Healthcare professionals in research (HPiR) Facebook community: a survey of U.K. doctoral and postdoctoral healthcare professionals outside of medicine.

BACKGROUND: Healthcare professionals outside of medicine (HCPs), including nurses, midwives and allied health professionals, are increasingly involved in research for patient benefit. Their challenge is to negotiate inter-professional or professionally isolated contexts. The aims of this study were to evaluate the 'Healthcare Professionals in Research' (HPiR) Facebook group (a self-directed and confidential peer support group for doctoral and postdoctoral HCPs) including engagement, the experiences of doctoral and postdoctoral HPiR members and to identify future career challenges using an on-line survey. METHODS: The HPiR Facebook group was launched in May 2019. Five HCP Community managers (CMs) were trained in on-line platform curation, moderation and screening. An on-line survey was designed to capture data from HPiR members. A purposive sampling approach was applied. Respondents were required to be doctoral and postdoctoral HCPs and a registered member of the HPiR group. Respondents represented a range of healthcare professions, 79 % of whom had over ten years clinical experience. Membership growth and engagement was analysed. Descriptive statistics were used to present numerical data. Qualitative data were analysed thematically. RESULTS: 96 members were admitted to the group within the first month. All members were actively engaged with group content. 34/96 doctoral and postdoctoral HCPs completed the survey. Most members joined for networking (88 %) and peer support (82 %) purposes. Analysis of text responses showed difficulties in balancing a clinical academic career and highlighted the consequences of undefined clinical academic roles and pathways. CONCLUSIONS: Doctoral and postdoctoral HCPs value the opportunities that HPiR provides for peer support and connection with fellow HCPs. HPiR has the potential to strengthen research capacity, support research skill development and drive change within the clinical academic community. Clinical academic roles and pathways need to be standardised. The creation of opportunities beyond doctoral studies is a priority.

Diagnostic and therapeutic practices in adult chronic nonbacterial osteomyelitis (CNO).

BACKGROUND: Chronic nonbacterial osteomyelitis (CNO) is a rare, and impactful auto-inflammatory bone disease occurring in children and adults. Clinical care for CNO is challenging, as the condition lacks validated classification criteria and evidence-based therapies. This study aimed to map the current diagnostic and therapeutic practices for CNO in adults, as a first step towards a standardized disease definition and future consensus treatment plans. METHODS: A primary survey was spread among global rheumatological/bone networks and 57 experts as identified from literature (May 2022), covering terminology, diagnostic tools (clinical, radiological, biochemical) and treatment steps. A secondary survey (sent to primary survey responders in August 2022) further queried key diagnostic features, treatment motivations, disease activity and treatment response monitoring. RESULTS: 36 and 23 physicians completed the primary and secondary survey respectively. Diagnosis was mainly based on individual physician assessment, in which the combination of chronic relapsing-remitting bone pain with radiologically-proven osteitis/osteomyelitis, sclerosis, hyperostosis and increased isotope uptake on bone scintigraphy were reported indicative of CNO. Physicians appeared more likely to refer to the condition as synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome in the presence of joint and skin pathology. MRI was most frequently performed, and the preferred diagnostic test for 47%. X-rays were second-most frequently used, although considered least informative of all available tools. Typical imaging features reported were hyperostosis, osteitis, osteosclerosis, bone marrow edema, while degeneration, soft tissue calcification, and ankylosis were not regarded characteristic. Inflammation markers and bone markers were generally regarded unhelpful for diagnostic and monitoring purposes and physicians infrequently performed bone biopsies. Management strategies diverged, including indications for treatment, response monitoring and declaration of remission. Step-1 treatment consisted of non-steroidal anti-inflammatory drugs/COX-2 inhibitors (83%). Common step 2-3 treatments were pamidronate, methotrexate, and TNF-a-inhibition (anti-TNFα), the latter two regarded especially convenient to co-target extra-skeletal inflammation in SAPHO syndrome. Overall pamidronate and anti-TNFα and were considered the most effective treatments. CONCLUSIONS: Following from our survey data, adult CNO is a broad and insufficiently characterized disease spectrum, including extra-osseous features. MRI is the favoured imaging diagnostic, and management strategies vary significantly. Overall, pamidronate and anti-TNFα are regarded most successful. The results lay out current practices for adult CNO, which may serve as backbone for a future consensus clinical guideline.

'Sink or swim': an evaluation of the clinical characteristics of individuals with high bone mass.

SUMMARY: High bone mineral density on routine dual energy X-ray absorptiometry (DXA) may indicate an underlying skeletal dysplasia. Two hundred fifty-eight individuals with unexplained high bone mass (HBM), 236 relatives (41% with HBM) and 58 spouses were studied. Cases could not float, had mandible enlargement, extra bone, broad frames, larger shoe sizes and increased body mass index (BMI). HBM cases may harbour an underlying genetic disorder. INTRODUCTION: High bone mineral density is a sporadic incidental finding on routine DXA scanning of apparently asymptomatic individuals. Such individuals may have an underlying skeletal dysplasia, as seen in LRP5 mutations. We aimed to characterize unexplained HBM and determine the potential for an underlying skeletal dysplasia. METHODS: Two hundred fifty-eight individuals with unexplained HBM (defined as L1 Z-score ≥ +3.2 plus total hip Z-score ≥ +1.2, or total hip Z-score ≥ +3.2) were recruited from 15 UK centres, by screening 335,115 DXA scans. Unexplained HBM affected 0.181% of DXA scans. Next 236 relatives were recruited of whom 94 (41%) had HBM (defined as L1 Z-score + total hip Z-score ≥ +3.2). Fifty-eight spouses were also recruited together with the unaffected relatives as controls. Phenotypes of cases and controls, obtained from clinical assessment, were compared using random-effects linear and logistic regression models, clustered by family, adjusted for confounders, including age and sex. RESULTS: Individuals with unexplained HBM had an excess of sinking when swimming (7.11 [3.65, 13.84], p < 0.001; adjusted odds ratio with 95% confidence interval shown), mandible enlargement (4.16 [2.34, 7.39], p < 0.001), extra bone at tendon/ligament insertions (2.07 [1.13, 3.78], p = 0.018) and broad frame (3.55 [2.12, 5.95], p < 0.001). HBM cases also had a larger shoe size (mean difference 0.4 [0.1, 0.7] UK sizes, p = 0.009) and increased BMI (mean difference 2.2 [1.3, 3.1] kg/m(2), p < 0.001). CONCLUSION: Individuals with unexplained HBM have an excess of clinical characteristics associated with skeletal dysplasia and their relatives are commonly affected, suggesting many may harbour an underlying genetic disorder affecting bone mass.

In vivo paracrine interaction between urokinase and its receptor: effect on tumor cell invasion.

Numerous studies have linked the production of increased levels of urokinase type plasminogen activator (uPA) with the malignant phenotype. It has also been shown that a specific cell surface receptor can bind uPA through a domain distinct and distant from the proteolytic domain. In an in vivo model of invasion, consisting of experimentally modified chorioallantoic membrane (CAM) of a chick embryo, only cells that concurrently expressed both uPA and a receptor for uPA, and in which the receptor was saturated with uPA, were efficient in invasion. To test whether uPA produced by one cell can, in a paracrine fashion, affect the invasive capacity of a receptor-expressing cell, we transfected LB6 mouse cells with human uPA (LB6[uPA]), or human uPA-receptor cDNA (LB6[uPAR]). LB6(uPA) cells released into the medium 1-2 Ploug units of human uPA per 10(6) cells in 24 h. The LB6(uPAR) cells expressed on their surface approximately 12,000 high affinity (Kd 1.7 x 10(-10) M uPA binding sites per cell. Unlabeled LB6(uPA) and 125-IUdR-labeled LB6(uPAR) cells were coinoculated onto experimentally wounded and resealed CAMs and their invasion was compared to that of homologous mixtures of labeled and unlabeled LB6(uPAR) or LB6(uPA) cells. Concurrent presence of both cell types in the CAMs resulted in a 1.8-fold increase of invasion of the uPA-receptor expressing cells. A four-fold stimulation of invasion was observed when cells were cocultured in vitro, prior to in vivo inoculation. Enhancement of invasion was prevented in both sets of experiments by treatment with specific antihuman uPA antibodies, indicating that uPA was the main mediator of the invasion-enhancing, paracrine effect on the receptor-expressing cells.

Cell-mediated immunity and serum blocking factors in cancer patients during chemotherapy and immunotherapy.

The leukocyte adherence inhibition test was used to monitor tumor-specific cell-mediated immunity in 15 patients who had a variety of malignant tumors and were undergoing chemotherapy alone or in combination with immunotherapy by Corynebacterium parvum. A rapid and prolonged loss of cell-mediated immunity in blood leukocytes was observed after treatment in all but one of the patients studied. Abolition of reactivity was due to the lack of production of the soluble lymphokine-like factor affecting leukocyte adherence to glass. A new phenomenon of adherence stimulation by antigen, also mediated by a soluble factor, was observed after treatment in some patients. A drop in titer or total abrogation of serum blocking factors occurred in six of six patients tested following chemotherapy or immunotherapy. The lowered levels of blocking activity persisted during treatment and, with the possible exception of one patient, were not correlated with clinical benefit.

Electrocardiographic monitoring of cardiac transplants in mice.

In the murine cardiac model for vascularised transplantation graft function may be monitored by direct palpation, electrocardiography, and graft histology. To assess the merits of these methods, and to measure ischaemic damage, isografts and allografts were examined at regular intervals from 0 to 60 days after grafting. Heart transplants were vascularised from the abdominal great vessels, using microsurgical techniques, with ischaemic times of less than 60 min. Isografts showed no decrease in heart rate over 60 days, as measured by palpation and electrocardiography, but the voltage of the ventricular complex fell progressively over the first 28 days after grafting then remained stable for more than 60 days. The voltage drop was associated with atrophy of myocardial tissue. Allografts in recipients treated with rabbit antimouse antilymphocyte serum were maintained for more than 60 days with little change in palpation rate or recorded heart rate but with significant falls in ventricular complex voltage, reflecting myocardial atrophy and fibrosis. Untreated allografts were rejected in 10-14 days and showed a rapid fall in palpated heart rate, measured heart rate, and ventricular complex voltage. Thus, in this study, palpation of the heart graft gave an accurate measure of the pulse rate and correlated with electrical activity in acutely rejecting grafts, but in long surviving grafts measurement of ventricular complex voltage showed myocardial damage that was not detectable by direct palpation.

Inhibition of whole blood antibody dependent cellular cytotoxicity by heat aggregated human IgG.

Inhibition of the whole blood antibody dependent cellular cytotoxicity (ADCC) of a lymphoblastoid cell line by heat aggregated human IgG (HAI) is described. Optimal sensitising antibody and effector cell concentrations were established to permit the detection of 0.1 microgram/ml HAI. Conditions which avoid the ADCC inhibitory effects of normal human sera were defined. Twelve paired normal human sera were stored at -70 degrees C for prolonged (greater than 3 years) and shorter (less than 6 months) periods of time. Sensitised sheep red cells were used to determine complement depletion in serum dilutions heated at 40 degrees C, 45 degrees C, 50 degrees C. Concentrations of human IgG (1 000-0.1 microgram/ml) were prepared in foetal calf serum before heating at 63 degrees C for 30 min to aggregate the IgG. ADCC inhibitory activity, frequently characteristic of normal human serum was minimised (less than 10%) when sera were stored at -70 degrees C and heated to 50 degrees C for 30 min to inactivate serum complement. This assay provides an economical, reproducible and sensitive test for the detection of circulating IgG complexes.

Leucocyte migration inhibition test in cadaveric renal transplantation.

The leucocyte migration inhibition test has been studied in a series of 192 renal allograft recipients. Seventy-seven patients showed no evidence of inhibition in the early post-transplant course, but 31 of these demonstrated clinical evidence of rejection, a false-negative rate of 16%. The remaining 115 recipients all demonstrated inhibition, with 13 of these showing no clinical evidence of rejection, a false-positive rate of 6.7%. Early antirejection therapy on the basis of inhibition did not result in improved kidney survival when compared with those recipients who did not receive specific therapy until there was clinical evidence of rejection. The leucocyte migration inhibition test did not detect changes attributable to humoral factors, which probably accounts for the high false-negative rate, and has not proved to be sufficiently reliable to be of value clinically as a single test. A combination of tests designed to detect both humoral and cellular factors responsible for rejection deserves further study.

T suppressor cells induced by transfusions and cyclosporine. Studies in the murine cardiac allograft model.

Pregraft transfusion combined with immunosuppression at the time of grafting improves the survival of clinical and experimental allografts. The mechanisms responsible for this effect were investigated in the murine model of cardiac transplantation, combining transfusions 7 to 30 days prior to transplantation with cyclosporine 100 mg/kg, 7 to 20 days pregraft or on days 0, 4, and 6 after grafting. Pregraft DST, third-party blood, and CsA all improved graft survival in the BALB/c-to-CBA donor-recipient combination. In animals treated with DST at 14 days pregrafting, 4/9 grafts survived for greater than 100 days. In those given C57BL/6 blood, or CsA on days 0, 4, 6 postgraft, 1/9 grafts survived for greater than 100 days. When 10(7) spleen cells from DST-treated CBA mice with long-surviving BALB/c heart grafts were transferred to naive CBA mice that then received a BALB/c heart 24 hr later, the transferred cells prolonged graft survival, with all grafts functioning at greater than 40 days, and 4/7 at greater than 100 days. Selective removal of T cells from the spleen cell population prior to transfer showed that L3T4+ T cells, but not Ly-2+ T cells, were required to maintain BALB/c allografts. Combining a short course of CsA with DST was more effective than either treatment alone. The most effective combined treatment was DST at day -14 with 100 mg/kg CsA given on days 0, 4, and 6 postgrafting (8/10 grafts survived greater than 100 days). This treatment also induced splenic suppressor T cells of the L3T4+ Ly-2- phenotype. These results clearly show that L3T4+ splenic T suppressor cells are induced by donor-specific blood transfusion with or without CsA treatment, and that these cells play a role in maintaining long-term tolerance to allografts in the mouse heart transplant model.

Adverse influence of recipient lymphoid resistance to in vitro immunosuppression on the outcome of kidney transplants.

The study investigated whether preoperative in vitro sensitivity of lymphocytes from potential renal transplant recipients could identify patients at increased risk of acute rejection following transplantation and immunosuppression with cyclosporine, azathioprine, and prednisolone. Mixed lymphocyte culture responses were measured preoperatively in the presence of methylprednisolone, CsA, and antithymocyte globulin, and without immunosuppressive agents in 50 transfused recipients of primary cadaver renal transplants. Patients were classified as sensitive if all three immunosuppressive agents produced more than 50% inhibition of their MLC responses, and as resistant if one or more agents failed to produce 50% inhibition. All patients received postoperatively a standardized triple immunosuppressive regimen. Acute rejection was confirmed histologically and treated with Pred with or without ATG or monoclonal antibody OKT3. A total of 29 patients (58%) were sensitive and 21 (42%) were resistant; 4 patients were resistant to 3 agents, 5 were resistant to MP and ATG, 6 were resistant to MP and CsA, and 6 were resistant to MP alone. Sensitive and resistant groups did not differ in age, sex, transfusion history, HLA A, B and DR mismatches or duration of follow-up. The resistant group had a higher rate of graft loss from acute rejection (chi 2 = 6.0, d.f. = 1, P less than 0.02), more episodes of acute rejection (chi 2 = 8.7, d.f. = 3, P less than 0.05), and a higher proportion of patients in whom reflux nephropathy was the cause of renal failure (chi 2 = 18.3, d.f. = 1, P less than 0.001). The resistant group also had a higher proportion of highly sensitized patients and higher serum creatinine concentrations than the sensitive group, although the differences did not reach statistical significance. The study indicates that patients at high risk of acute rejection of renal allografts can be identified by a pretransplant in vitro assay, a finding that could influence recipient selection and immunosuppression.

Evidence that an anthracycline-anti-CD8 immunoconjugate, idarubicin-anti-Ly-2.1, prolongs heart allograft survival in mice.

To examine the potential use of immunoconjugates of drugs and antibodies as immunosuppressive agents, mice were treated with a short course (4 days) of T-cell-specific anti-Ly-2.1 monoclonal antibody, or MAB conjugated to an anthracycline, idarubicin (IDA). The anti-Ly-2.1 MAB had no significant effect on the survival of BALB/c (Ly-2.2) heart allografts in CBA (Ly-2.1) mice, but was a potent immunosuppressive agent when coupled to IDA, with most grafts surviving for > 100 days following treatment with doses ranging from 10 to 120 micrograms IDA, covalently coupled to 1-8 mg MAB. IDA-MAB treated mice with long-surviving heart grafts showed donor-specific tolerance. They did not reject donor-type skin grafts (these survived for > 50 days), but rejected third-party skin in 10-14 days. Heart allografts in these mice survived for > 100 days. Allografts placed 30 days after treatment were rejected, showing a recovery of peripheral T cell function at this time. Newly derived thymic T cells were, however, not required for this recovery since adult thymectomized, IDA-MAB treated animals also recovered T cell function and rejected heart allografts. FACScan analysis of T cells from mice treated with 80 micrograms IDA-4 mg MAB, which had received a heart allograft, showed 95% T cell depletion in the spleen compared with ungrafted, IDA-MAB treated animals, and untreated controls with or without allografts. Splenic T cell depletion was however not significant in CBA mice immunosuppressed with the lower dose of 10 micrograms IDA-MAB. Thus rapid depletion of splenic T cells was not required for immunosuppression induced by IDA-MAB conjugates. However, the minor subpopulation of Ly-2+, which was activated by alloantigen while carrying IDA-MAB, may be depleted during the T cell response to the allograft, resulting in a state of alloantigen-specific tolerance in mice with long-surviving heart allografts.

Technetium-99m-MDP patterns in patients with painful shoulder lesions.

UNLABELLED: There is no consensus on the optimum mode of imaging in patients with painful shoulder lesions. There is a particular paucity of scintigraphic data. As a result, the strengths and weaknesses of scintigraphy cannot be adequately compared to other imaging techniques used in shoulder imaging. This study evaluated whether specific patterns of scintigraphic abnormality could be detected in patients with painful shoulders seen in rheumatological practice using 99mTc-methylene diphosphonate (MDP). METHODS: Scintigraphic abnormalities were recorded in consecutive patients presenting to a rheumatology clinic with unilateral shoulder pain. Patients were subdivided according to patterns of clinical abnormality consistent with a working diagnosis of a lesion located in the subacromial region, adhesive capsulitis (frozen shoulder) or a lesion likely to be located in the glenohumeral joint. Patterns of radiopharmaceutical distribution in different regions of the shoulder were evaluated in the light of clinical data and the results of shoulder radiographs. RESULTS: Technetium-99m-MDP scans were abnormal in 19 of 24 (79%) patients, and radiographs were abnormal in 8 of 24 (33%) patients. Distinct patterns of 99mTc-MDP image abnormality were identified: an increase in 99mTc-MDP uptake in the coracoid, acromion and medial humeral head on anterior planar images, together with an absence of posterior planar image abnormality, frequently occurred in association with a working diagnosis of a lesion located in the subacromial region. Posterior planar 99mTc-MDP image abnormalities always occurred in patients with clinical features consistent with a diagnosis of adhesive capsulitis. There was an 85% agreement between two observers' scores when 99mTc-MDP distribution in specific shoulder regions was graded. CONCLUSION: Distinct patterns of 99mTc-MDP distribution may be associated with clinically-distinct patterns of abnormality in patients with painful shoulder lesions. Further studies to elucidate a role for 99mTc-MDP scintigraphy in this patient group are warranted.

Samarium-153-particulate hydroxyapatite radiation synovectomy: biodistribution data for chronic knee synovitis.

UNLABELLED: Biodistribution data for the radiation synovectomy agent samarium-153-particulate hydroxyapatite (153Sm-PHYP) are reported. METHODS: Mean extra-articular activity accumulation calculated from serial whole-body scans in 13 patients treated for chronic knee synovitis was 0.74% of injected activity (range 0%-3%). RESULTS: In four patients (31%), activity was noted in the lung (mean 0.68% of injected activity). In six patients (46%), 0.29% of injected activity accumulated in the regional lymph nodes and in three patients (23%), 0.62% of injected dose accumulated in the liver. Absorbed dose estimates were lung: 14 mGy, regional lymph nodes; 50 mGy, liver; 4 mGy. SPECT demonstrated good distribution of 153Sm-PHYP throughout the anterior knee compartments, although distribution to the posterior compartment was variable. CONCLUSION: Distribution is dependent on adequate knee flexion immediately following injection and may be influenced by the size range of labeled particles. Favorable biodistribution data suggest that 153Sm-PHYP is a potentially useful radiation synovectomy agent.

Acceleration of B16 melanoma growth in mice after blood transfusion.

Evidence suggests that blood transfusions depress immunologic reactivity; as some tumors are influenced by the immune status of their host, it is possible that transfusions could promote tumor growth by impairing host immunity. The influence of blood transfusion on the growth of a transplantable B16 melanoma was examined in nude (athymic) CBA mice and immunocompetent C57 BL/6J mice. Recipients were given infusions of saline solution or syngeneic or H-2-incompatible allogeneic blood transfusions on two occasions 3 days apart. Infusions were begun 10 days before inoculation of a single cell suspension of B16 melanoma. Growth was determined by measurements of primary tumor volume and tumor weight after excision. There was no statistically significant difference in tumor size or weight between the three recipient groups of athymic mice. However, immunocompetent mice given H-2-incompatible allogeneic blood had higher rates of tumor engraftment--saline solution recipients versus allogeneic recipients: chi 2 = 13.2, df = 1, p less than 0.001; syngeneic recipients versus allogeneic recipients: chi 2 = 2.97, df = 1, p greater than 0.05. In the allogeneic group significantly larger and heavier tumors developed than in mice given syngeneic blood or saline solution. The study indicates that H-2-incompatible allogeneic blood transfusions can influence the growth of a transplantable murine tumor by a mechanism that involves a cell-mediated immune response.

The effect of operative ischemia in murine cardiac transplantation: isograft control studies.

Isograft studies were performed in the murine model of cardiac transplantation to investigate the morphologic effects of operative ischemia. Primarily vascularized CBA mouse hearts were grafted heterotopically into the recipient CBA mouse's abdomen with standard microsurgical techniques. After ischemia times of 30 and 60 minutes, histologic examination showed minimal myocardial damage, with necrosis or scarring occupying less than 5% of the cross-sectional area of hearts bisected from apex to base after grafts had been removed on the seventh day after transplantation. Maximal ischemic damage was seen at 7 days after transplantation after 120 minutes of ischemia, with more than 30% myocardial necrosis or scarring of myocardial tissue. Isografts performed with ischemia times of less than 60 minutes were followed for more than 100 days. All hearts showed a fine, generalized, perimyocytic fibrosis, which was maximal at 28 days after transplantation and did not progress thereafter. These results will serve as important control measures for future studies in this model because ischemic damage must be considered in examining histologic samples from long-surviving cardiac allografts maintained in immunosuppressed recipients.

Skin cancer in Caucasian renal allograft recipients living in a subtropical climate.

Between September, 1969, and December, 1978, 290 patients received 325 cadaveric renal allografts; 11 others transplanted elsewhere were also observed. Cancers developed in 28 patients (9.3%); 26 of these (93%) had skin cancers. The incidence of skin cancer increased by 5% annually after the first year of graft function, to a cumulative 44% in those surviving 9 years with functioning grafts. This represents an incidence of 4,356/100,000 person years of post-transplant risk--20.6 times the annual incidence of skin cancer in the general population of Southern Queensland. Half of the patients had multiple tumors when the first skin cancer was diagnosed, after a mean latent interval of 34 months. A total of 138 skin cancers occurred in 26 patients (average, 5.3 per patient), with a maximum of 19 in one individual. The ratio of basal to squamous cell carcinoma was reversed from 4:1, in the general population, to 1:1.7. Conventional surgical excision gave satisfactory results, with the one local recurrence being controlled by reexcision. Two patients (7%) died of melanoma and metastatic squamous cell carcinoma, respectively, whereas two of the other four patients who died from cancer had coincidental skin cancer. The two skin cancer deaths represent only 2% of all deaths in allograft recipients. These results suggest that the problem of skin cancer in these patients can be controlled and thus is not a significant contraindication to the continued clinical use of cadaveric renal transplantation.

Surgery in Australia.

More than 4000 surgeons in Australia provide services to 17.6 million people living in the world's driest continent, with a land mass comparable to that of the United States. The problem of distance has been overcome in large part for the 17% of the population who live in remote areas by modern communication systems and by the Flying Doctor and Flying Surgeon services. For the remaining population, largely clustered on the fertile eastern seaboard, surgical services rival the best in the world, and surgical training, under the control of The Royal Australasian College of Surgeons, has set an example for which Australia can be justifiably proud.

The Annual Scientific Congress of the Royal Australasian College of Surgeons.

The Royal Australasian College of Surgeons (RACS) is responsible for the training, examination, and recertification of its fellows, who make up the great majority of the practicing specialist surgeons in Australia and New Zealand. One of the 16 Objects of the College is "To bring together the surgeons of Australia and New Zealand periodically for scientific discussion and practical demonstration of surgical subjects." In the furtherance of this object, there are many local and national meetings each year, but the highlight is the Annual Scientific Congress (ASC), held in each of the major cities on rotation, traditionally in the month of May, which is late autumn in the southern hemisphere.