Anemia in salmon aquaculture: Scotland as a case study.

Anemia in salmonid aquaculture is a recognized blood disorder resulting from the reduction of hemoglobin concentration and/or erythrocyte count. Because of sub-optimal oxygen supply to the tissues, as a negative impact of anemia fish will experience reduced growth and poor health. This health challenge may be linked with several factors including anthropogenic changes in the marine environment, infectious etiology (viral, bacterial, and parasitic), nutritional deficiencies, or hemorrhaging. From the mid-late summer of 2017 to 2019, Scottish salmon farming companies began to report the occurrence of anemic events in open-net marine sites. At that time, the industry had little understanding of the pathogenesis and possible mechanisms of anemia and limited the ability to formulate effective mitigation strategies. Clinical examination of fish raised suspicion of anemia and this was confirmed by generating a packed cell volume value by centrifugation of a microhematocrit tube of whole anticoagulated blood. Company health team members, including vets and biologists, reported discoloration of gills and local hemorrhages. This paper reviews various commercially significant cases and lesser-known cases of anemia in cultured salmonid species induced by various biological factors. The current methods available to assess hematology are addressed and some future methods that could be adopted in modern day fish farming are identified. An account of the most recent anemic event in Scottish farmed Atlantic salmon (Salmo salar) is presented and discussed as a case study from information provided by two major Scottish salmon producers. The percent of total marine sites (n = 80) included in this case study, that reported with suspected or clinical anemia covering the period mid-late summer 2017 to 2019, was between 1 and 13%. The findings from this case study suggest that anemia experienced in most cases was regenerative and most likely linked to blood loss from the gills.

Internal jugular vein thrombosis following functional neck dissection.

Twenty-five patients on whom 27 functional neck dissections were performed for upper aerodigestive tract squamous carcinoma were prospectively investigated to determine the frequency of venous thrombosis on the side of the neck dissection. Retrograde venography, performed within 1 month postoperatively, was used to determine the status of the internal jugular vein. Nineteen veins were patent at venography, but ipsilateral occlusion was demonstrated in 8. In 5 of the 8 patients, venous thrombosis followed major wound sepsis or fistula formation. No causes for the remaining 3 cases of internal jugular vein thromboses were identified. Possible mechanisms for "spontaneous" internal jugular vein occlusion following functional neck dissection are endothelial trauma, reduction in venous flow during anesthesia, and the altered coagulability profile of some cancer patients. The finding that functional neck dissection does not always maintain patency of the internal jugular vein is especially important when surgical treatment to the opposite side of the neck is planned, as the surgeon may be faced with an unexpectedly complicated postoperative course.

Human balantidiasis. A case report.

A 58-year-old woman, who presented to hospital with melaena and faecal peritonitis due to a perforated terminal ileum, was found to be infected with Balantidium coli. This protozoan parasite is commonly found in pigs, but can infect man, and may mimic amoebic infection. The diagnosis may be missed unless fresh stools are examined immediately. The patient died from septicaemia.

The Edinburgh intercalated honours BSc in pathology: evaluation of selection methods, undergraduate performance, and postgraduate career.

In a study of 60 students who entered the intercalated honours BSc course in pathology at the University of Edinburgh over 10 years the conventional criteria of academic excellence and motivation were shown to be appropriate for the selection of honours students. When compared with classmates who did not take the intercalated year but who had shown similar high academic ability in the preclinical course the students who had taken the honours BSc did better in the remainder of the undergraduate curriculum. Of 42 honours students, 18 (43%) entered academic careers, particularly in pathology and medicine, but there was no observed tendency for students without honours BSc to do so. Although it is impossible to establish a causal relation between taking the honours course and subsequent academic distinction, the results suggest that the intercalated honours BSc in pathology serves a useful function in introducing able students into academic careers. The findings justify the financial support made available to such students during their intercalated year by the Medical Research Council and the Scottish Education Department.

A comparison of the effects of prednisolone and methylprednisolone on human lymphoblastoid cells.

Methylprednisolone is more effective than prednisolone in mediating long-term cytolysis and immediate inhibition of nucleoside uptake in human lymphoblastoid cells. This suggests that methylation of prednisolone makes it more potent by aiding interaction with a cellular target rather than increasing its stability.

Case report: computed tomographic and scintigraphic appearances of dermatofibrosarcoma protuberans.

The computed tomographic and scintigraphic appearances of dermatofibrosarcoma protuberans involving the mental region are presented. The tumour was demonstrated as a moderately well-defined vascular mass extending from the skin to invade the subcutaneous tissue and strap muscles. Only one case of the imaging features of this rare tumour has been reported previously.

Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.

The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations. Its morphological features suggest that it is an active, inherently programmed phenomenon, and it has been shown that it can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological.The structural changes take place in two discrete stages. The first comprises nuclear and cytoplasmic condensation and breaking up of the cell into a number of membrane-bound, ultrastructurally well-preserved fragments. In the second stage these apoptotic bodies are shed from epithelial-lined surfaces or are taken up by other cells, where they undergo a series of changes resembling in vitro autolysis within phagosomes, and are rapidly degraded by lysosomal enzymes derived from the ingesting cells.Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development. It occurs spontaneously in untreated malignant neoplasms, and participates in at least some types of therapeutically induced tumour regression. It is implicated in both physiological involution and atrophy of various tissues and organs. It can also be triggered by noxious agents, both in the embryo and adult animal.

Effect of methylprednisolone on the nucleoside metabolism of a human lymphoblastoid cell line.

Concentrations of methylprednisolone which have lethal effects on human lymphoblastoid cell lines in vitro cause a reduction both in the uptake of uridine and thymidine into acid-soluble material and their incorporation into acid-insoluble material. These effects are virtually instantaneous, which indicates that they do not depend on alterations in gene activity. Normal uptake of nucleosides into cells is by both simple and facilitated diffusion, and methylprednisolone appears to act directly on the cell surface to inhibit only facilitated diffusion uptake.

Morphological aspects of glucocorticoid-induced cell death in human lymphoblastoid cells.

Morphological aspects of cell death associated with a cytolethal concentration of methylprednisolone sodium succinate (500 micrograms/ml) on the BLA1 lymphoblastoid cell line were studied over a 48-hr incubation period by light, transmission and scanning electron microscopy. Studies revealed two distinctive morphological changes induced by the steroid from 1 hr onwards after treatment. One showed contortion and "blebbing" of the cytoplasm and nucleus accompanied or followed by nuclear pyknosis, resulting in the formation of membrane-bounded bodies containing apparently normal cytoplasmic organelles with or without nuclear fragments. The other showed "rounding up" of the cell with loss of cytoplasmic protrusions and long slender surface processes, aggregation of well-preserved cytoplasmic organelles, accompanied by nuclear pyknosis and fragmentation. In both cases many of the features are typical of apoptosis. The subsequent degeneration of cells and fragments not unexpectedly resembled in vitro autolysis. This in-vitro system is suitable for studying the early biochemical events and intracellular control mechanisms of apoptosis.

Pitfalls in the management of preauricular sinuses.

A total of 159 operations for the excision of a preauricular sinus carried out in 117 patients over an 8-year period were reviewed. Previous excision, the use of a probe to delineate the sinus and operating under local anaesthesia all increased the chance of recurrence. The condition recurred more often in patients who developed post-operative wound sepsis than in those who healed primarily. Means of decreasing the recurrence rate include: (1) meticulous dissection of the sinus by an experienced head and neck surgeon under general anaesthesia; (2) the use of an extended preauricular incision; (3) clearance down to the temporalis fascia to ensure complete removal of all epithelial components; (4) avoidance of sinus rupture; and (5) closure of wound dead space.

Protection from the embryopathic effects of 7-hydroxymethyl-12-methylbenz(a)anthracene by 2-methyl-1,2-bis-(3-pyridyl)1-propanone(metopirone, Ciba) and beta-diethylaminoethyldiphenyl-n-propyl acetate (SKF 525-A).

Pretreatment with Metopirone (40 mg.) or SKF 525-A (2 mg./100 g. maternal body weight) protected aganist the embryotoxic and teratogenic actions of7-OHM-12-MBA) (2.5 mg/100 g. maternal body weight) in the Sprague-Dawley rat. At the doses administered SKF-525-A was a more efficient protector than Metopirone. The adrenocorticolytic actions of 7-OHM-12-MBA in the maternal adrenal glands were also prevented by these compounds and a close correlation existed between the degree of protection of the maternal adrenals and of the foetuses. It is suggested that the ultimate embryopathic substance is a metabolite of 7-OHM-12-MBA.

Reciprocal relationship between the production of adrenal damage by 7,12-dimethylbenz(a)anthracene in rats and the induction of liver damage by various treatments.

Further investigations into the mechanism by which CCl(4) administration to Sprague-Dawley rats protects them against the adrenocorticolytic action of dimethylbenz(a)anthracene (DMBA) are reported. The results show that CCl(4) must be given shortly before DMBA to achieve the best protection and that treatments given after DMBA are ineffective. It was established that the hepatotoxicity of CCl(4) in these experiments was related reciprocally to the adrenocorticolytic effect of DMBA.Protection with butter yellow (DAB) was achieved only when sufficient time elapses for drug metabolism to be stimulated in the liver. Butter yellow given after DMBA has no protective effect but the prior exposure of the rats to DMBA potentiates the hepatotoxic effects of DAB.Partial hepatectomy gives protection when performed 1 day before DMBA; shorter intervals give no protection. Some protection can be achieved with resection 6 or 24 hours after DMBA.

Cytolethal effects of glucocorticoids in human lymphoblastoid cell lines.

Glucocorticoid hormones penetrate rapidly into intact lymphoblastoid cells and are retained with the same high affinity and specificity as with cytoplasmic extracts. Optimal conditions for lethal glucocorticoid responses in vitro were determined for a series of human lymphoblastoid cell lines by using different glucocorticoid preparations, and steroid solvents and by varying the cell density. Kinetic studies revealed that lethal glucocorticoid effects are dose-dependent and that continuous exposure of cells to steroid is necessary for progression of lethal effects to occur. Even under optimal conditions, human lymphoblastoid cells only exhibit a marked cytolethal response to glucocorticoids at concentrations which greatly exceed both physiological and therapeutically attainable steroid levels. They are also greatly in excess of steroid levels required to saturate the cytoplasmic receptors of intact or disrupted lymphoblastoid cells. It is suggested that either lethal steroid mechanisms in vitro differ fundamentally from those in vivo or the pharmacological activity of glucocorticoids in vivo does not involve a direct cytolethal action.

Cytoplasmic receptor levels and glucocorticoid response in human lymphoblastoid cell lines.

The cytolethal response to treatment with prednisolone was investigated in vitro in eight human lymphoblastoid cell lines containing varying concentrations of specific cytoplasmic glucocorticoid receptors. A similar response was observed in seven of the lines irrespective of their concentration of cytoplasmic receptors and pharmacological doses of steroid, well above those required to saturate receptors in cell-free extracts, were required for a massive lethal response. One cell line derived from Burkitt's lymphoma was refractory to lethal effects even with pharmacological doses of steroid. A similar unresponsiveness to the cytolethal effect of prednisolone in vitro was observed in fresh lymphoblasts derived from patients with acute lymphoblastic leukaemia despite evidence of a satisfactory clinical response to therapy which included steroid. The resistance of human lymphoblastoid cells to treatment with glucocorticoids in vitro may result from a defect in activation subsequent to the binding of steroid to cytoplasmic receptors.