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We present a study on the optical losses of Fabry-Pérot cavities subject to realistic transverse mirror misalignment. We consider mirrors of the two most prevalent surface forms: idealised spherical depressions, and Gaussian profiles generated by laser ablation. We first describe the mode mixing phenomena seen in the spherical mirror case and compare to the frequently-used clipping model, observing close agreement in the predicted diffraction loss, but with the addition of protective mode mixing at transverse degeneracies. We then discuss the Gaussian mirror case, detailing how the varying surface curvature across the mirror leads to complex variations in round trip loss and mode profile. In light of the severe mode distortion and strongly elevated loss predicted for many cavity lengths and transverse alignments when using Gaussian mirrors, we suggest that the consequences of mirror surface profile are carefully considered when designing cavity experiments.

We explore coherent multi-photon processes in 87Rb133Cs molecules using 3-level lambda and ladder configurations of rotational and hyperfine states, and discuss their relevance to future applications in quantum computation and quantum simulation. In the lambda configuration, we demonstrate the driving of population between two hyperfine levels of the rotational ground state via a two-photon Raman transition. Such pairs of states may be used in the future as a quantum memory, and we measure a Ramsey coherence time for a superposition of these states of 58(9) ms. In the ladder configuration, we show that we can generate and coherently populate microwave dressed states via the observation of an Autler-Townes doublet. We demonstrate that we can control the strength of this dressing by varying the intensity of the microwave coupling field. Finally, we perform spectroscopy of the rotational states of 87Rb133Cs up to N = 6, highlighting the potential of ultracold molecules for quantum simulation in synthetic dimensions. By fitting the measured transition frequencies we determine a new value of the centrifugal distortion coefficient Dv = h × 207.3(2) Hz.

We show that the lifetime of ultracold ground-state ^{87}Rb^{133}Cs molecules in an optical trap is limited by fast optical excitation of long-lived two-body collision complexes. We partially suppress this loss mechanism by applying square-wave modulation to the trap intensity, such that the molecules spend 75% of each modulation cycle in the dark. By varying the modulation frequency, we show that the lifetime of the collision complex is 0.53±0.06  ms in the dark. We find that the rate of optical excitation of the collision complex is 3&#95;{-2}^{+4}×10^{3}  W^{-1} cm^{2} s^{-1} for λ=1550  nm, leading to a lifetime of <100  ns for typical trap intensities. These results explain the two-body loss observed in experiments on nonreactive bialkali molecules.

Understanding and controlling collisions is crucial to the burgeoning field of ultracold molecules. All experiments so far have observed fast loss of molecules from the trap. However, the dominant mechanism for collisional loss is not well understood when there are no allowed 2-body loss processes. Here we experimentally investigate collisional losses of nonreactive ultracold 87 Rb 133 Cs molecules, and compare our findings with the sticky collision hypothesis that pairs of molecules form long-lived collision complexes. We demonstrate that loss of molecules occupying their rotational and hyperfine ground state is best described by second-order rate equations, consistent with the expectation for complex-mediated collisions, but that the rate is lower than the limit of universal loss. The loss is insensitive to magnetic field but increases for excited rotational states. We demonstrate that dipolar effects lead to significantly faster loss for an incoherent mixture of rotational states.

The serum "uracil+uridine" levels, expressed as uracil, have been measured in 10 cases of pernicious anaemia both before and after treatment, and compared with the levels in 97 normal subjects. The mean pre-treamtent value (8.82 mumol/1., range 6.0-12.0 mumol/1.) differed significantly from that of the normal controls (15.7 mumol/1., range 5.7-40.5 mumol/1., t = 8.8, P less than 0.001). This confirms the low serum uracil level previously reported in pernicious anaemia relapse. The level rose progressively after treatment, reaching a maximum on the fourth day (mean 17.85 mumol/1., range 9.3-23.4 mumol/1.). This was not significantly different from the mean of the normal control group. The difference between the pre- and post-treatment levels was significant on days 3,4 and 5 (P less than 0.005, P less than 0.001 and P less than 0.005 respectively) and the rise preceded the reticulocyte response by 24 h. A further case was treated with pysiological doses of vitamin B12 (2 mug daily for 6 d) and a similar rise in the serum uracil level noted. These results are not explained by any of the known functions of vitamin B12. They are, however, similar to the changes in the serum methionine levels previously reported in pernicious anaemia. The latter were readily explained by the known action of vitamin B12 on "de novo" methionine synthesis and it is suggested that the synthesis of uracil, like that of methionine, might be influenced by vitamin B12 in man.

The serum "uracil+uridine" level, expressed as uracil, has been measured in 21 cases of vitamin B12 deficiency, in which the serum folate was normal, and compared with the level in 97 normal subjects. The level in the vitamin B12 deficient group (11.9 mumol/1). was significantly lower than in the controls (15.7 mumol/1., P less than 0.005). Nine of the former were complicated by stystemic illness but the clinical and haematological features in the remaining 12 were consistent with the diagnosis of pernicious anaemia in relapse. The serum uracil level in this group was even lower (10.21 mumol/1., P less than 0.01). This finding is unexpected in view of the generally accepted indirect role of vitamine B12 in the methylation of deoxyuridine monophosphate to deoxythymidine monophosphate. Reasons are given for not accepting these results as reflecting the main biochemical lesion in vitamin B12 deficiency. Although they do not give direct support to an impairment in the methylation of deoxyuridine monophosphate, they do not exclude it as they test only one possible metabolic pathway and moreover they could represent the result of more than one action of vitamin B12 on uracil metabolism. They do show, however, that some aspect of uracil metabolism other than methylation is affected in vitamin B12 deficiency in man.

Vasospasm of the vertebrobasilar system was induced in seven dogs by the intracisternal injection of autologous blood. Somatosensory and brain stem auditory evoked potentials were recorded before and after the induction of angiographically confirmed vasospasm. Additionally, somatosensory evoked potentials were monitored during graded hypotension to 40 mm Hg. There was no significant alteration in the evoked potentials by vasospasm or hypotension. Detailed clinical examination and postmortem histopathological studies did not demonstrate any focal neurological deficit or infarction attributable to vasospasm. Previous studies have noted close correlations between decreased cerebral blood flow and evoked potential alterations. Induced hypotension to a mean arterial pressure of 40 mm Hg in the presence of documented vasospasm was not sufficient to cause evoked potential changes, focal neurological deficit, or pathological evidence of infarction in the canine model.

Serum methionine and valine have been assayed microbiologically in 31 patients anaesthetized with and in 13 controls anaesthetized without nitrous oxide. Isoleucine has been similarly assayed in five cases and three controls. The preinduction levels of both methionine and valine were considerably below those of semifasting healthy adults. Serum methionine fell significantly in both groups as did valine and isoleucine in the controls. These findings are attributed to dietary restriction before and during the operation. Serum valine was significantly elevated in patients anaesthetized with nitrous oxide but only in those anaesthetized for 3 h or longer. Isoleucine also was elevated in two of the five cases exposed to nitrous oxide. Reasons are given for attributing these elevated levels to the direct action of nitrous oxide. Valine is entirely and isoleucine is partly catabolized along the adenosylcobalamin dependent propionyl-CoA-succinyl-CoA pathway. It is concluded that their elevated levels are caused by the inactivation of adenosylcobalamin by nitrous oxide thereby inducing the methylmalonyl mutase block in this pathway. It is suggested also that the relief of this block by adenosylcobalamin in pernicious anaemia could provide a possible metabolic basis for the well recognized early subjective improvement encountered in this disease following vitamin B12 therapy.

A microbiological method for the assay of uracil is described. The growth of the test organism is supported by uracil and also by uridine but not by uridylic acid. The method therefore measures uracil and uridine together. The ;uracil + uridine' level, expressed as uracil, has been measured in blood from 144 normal subjects ranging in age from cord blood to the eighth decade. The mean level of 22 mu mol/l (0.25 mg%) in cord blood decreases to 15 mumol/l (0.17 mg%) in adults over the age of 20. There is no difference between the sexes. Uracil is of interest because (a) it is a constituent base of RNA, (b) it is the precursor of two of the bases thymine and cytosine that enter into the composition of DNA, and (c) under certain circumstances it has mutagenic properties. The last is dependent upon the existence of two tautomeric forms of uracil, the common keto form which pairs normally with adenine and the rare enol form which pairs with guanine. A mistake in base pairing which allows uracil in its enol form to enter the DNA molecule and pair with guanine can result in a G = C --> A = T base transition in the DNA molecule. The molecular mechanism involved as well as the possible bearing on somatic mutation are discussed.

A microbiological method for the assay of valine, leucine, and methionine in serum is described and its accuracy and reproducibility are assessed. Under the conditions specified the L-isomers only of the three amino acids are measured. The serum levels of the three amino acids in 60 normal subjects are presented.