) = 0.71069 angstrom, mu = 0.081 mm-1, F(000) = 1792, T = 297 K. The final R value for 4925 [I greater-than-or-equal-to 3sigma(I)] reflections is 0.065 (wR = 0.067). The peptide backbone of the two independent molecules in the asymmetric unit is folded at the -Aib-Pip- sequence to form a type-I (I') beta-bend stabilized by a 1 <-- 4 intramolecular N-H...O=C hydrogen bond between the Aib(3) peptide N-H and Boc urethane C=O groups.

Structure of 7-ethylamino-6-methyl-4-trifluoromethylcoumarin

C13H12F3NO2, M(r) = 271.2, triclinic, P1BAR, a = 5.029 (2), b = 7.479 (2), c = 17.073 (5) angstrom, alpha = 97.98 (2), beta = 95.54 (3), gamma = 103.62 (3)-degrees, V = 612.4 (4) angstrom 3, Z = 2, D(m) = 1.463, D(x) = 1.471 g cm-3, lambda(Mo K-alpha) = 0.71069 angstrom, mu = 1.23 cm-1, F(000) = 280, T = 298 K, final R value is 0.041 for 2047 observed reflections with \F(omicron)\ greater-than-or-equal-to 6-sigma(\F(omicron)\). The N-C(sp2) bond length is 1.356 (2) angstrom. The N and C atoms of the ethylamino group deviate by < 0.15 angstrom from the plane of the aromatic ring. Short intramolecular contacts, C(3)...F(17) 2.668 (3) angstrom [H(3)...F(17) 2.39 (2) angstrom, C(3)-H(C3)...F(17) 98 (1)-degrees], C(5)...F(18) 3.074 (3) and C(5)...F(19) 3.077 (3) angstrom exist in the structure. The crystal structure is stabilized by intermolecular N-H...O hydrogen bonds with N(12)-H(N12) 0.79 (3), H(N12)...O(11)' 2.36 (3), N(12)...O(11)' (x - 1, y + 1, z) 3.105 (3) angstrom and N(12)-H(N12)...O(11)' 155 (2)-degrees.

Efecto de la edad de destete y del sistema de alimentación sobre el crecimiento en terneras de lechería

Se efectuó una prueba de alimentación usando el diseño de parcela dividida con un arreglo completamente al azar, con 36 terneras provenientes del cruce Holstein y Pardo Suizo, para comparar el efecto de dos edades de destete 4 y 8 semanas, y tres sistemas de alimentación en el crecimiento de terneras de lecheria. Los tratamientos fueron los siguientes: a) leche integra suministrada en forma gradual y el destete a las 4 semanas; b) leche integra suministrada en forma constante y el destete a las 4 semanas; c) sustituto de leche por 4 semanas; d, e y f, similares a los tratamientos anteriores en lo referente al alimento liquido pero con destete a las 8 semanas. El resto de la racion consistio en alimentos concentrados; iniciador, desarrollo y heno. Desde las 9 a las 20 semanas las terneras pasaron en grupos de seis a corrales comunes. El iniciador suministrado a las terneras de los tratamientos a y d se ofreció a razón de 144 gr. por litro de leche integra, previa disolución en agua, y el iniciador que consumieron las terneras de los tratamientos c y f se administro a razón de 0.90 kg hasta el destete. El concentrado de desarrollo se ofreció a los tratamientos a, b, d y a donde la 1 a las 20 semanas y en los tratamientos c y f después del destete hasta alcanzar un máximo de 2.7 kg. Todos los tratamientos tuvieron a disposición a partir del destete heno de estrella (Cynodon sp). La ganancia de peso vivo promedio total, de 66.48 kg obtenida por las terneras del tratamiento e, fue similar a las de 56.84, 50.74, 53.72 y 55.53 kg logradas por las terneras de los tratamientos b, c,d y f, pero significativamente diferente (P<0.05), a 43.42 kg alcanzada por las terneras del tratamiento a. El promedio de ganancias de peso vivo por día desde la 1 hasta las 20 semanas de edad fue 0.31, 0.41, 0.36, 0.38, 0.47 y 0.40 kg para los tratamientos a al f respectivamente. La mayor ganancia promedio en altura a la cruz 20.32 cm lograda por las terneras del tratamiento II fue similar a la de 17.97 cm obtenida por las terneras del tratamiento III, pero significativamente diferentes (P<0.01), con la de 15.94 cm alcanzada por las terneras del sistema I. El promedio de ganancia en perímetro toraxico fue 22.23, 27.30, 26.29, 26.29, 30.35 y 26.29 cm para los tratamientos a al f respectivamente. Estas ganancias no fueron significativas (P<0.05). Los costos totales de alimentación por ternera desde la 1 hasta las 20 semanas fueron 245.98, 315.74, 283.41, 318.41, 457.48 y 335.33 córdobas para los tratamientos a al f respectivamente. Los costos correspondientes por kg de aumento en peso vivo, fueron 5.67, 5.55, 5.59, 5.93, 6.88 y 6.04 respectivamente.

NOAA Coastal Change Analysis Program (C-CAP): Guidance for Regional Implementation

EXECUTIVE SUMMARY: The Coastal Change Analysis Programl (C-CAP) is developing a nationally standardized database on landcover and habitat change in the coastal regions of the United States. C-CAP is part of the Estuarine Habitat Program (EHP) of NOAA's Coastal Ocean Program (COP). C-CAP inventories coastal submersed habitats, wetland habitats, and adjacent uplands and monitors changes in these habitats on a one- to five-year cycle. This type of information and frequency of detection are required to improve scientific understanding of the linkages of coastal and submersed wetland habitats with adjacent uplands and with the distribution, abundance, and health of living marine resources. The monitoring cycle will vary according to the rate and magnitude of change in each geographic region. Satellite imagery (primarily Landsat Thematic Mapper), aerial photography, and field data are interpreted, classified, analyzed, and integrated with other digital data in a geographic information system (GIS). The resulting landcover change databases are disseminated in digital form for use by anyone wishing to conduct geographic analysis in the completed regions. C-CAP spatial information on coastal change will be input to EHP conceptual and predictive models to support coastal resource policy planning and analysis. CCAP products will include 1) spatially registered digital databases and images, 2) tabular summaries by state, county, and hydrologic unit, and 3) documentation. Aggregations to larger areas (representing habitats, wildlife refuges, or management districts) will be provided on a case-by-case basis. Ongoing C-CAP research will continue to explore techniques for remote determination of biomass, productivity, and functional status of wetlands and will evaluate new technologies (e.g. remote sensor systems, global positioning systems, image processing algorithms) as they become available. Selected hardcopy land-cover change maps will be produced at local (1:24,000) to regional scales (1:500,000) for distribution. Digital land-cover change data will be provided to users for the cost of reproduction. Much of the guidance contained in this document was developed through a series of professional workshops and interagency meetings that focused on a) coastal wetlands and uplands; b) coastal submersed habitat including aquatic beds; c) user needs; d) regional issues; e) classification schemes; f) change detection techniques; and g) data quality. Invited participants included technical and regional experts and representatives of key State and Federal organizations. Coastal habitat managers and researchers were given an opportunity for review and comment. This document summarizes C-CAP protocols and procedures that are to be used by scientists throughout the United States to develop consistent and reliable coastal change information for input to the C-CAP nationwide database. It also provides useful guidelines for contributors working on related projects. It is considered a working document subject to periodic review and revision.(PDF file contains 104 pages.)