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Parotidectomy is the definitive procedure for diagnosis and treatment of most parotid masses but, due to the risk of haematoma and seroma formation, has traditionally included a drain. The drain itself comes with its own risks and, in most hospitals, the need for overnight admission, which has significant cost implications (Mallon et al. Ann R Coll Surg Engl 95(4):258–262; 2013). Fibrin glue, with its haemostatic and adhesive properties, reduces the risk of collection or haematoma and therefore may negate the need for a drain. This is the first study to look at the use of ARTISS as an alternative to drains in parotidectomy. We performed a retrospective study of all the patients who underwent a partial parotidectomy over a 4-year period from 2014 until 2018 under the same senior surgeon. Patients were divided into those that had a drain and those that had ARTISS. Their operative record, inpatient notes and clinic letters were reviewed to record information regarding length of stay, histology, complications and recurrence. A total of 34 patients were identified; 17 ARTISS and 17 drain patients. We showed that the mean length of stay improved significantly from 1.6 days with the drain to 0.5 days with ARTISS (Fig. 1) but without a difference in complication rate (Fig. 2), which was 5/17 (29%) in each group. In conclusion, parotidectomy can be undertaken safely as a day-case procedure with the application of ARTISS. This new approach to parotid surgery not only offers less morbidity for patients but also positive financial revenue for public health institutions.

A BSTRACT.— Reef fish movements over short and long time frames have important consequences for identifying essential fish habitat, quantifying ecological flows across the seascape and designing marine reserves. We use grunts (Haemulidae) as a representative model group for quantifying movement in terms of distances, time scales, temporal patterns, habitat associations and controls. Here, we provide a review based on recent studies and our own experience. The ritualized, twilight feeding migrations of grunts represent an important mechanism for transferring nutrients and organic matter across habitat boundaries, with movements on the order of 100-300 m. Both compass orientation and vision are used for navigation during feeding migrations. Feeding movements of adults are less ritualized in both space and time and typically occur on the same scale of distance as juveniles, although longer excursions have been documented. Ontogenetic migrations occur over years and take the form of discrete habitat shifts, with most individuals moving progressively offshore. Distances and pathways followed by fish will depend on the exact width of the shelf and distribution of suitable habitats. Transplant experiments suggest there are significant barriers to fish migration, and migration corridors, especially reef margins, seem to be important in determining the direction of ontogenetic habitat shifts, but these may be disrupted by environmental perturbations. Theoretical considerations relative to barrier perception and growth-survival trade-offs appear to explain normal movements of grunts and their responses to environmental perturbations, but lack of information on how fish may sense new locations at distance prevents the full use of theory to generate rules of migration covering timing, distance and direction.

The in vitro metabolism of SDZ HDL 376, a thiocarbamide developed for the treatment of atherosclerosis, was investigated in rat, dog, monkey, and human liver microsomes, as well as in rat and human liver slices. [14C]SDZ HDL 376 was extensively metabolized in all the species except human. In rat liver microsomes an S-oxide was the major metabolite. In human and monkey microsomes, carbon hydroxylation was favored. The NADPH-dependent oxidation of SDZ HDL 376 resulted in covalent binding to microsomal protein. Addition of GSH to the incubations decreased protein binding in a concentration-dependent manner and resulted in a novel SDZ HDL 376-GSH adduct. Adduct formation required NADPH and was mediated predominantly by cytochrome P450. Inhibition of cytochrome P450 by 1-aminobenzotriazole resulted in a 95% decrease in adduct formation, while heat inactivation of flavin-containing monooxygenases resulted in a 10% decrease. Unlike other thiocarbamides which form disulfide adducts with GSH, the SDZ HDL 376 adduct contained a thioether linkage as characterized by LC/MS/MS and reference to a synthetic standard. Reactions performed with [35S]GSH resulted in a [35S]SDZ HDL 376-GSH adduct, demonstrating the sulfur was derived from GSH. Adduct formation was faster in rat microsomal reactions compared to human microsomes. Other structurally unrelated thiocarbamides (phenylthiourea, methimazole, 2-mercaptobenzimidazole, 2-mercaptoquinazoline, and 2-propyl-6-thiouracil) did not form similar adducts in rat liver microsomes supplemented with GSH. Therefore, the GSH adduct of SDZ HDL 376 is unique for this type of thiocarbamide. These results suggest that the bioactivation and detoxification of SDZ HDL 376 differ significantly from other thiocarbamides. Furthermore, the in vitro formation of S-oxides and GSH adducts in rat hepatic tissue, and ring hydroxylation and glucuronidation in human hepatic tissue, suggests rats may be more susceptible to the toxicity of SDZ HDL 376 compared to humans.

We developed a technique for applying forced oscillations in flow between 5 and 200 Hz to the lung through an alveolar capsule. This provided measures of the complex alveolar imput impedance of the lung, which we modelled in terms of an elastic alveolar unit connected to the rest of the lung by a peripheral airway. The estimated elastance of the alveolar compartment in 6 normal dogs was about 5 orders of magnitude greater than the elastance of the entire lung. The resistance of the airway leading into the compartment from the rest of the lung was about 5 orders of magnitude greater than the resistance of the entire airway tree. The capsule oscillation technique thus gives mechanical information about an extremely small region of the lung (in the order of 10 mm3 in volume) just under the capsule. A bolus i.v. injection of methacholine caused a variable response in the alveolar regions studied, with some regional elastances and resistances increasing while others decreased, despite the fact that overall lung resistance and elastance always increased. We conclude that our capsule oscillator technique yields precise mechanical information about very small distal regions of the lung, and that these regions respond heterogeneously to injected methacholine.

A description is provided for Verticillium fungicola . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Cultivated mushrooms (the fungus has also been recorded from decaying leaf litter and from the sporophores of other larger Basidiomycetes). DISEASE: Dry bubble, brown spot of mushrooms; ' mole '. Causes light brown superficial irregular spots on caps, later enlarging and coalescing into dark brown blotches. Severe attacks cause mushrooms to become distorted with abnormal swelling of the stipe and the tissues drying out and becoming leathery. The disease occurs either in single or clumps of sporophores. GEOGRAPHICAL DISTRIBUTION: Europe (UK, France, Germany, Switzerland, Netherlands, Romania, Bulgaria, Austria, Denmark); North America (USA); Asia (China, India, Japan); Australia; Africa (S. Africa, Rhodesia). TRANSMISSION: By splash dispersed conidia and contaminated casing soil.

A description is provided for Ascosphaera apis . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Apis mellifera and Megachile spp. DISEASE: Chalkbrood of the honey bee ( Apis mellifera ) with a few poorly documented records on leaf cutting bees Megachile spp. (Melville & Dade, 1944) and M . internis (Baker & Torchio, 1968). The spores are ingested by young larvae and germinate in the gut, breaking out of the hind end when larvae are sealed in their cells prior to pupation. If one strain only is present this forms the typical chalkbrood. If both strains are present a layer of grey cysts forms on the surface of the larva. Larvae are most susceptible at 3-4 days old and are then chilled briefly immediately after sealing. Although fatal to the larvae, this rarely destroys a whole colony and individual dead larvae are ejected by the bees. Ascospores persist many years providing periodic trouble in adverse conditions. GEOGRAPHICAL DISTRIBUTION: Europe; USA. Until 1968 chalkbrood was considered to be a European disease and it was only in 1971 that it became recognised as of economic importance in USA (Hitchcock & Christensen, 1972). TRANSMISSION: By ascospores within the cells of the comb to young larvae. From hive to hive probably by robber bees. More prevalent in cold, wet summers.

A description is provided for Mycogone rosea . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Cultivated mushrooms, Amanita rubescens, A. caesaraea, Inocybe sp., Trichloma terreum , termite fungus garden. DISEASE: A disease of mushroom similar to 'wet bubble' in some respects. Causes dark brown discoloration of caps with underlying tissues stained yellow. May cause small depressions in the cap under which the tissues are discoloured dark brown; alternate zoning of white and brown on the affected area is also sometimes found (18, 570). GEOGRAPHICAL DISTRIBUTION: Reported from Britain, Germany, Uganda, Hungary and (?) New South Wales (Australia), but probably more widely distributed in regions where edible fungi are cultivated (49, 1869; 41, 275). TRANSMISSION: Probably by spores and mycelium in soil. Mycelium and spores have been shown to be infective (570).

A description is provided for Entomophthora grylli . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Orthoptera; nymph and adults of grasshoppers and locusts; there have also been records on Lepidoptera, Diptera and Coleoptera (MacLeod & Muller-Kogler, 1973). GEOGRAPHICAL DISTRIBUTION: Europe, including Britain; Canada; East, Central and South Africa. Fresenius quotes a record at 6000 ft near St. Moritz. DISEASE: The disease, causing epizootics in red locusts, Cyrtacanthacra septemfasciata ( Nomadacris septemfasciata ), in S. Africa is described by Skaife (1925). Infection is by germinating conidia which penetrate the integument. Dying insects characteristically climb up grass stems and die, apparently embracing the stem. The body becomes soft and easily disintegrates. The abdomen curls upward and backwards. Shortly after death a white, buff or greenish furry growth appears from the intersegmental membrane, leg joints, junction of the head and thorax and at the base of the antennae. The growth is made up of club-shaped conidiogenous cells which forcibly discharge conidia around the dead insect. Conidia, coated with the sticky contents of the conidiophore, are discharged in the evening, when the insects are clustered together and adhere to the surface of healthy individuals. A total of about 1% of locusts throughout the season die showing no external growth but are filled with resting spores; other individuals appear to be immune.

A description is provided for Cordyceps militaris . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: A wide range of Lepidoptera , larvae and pupae; has also been reported on pupae of Coleoptera and on certain Hymenoptera (Willis, 1959). Experimental infection of Bombyx mori by conidia is reported by Latge & Vey (1974). GEOGRAPHICAL DISTRIBUTION: World wide. DISEASE: Ascospore parts germinate on a suitable host by one or more germ tubes which penetrate the integument. Hyphal bodies form in the haemocoel which bud, filling it with unicellular bodies which finally adhere in chains filling the entire body cavity. The host dies and its cadaver shrinks, the hyphal chains becoming compact. Slender hyphae penetrate the gut and other tissues, the mass becomes hardened into an endosclerotium and the integument distended to near normal size. Stromata later arise from the sclerotium.

A description is provided for Cordyceps dipterigena . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Diptera ( Muscidae ). GEOGRAPHICAL DISTRIBUTION: Widespread in tropical countries; Sri Lanka, Indonesia, New Guinea, North, Central and South America, Japan, Ghana.

A description is provided for Metarhizium anisopliae . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Wide range of insects, including Orthoptera, Coleoptera, Lepidoptera, Hemiptera and Hymenoptera , also Arachnida , from soil and from a crocodile (Austwick in Tulloch, 1976). Latch (1965) quotes 166 insect species attacked in nature, and Veen (1968) lists 204 hosts under their respective orders from the literature up to 1965. GEOGRAPHICAL DISTRIBUTION: World wide. DISEASE: The green muscardine fungus. Entry is probably both by ingestion of spores and by penetration through the integument. For an account of the work of Zacharuk (1970-1974) on the germination of spores, formation of appressorial cells, penetrant pegs through the epicuticle and sub-epicuticular penetrant plates giving rise to hyphal bodies that circulate in thehaemolymph, see Ferron (1978). All stages of the host are affected, chlamydospores forming in the cadaver and subsequently germinating to produce the familiar green spores on the surface. On a given host, strains vary in their virulence (Ferron, 1978). The fungus causes an economically important disease of silkworms, and Veen (1968) gives an account of the disease in the locust.

A description is provided for Gibellula pulchra . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Spiders. The conspicuous synnemata only develop after the host has died and are frequently found on the under side of leaves. GEOGRAPHICAL DISTRIBUTION: World wide but especially in the tropics where it is thought to exert a natural control over the spider population in the forests (Evans, 1974).

A description is provided for Sarocladium attenuatum . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Oryza sativa (rice). DISEASE: Sheath rot. The symptoms are similar to those of sheath rot associated with S. oryzae . GEOGRAPHICAL DISTRIBUTION: India, Sri Lanka, Nigeria, Gambia, Mexico, USA. The distributions of S. attenuatum and S. oryzae overlap and many records of S. attenuatum must have been included in that of ' Acrocylindrium oryzae ' before a distinction between the two species had been drawn, but S. attenuatum alone has been recorded for America and S. oryzae only in S.E. Asia. TRANSMISSION: Sarcocladium attenuatum has been isolated from Nilaparvata lugers , the brown plant hopper of rice (CMI records), which might suggest a similar role to that suggested for other rice pests and S. oryzae . Seedborne (56, 5628).

A description is provided for Beauveria brongniartii . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Attacks all stages of a wide range of insects; man. DISEASE: The 'white muscardine' as used by early workers. GEOGRAPHICAL DISTRIBUTION: World wide.

A description is provided for Hirsutella citriformis . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: H. citriformis has been recorded mainly from Hemiptera . GEOGRAPHICAL DISTRIBUTION: Africa, Asia, New Zealand, Hawaii, Solomon Islands. DISEASE: Hirsutella citriformis parasitises the brown plant hopper of rice, Nilaparvata lugens . As N. lugens causes serious outbreaks in the Solomon Islands and elsewhere, and is the vector of the grassy stunt virus of rice, H. citriformis has been considered for its control. Strains are listed as available at the Institute fur Biologische Schfidlingsbekfimpfung, Heinrichstrasse 243, 61 Darmstadt, German Federal Republic (Bulletin SROP 1973/3).

A description is provided for Verticillium psalliotae . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On cultivated mushrooms ( Agaricus spp.), on rust fungi, and in soil, and as an endoparasite of Rhophalomyces elegans (Phycomycetes). DISEASE: Causes brown spotting of the cap and pileus of cultivated mushrooms, often with distorted growth and subsequent shrivelling of the fruit bodies resulting in large losses. Similar in effects on the host to V. fungicola . GEOGRAPHICAL DISTRIBUTION: North America and Europe. TRANSMISSION: By spores in water and air, and by mycelial contamination of compost and casing soil.

A description is provided for Beauveria bassiana . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS & SUBSTRATA: All stages of insects of all groups; lungs of wild rodents, nasal swab of horse; man; giant tortoise. The fungus overwinters in vegetable matter and is found in the soil. DISEASE: The fungus has been known since 1835 as the cause of the muscardine disease of silkworms. Although B. bassiana has multiplied in bees in laboratory tests it has so far not been recorded from bees in nature (Bailey, 1971). According to Wasti & Hartman (1975) penetration of the cuticle of gypsy moth ( Porthetria dispar [Lymantria dispar] ) larvae takes place 24 h after 2nd instar larvae have crawled over a culture of B. bassiana and within 64h the interior of the insect is completely filled with hyphae. These authors also note penetration of the gut wall. Fargues & Vey (1974), who sprayed conidia on to 3rd instar larvae of Leptinostarsa decemlineata (Colorado beetle), showed that conidia germinate on the surface of the integument, penetrate the loosening skin, and blastospores develop in the moulting fluid, infecting the new integument as it forms. Some individuals cannot finish the moult, in others the delicate new skin ruptures and hyphae enter the haemolymph. GEOGRAPHICAL DISTRIBUTION: World wide.

A description is provided for Verticillium lecanii . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS & SUBSTRATA: Parasitises all stages of development of insects of all groups and Arachnida ; hyperparasitises rust fungi and macrofungi; found on plant material, soil, surface of optical glass. For the literature of fungal hypoparasitism see Domsch & Gams. GEOGRAPHICAL DISTRIBUTION: World wide. DISEASE: Referring to it as the 'farmer's friend', Viegas described the white halo formed by the fungus around dead Coccus (Lecanium) viridis scale insects on the coffee plant. Aerial hyphae arising from dead hosts and covering the body are characteristic.

A description is provided for Metarhizium flavoviride . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Larvae and pupae of the curculionids (weevils), Ceutorrhynchus macula-alba and C. albovittatus, Otiorhynchus sulcatus and soil. GEOGRAPHICAL DISTRIBUTION: Europe (France, Germany, Netherlands, Czechoslovakia).

A description is provided for Sarocladium oryzae . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Oryza sativa (rice). DISEASE: Sheath rot. This occurs in the upper leaf sheath enclosing young panicles and starts as oblong or irregular lesions with brownish margins and greyish centres, 0.5-1.5 cm long, which later enlarge and coalesce. Whitish mycelium may be seen in the centre of the lesions and occasionally inside the rotted sheaths. Severely affected panicles do not emerge, the effect being known as choking. The symptoms are evidently indistinguishable from those associated with S. attenuatum . GEOGRAPHICAL DISTRIBUTION: India, Bangladesh, Brunei, Kenya, Nigeria. Although it is not always possible when ' Acrocydndrium oryzae ' is reported in the earlier literature to know whether S. oryzae or S. attenuatum is intended, the distribution of the former extends into S.E. Asia and the latter into N. America. TRANSMISSION: By conidial dispersal. Fungal attack is often associated with damage by pests - the boring beetle, Corticarina gibbosa (Amin et al. ) or the mite Steneotarsonemus madecassus (Hsieh et al. , 1977 with ' Acrocylindrium oryzae ') and S. spinki (Chien & Huang, 1979).

A description is provided for Mycogone perniciosa . Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Cultivated mushrooms, Pluteus sp., Coprinus sp., Panaeolus campanulatus, P. campestris . DISEASE: Wet bubble disease, white mould. A serious mushroom disease appearing at an early stage as a white mycelial growth causing deformation of the gills and covering the cap. Total mycelial disorganization ensues with diseased carpophores exuding a brown malodorous liquid. GEOGRAPHICAL DISTRIBUTION: In most parts of Europe, North America, Asia and Australasia where mushrooms are cultivated on a large scale. TRANSMISSION: By spread of spores and mycelial inoculum through watering and use of conlaminated compost, soil and implements. Air-borne spore dispersal is not considered important (47, 3661). Experimental inoculation through soil has been found to be more effective than direct application of the fungus to the sporophore (47, 1742).