Dewetting of polystyrene films on a silicon substrate is investigated as a function of film thickness h. We observe the nucleation of holes in the early stage of dewetting for relatively thick films ͑h. 100 Å͒, as observed previously, but the breakup of thinner films occurs through the growth of uniformly distributed surface undulations ("spinodal dewetting"). The average amplitude dh of these undulations increases exponentially up to the film rupture point where dh becomes comparable to h, as predicted by a capillary wave instability model. [S0031-9007(98)06787-8]

The polypeptide composition of epidermal keratin varies in disease . To better understand the biological meaning of these variations, we have analyzed keratins from a number of human epidermal diseases by the immunoblot technique using AE1 and AE3 monoclonal antikeratin antibodies . The results reveal a continuous spectrum of keratin expression ranging from one closely resembling the normal in vivo pattern to one almost identical to cultured epidermal keratinocytes . Specifically, a 50-kilodalton (kd) (AEl-positive) and a 58-kd (AE3-positive) keratin are present in all diseases, supporting the concept that they represent "permanent" markers for keratinocytes . A 56.5-kd (AE1) and a 65-67-kd (AE3) keratin, previously shown to be markers for keratinization, are expressed only by lesions retaining a keratinized morphology . A 48-kd (AE1) and a 56-kd (AE3) keratin are present in all hyperproliferative (para-or nonkeratinized) disorders, but not in normal abdominal epidermis or in ichthyosis vulgaris which is a non hyperproliferative disease . These two keratins have previously been found in various nonepidermal keratinocytes undergoing hyperproliferation, suggesting that these keratins are not epidermis-specific and may represent markers for hyperproliferative keratinocytes in general . In various epidermal diseases, there is a reciprocal expression of the (keratin) markers for hyperproliferation and keratinization, supporting the mutual exclusiveness of the two cellular events . Moreover, our results indicate that, as far as keratin expression is concerned, cultured human epidermal cells resemble and thus may be regarded as a model for epidermal hyperplasia. Finally, the apparent lack of any major, diseasespecific keratin changes in the epidermal disorders studied so far implies that keratin abnormalities probably represent the consequence, rather than the cause, of these diseases.The keratins are a group of water-insoluble proteins (40-70 Kdaltons [kd])' that form 10-nm desmosome-associated tonofilaments in all epithelia (15,17,18,61,63,64). Four major keratins (50, 56.5, 58, and 65-67 kd) have been identified in normal human epidermis (7, 21, 40, 72; cf. 4, 49, 62); significant alterations in epidermal keratin composition can occur, however, as a result of disease (1,3,5,25,26,28,33,34,36,37,40,50,52,54,66,71) as well as changes in cellular growth environment (10,20,29,55,61,62 -67-kd keratins (1, 5, 8, 37, 50, 54, 66). In addition, Thaler et al. (65,66) reported that two water-insoluble proteins of -54 and 57 kd are unique to psoriatic scale, although Baden et al. (5) found no "psoriasis-specific" keratin changes . Hunter and Skerrow (26) reported that certain abnormal keratin polypeptides ranging from 55-63 kd (probably corresponding to 50-58 kd in our gel system) are present in the scales of psoriasis, atopic dermatitis, and seborrheic dermatitis, as well as in the stratum comeum oftape-stripped epidermis . Interestingly, Kubilus et al. (28) found that keratins of another disease, basal cell 13...

The cover picture shows a single‐walled carbon nanotube (SWNT) functionalized with nucleophilic carbenes at the sidewall. Normally, single‐walled nanotubes exist in the form of insoluble bundles. The sidewall addition of reactive organic groups such as radicals, nitrenes, or carbenes such as the ones shown in the cover picture disrupts the bundles. The background of the picture shows a typical AFM image of such derivatized SWNTs. The isolated SWNTs are soluble in organic solvents giving black solutions. This enables a spectroscopic characterization of nanotubes in solution. With this versatile sidewall functionalization the decisive requirements for the development of technological applications such as the production of ultrathin films or the processing to polymer composites with new electronic and mechanic properties have been compiled. Details about this new chemical funtionalization of SWNTs is described by Hirsch et al. on pp. 4002 ff.

Linear viscoelasticity (LVE) of low-ion-content and lowmolecular-weight (nonentangled) randomly sulfonated polystyrene shows a sol−gel transition when the average number of ionic groups per chain approaches unity. This transition can be well understood by regarding the number of ionizable sites over a chain as the relevant functionality for crosslinking. For ionomers below but very close to the gel point, the LVE shows power law relaxation similar to gelation of chemical cross-linking. Nevertheless, ionomers near and beyond the gel point also show terminal relaxation not seen in chemically cross-linking systems, which is controlled by ionic dissociation. Careful analysis of the power law region of the frequency dependence of complex modulus close to the gel point shows a change in exponent from ∼1 at high frequency to ∼0.67 at low frequency, which strongly suggests a transition from mean-field to critical percolation known as the Ginzburg point. A mean-field percolation theory by Rubinstein and Semenov for gelation with effective breakup has been modified to include critical percolation close to the gel point and predicts well the observed LVE of lightly sulfonated polystyrene oligomers.

CAE was proven to be noninferior to RFA for the treatment of incompetent GSVs at month 3 after the procedure. Both treatment methods showed good safety profiles. CAE does not require tumescent anesthesia and is associated with less postprocedure ecchymosis.