Development of school connectedness as a component of an injury prevention program for early adolescents

The current program of research addresses the need for multi-level programs to target the major increase in injury rates that occurs throughout adolescence. Specifically, it involves the investigation of school connectedness as a protective factor for adolescent injury, and the development of school connectedness as a component of an injury prevention program. To date, school-based risk taking and injury prevention has frequently been limited to addressing adolescents' knowledge and attitudes to risk behaviours, and has largely overlooked the importance of the wider school social context as a protective factor in adolescent development. Additionally, school connectedness has been primarily studied in terms of its impact on student achievement, wellbeing and risk taking behaviour, and research has not yet addressed possible links with injury. Further, school connectedness intervention programs have targeted risk taking behaviours without evaluating their potential impact on injury outcomes. This is the first reported research to develop strategies to increase school connectedness as part of a school-based injury prevention program. The research program was conceptualised as three distinct stages. The development of these research stages was informed by a comprehensive review of the literature on adolescent risk taking, injury and school-based prevention, as well as on school connectedness and its importance in adolescence. A review of the school connectedness literature indicated that students' connectedness is largely influenced by relationships within the school context including with teachers and other school staff, and is therefore a potentially modifiable factor that may be targeted in school-based programs. Overall, the literature shows school connectedness to be a key protective factor in adolescent development. This review established a foundation from which the current program of research was designed. The first stage of the research involved an empirical investigation of the relationship between adolescent risk taking-related injuries and school connectedness. Stage one incorporated two studies. The first involved the development of a measure of adolescent injury, the Extended Adolescent Injury Checklist (E-AIC), for use in the current research as well as in future school-based studies and program evaluation. The results of this study also highlighted the extent of the problem of risk-related injury in adolescence. The second study in Stage one examined the relationship between students' reports of school connectedness, risk taking behaviour and risk taking-related injuries on the E-AIC. The results of this study showed significant relationships between increased school connectedness and reduced reported engagement in transport and violence risk taking, and fewer associated injuries. This study therefore suggested the potential for school-based injury prevention programs to incorporate strategies targeting increased adolescent connectedness to school. The second stage of this research involved the compilation of an evidence base to inform the design of a school connectedness intervention. Stage two also incorporated two studies. The first study in Stage two involved a systematic review of programs that have targeted school connectedness for reduced risk taking and injury. The results of this study revealed that interventions targeting school connectedness can be effective in reducing adolescent risk taking behaviour, and also provided an evidence base for the design of the current school connectedness intervention. The second study in Stage two examined teachers' understanding and perceptions of school connectedness. This qualitative study indicated that teachers consider students' connectedness to be an important factor that relates to their risk taking behaviour; and also provided directions and content for the intervention design stage. The third stage of this research built upon the findings of each of the previous studies, and involved the design, implementation and evaluation of a school connectedness intervention as a component of an adolescent injury prevention program, Skills for Preventing Injury in Youth (SPIY). This connectedness intervention was designed as a professional development workshop for teachers of 13 to 14 year old adolescents, and was developed as a complementary component to the curriculum-based SPIY program. The SPIY connectedness component was implemented and evaluated using process and six-month impact evaluation methodologies. The results of this study revealed that teachers saw value in the program and made use of the strategies presented, and that program school students' self-reported violence risk behaviour was reduced at six-month follow-up. Despite these promising findings, the results of this study did not demonstrate a significant impact of the program on change in students' connectedness to school, relative to comparison schools. The positive impact on self-reported violence risk behaviour was however replicated in additional analyses comparing students participating in the connectedness version of SPIY with students participating in an earlier curriculumonly version of the program. This finding indicated that the connectedness component has additional benefits relating to reduction in violence risks, over and above a curriculum-only version of the program. This research was the first reported to address the relationship between school connectedness and adolescent injury outcomes, and to develop school connectedness as a component of an adolescent injury prevention program. Overall, the results of this program of research have demonstrated the importance of incorporating strategies targeting the wider school social context, including school connectedness, in adolescent injury prevention programs. This research has important implications for future research and practice in adolescent injury prevention.

The role of the Eph and ephrin proteins in prostate cancer

Prostate cancer is the most commonly diagnosed malignancy and the second leading cause of cancer related deaths in Australian men. Treatment in the early stages of the disease involves surgery, radiation and/or hormone therapy. However, in late stages of the disease these treatments are no longer effective and only palliative care is available. Therefore, there is a focus on exploration of novel therapies to increase survival and treatment efficacy. Advanced prostate cancer is characterised by bone or other distant metastasis. Spreading of the primary tumour to a secondary location is a complex process requiring an initial loss in cell-cell adhesion followed by increased cell migration and invasion. One gene family that has been known to affect cell-to-cell contact in other model systems are the Eph receptor tyrosine kinases. They are the largest family of receptor tyrosine kinases made up of 14 vertebrate Eph receptors that bind to nine cell membrane bound ephrin ligands. Eph-ephrin interaction is crucial in regulating cell behaviour in developmental processes and it is now thought that the underlying mechanisms involved in development may also be involved in cancer. Aberrant expression has been reported in many human malignancies including prostate cancer. Furthermore, expression has been linked with metastasis and poor prognosis in other tumour models. This study explores the potential role of the Eph receptor family in prostate cancer, in particular the roles of EphA2, EphA3 and ephrin-A5. Gene expression profiles were established for the Eph family in a series of prostate cancer cell lines using quantitative real time RT-PCR. A smaller subset of the most prominently expressed genes was chosen to screen a cohort of clinical samples. Elevated levels of EphA2, EphA3 and their ligands, ephrin-A1 and ephrin-A5 were observed in individual cell lines. Interestingly high EphA3 expression was observed in the androgen responsive cell lines while EphA2 was more prominent in the androgen independent cell lines. However, studies using 5-dihydrotestosterone suggest that EphA3 expression in not regulated by androgen. Cells expressing EphA2 showed a greater ability for migration and invasion while cells expressing EphA3 showed poor migration and invasion. Forced expression of EphA2 in the LNCaP cell line resulted in a more invasive phenotype while forced expression of EphA3 in the PC-3 cell line suggests a possible negative effect for EphA3 on cell migration and invasion. Cell signalling studies show activation of EphA2 decreases activity of proteins thought to be involved in pathways regulating cell movement including Akt, Src and FAK. Changes to the activation status of Rho family members, including RhoA and Rac1, associated with reorganisation of the actin cytoskeleton, an important part of cell migration was also observed. As a result, activation of EphA2 in PC-3 cells resulted in a less invasive phenotype. A novel finding in this study was the discovery of a combination of two EphA2 Mabs able to activate EphA2. Preliminary results show a potential for this antibody combination to reduce prostate cancer invasion in vitro. A unique aspect of Eph-ephrin interaction is the resulting bi-directional signalling that occurs through both the receptor and ligand. In this study a potential role for ephrin-A5 mediated signalling in prostate cancer was observed. LNCaP cells express high levels of EphA3 and its high affinity ligand ephrin-A5. In stripe assays, used to study guidance cues, LNCaP cells show strong attraction/migration to EphA3-Fc stripes but not ephrin-A5-Fc stripes suggesting ephrin-A5 mediated reverse cell signalling is involved. Knockdown of ephrin-A5 using shRNA resulted in a decrease in attraction/migration to EphA3-Fc stripes. Furthermore a reduction in proliferation was also observed in vitro. A subcutaneous xenograft model using ephrin-A5 shRNA cells versus controls showed a decrease in tumour formation. This study demonstrates a difference in EphA2 and EphA3 function in prostate cancer migration/invasion and a potential role for ephrin-A5 in prostate cancer cell adhesion and growth.

State-of-the-art : track degradation at bridge transitions

Transition zones between bridge decks and rail tracks suffer early failure due to poor interaction between rail vehicles and sudden changes of stiffness. This has been an ongoing problem to rail industry and yet still no systematic studies appear to have been taken to maintain a gradually smoothening transmission of forces between the bridge and its approach. Differential settlement between the bridge deck and rail track in the transition zone is the fundamental issue, which negatively impacts the rail industry by causing passenger discomfort, early damage to infrastructure and vehicle components, speed reduction, and frequent maintenance cycles. Identification of mechanism of the track degradation and factors affecting is imperative to design any mitigation method for reducing track degradation rate at the bridge transition zone. Unfortunately this issue is still not well understood, after conducting a numbers of reviews to evaluate the key causes, and introducing a wide range of mitigation techniques. In this study, a comprehensive analysis of the available literature has been carried out to develop either a novel design framework or a mitigation technique for the bridge transition zone. This paper addresses three critical questions in relation to the track degradation at transition zone: (1) what are the causes of bridge transition track degradation?; (2) what are the available mitigation techniques in reducing the track degradation rate?; (3) what are the factors affecting on poor performance of the existing mitigation techniques?. It is found that the absence of soil-water response, dynamic loading response, and behaviour of geotechnical characteristics under long-term conditions in existing track transition design frameworks critically influence on the failures of existing mitigation techniques. This paper also evaluates some of the existing design frameworks to identify how each design framework addresses the track degradation at the bridge transition zone.

Not drowning, (hand)waving? Molecular phylogenetics, biogeography and evolutionary tempo of the ‘Gondwanan’ midge Stictocladius Edwards (Diptera: Chironomidae)

Many insect clades, especially within the Diptera (true flies), have been considered classically ‘Gondwanan’, with an inference that distributions derive from vicariance of the southern continents. Assessing the role that vicariance has played in the evolution of austral taxa requires testing the location and tempo of diversification and speciation against the well-established predictions of fragmentation of the ancient super-continent. Several early (anecdotal) hypotheses that current austral distributions originate from the breakup of Gondwana derive from studies of taxa within the family Chironomidae (non-biting midges). With the advent of molecular phylogenetics and biogeographic analytical software, these studies have been revisited and expanded to test such conclusions better. Here we studied the midge genus Stictocladius Edwards, from the subfamily Orthocladiinae, which contains austral-distributed clades that match vicariance-based expectations. We resolve several issues of systematic relationships among morphological species and reveal cryptic diversity within many taxa. Time-calibrated phylogenetic relationships among taxa accorded partially with the predicted tempo from geology. For these apparently vagile insects, vicariance-dated patterns persist for South America and Australia. However, as often found, divergence time estimates for New Zealand at c. 50 mya post-date separation of Zealandia from Antarctica and the remainder of Gondwana, but predate the proposed Oligocene ‘drowning’ of these islands. We detail other such ‘anomalous’ dates and suggest a single common explanation rather than stochastic processes. This could involve synchronous establishment following recovery from ‘drowning’ and/or deleteriously warming associated with the mid-Eocene climatic optimum (hence ‘waving’, which refers to cycles of drowning events) plus new availability of topography providing of cool running waters, or all these factors in combination. Alternatively a vicariance explanation remains available, given the uncertain duration of connectivity of Zealandia to Australia–Antarctic–South America via the Lord Howe and Norfolk ridges into the Eocene.

Domestication for Conservation of an Endangered Species: The Case of the Wollemi Pine

A small population of tall slender conifers was discovered in 1994 in a deep rainforest canyon of the Wollemi National Park, New SouthWales, Australia. The living trees closely resembled fossils that were more than 65 million years old, and this ‘living fossil’ was recognised as a third extant genus in the Araucariaceae (Araucaria, Agathis and now Wollemia). The species was named the Wollemi pine (W. nobilis). Extensive searches uncovered very few populations, with the total number of adult trees being less than 100. Ex situ collections were quickly established in Sydney as part of the Wollemi Pine Recovery Plan. The majority of the ex situ population was later transferred to our custom-built facility in Queensland for commercial multiplication. Domestication has relied very heavily on the species’ amenability to vegetative propagation because seed collection from the natural populations is dangerous, expensive, and undesirable for conservation reasons. Early propagation success was poor, with only about 25% of cuttings producing roots. However, small increases in propagation success have a very large impact on a domestication program because plant production can be modelled on an exponential curve where each rooted cutting develops into a mother plant that, in turn, provides more rooted cuttings. An extensive research program elevated rooting percentages to greater than 80% and also provided in vitro methods for plant multiplication. These successes have enabled international release of the Wollemi pine as a new and attractive species for ornamental horticulture.

Characterization of the mitochondrial active-site serine protein LACTB: filaments in the mitochondrial intermembrane space

Mitochondria have evolved from endosymbiotic alpha-proteobacteria. During the endosymbiotic process early eukaryotes dumped the major component of the bacterial cell wall, the peptidoglycan layer. Peptidoglycan is synthesized and maintained by active-site serine enzymes belonging to the penicillin-binding protein and the β-lactamase superfamily. Mammals harbor a protein named LACTB that shares sequence similarity with bacterial penicillin-binding proteins and β-lactamases. Since eukaryotes lack the synthesis machinery for peptidoglycan, the physiological role of LACTB is intriguing. Recently, LACTB has been validated in vivo to be causative for obesity, suggesting that LACTB is implicated in metabolic processes. The aim of this study was to investigate the phylogeny, structure, biochemistry and cell biology of LACTB in order to elucidate its physiological function. Phylogenetic analysis revealed that LACTB has evolved from penicillin binding-proteins present in the bacterial periplasmic space. A structural model of LACTB indicates that LACTB shares characteristic features common to all penicillin-binding proteins and β-lactamases. Recombinat LACTB protein expressed in E. coli was recovered in significant quantities. Biochemical and cell biology studies showed that LACTB is a soluble protein localized in the mitochondrial intermembrane space. Further analysis showed that LACTB preprotein underwent proteolytic processing disclosing an N-terminal tetrapeptide motif also found in a set of cell death-inducing proteins. Electron microscopy structural studies revealed that LACTB can polymerize to form stable filaments with lengths ranging from twenty to several hundred nanometers. These data suggest that LACTB filaments define a distinct microdomain in the intermembrane space. A possible role of LACTB filaments is proposed in the intramitochondrial membrane organization and microcompartmentation. The implications of these findings offer novel insight into the evolution of mitochondria. Further studies of the LACTB function might provide a tool to treat mitochondria-related metabolic diseases.

The Pathobiology of the Saccular Cerebral Artery Aneurysm Rupture and Repair : A Clinicopathological and Experimental Approach

Backround and Purpose The often fatal (in 50-35%) subarachnoid hemorrhage (SAH) caused by saccular cerebral artery aneurysm (SCAA) rupture affects mainly the working aged population. The incidence of SAH is 10-11 / 100 000 in Western countries and twice as high in Finland and Japan. The estimated prevalence of SCAAs is around 2%. Many of those never rupture. Currently there are, however, no diagnostic methods to identify rupture-prone SCAAs from quiescent, (dormant) ones. Finding diagnostic markers for rupture-prone SCAAs is of primary importance since a SCAA rupture has such a sinister outcome, and all current treatment modalities are associated with morbidity and mortality. Also the therapies that prevent SCAA rupture need to be developed to as minimally invasive as possible. Although the clinical risk factors for SCAA rupture have been extensively studied and documented in large patient series, the cellular and molecular mechanisms how these risk factors lead to SCAA wall rupture remain incompletely known. Elucidation of the molecular and cellular pathobiology of the SCAA wall is needed in order to develop i) novel diagnostic tools that could identify rupture-prone SCAAs or patients at risk of SAH, and to ii) develop novel biological therapies that prevent SCAA wall rupture. Materials and Methods In this study, histological samples from unruptured and ruptured SCAAs and plasma samples from SCAA carriers were compared in order to identify structural changes, cell populations, growth factor receptors, or other molecular markers that would associate with SCAA wall rupture. In addition, experimental saccular aneurysm models and experimental models of mechanical vascular injury were used to study the cellular mechanisms of scar formation in the arterial wall, and the adaptation of the arterial wall to increased mechanical stress. Results and Interpretation Inflammation and degeneration of the SCAA wall, namely loss of mural cells and degradation of the wall matrix, were found to associate with rupture. Unruptured SCAA walls had structural resemblance with pads of myointimal hyperplasia or so called neointima that characterizes early atherosclerotic lesions, and is the repair and adaptation mechanism of the arterial wall after injury or increased mechanical stress. As in pads of myointimal hyperplasia elsewhere in the vasculature, oxidated LDL was found in the SCAA walls. Immunity against OxLDL was demonstrated in SAH patients with detection of circulating anti-oxidized LDL antibodies, which were significantly associated with the risk of rupture in patients with solitary SCAAs. Growth factor receptors associated with arterial wall remodeling and angiogenesis were more expressed in ruptured SCAA walls. In experimental saccular aneurysm models, capillary growth, arterial wall remodeling and neointima formation were found. The neointimal cells were shown to originate from the experimental aneurysm wall with minor contribution from the adjacent artery, and a negligible contribution of bone marrow-derived neointimal cells. Since loss of mural cells characterizes ruptured human SCAAs and likely impairs the adaptation and repair mechanism of ruptured or rupture-prone SCAAs, we investigated also the hypothesis that bone marrow-derived or circulating neointimal precursor cells could be used to enhance neointima formation and compensate the impaired repair capacity in ruptured SCAA walls. However, significant contribution of bone marrow cells or circulating mononuclear cells to neointima formation was not found.

Pathophysiology of Congenital Nephrotic Syndrome of the Finnish type

Congenital nephrotic syndrome of the Finnish type (NPHS1) is an autosomal recessive disease which is highly enriched in the Finnish population. It is caused by mutations in the NPHS1 gene encoding for nephrin, which is a major component of the glomerular filtration barrier in the kidney. Patients with NPHS1 have heavy proteinuria and nephrotic syndrome (NS) from birth and develop renal fibrosis in early childhood. Renal transplantation (TX) is the only curative treatment for NPHS1. These patients form the largest group of pediatric kidney transplant children in our country. The NPHS1 kidneys are removed in infancy and they serve as an excellent human material for studies of the pathophysiology of proteinuric kidney diseases. Sustained proteinuria is a major factor leading to end-stage renal failure and understanding this process is crucial for nephrology. In this study we investigated the glomerular and tubulointerstitial changes that occur in the NPHS1 kidneys during infancy as well as the expression of nephrin in non-renal tissues. We also studied the pathology and management of recurrent proteinuria in kidney grafts transplanted to NPHS1 children. Severe renal lesions evolved in patients with NPHS1 during the first months of life. Glomerular sclerosis developed through progressive mesangial sclerosis, and capillary obliteration was an early consequence of this process. Shrinkage of the glomerular tuft was common, whereas occlusion of tubular opening or protrusion of the glomerular tuft into subepithelial space or through the Bowman's capsule were not detected. Few inflammatory cells were detected in the mesangial area. The glomerular epithelial cells (podocytes) showed severe ultrastructural changes and hypertrophy. Podocyte proliferation and apoptosis were rare, but moderate amounts of podocytes were detached and ended up in the urine. The results showed that endocapillary lesions not extracapillary lesions, as generally believed were important for the sclerotic process in the NPHS1 glomeruli. In the tubulointerstitium, severe lesions developed in NPHS1 kidneys during infancy. Despite heavy proteinuria, tubular epithelial cells (TECs) did not show transition into myofibroblasts. The most abundant chemokines in NPHS1 tissue were neutrophil activating protein-2 (NAP-2), macrophage inhibiting factor (MIF), and monocyte chemoattractant protein-1 (MCP-1). Interstitial inflammation and fibrosis were first detected in the paraglomerular areas and the most abundant inflammatory cells were monocytes/macrophages. Arteries and arterioles showed intimal hypertrophy, but the pericapillary microvasculature remained quite normal. However, excessive oxidative stress was evident in NPHS1 kidneys. The results indicated that TECs were relatively resistant to the heavy tubular protein load. Nephrin was at first thought to be podocyte specific, but some studies especially in experimental animals have suggested that nephrin might also be expressed in non-renal tissues such as pancreas and central nervous system. The knowledge of nephrin biology is important for the evaluation of nephrin related diseases. In our study, no significant amounts of nephrin protein or mRNA were detected in non-renal tissues of man and pig as studied by immunohistochemistry and in situ hybridization. The phenotype analysis of NPHS1 children, who totally lack nephrin, revealed no marked impairment in the neurological, testicular, or pancreatic function speaking against the idea that nephrin would play an important functional role outside the kidney. The NPHS1 kidneys do not express nephrin and antibodies against this major glomerular filter protein have been observed in NPHS1 children after renal TX most likely as an immune reaction against a novel antigen. These antibodies have been associated with the development of recurrent NS in the kidney graft of NPHS1 patients. In our study, a third of the NPHS1 patients homozygous for Fin-Major mutation developed recurrent NS in the transplanted graft. Re-transplantations were performed to patients who lost their graft due to recurrent NS and heavy proteinuria immediately developed in all cases. While 73% of the patients had detectable serum anti-nephrin antibodies, the kidney biopsy findings were minimal. Introduction of plasma exchange (PE) to the treatment of recurrent nephroses increased the remission rate from 54% to 89%. If remission was achieved, recurrent NS did not significantly deteriorate the long term graft function. In conclusion, the results show that the lack of nephrin in podocyte slit diaphragm in NPHS1 kidneys induces progressive mesangial expansion and glomerular capillary obliteration and inflicts interstitial fibrosis, inflammation, and oxidative stress with surprisingly little involvement of the TECs in this process. Nephrin appears to have no clinical significance outside the kidney. Development of antibodies against nephrin seems to be a major cause of recurrent NS in kidney grafts of NPHS1 patients and combined use of PE and cyclophosphamide markedly improved remission rates.

Comparative Nucleotide and Amino Acid Sequence Analysis of the Sequence-Specific RNA-Binding Rotavirus Nonstructural Protein NSP3

NSP3, an acidic nonstructural protein, encoded by gene 7 has been implicated as the key player in the assembly of the 11 viral plus-strand RNAs into the early replication intermediates during rotavirus morphogenesis. To date, the sequence or NSP3 from only three animal rotaviruses (SA11, SA114F, and bovine UK) has been determined and that from a human strain has not been reported. To determine the genetic diversity among gene 7 alleles from group A rotaviruses, the nucleotide sequence of the NSP3 gene from 13 strains belonging to nine different G serotypes, from both humans and animals, has been determined. Based on the amino acid sequence identity as well as phylogenetic analysis, NSP3 from group A rotaviruses falls into three evolutionarily related groups, i.e., the SA11 group, the Wa group, and the S2 group. The SA 11/SA114F gene appears to have a distant ancestral origin from that of the others and codes for a polypeptide of 315 amino acids (aa) in length. NSP3 from all other group A rotaviruses is only 313 aa in length because of a 2-amino-acid deletion near the carboxy-terminus, While the SA114F gene has the longest 3' untranslated region (UTR) of 132 nucleotides, that from other strains suffered deletions of varying lengths at two positions downstream of the translational termination codon. In spite of the divergence of the nucleotide (nt) sequence in the protein coding region, a stretch of about 80 nt in the 3' UTR is highly conserved in the NSP3 gene from all the strains. This conserved sequence in the 3' UTR might play an important role in the regulation of expression of the NSP3 gene. (C) 1995 Academic Press, Inc.

Biology, ecology, control and management of the invasive Indo-Pacific lionfish: An updated integrated assessment

Venomous Indo-Pacific lionfish (Pterois miles and P. volitans) are now established along the Southeast U.S.A. and parts of the Caribbean and pose a serious threat to reef fish communities of these regions. Lionfish are likely to invade the Gulf of Mexico and potentially South America in the near future. Introductions of lionfish were noted since the 1980s along south Florida and by 2000 lionfish were established off the coast of North Carolina. Lionfish are now one of the more numerous predatory reef fishes at some locations off the Southeast U.S.A. and Caribbean. Lionfish are largely piscivores that feed occasionally on economically important reef fishes. The trophic impacts of lionfish could alter the structure of native reef fish communities and potentially hamper stock rebuilding efforts of the Snapper –Grouper Complex. Additional effects of the lionfish invasion are far-reaching and could increase coral reef ecosystem stress, threaten human health, and ultimately impact the marine aquarium industry. Control strategies for lionfish are needed to mitigate impacts, especially in protected areas. This integrated assessment provides a general overview of the biology and ecology of lionfish including genetics, taxonomy, reproductive biology, early life history and dispersal, venom defense and predation, and feeding ecology. In addition, alternative management actions for mitigating the negative impacts of lionfish, approaches for reducing the risk of future invasions, and directions for future research are provided.

A molecular genetic investigation of the population structure of Atlantic menhaden (Brevoortia tyrannus)

Atlantic menhaden (Brevoortia tyrannus), through landings, support one of the largest commercial fisheries in the United States. Recent consolidation of the once coast-wide reduction fishery to waters within and around Chesapeake Bay has raised concerns over the possibility of the loss of unique genetic variation resulting from concentrated fishing pressure. To address this question, we surveyed variation at the mitochondrial cytochrome c oxidase subunit I (COI) gene region and seven nuclear microsatellite loci to evaluate stock structure of Atlantic menhaden. Samples were collected from up to three cohorts of Atlantic menhaden at four geographic locations along the U.S. Atlantic coast in 2006 and 2007, and from the closely related Gulf menhaden (B. patronus) in the Gulf of Mexico. Genetic divergence between Atlantic menhaden and Gulf menhaden, based on the COI gene region sequences and microsatellite loci, was more characteristic of conspecific populations than separate species. Hierarchical analyses of molecular variance indicated a homogeneous distribution of genetic variation within Atlantic menhaden. No significant variation was found between young-of-the-year menhaden (YOY) collected early and late in the season within Chesapeake Bay, between young-of-the-year and yearling menhaden collected in the Chesapeake Bay during the same year, between YOY and yearling menhaden taken in Chesapeake Bay in successive years, or among combined YOY and yearling Atlantic menhaden collected in both years from the four geographic locations. The genetic connectivity between the regional collections indicates that the concentration of fishing pressure in and around Chesapeake Bay will not result in a significant loss of unique genetic variation.

Assessment and possible development of the fishery resources of Pedro Bank

Pedro Bank is about 1,300 square miles in extent and lies at the mouth of the Palk Strait close to the mainland, enabling smaller boats to exploit it. Trawl surveys indicated the presence of substantial demersal varieties on the Pedro Bank, but the results of the early commercial operations indicate that a 135-foot trawler may not be operated continuously on the bank without diminishing returns. Subsequent to the commercial operations extensive surveys with smaller boats and various types of gear were carried out. Of the various types of gear tried out, results from bottom long lining and hand lining operations were promising. Trials were carried out to compare these two types of gear. Though not extensive, these trials indicated that at the initial stages of exploitation of the Bank, hand lining, which is extensively practiced in Ceylon, may be better but as exploitation progresses; with more experience, it should be possible to overcome some of the present disadvantages of bottom long lining and eventually bottom long lining should produce better results. The recently introduced mechanised craft are exploiting only the fringe of the bank and it should be possible to exploit its stocks fully with slightly bigger boats with a 35-40 mile range.

Evolution of the black muntjac (Muntiacus crinifrons) karyotype revealed by comparative chromosome painting

The black muntjac (Muntiacus crinifrons) has an unusual karyotype of 2n = 8 in females and 2n = 9 in males. We have studied the evolution of this karyotype by hybridising chromosome-specific paints derived from flow-sorted chromosomes of the Chinese muntjac (M. reevesi, 2n = 46) to chromosomes of the black muntjac. The hybridisation pattern allowed us to infer chromosomal homologies between these two species. Tandem and centromeric fusions, reciprocal translocations, and insertions are involved in the reduction of the diploid number from 2n = 46 to 2n = 8, 9. The painting patterns further show complex chromosomal rearrangements in the male black muntjac which involve more than half the karyotype, including both sex chromosomes. Since early meiosis is reported to be normal without any visible inversion loops of the synaptonemal complex, the observed chromosomal rearrangements would lead to heterosynapsis and, therefore, leave a large fraction of the male black muntjac karyotype balanced between the two sexes.

An approach to prediction of the South China Sea summer monsoon onset

In the present paper, correlation between the South China Sea summer monsoon (SCSSM) onset and heat content in the upper layer of the warm pool in the western Pacific Ocean is examined using the Scripps Institution of Oceanography dataset for the period of 1955-1998 and an approach to prediction the SCSSM onset is proposed. Correlation showes that there exists interdecadal variability of the SCSSM onset demarcated by 1970 with the largest correlation coefficient in the area west of the center of the warm pool rather than near its centers, implying certain effect from other factors involved besides ENSO. As the correlation is poor for the period before 1970, the heat content anomaly of the warm pool after 1970 is used to indicate early or late onset of the SCSSM beforehand. An ideal representative area (1A degrees x1A degrees) for the warm pool heat content was determined with its center at 3A degrees N/138A degrees E. The nearest TAO (TAO-Tropical Atmosphere Ocean-array) mooring to the center is at 2A degrees N/137A degrees E, and chosen to calculate the heat content for prediction. It is suggested that the TAO mooring at 2A degrees N/137A degrees E could be used to predict the SCSSM onset with the heat content in the upper layer, if the correlation between the SCSSM onset and the heat content of the warm pool runs like that of after 1970. On the other hand, if the situation does like the one before 1970, the representative station is determined at 13A degrees S/74A degrees E with relatively poor correlation, meaning that the warm pool in the western Pacific Ocean plays more important role in the SCSSM onset than the Indian Ocean.

Highly sensitive determination of the methylated p16 gene in cancer patients by microchip electrophoresis

The p16 tumor suppressor gene is inactivated by promoter region hypermethylation in many types of tumor. Recent studies showed that aberrant methylation of the p16 gene is an early event in many tumors, especially in lung cancer, and may constitute a new biomarker for early detection and monitoring of prevention trials. We detected tumor-associated aberrant hypermethylation of the p16 gene in plasma and tissue DNA from 153 specimens using a modified semi-nested methylation-specific PCR (MSP) combining plastic microchip electrophoresis or slab gel electrophoresis, respectively. Specimens were from 79 lung cancer patients, 15 abdominal tumor patients, 30 positive controls and 30 negative controls. The results showed that the positive rate obtained by microchip electrophoresis was more than 26.6% higher and the same speciticity was kept when compared with slab gel electrophoresis. The microchip electrophoresis can rapidly and accurately analyze the PCR products of methylated DNA and obviously improve the positive rate of diagnosis of cancer patients when compared with gel electrophoresis. This method with the high assay sensitivity might be used for detection of methylation of p16 gene and even to facilitate early diagnosis of cancer patients. (C) 2004 Elsevier B.V. All rights reserved.