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The structures formed by adsorption of carboxyalkylphosphonic acids on metal oxide powders were characterized by solid-state NMR and FTIR-PAS (Fourier transform infrared photoacoustic spectroscopy). A series of diacids, HO2C(CH2)nPO3H2 (n = 2, 3, 11, and 15), were deposited on nonporous TiO2 and ZrO2 powders and nanocrystalline ZrO2 with average particle diameters of 21, 30, and 5 nm, respectively. Solid-state ³¹P NMR, combined with FTIR-PAS, indicates that the phosphonic acid group binds selectively to the surface, producing a monolayer of carboxylic acid terminated chains. The average chain conformation depends on the substrate in addition to the chain length. Ordered samples display thermal order/disorder transitions similar to other self-assembled monolayer systems. The more restricted chain mobility relative to analogous methyl-terminated chains is attributed to hydrogen-bonding among the pendant carboxylic acid groups. These results demonstrate that phosphonic acids are useful for selectively introducing pendant polar functional groups on metal oxide surfaces.

Deuterium NMR spectroscopy has been used to probe the dynamics of deuterated octadecylphosphonate (−1,1−d2) (ODPA−d2) monolayers on nonporous ZrO2 powder (surface area ≈ 40 m²/g) over the temperature range of 200−340 K. At 200 K, a broadened Pake doublet with distinct nonrigid characteristics and a horn splitting of approximately 120 kHz was observed. With increasing temperature, the ²H spectrum gradually transforms into a relatively narrow and featureless peak. Spectral simulations are performed with the help of plausible motional models, and the results show that, over the whole temperature range studied, the C1−D bonds have substantial motional freedom with respect to the characteristic ²H NMR time scale. In addition, at each temperature, a weighted superposition of several simulated line shapes with different rates and site populations is required to account for the observed spectral features, indicating the presence of considerable motional heterogeneity within the ODPA monolayers. The results are further discussed in terms of the known characteristics of the ZrO2 surface and of the conformational transitions in the octadecyl chain.

Long-chain alkanoic acids (CH3(CH3)nCO2H, n > 15) form conformationally ordered monolayers on zirconium oxide powder via a chelating bidentate zirconium carboxylate surface bond. ω-Hydroxyalkanoic acids (HO(CH3)15CO2H) produce hydrophilic monolayers, with no evidence of looping to the metal oxide surface. Variable temperature and two-dimensional solid-state NMR experiments demonstrate that alkanoate monolayers display chain dynamics similar to other self-assembled monolayers (SAMs). The thermal behavior of alkanoate SAMs is also compared to analogous fatty acid salt Langmuir−Blodgett monolayers which undergo pretransitional chain disordering.

BLOOM'S syndrome (BS) is a rare, autosomal recessive condition of pre-natal and post-natal growth retardation, sun-induced telangiectatic erythema, impaired immunological function and predisposition to cancer1,2. BS cells show a high incidence of chromosome breakage and rearrangement often with abnormal nuclear morphology. Chromosome exchanges appear mainly to involve homologous chromosomes, while sister chromatid exchanges are abnormally frequent3. These features suggest a defect of DNA replication or repair. In particular, the high incidence of sister chromatid exchanges may be explained if free ends in the DNA, resulting from abnormalities of DNA synthesis and/or repair, act as initiation points for exchange4. We report here that BS fibroblasts are abnormally sensitive to ultraviolet irradiation in vitroand show a rate of DNA synthesis and DNA chain maturation lower than controls. They do not, however, have defective bypass of ultraviolet light-induced lesions during DNA replication as xeroderma pigmentosum (XP) variants5.

Patients with Xeroderma pigmentosum and defective DNA excision repair can be distinguished as a rapid (r-XP) and slow (s-XP) complementing variety. When fused with normal cells, fibroblasts from the r-XP are complemented rapidly and in the absence of protein synthesis while those from the s-XP are complemented slowly by a process partly, but not entirely, dependent on protein synthesis. Heterokaryons with different ratios of r-XP to s-XP nuclei (i.e. 1:1–5 and 1–5:1) and control heterokaryons containing one normal and 1–5 r- or s-XP nuclei show that if cell fusion and incubation is conducted in medium preventing protein synthesis, the r-XP cells do not complement the 8-XP partner at all and, conversely, that the latter is not as effective as normal cells at complementing the r-XP partner. On the contrary, if protein synthesis is permitted, the 2 types of XP cells complement each other in a gene dose-dependent manner and to an extent similar to that observed in the control heterokaryons. These findings indicate that the r- and 8-XP varieties are caused by mutations at different loci and suggest that the products of these loci interact to produce a functional unit which is present in normal control cells but absent in the XP strains. The relationship between the complementation groups described here and those already reported in the literature is being investigated.

Measured wave force data from the Conoco test structure in hurricane Carmen have been analyzed on a wave‐by‐wave basis to determine the total hydrodynamic forces exerted on the platform. These measurements are compared with calculated total forces. The calculated forces are based on a conventional API wave‐current force determination procedure. Observations made on the basis of the Conoco test structure (CTS) data are compared with those from the Exxon ocean test structure (OTS). The comparisons indicate that the two data sets indicate similar trends if it is recognized that in contrast with the CTS data, the OTS data did not involve high storm waves; that these waves were long‐crested and unidirectional; and that there were no significant currents. The data indicate that the present API RP 2A guideline wave‐force formulation will given an unbiased estimate of maximum total hydrodynamic forces developed on small‐diameter membered structures located in deep water in intense hurricanes. Directional spreading associated with the intense, central portions of hurricanes can lead to substantial reductions in wave forces, as compared with unidirectional waves of identical heights and periods.

Patients with the light-sensitive disease xeroderma pigmentosum (XP) are genetically heterogeneous. Most patients are defective in the excision repair of u.v.-induced DNA damage while some, the XP-variants, seem proficient in excision repair but replicate u.v.-damaged DNA with difficulty. The former have so far been assigned to 5 complementation groups (A-E) of which B and E are extremely rare. Information on the nature of the defect in XP is contradictory. Studies based on the sedimentation of DNA in alkaline gradients suggest that patients of complementation group A can perform the first step of excision repair (‘incision’) while others, based on the elution by alkali of the DNA of cells lysed on filters, suggest that they cannot. We have therefore investigated the repair of DNA damaged by u.v. irradiation using a method based on a precisely defined theoretical approach. A single break in one of the strands of a double-stranded and supercoiled circle of DNA releases supercoiling and reduces its rate of sedimentation in sucrose gradients. Structures resembling nuclei (‘nucleoids’) containing superhelical DNA may be obtained from human lymphocytes and their rate of sedimentation is influenced by the integrity of their DNA. Analysis of the sedimentation of nucleoids from normal and XP lymphocytes in sucrose gradients containing different concentrations of ethidium indicates that their DNA is similarly supercoiled. The lymphocytes of patients of complementation groups A, C and D repair damage induced by γ-rays just like controls. However, they cannot repair normally DNA damaged by u.v. irradiation; the cells are defective in the first step of excision repair. The XP-variant and XP-heterozygous cells repaired u.v.- and γ-ray-induced damage like controls. Some problems regarding the nature of the defect in XP are discussed.

We report clinical, genetic and biochemical findings in 13 families with the photosensitive genodermatosis, xeroderma pigmentosum. All patients had a defect in repair of DNA damage provoked by ultraviolet radiation. Eleven patients and their three affected sibs were defective in the excision repair of UVR induced DNA lesions while the other two were defective in post-replication repair. One in the former group was diagnosed prior to the development of permanent skin abnormalities and preventive measures succeeded for almost five years in maintaining a normal appearing skin. In addition, two cases were diagnosed prenatally and aborted therapeutically. Some patients' parents showed slightly reduced repair of UVR induced DNA damage. In xeroderma pigmentosum (XP), the defect in the excision of DNA lesions appears to be due to homozygosity for one of at least seven different mutations and, accordingly, XP patients can be assigned to seven so-called complementation groups, A to G. Of these, groups A, C and D are the most common. Somatic cell fusion allowed three of the families reported here to be assigned to group A, four to group C and four to group D. Fibroblasts of patients from these three groups were shown to differ not only in the degree and kinetics of their residual DNA repair but also in the kinetics with which their defect is complemented by fusion with normal or XP cells of other groups. This confirms that mutations of different genes play a role in XP and provides a basis for understanding how such genes interact to secure repair of DNA lesions in normal cells. We discuss the phenotype of XP from different complementation groups in relation to the severe neurological abnormalities which may develop and must be considered in genetic counselling. We also discuss the biochemical anomalies of XP and the cellular effects of physical and chemical agents which damage DNA. In the practical management of XP, the importance of early differential diagnosis and prompt initiation of treatment is emphasized. Lastly we review the relationship between DNA repair and skin cancer in XP.