The GroES heptamer forms a dome, approximately 75 A in diameter and 30 A high, with an 8 A orifice in the centre of its roof. The 'mobile loop' segment, previously identified as a GroEL binding determinant, is disordered in the crystal structure in six subunits; the single well-ordered copy extends from the bottom outer rim of the GroES dome, suggesting that the cavity within the dome is continuous with the polypeptide binding chamber of GroEL in the chaperonin complex.

p23 is a co-chaperone for the heat shock protein, hsp90. This protein binds hsp90 and participates in the folding of a number of cell regulatory proteins, but its activities are still unclear. We have solved a crystal structure of human p23 lacking 35 residues at the COOH terminus. The structure reveals a disulfide-linked dimer with each subunit containing eight ␤-strands in a compact antiparallel ␤-sandwich fold. In solution, however, p23 is primarily monomeric and the dimer appears to be a minor component. Conserved residues are clustered on one face of the monomer and define a putative surface region and binding pocket for interaction(s) with hsp90 or protein substrates. p23 contains a COOH-terminal tail that is apparently less structured and is unresolved in the crystal structure. This tail is not needed for the binding of p23 to hsp90 or to complexes with the progesterone receptor. However, the tail is necessary for optimum active chaperoning of the progesterone receptor, as well as the passive chaperoning activity of p23 in assays measuring inhibition of heat-induced protein aggregation.p23 is a ubiquitous, highly conserved protein which functions as a co-chaperone for the larger molecular chaperone, hsp90.

In a nine‐year period 101 dogs which were available for subsequent follow‐up studies, were subjected to perineal hernia surgery. In thirty‐six dogs the hernia was bilateral and, therefore, 137 hernias were initially operated. In 111 operations the standard perineal technique was adopted. In twenty‐six operations the superficial gluteal muscle was reflected and sutured into the hernial defect (‘gluteal flap’). Later, following recurrence of hernia or new development on the second side, a further sixteen operations were done, including three anal splitting procedures. In all cases the deep sutures were of monofilament nylon. A post‐operative follow‐up was carried out for a minimum period of 12 (average 39) months. The operative and post‐operative complications included superficial and deep wound infection, partial or complete sciatic paralysis, rectal prolapse and recurrence of the hernia following breakdown of the repair, as well as occurrence of the hernia on the opposite side. The success rate (75 per cent excluding six immediate post‐operative fatalities) judged by remission of signs and lack of recurrence was higher in the standard technique (81 per cent) than the gluteal flap method (64 per cent). Anal splitting was unsuccessful and resulted in faecal incontinence. The standard technique was slow, sometimes gave limited exposure but was rarely associated with wound breakdown (13 per cent of operations), though sciatic paralysis was only noted in this procedure. The gluteal flap method was longer, gave excellent exposure with no risk of sciatic nerve damage, but was often associated with wound breakdown (58 per cent). Both techniques led sometimes to rectal prolapse. Castration with hernial repair resulted in a lower recurrence rate (13 per cent v. 20 per cent). Castration should be carried out in all cases of perineal hernia.

Abstract. Ten melanocytomas from 10 cattle were diagnosed by histopathologic examination of biopsy specimens submitted to the Veterinary Medical Diagnostic Laboratory, University of Missouri, between I January 1986 and 3 1 December 1993. One tumor was congenital; the others were first noticed between 2 months and 2 years of age (x = 9.9 months). Six tumors occurred in purebred (3) or crossbred (3) Angus cattle; one tumor each occurred in a Holstein, a Shorthorn, a Simmental, and a beef calf of unrecorded breed or coat color. Five calves were female, and five were male. Five tumors occurred in truncal dermis or subcutis (three in abdominal skin), four occurred on a limb, and one occurred on the jaw. Tumors varied in histologic appearance, but all were pigmented and all had few mitotic figures. Outcome was known for 8/10 cattle. In four cattle followed for at least 1 year, the tumor did not recur after surgical excision. Another heifer had residual gray tissue at the tumor site after surgery but remained in the herd without regrowth of the tumor 30 months after excision. Three other calves were slaughtered within 6 months of excision without apparent recurrence of the tumor.Key words: Cattle; congenital tumor; juvenile; melanocytic nevi; melanocytoma; neoplasia.Melanocytic tumors usually account for 5-6% of all tumors in surveys of bovine n e~p l a s m s~J~,~~,~* and occur most commonly in the s k h 6 J 4 A disproportionate number of reported cases have occurred in India,7,12,16,19,21,23,24,31,32,37 where predominantly gray cattle were affected.23 Black or red cattleI4 have been affected more commonly in Europe and North America. Although melanocytic tumors have been reported in older ~a t t l e ,~J~J~,~~ most cases have occurred in calves younger than 2 years.4,6J4J7Js,29,34,37,39 Neither site nor gender predilection has been apparent. In only a few reported cases has the tumor invaded deeper than the ~u b c u t i s~~~~~ or m e t a~t a s i z e d .~~,~~ The purpose of this retrospective study was to evaluate risk factors, pathologic features, and biologic behavior of bovine cutaneous melanocytic tumors. Materials and MethodsThe Veterinary Medical Diagnostic Laboratory files were searched retrospectively for all cases of melanocytic tumors in cattle from 1 January 1986 through 3 1 December 1993. Ten such tumors were encountered; all were biopsies of cutaneous masses submitted in 10% neutral buffered formalin for routine histologic processing. Paraffin-embedded sections were stained with hematoxylin and eosin. Serial sections of each tumor were also treated with 0.25% potassium permanganate and washed in 5% oxalic acid to bleach melanin before staining with hematoxylin and eosin. Tumors were classified30 as junctional or dermal when possible.