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Low‐temperature thermochronometry is widely used to measure the timing and rate of slip on normal faults. Rates are often derived from suites of footwall thermochronometer samples, but regression of age versus structural depth fails to account for the trajectories of samples during fault slip. We demonstrate that in rotating fault blocks, regression of age‐depth data is susceptible to significant errors (>10%) in the identification of the initiation and rate of faulting. Advection of heat and topographic growth influence the thermal histories of exhumed particles, but for a range of geologically reasonable fault geometries and rates these effects produce Apatite (U‐Th)/He ages comparable to those derived from rotation through fixed isotherms. We apply the fixed‐isotherm model to published data from the Pine Forest Range and the East Range, Nevada, by incorporating field and thermochronologic constraints into a Markov chain Monte Carlo model. Modeled parameters for the Pine Forest Range are described by narrow ranges of geologically reasonable values. Compared to slip rates of 0.3–0.8 km/Myr and an initiation of faulting ca. 11–12 Ma derived from visual inspection, the model predicts an average slip rate of ~1.1 km/Myr and an onset of faulting ca. 9–10 Ma. For the East Range fault block the model suggests that faulting began ~17 Ma with an extension rate of ~3 km/Myr and slowed to an extension rate of ~0.5 km/Myr at ~14 Ma. The absence of a preserved partial retention zone in the East Range sample set limits how well the model can predict fault block geometry. Normal faults form in settings where the crust is extending and can be associated with both seismic hazards and natural resource emplacement. To learn about the history of normal faults we often turn to minerals that record the history of cooling that occurs as fault slip carries rocks from depth to the relatively cool surface of the Earth. To interpret these cooling histories, it is common practice to treat the cooling of these minerals as resulting from the vertical translation of a series of samples through the crust. However, this ignores the basic geologic observation that sets of samples are often collected from areas that have undergone rotation as well as vertical translation. Here we investigate how this rotation may complicate the interpretations we make about fault histories by simulating the cooling histories of minerals that undergo faulting and associated rotation. We find that traditional methods for inferring slip histories on faults may be significantly biased and propose a relatively simple alternative for investigating these systems that is consistent with our geologic observations. Curved particle trajectories in tilted normal fault blocks complicate the interpretation of thermochronometer agesSimple interpretation of age‐versus‐structural depth plots can significantly mispredict the onset and rate of faultingTwo examples from the Basin and Range Province of Nevada reveal promise for quantitative inference of slip history from kinematic descriptions of sample paths

This report describes 7‐year‐old Afro‐Caribbean monozygotic twin boys who both presented with bilateral unerupted mesiodentes palatal to the central incisors. There have been two previous similar reports. From this case and previous reports it was concluded that mesiodentes in monozygotic twins are likely to be concordant with respect to the numberof supernumerary teeth. Unilateral mesiodens usually have been mirror imaged in each twin. Minor discordance between monozygotic twins is common with respect to the shape(conical, incisiform or tuberculate) and orientation(inverted or normal) of individual mesiodens within and between each twin.

Improvement of the M20 Maidstone bypass, junctions 518 G.J. H l , i l BSc, MICE, MIHT,and S. P. Johnstone, BSc, MICE, MIHT The M20 Maidstone bypass was a 30-year oldhighway rendered substandard by traffic growth and enhancement of design requirements. A commitment was madethat it would be improved froma dualtwo-lane to at least a dual three-lane carriageway would be operational by the and scheduled opening of the Channel Tunnel in 1993. This Paper outlines the improvement study and gives a commentary on the factors which conditioned the final engineering solution...

Telephone subscribers require a service which is reliable and offers a wide range of facilities. System design is of vital importance in determining the ability of an administration to meet these requirements economically, and processor controlled exchanges can be designed to provide the necessary qualities of reliability and flexibility. This paper describes in outline the operation of the TXE4 system, and shows how it incorporates features which will enable an administration both to meet its present commitments and to look ahead to providing an enhanced service in the future.

SummaryWhen BALB/c mice and athymic (nude) mice are injected intraperitoneally (i.p.) with pneumococcal type III polysaccharide (SIII), their antibodies as measured by passive haemagglutination (HA) are inhibited more easily by high doses of SIII than antibody measured by passive haemolysis (HL). The HA activity, due mainly to a highly avid non-complement-fixing (NCF) type of IgM, was further distinguished from the HL activity (CF-IgM, or CF-IgM plus CF hybrid IgM/A anti-SIII antibodies) by the failure of the NCF-IgM anti-SIII to bind to protein-A of Staphylococcus aureus (Sa). High-dose tolerance in the HL anti-SIII antibody response of BALB/c and athymic mice was induced only in the absence of circulating NCF-IgM anti-SIII antibodies. The presence of NCF-IgM anti-SIII antibodies formed to multiple daily increasing amounts of SIII, commencing with 0·01 μg SIII, decreased the magnitude of the HL anti-SIII response to subsequent daily increments of SIII antigen injected into BALB/c and athymic (nude) mice. Thus, the effect on the HL anti-SIII response was independent of T-cells. The concomitant administration of NCF-IgM anti-SIII rendered SIII less tolerogenic in primed mice. In contrast to the HL activity, the NCF-IgM anti-SIII antibodies were induced to low doses of SIII, conferred protection against viable pneumococci, but did not precipitate the soluble antigen in agar. It is proposed that immune paralysis (as defined by the failure of SIII-injected mice to resist pneumococci challenge) is not necessarily a condition of total unresponsiveness but is due to an absence of protective NCF-IgM anti-SIII antibodies. Thus, immune paralysis can co-exist with either the presence or absence of non-protective CF-IgM or CF-IgM/A anti-SIII antibodies.Australian Journal of Experimental Biology and Medical Science (1985) 63, 19–32; doi:10.1038/icb.1985.3

SummaryThe influence of hereditary absence of thymus upon the synthesis of IgA, complement-fixing (CF) hybrid IgM/A, CF-IgM and non-CF-IgM antibodies to pneumococcal type III polysaccharide (SIII) injected into BALB/c and athymic nude mice was studied. Techniques Involved the differential absorption of the serum antibodies by protein-A of Staphylococcus aureus (Sa), co-precipitation in gels with 125I-SIII and autoradiography. IgM/A anti-SIII activity was not demonstrable in nude mice but was produced in significant amounts, by day 5 in BALB/c mice injected with SIII. By day 8, node mice produced more IgA anti-SIII antibodies than BALB/c mice injected with the same antigen. IgA anti-SIII antibodies were not detected in either strain 5 days after SIII administration. The absence of hybrid IgM/A anti-SIII antibodies in athymic mice, prior to the appearance of monotypic IgA anti-SIII antibodies at day 8, suggests that IgM/A and not IgA synthesis is largely T cell-dependent The evidence also implies that hybrid IgM/A antibody production, maximal on day 5 in BALB/c mice, and absent from nude mice, is not an essential produced in the switching from IgM to IgA synthesis. Both strains of mice produced comparable amounts of complement-fixing (CF)-IgM and NCF-IgM anti-SIII antibodies, with the production of non-complement-fixing (NCF)-IgM anti-SIII in athymic mice being delayed. Results indicate that attemptS to quantitate the levels of IgA by assays incorporating anti-IgA anti-sera may be complicated by the presence of IgM/A hybrid antibody. The lower levels of IgA in nude mice may not necessarily imply T cell dependency of IgA synthesis. Since cells producing the T cell-dependent IgM/A antibodies are visualized by direct plagues, the present findings have important implications in studies where the calculation of the number of indirect plaque-forming cells is based on the assumption that direct plaques are due only to thymus-independent CF-IgM antibodies.Australian Journal of Experimental Biology and Medical Science (1984) 62, 701–709; doi:10.1038/icb.1984.66

SummaryPrior treatment (priming) with a weakly immunogenic dose of Type III pneumococcal polysaccharide (SIII) results in the development of an antigen-specific state of unresponsiveness termed low-dose paralysis which is believed to be mediated by suppressor T cells. The present findings show that the passive administration of functionally distinct non-complement-fixing (NCF) IgM anti-SIII antibodies either in monoclonal form or from protein-A absorbed immune serum could significantly suppress the direct plaque-forming cell (PFC) response to an immunogenic dose of SIII administered concurrently. The degree of suppression was comparable with that induced by low–dose paralysis. Low-dose paralysis was consistently induced in athymic (nude) mice 4 days, but not 3 days, after priming with a low dose of SIII, and was associated with the delayed appearance of NCF-IgM anti-SIII in the serum of athymic mice. In contrast, low-dose paralysis was readily induced in normal BALB/c mice 3 days after priming when NCF-IgM anti-SIII antibodies were present. Comparable inhibiton of the direct anti-SIII PFC response was observed when Concanavalin A (Con A) or NCF-IgM anti-SIII serum was administered with SIII antigen. That Con A and NCF-IgM anti-SIII together did not produce additive suppression was attributed to the adsorption of NCF-IgM anti-SIII antibodies to Con A. Complement-dependent single radial haemolysis mediated by CF hybrid IgM/A or CF-IgM anti-SIII serum was blocked by monoclonal NCF-IgM or IgA anti-SIII antibodies and indicated that each of the antibodies was specific for the same SIII-determinant. Evidence is presented to show that low-dose paralysis in the CF-IgM response to SIII is not mediated by suppressor T cells but can be attributed to highly avid NCF-IgM anti-SIII antibodies, formed preferentially to low doses of SIII, being able to reduce the immunogenicity of SIII administered subsequently.We propose that low-dose paralysis to SIII is the result of an immunobiological function of highly avid NCF-IgM anti-SIII antibodies which not only confer resistance against capsulated pneumococci but preferentially bind soluble SIII-antigen to reduce its immunogenicity and thereby protect specific CF-IgM positive B cells from being rendered tolerant by direct contact with higher doses of SIII antigen.Australian Journal of Experimental Biology and Medical Science (1986) 64, 19–35; doi:10.1038/icb.1986.3

Annexin I is a member of the annexin family of Ca(2+)- and phospholipid-binding proteins. The ability of this protein to aggregate and to mediate the fusion of various types of vesicles has supported the hypothesis that this protein might be involved in intracellular membrane fusion processes such as exocytosis. Although annexin I has been described as a major in vitro substrate of both protein kinase C and the epidermal-growth-factor-receptor protein tyrosine kinase, the functional consequences of these phosphorylation events have not been investigated. In this paper we examine the effect of the phosphorylation of annexin I by protein kinase C on the phospholipid aggregation activity of the protein. The stoichiometry of phosphorylation of the protein was affected by the method of preparation of the phospholipid. Under optimal assay conditions protein kinase C catalysed the incorporation of 2.83 +/- 0.23 mol of phosphate/mol of annexin I (mean +/- S.E.M., n = 21). Studies with the Ca(2+)- and phospholipid-independent form of protein kinase C suggested that the phosphorylation of annexin I was stimulated by phospholipid in the absence of Ca2+, although maximal phosphorylation was achieved in the presence of both phospholipid and Ca2+. Phosphorylation of annexin I resulted in a dramatic decrease in the rate and extent of phospholipid vesicle aggregation, without significantly disrupting the binding of the protein to the phospholipid vesicles. The phosphorylation of annexin I increased the EC50 (Ca2+) of phospholipid vesicle aggregation from 19 +/- 10 microM (mean +/- S.D., n = 7) for the native protein to 290 +/- 95 microM (mean +/- S.D., n = 5) for the phosphorylated protein. These results suggest that protein kinase C may act to inhibit the phospholipid vesicle aggregation activity of annexin I.

The complete primary structure of the core protein of rat NG2, a large, chondroitin sulfate proteoglycan expressed on O2A progenitor cells, has been determined from cDNA clones. These cDNAs hybridize to an mRNA species of 8.9 kbp from rat neural cell lines. The total contiguous cDNA spans 8,071 nucleotides and contains an open reading frame for 2,325 amino acids. The predicted protein is an integral membrane protein with a large extracellular domain (2,224 amino acids), a single transmembrane domain (25 amino acids), and a short cytoplasmic tail (76 amino acids). Based on the deduced amino acid sequence and immunochemical analysis of proteolytic fragments of NG2, the extracellular region can be divided into three domains: an amino terminal cysteine-containing domain which is stabilized by intrachain disulfide bonds, a serine-glycine-containing domain to which chondroitin sulfate chains are attached, and another cysteine-containing domain. Four internal repeats, each consisting of 200 amino acids, are found in the extracellular domain of NG2. These repeats contain a short sequence that resembles the putative Ca(++)-binding region of the cadherins. The sequence of NG2 does not show significant homology with any other known proteins, suggesting that NG2 is a novel species of integral membrane proteoglycan.

The Dixie Valley fault bounds the east side of the Stillwater Range in west‐central Nevada and last ruptured in 1954. Offset basalts indicate that slip began more recently than ~14 Ma, and prior work has interpreted the southern segment as an active low‐angle normal fault. Oligocene igneous rocks in the southern Stillwater Range were steeply tilted during large‐magnitude extension prior to ~14 Ma. To refine the timing of early extension and the onset of slip on the Dixie Valley fault, we collected two transects of samples for apatite fission track, apatite and zircon (U‐Th)/He (AHe and ZHe), and apatite 4He/3He thermochronometry. Apatite fission track ages from the Oligocene IXL pluton indicate rapid cooling ~18–14 Ma, and AHe and ZHe ages from the Cretaceous La Plata Canyon pluton indicate rapid cooling ~16–19 Ma. We interpret these data to record cooling during rapid extension. AHe ages from the IXL pluton are ~6–8 Ma and record cooling during slip on the Dixie Valley fault. We modeled these ages and 4He/3He spectra from one sample as the result of cooling during exhumation of a tilted fault block at a constant extension rate. The model predicts slip on the Dixie Valley fault beginning ~8 Ma. Although it does not constrain the initial fault dip, the model illustrates how a low‐angle fault requires a higher extension rate to reproduce cooling ages. Consequently, we prefer a high‐angle southern Dixie Valley fault for strain compatibility with the high‐angle northern segment. Oligocene volcanic rocks in the southern Stillwater Range were tilted during Miocene (18–14 Ma) extensionSlip on the Dixie Valley fault began ~8 Ma

We describe the use of MRI to establish the exact diagnosis in a swollen elbow in a neonate. Urgent diagnosis was needed for medical and social reasons. We accomplished this without the use of an invasive procedure or anaesthesia for a fracture that is recognised to be difficult to diagnose in patients of this age group.

IntroductionThe ‘Getting it right first time’ (GIRFT) programme will require endoscopy units to demonstrate improvements in efficiency and quality of patient care. Data collection in endoscopy beyond that recorded in the endoscopy report is difficult (e.g. patient flow, coding, use of consumables, externally validated quality markers and complications occurring outside of the room). Barcode technology offers an exciting way to achieve this.MethodBetween July-October 2016, patients undergoing bowel cancer screening colonoscopy or ERCP at our hospital were ‘tracked’ through their journey in endoscopy using hTrak barcode technology. The following data were collected: patient co-morbidities; patient location; endoscopy equipment used including disposable items; endoscopy personnel; drugs used; reasons for procedure or equipment failure; complications; and route of discharge.ResultsIn the 3 month period 268 bowel cancer screening colonoscopies and 141 ERCPs were tracked Co-morbidity data were successfully gathered on all patients taking <30s per patient (previously this was not done for out-patient endoscopies in our hospital due to the large volume of procedures). Consumable costs were as follows (per procedure):Diagnostic colonoscopy £13.95 Therapeutic colonoscopy £34.85 Diagnostic ERCP £305.41 Intermediate therapeutic ERCP £365.46 Major therapeutic ERCP £568.61 Tracking also allowed consumables to be reordered in a timely fashion and reduced loss of out-of-date stock.Equipment failure was recorded 16 cases including both endoscope and stack failures.32 complications were recorded, 17 in-room and 16 out-of-room. Out-of-room complications included 10 bleeding episodes, 1 use of flumazenil and 2 episodes of patient distress requiring pain relief. In the 3 months prior to tracking only 3 complications had been recorded for 1080 colonoscopies (including screening and symptomatic) and 127 ERCPs.ConclusionBarcode technology has revolutionised data collection in our department allowing us to meet the aims of the GIRFT programme, saving money and (most importantly) improving patient safety.Disclosure of InterestA. Goddard: None Declared, S. Johnstone: None Declared, J. Green: None Declared, J. Mayne: None Declared, K. Downs Conflict with: GS1 Board Member

IT is well established that high-purity chromium can be produced by electrolysing an aqueous solution of chromic acid containing a small sulphate addition, and that a significant factor governing the purity of such material is the temperature of the electrolyte1. Oxygen and nitrogen contents of 0.02 and 0.001 weight per cent respectively or better can be attained provided the bath temperature is high, that is, in the vicinity of 80° C. Under optimum conditions the metallic impurity is extremely low.

Nitration of thieno(3,2‐b)pyridine oxide (I) is accompanied by N‐deoxygenation to yield the 3,7‐dinitro derivative (II), whereas nitration of 7‐nitrothieno(3,2‐b)pyridine oxide (III) with a large excess of nitrating agent introduces a second nitro group to yield the 3,7‐dinitro derivative (IV).

In the solid state, the enol chelate (III) is found to be the only existing tautomer, whereas in solution minor amounts of the keto tautomer are also present.

UNUSUAL features observed during work on the ductility of chromium were the difficulty of detecting the completion of recrystallization of cold-worked material and the sensitivity of the ductile/brittle transition temperature of recrystallized material to small amounts of deformation, either residual or imposed.