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Turner syndrome (TS) is a chromosomal disorder with various complications, including congenital anomaly of the kidney and urinary tract (CAKUT). However, its renal function remains poorly known. Therefore, this study aimed to evaluate renal function in TS of various ages from childhood to adulthood.

We retrospectively analyzed 63 patients with TS who visited our hospital between 1989 and 2020, examined their renal morphology, and analyzed renal function by calculating the estimated glomerular filtration rate (eGFR) using formulas applicable for Japanese populations.

Renal morphological abnormality was observed in 22 cases (35.0%) (horseshoe kidney, 7 [11.1%]; hydronephrosis, 11 [17.5%]; duplex collecting system, 3 [4.8%]; and single unilateral kidney, 1 [1.6%]). We evaluated the eGFR of 47 subjects aged 2.8-39.3years and classified them into Group 1 (with CAKUT, n = 15) and Group 2 (without CAKUT, n = 32). The eGFR at the first visit and the final follow-up was not statistically different between these groups. In Group 1 with CAKUT, the eGFR was not significantly different between that at the first visit and that at the final follow-up (p = 0.21). H-151 clinical trial During the observation period (median, 7.9years), the eGFR of all individuals in both groups gradually decreased with age, but did not fall < 60mL/min/1.73m

, which defines chronic kidney disease (CKD).

The renal function of TS remained normal in all cases during our investigation period, and no one developed CKD by the age of 40years.

The renal function of TS remained normal in all cases during our investigation period, and no one developed CKD by the age of 40 years.

To examine the association between (GWG) and epithelial ovarian cancer (EOC).

We compared GWG between 670 incident EOC cases and1,551 community controls from a population-based, case-control study conducted in Pennsylvania, Ohio, and New York from 2003 to 2008. Multivariable unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) associated with GWG adjusting for potential confounders. To explore the potential effect of maternal long-term weight retention after childbearing, we restricted analyses to women who began their childbearing years as normal/underweight and examined differences in EOC risk between those who were normal/underweight versus those who were overweight/obese at study baseline reference date.

Average GWG per full-term pregnancy did not differ between cases and controls. Among women who were normal/underweight at study baseline, greater average GWG was not associated with EOC (OR = 0.9, 0.8, 0.7 for quartiles 2, 3 and 4 of GWG gain, uld provide another means to help women reduce their risk of this often-fatal malignancy.

Guidelines recommend endoscopy with biopsies to stratify patients with gastric premalignant lesions (GPL) to high and low progression risk. High-risk patients are recommended to undergo surveillance. We aimed to assess the accuracy of guideline recommendations to identify low-risk patients, who can safely be discharged from surveillance.

This study includes patients with GPL. Patients underwent at least two endoscopies with an interval of 1-6years. Patients were defined ‘low risk’ if they fulfilled requirements for discharge, and ‘high risk’ if they fulfilled requirements for surveillance, according to European guidelines (MAPS-2012, updated MAPS-2019, BSG). Patients defined ‘low risk’ with progression of disease during follow-up (FU) were considered ‘misclassified’ as low risk.

334 patients (median age 60years IQR11; 48.7% male) were included and followed for a median of 48months. At baseline, 181/334 (54%) patients were defined low risk. Of these, 32.6% were ‘misclassified’, showing progression of disease during FU. If MAPS-2019 were followed, 169/334 (51%) patients were defined low risk, of which 32.5% were ‘misclassified’. If BSG were followed, 174/334 (51%) patients were defined low risk, of which 32.2% were ‘misclassified’. Seven patients developed gastric cancer (GC) or dysplasia, four patients were ‘misclassified’ based on MAPS-2012 and three on MAPS-2019 and BSG. By performing one additional endoscopy 72.9% (95% CI 62.4-83.3) of high-risk patients and all patients who developed GC or dysplasia were identified.

One-third of patients that would have been discharged from GC surveillance, appeared to be ‘misclassified’ as low risk. One additional endoscopy will reduce this risk by 70%.

One-third of patients that would have been discharged from GC surveillance, appeared to be ‘misclassified’ as low risk. One additional endoscopy will reduce this risk by 70%.

Ischemic colitis is a common disease; however, its pathophysiology remains unclear, especially in ischemic proctitis after sigmoidectomy. We present a rare case of ischemic proctitis 6months after laparoscopic sigmoidectomy.

The patient was a 60-year-old man with hypertension, type 2 diabetes, and hyperlipidemia. He was a smoker. He underwent laparoscopic sigmoidectomy for pathological stage I sigmoid colon cancer and was followed up without any adjuvant therapy. Six months after his surgery, he complained of lower abdominal discomfort, bloody stools, and tenesmus. Colonoscopy showed extensive rectal ulcers between the anastomotic site and the anal canal, which was particularly severe on the anal side several centimeters beyond the anastomosis. We provided non-surgical management, including hyperbaric oxygen therapy. The rectal ulcers had healed 48days after the therapeutic intervention. He has not experienced any recurrence for 3.5years.

While performing sigmoidectomy, it is important to consider the blood backflow from the anal side of the bowel carefully, especially for patients with risk factors of ischemic proctitis.

While performing sigmoidectomy, it is important to consider the blood backflow from the anal side of the bowel carefully, especially for patients with risk factors of ischemic proctitis.

The degree of cell proliferation is important for subclassification of breast cancers into prognostic and therapeutic groups. DTX3 has been identified as a driver of proliferation in luminal breast cancer. In this study, we describe DTX3 copy number in breast cancer primary tumours and corresponding axillary lymph node metastases, and studied associations with molecular subtype, proliferation and prognosis.

Using fluorescence in situ hybridization, we assessed DTX3 and chromosome 12 centromere (CEP12) copy number in 542 primary breast cancers and 117 lymph node metastases, from a well-described cohort of Norwegian breast cancer patients. Proliferation was expressed as mitotic counts and Ki67 score. Associations between DTX3 copy number and molecular subtype and proliferation were assessed using Pearson’s χ

test. We studied the effect of copy number increase on prognosis estimating cumulative incidence of breast cancer death and hazard ratios.

Mean DTX3 copy number ≥ 4 was found in 23 tumours (4%), and mean ≥ 5 in 9 tumours (1.7%). Copy number increase was found within all molecular subtypes except the 5 negative phenotype and the Luminal B (HER2 +) subtype. DTX3 copy number increase was not accompanied by an increase in CEP12. Point estimates showed that there were associations between DTX3 copy number increase and high proliferation and poor prognosis; however, precision depended on copy number cut-off.

DTX3 copy number increase was present in a small proportion of breast cancer cases. There was an association between copy number increase and high tumour cell proliferation and poor prognosis.

DTX3 copy number increase was present in a small proportion of breast cancer cases. There was an association between copy number increase and high tumour cell proliferation and poor prognosis.

Cardiac function assessment is important for detecting and managing trastuzumab-associated cardiotoxicity. Our study estimates rates and predictors of cardiac assessment among patients receiving trastuzumab for HER2-positive early breast cancer (HER2+EBC) in Australia.

We conducted a retrospective cohort study of Australians initiating (neo)adjuvant trastuzumab for HER2+EBC between 1 January 2015 and 15 April 2019. We used administrative claims to determine the number of patients receiving guideline-recommended assessment, i.e. evidence of baseline cardiac assessment (between 120days before and 30days after trastuzumab initiation) and regular on-treatment cardiac assessments (at least every 120days). We examined factors associated with baseline and regular on-treatment cardiac assessment.

Our study includes 5621 patients (median age 56years), of whom 4984 (88.7%) had a baseline cardiac function test. Among 4280 patients with at least 12months of follow-up, 2702 (63.1%) had guideline-recommended cardiac as year of diagnosis and geography, rather than individual patient factors.

Triple negative breast cancer (TNBC) is characterized by invasiveness and short survival. Identifying novel TNBC-targeted therapies, to potentiate standard of care (SOC) therapy, is an unmet need. Progranulin (PGRN/GP88) is a biological driver of tumorigenesis, survival, and drug resistance in several cancers including breast cancer (BC). PGRN/GP88 tissue expression is an independent prognostic factor of recurrence while elevated serum PGRN/GP88 level is associated with poor outcomes. Since PGRN/GP88 expression is elevated in 30% TNBC, we investigated the involvement of progranulin on TNBC.

The effect of inhibiting PGRN/GP88 expression in TNBC cells by siRNA was investigated. The effects of a neutralizing anti-human PGRN/GP88 monoclonal antibody AG01 on the proliferation and migration of two TNBC cell lines expressing PGRN/GP88 were then examined in vitro and in vivo.

Inhibition of GP88 expression by siRNA and AG01 treatment to block PGRN/GP88 action reduced proliferation and migration in a dose-dependent fashion in MDA-MB-231 and HS578-T cells. Western blot analysis showed decreased expression of phosphorylated protein kinases p-Src, p-AKT, and p-ERK upon AG01 treatment, as well as inhibition of tumor growth and Ki67 expression in vivo.

PGRN/GP88 represents a therapeutic target with companion diagnostics. Blocking PGRN/GP88 with antibody treatment mayprovide novel-targeted solutions in TNBC treatment which could eventually address the issue of toxicity and unresponsiveness associated with SOC.

PGRN/GP88 represents a therapeutic target with companion diagnostics. Blocking PGRN/GP88 with antibody treatment may provide novel-targeted solutions in TNBC treatment which could eventually address the issue of toxicity and unresponsiveness associated with SOC.As witnessed over the last year, immunity emerged as one of most highly debated topics in the current Covid-19 pandemic. Countries around the globe have been debating whether herd immunity or lockdown is the best response, as the race continues for the development and rollout of effective vaccines against coronavirus and as the economic costs of implementing strict containment measures are weighed against public health costs. What became evident all the more is that immunity is precisely what bridges between biological life and political life in the current climate, be it in terms of the contentious notion of herd immunity, the geopolitical struggle for vaccines, or the possible emergence of “Covid-elite”, i.e. holders of so-called “immunity passports”. Immunity, as such, is certainly not only a matter of science and biology alone, but is inherently political in the way that pandemics themselves are often highly politicised. Drawing on the work of Roberto Esposito and other literature from the field of biopolitics and immunology, this paper provides a critical examination of the concept of immunity in light of the recent events, highlighting the intersections between the politics of defence and the politics of sacrifice which animate governments’ immunitary responses to the Covid-19 pandemic.