Globalization of medicine is increasing, as manifested by the growing number of migrating doctors and cross-border education providers. In addition, new medical schools of dubious quality are proliferating. This situation accentuates the need to define standards and introduce effective and transparent accreditation systems. With this background, and reflecting the important interface between medical education and health care delivery, a World Health Organization (WHO)/World Federation for Medical Education (WFME) Strategic Partnership to improve medical education was formed in 2004. In addition to working on reform processes, capacity building, and evaluation of medical education at the regional and national levels, the partnership in 2005 published guidelines for accreditation of basic medical education. Only a minority of countries have quality assurance systems based on external evaluation, and most of these use only general criteria for higher education. The WHO/WFME Guidelines recommend establishing accreditation that is effective, independent, transparent, and based on criteria specific to medical education. An important prerequisite for this development was the WFME Global Standards program, initiated in 1997 and widely endorsed. The standards are now being used in all regions as a basis for improving medical education throughout its continuum and as a template for national and regional accreditation standards. Promotion of national accreditation systems will pivotally influence future international appraisal of medical education. Information about accreditation status--agencies involved and criteria and procedures used--will be essential to future databases of medical schools and will be a foundation for international "meta-recognition" of institutions and programs ("accrediting the accreditors").

The binding of iron-saturated 125I-lactoferrin to human monocytes was studied at pH 7.4 and 37 degrees C. Monocytes in suspension bound 125I-lactoferrin by a reversible, saturable and specific binding indicating the presence of a receptor. The dissociation constant (KD) of the binding was estimated at about 4.5 x 10(-9) M and the number of receptors was about 1.6 x 10(6) per monocyte. The affinity of native lactoferrin (20% iron saturated) was only slightly below that of iron-saturated lactoferrin (KD about 7.9 x 10(-9) M). Human transferrin, horse cytochrome c and human immunoglobulin G were without inhibitory effect on the binding of 125I-lactoferrin. The majority of cell-bound 125I-lactoferrin was dissociable. The dissociation rate was not affected by addition of unlabelled lactoferrin to the dissociation medium. The binding of 125I-lactoferrin to adherent mononuclear blood cells showed an about 100-fold lower affinity (KD about 2.5 x 10(-7) M) than to cells in suspension, but the specificity of the binding was the same. These results are compatible with the idea that lactoferrin exerts a biological effect mediated by an interaction with cells of the monocyte/macrophage lineage.

ABSTRACT. Neutrophil granulocyte chemotaxis and intraneutrophilic and plasma levels of lysozyme as well as the number of T and B lymphocytes and lymphocyte transformation in vitro on stimulation with mitogens and microbial antigens were studied in four groups of patients with diabetes mellitus (DM). Twelve patients with insulin‐dependent diabetes mellitus (IDDM) and ketoacidosis and 4 patients with non‐insulin‐dependent diabetes mellitus were studied at the time of diagnosis and before and after start of treatment. Ten patients with IDDM of less than 10 years' duration which had been difficult to regulate well and 10 patients with IDDM well regulated for more than 20 years were studied at their regular outpatient visits. Apart from a slight increase in plasma lysozyme in group 1 from the first to the second examination, we found no differences between diabetics and healthy control persons. It is concluded that if patients with DM are more susceptible to infections, it is probably caused by elements of neutrophil or lymphocyte function not examined in this study or by factors unrelated to immunity.

Medical doctors constitute a profession which embraces trust from and accountability to society.This responsibility extends to all medical educational institutions. Social accountability of medical education means a willingness and ability to adjust to the needs of patients and health care systems both nationally and globally. But it also implies a responsibility to contribute to the development of medicine and society through fostering competence for research and improvement. Accreditation is a process by which a statutory body evaluates and recognises an educational institution and/or its programme with respect to meeting approved criteria. It is a means for quality assurance, but also a strong power to reinforce the need for improvement and reforms. It must be performed through internationally recognized and transparent standards and should foremost promote quality development. The social accountability of medical education must be included in all accreditation processes at all levels.The WFME global standards programme provides tools for national or regional accreditation but also guidance for reforms and quality improvement. The standards are used worldwide and have been adopted to local needs in most parts of the world. They are framed to specify attainment at two levels; basic standards or minimum requirements and standards for quality development. The concept of social accountability is embedded in all parts of the WFME standards documents. In 2011, a revision of the Standards for undergraduate education has been instituted. Strengthening of aspects on social accountability of medical education will be a particular concern.3

ter region characteristic of CML. In December 1996, the patient was treated with high-dose cyclophosphamide plus total body irradiation 11.9 Gy followed by allogeneic bone Exposure to ionizing radiation is known to result in a dosemarrow transplantation from an HLA-DR-type identical sister. dependent increased risk of acute leukemias and of CML He is still being followed with both malignancies in characteristically carrying the Philadelphia chromosome complete remission. translocation t(9;22)(q34;q11). Treatment with alkylating Late occurrence of the Philadelphia chromosome has preagents is associated with a dose-dependent increased risk of viously been observed, but only rarely, in myeloid disorders AML, in most cases presenting as myelodysplasia (MDS) with and in acute lymphoblastic leukemia (ALL), both in previously loss of a part of or the whole long arm of chromosomes 5 or 7.untreated patients and after radiotherapy and chemotherapy. During the past few years some epipodophyllotoxins, some A review of the literature of chemotherapy-related cases, howanthracyclines and other DNA topoisomerase II inhibitors ever, reveals 26 patients including our case, with Philadelphia have been shown to be leukemogenic, in most cases adminischromosome-positive CML, AML or ALL following chemotered in combination with an alkylating agent or a platinum therapy of a Philadelphia chromosome-negative leukemia or derivative. 1 Two independent studies have demonstrated a another malignancy, most often Hodgkin's disease 4-22 significant association between this type of combination (Table 1). One of these 26 patients was treated for Hodgkin's chemotherapy and the development of AML with balanced disease with radiotherapy and single agent chemotherapy with translocations involving chromosome bands 11q23 and vinblastin and developed CML as late as 192 months after 21q22. 2,3 However, other balanced aberrations such as the therapy. 7 For these reasons this particular case is considered t(15;17)(q22;q12) and the inv(16)(p13q22) more rarely as unrelated to chemotherapy and excluded in our evaluation. observed in t-AML have also been related to previous chemoOf the remaining 25 patients, 22 patients had previously therapy with DNA topoisomerase II inhibitors. 1 received DNA topoisomerase II inhibitors, daunorubicin in 10 Recently, we observed a patient with Philadelphia chromocases, 13 patients had received alkylating agents and 10 some-positive CML after therapy with etoposide, cisplatin and patients radiotherapy (Table 1). These findings raise the quesbleomycin for a germ cell tumor. This case, together with tion of a causal relationship between chemotherapy with other sporadic case reports of chemotherapy-related, late DNA topoisomerase II inhibitors and subsequent development occurring Philadelphia chromosome-positive leukemias of of leukemia with a t(9;22). various types, leads us to suggest that the development of Most of the chemotherapy-related leukemias with t(9;22) t(9;22)(q34;q11) in some of these rather rare cases may also coul...

A B S T R A C T Lysozyme turnover studies with Ilabeled human lysozyme were carried out on 22 patients, viz. nine control patients, seven nephrological patients with varying degrees of renal insufficiency, including three bilaterally nephrectomized patients, and six hematological patients with disturbed turnover of the neutrophilic granulocytes.It was found that plasma lysozyme has a rapid turnover with a fractional catabolic rate of 76%/hr of the plasma content. Lysozyme catabolism varied with the endogenous creatinine clearance; in addition however, extrarenal sites of catabolism were demonstrated since lysozyme could be broken down in the anephric patients, although only at a rate amounting to about 15% of the rate found in persons with intact kidneys.In the uremic patients the increased plasma lysozyme concentration was due to decreased rates of catabolism; in the hematological patients the increased plasma lysozyme level was due to increased rates of synthesis which supports the hypothesis that plasma lysozyme mainly stems from disintegrating neutrophilic granulocytes. Furthermore, it was shown that in the nonhematological patients examined, the rate of synthesis varied with the endogenous creatinine clearance.

No abstract

A B S T R A C T Lysozyme turnover in the rat was studied with 'I-labeled rat lysozyme. It was found that plasma lysozyme has a rapid disappearance rate with a half-life of 75 min. The rate of synthesis was calculated at 3.4 /Ag/min per 100 g rat. This rate of synthesis was compared with figures from the literature for the turnover rate of neutrophilic granulocytes, and the data were consistent with the concept that disintegrating neutrophils are the main source of plasma lysozyme.The distribution of enzymatic lysozyme activity and of radioactive lysozyme was studied in several organs. Very high enzymatic activity was found in leukocytes as were considerable activities in lungs, kidneys, bone marrow, spleen, and intestine; little enzymatic activity was found in the urine. High radioactive levels as compared with plasma radioactivity were demonstrated only in the kidneys. This indicates that of the organs studied, the kidney is the predominant site of storage and destruction of plasma lysozyme.Lysozyme was found to disappear only slowly from the kidneys over a period of 4 days. The data obtained seem to indicate that lysozyme or a lysozyme degradation product precipitable by trichloroacetic acid was released in small amounts from the kidneys to plasma throughout this period. INTRODUCTIONIncreasing interest in lysozyme (muramidase) as a diagnostic tool in hematology and nephrology has stressed the importance of knowledge of the metabolism of this enzyme. However, few turnover studies of lysozyme have been carried out, and these were performed either with xenogeneic lysozyme (from hen egg white) or with unphysiological amounts of endogenous lysozyme (1-3). The aim of the present study was to investigate lysozyme turnover in the rat using radioactively labeled rat lysozyme.