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Background: 131 I-metaiodobenzylguanidine ( 131 I-mIBG) effectiveness in children with metastasised neuroblastoma (NB) is linked to the effective dose absorbed by the target; a target of 4 Gy whole-body dose threshold has been proposed. Achieving this dose often requires administering 131 I-mIBG twice back-to-back, which may cause haematological toxicity. In this study, we tried identifying the factors predicting the achievement of 4 Gy whole-body dose with a single radiopharmaceutical administration., Materials and Methods: Children affected by metastatic NB and treated with a high 131 I-mIBG activity (>450 MBq (megabecquerel)/kg) were evaluated retrospectively. Kinetics measurements were carried out at multiple time points to estimate the whole-body dose, which was compared with clinical and activity-related parameters., Results: Seventeen children (12 females, median age 3 years, age range: 1.5-6.9 years) were included. Eleven of them still bore the primary tumour. The median whole-body dose was 2.88 Gy (range: 1.63-4.22 Gy). Children with a 'bulky' primary (>30 mL) received a higher whole-body dose than those with smaller or surgically removed primaries (3.42 ± 0.74 vs. 2.48 ± 0.65 Gy, respectively, p = .016). Conversely, the correlation between activity/kg and the whole-body dose was moderate (R: 0.42, p = .093). In the multivariate analysis, the volume of the primary tumour was the most relevant predictor of the whole-body dose (p = .002)., Conclusions: These data suggest that the presence of a bulky primary tumour can significantly prolong the 131 I-mIBG biological half-life, effectively increasing the absorbed whole-body dose. This information could be used to model the administered activity, allowing to attain the target dose without needing a two-step radiopharmaceutical administration., (© 2023 Wiley Periodicals LLC.)

Hypertension induced by long-term infusion of angiotensin II (Ang II) is associated with augmented intrarenal Ang II levels to a greater extent than can be explained on the basis of the circulating Ang II levels. Although part of this augmentation is due to AT(1) receptor-dependent internalization, the intracellular compartments involved in this Ang II accumulation remain unknown. In the present study, we sought to determine whether Ang II trafficking into renal cortical endosomes is increased during Ang II hypertension, and if so, whether the AT(1) receptor antagonist, candesartan, prevents this accumulation. Compared with controls (n=12; 114+/-2 mm Hg), Ang II-infused rats (n=12; 80 ng/kg/min, SC, for 13 days) developed hypertension with systolic blood pressure rising to 185+/-4 mm Hg by Day 12. In Ang II hypertensive rats, plasma renin activity was suppressed, whereas plasma and kidney Ang II levels were increased by 3-fold (348+/-58 versus 119+/-16 fmol/mL) and 2-fold (399+/-39 versus 186+/-26 fmol/g). Intracellular endosomal Ang II levels were increased by more than 10-fold (1100+/-283 versus 71+/-12 fmol/mg protein), whereas intermicrovillar cleft Ang II levels were increased by more than 2-fold (88+/-22 versus 37+/-7 fmol/mg protein). Flow cytometric analysis detected significant increases in AT(1A) receptor antibody binding in endosomal and intermicrovillar clefts of Ang II-infused rats. The hypertension induced by Ang II was prevented in rats treated concurrently with candesartan (2 mg/kg/d, 119+/-3 mm Hg). Candesartan treatment (n=8) also prevented increases in kidney (215+/-19 fmol/g), endosomal (96+/-29 fmol/mg protein), and intermicrovillar cleft Ang II levels (11+/-2 fmol/mg protein). These results indicate that there is substantial intracellular accumulation of angiotensin peptides in renal cortical endosomes during Ang II-dependent hypertension via an AT(1) receptor-mediated process.

The NIDEK EAS-1000 is a camera and computer system designed to facilitate measurement and analysis of the anterior segment of the eye. To evaluate the interobserver reproducibility of the system, three examiners assessed the anterior chamber depth and peripheral angle measurement in 20 disease-free eyes. Intraobserver reproducibility was determined by each investigator's photographing and analyzing the same eye on three different occasions. Interobserver correlation for the anterior chamber depth (using the first three readings of the same eye made by each examiner) was 0.97, with an 95% CI of 0.94 to 0.98. Interobserver correlation for angle measurement (again using the first three readings of the same eye made by each examiner) was 0.89, with a 95% confidence interval (CI) of 0.81 to 0.95. Intraobserver correlations for anterior chamber depth were 0.98 for each of the three examiners (mean, 0.98), wiht a 95% CI of 0.91 to 0.99. Intraobserver correlations for anterior chamber depth were 0.98 for each of the three examiners (mean, 0.98), with a 95% CI of 0.91 to 0.99. The intraobserver CI for angle measurement was 0.97 (range, 0.95 to 0.99). The intraobserver and interobserver reproducibility of the NIDEK EAS-1000 system was excellent.

Osteopetrosis is a rare congenital disorder of bone metabolism characterized by generalized sclerotic bone resulting from osteoclast dysfunction. There are several ocular manifestations, one of which is nasolacrimal duct obstruction from osteosclerosis of the nasolacrimal foramen. The surgeon must anticipate and prepare for the difficulties of working with marbleized, ultra-dense bone, alternating technique accordingly. In nasolacrimal duct obstruction, surgical management produces seemingly stable long-term results. However, if ossification recurs at the operative site, reoperation may become necessary for either optic nerve decompression or dacryocystorhinostomy.

Fifty-five patients with Mycobacterium kansasii isolates (47 pulmonary and eight disseminated) were identified at a large Texas hospital from 1975 to 1985. The mean age of patients was 60 years, and there was a slight male predominance. Isolation of M. kansasii usually represented disease. The great majority of patients with pulmonary infection due to M. kansasii had underlying pulmonary diseases, and 70% had nonpulmonary predisposing factors. M. kansasii pulmonary disease clinically and radiographically resembled pulmonary tuberculosis. Disseminated M. kansasii infection occurred in severely immunocompromised patients, who frequently had pulmonary predispositions as well. Disseminated infection most of ten involved the lung, reticuloendothelial system, bone, joint, and skin and presented with signs and symptoms related to these organs. Despite only moderate in vitro susceptibility of M. kansasii to routine antituberculous drugs, most patients responded to rifampin-containing regimens. The prognosis of patients with M. kansasii disease was determined primarily by their underlying diseases.