The Lymphoedema Genitourinary Cancer Questionnaire in urology follow‐up clinics

Is the Lymphoedema Genitourinary Cancer Questionnaire (LGUCQ) useful to men treated for genitourinary cancer through facilitating symptom disclosure? Lymphoedema can be debilitating and progressive and its association with bladder, prostate, testicular and penile cancer, either as a consequence of treatment or progressive disease is well recognized. However, lymphoedema is generally unrecognized during follow‐up. Research on genitourinary cancer‐related lymphoedema is sparse with a lack of reliable prevalence figures. A lack of empirical understanding of the experiences of these men led to the development of the LGUCQ, a simple two‐sided tool to facilitate self‐reporting of symptoms and difficulties associated with lymphoedema. Related pilot work suggests that written self‐report tools enable men to disclose more sensitive information than they would verbally. However, the LGUCQ had not been formally evaluated in an uro‐oncology department to identify the benefits from the perspective of the patients and health professionals. Thematic analysis of completed LGUCQs and interviews with patients and staff were performed. Emergent themes included the perceived barriers to symptom disclosure, the LGUCQ as facilitator and pragmatic addition, the support needs of patients and health professionals and refinements required for roll out. Issues limiting identification of lymphoedema within uro‐oncology services existed. Findings suggest the inclusion of the LGUCQ within uro‐oncology clinics could lead to earlier identification of lymphoedema. Patients could identify genital oedema problems with the LGUCQ increasing prompt and accurate disclosure and normalizing the experience.     

Distribution of ABO and Rh-D blood groups among blood donors in a tertiary care centre in South India

The distribution of ABO and Rh-D blood groups was studied among 150,536 blood donors screened at the Dr John Scudder Memorial Blood Bank, Christian Medical College Hospital, Vellore, over a period of 11 years (April 1988 to March 1999).The most common blood group was found to be group O [58,330 (38.75%)], followed by group B [49,202 (32.69%)], and group A [28,372 (18.85%)]. The least common blood group was AB group [7,930 (5.27%)]. A2 or A2B groups were found in 3.01% and 1.43% of donors, respectively.The prevalence of Rh-D negative group was found in 8,225 (5.47%) donors. Bombay group (H negative non-secretor, genotype hh phenotype Oh) was found in six donors (0.004%). Although the incidence of Rh-D negative group was identical to previously published data from North India, the most common blood group was O group in our study as opposed to B group.     

GlideScope videolaryngoscope-assisted retrieval of an intratracheal foreign body

Postintubation tracheal stenosis presents major challenges to the anesthesiologist, especially in situations where the airway is shared with the surgeon. The airway management of a patient with severe postintubation subglottic stenosis, who developed complete airway obstruction during attempted tracheal dilatation, is presented.     

Haemoglobin drives inflammation and initiates antigen spread and nephritis in lupus

Haemoglobin (Hb) has well-documented inflammatory effects and is normally efficiently scavenged; clearance mechanisms can be overwhelmed during erythrocyte lysis. Whether Hb is preferentially inflammatory in lupus and triggers broad anti-self responses was assessed. Peripheral blood mononuclear cells (PBMCs) derived from SLE patients secreted higher levels of lupus-associated inflammatory cytokines when incubated with human Hb than did PBMCs derived from healthy donors, an effect negated by haptoglobin. Ferric murine Hb triggered the preferential release of lupus-associated cytokines from splenocytes, B cells, CD4 T cells, CD8 T cells and plasmacytoid dendritic cells isolated from ageing, lupus-prone NZM2410 mice, and also had mitogenic effects on B cells. Pull-downs, followed by mass spectrometry, revealed interactions of Hb with several lupus-associated autoantigens; co-incubation of ferric Hb with apoptotic blebs (structures that contain packaged autoantigens) revealed synergies—in terms of cytokine release and autoantibody production in vitro—that were also restricted to the lupus genotype. Murine ferric Hb activated multiple signalling pathways and, in combination with apoptotic blebs, preferentially triggered MAP kinase signalling specifically in splenocytes isolated from lupus-prone mice. Infusion of murine ferric Hb into lupus-prone mice led to enhanced release of lupus-associated cytokines, the generation of a spectrum of autoantibodies and enhanced-onset glomerulosclerosis. Given that the biased recognition of ferric Hb in a lupus milieu, possibly in concert with lupus-associated autoantigens, triggers inflammatory responses and the generation of lupus-associated cytokines, and also stimulates the generation of potentially pathogenic lupus-associated autoantibodies, neutralization of Hb could have beneficial effects.     

Lysozyme: a mediator of myocardial depression and adrenergic dysfunction in septic shock in dogs

The objective of the present study was to identify the nature of a filterable cardiodepressant substance (FCS) that contributes to myocardial dysfunction in a canine model of Escherichia coli septic shock. In a previous study, it was found that FCS increased in plasma after 4 h of bacteremia (Am J Physiol 1993;264:H1402) in which FCS was identified by a bioassay that included a right ventricular trabecular (RVT) preparation. In that study, FCS was only partially identified by pore filtration techniques and was found to be a protein of molecular weight between 10 and 30 K. In the present study, FCS was further purified by size exclusion high-pressure liquid chromatography, until a single band was identified on one-dimensional gel electrophoresis. This band was then subjected to tandem mass spectrometry and protein-sequencing techniques and both techniques identified FCS as lysozyme c (Lzm-S), consistent with that originating from the canine spleen. Confirmatory tests showed that purified Lzm-S produced myocardial depression in the RVT preparation at concentrations achieved during sepsis in the in vivo preparation. In addition, Lzm-S inhibited the adrenergic response induced by field stimulation and the beta- agonist isoproterenol in in vitro preparations, these results suggesting that Lzm-S may inhibit the sympathetic response in sepsis. The present findings indicate that Lzm-S originating from disintegrating leukocytes from organs such as the spleen contributes to myocardial dysfunction in this model. The mechanism may relate to its binding or hydrolysis of a cardiac membrane glycoprotein thereby interfering with myocardial excitation-contraction coupling in sepsis.     

Emerging translational science discoveries,clonal approaches,and treatment trends in chronic myeloproliferative neoplasms

The 60th American Society of Hematology (ASH) held in San Diego in December 2018 was followed by the 13th Post‐ASH chronic myeloproliferative neoplasms (MPNs) workshop on December 4 and 5, 2018. This closed annual workshop, first introduced in 2006 by Goldman and Mughal, was organized in collaboration with Alpine Oncology Foundation and allowed experts in preclinical and clinical research in the chronic MPNs to discuss the current scenario, including relevant presentations at ASH, and address pivotal open questions that impact translational research and clinical management. This review is based on the presentations and deliberations at this workshop, and rather than provide a resume of the proceedings, we have selected some of the important translational science and treatment issues that require clarity. We discuss the experimental and observational evidence to support the intimate interaction between aging, inflammation, and clonal evolution of MPNs, the clinical impact of the unfolding mutational landscape on the emerging targets and treatment of MPNs, new methods to detect clonal heterogeneity, the challenges in managing childhood and adolescent MPN, and reflect on the treatment of systemic mastocytosis (SM) following the licensing of midostaurin.