Dietary Salt Intake and Discretionary Salt Use in Two General Population Samples in Australia: 2011 and 2014

The limited Australian measures to reduce population sodium intake through national initiatives targeting sodium in the food supply have not been evaluated. The aim was, thus, to assess if there has been a change in salt intake and discretionary salt use between 2011 and 2014 in the state of Victoria, Australia. Adults drawn from a population sample provided 24 h urine collections and reported discretionary salt use in 2011 and 2014. The final sample included 307 subjects who participated in both surveys, 291 who participated in 2011 only, and 135 subjects who participated in 2014 only. Analysis included adjustment for age, gender, metropolitan area, weekend collection and participation in both surveys, where appropriate. In 2011, 598 participants: 53% female, age 57.1(12.0)(SD) years and in 2014, 442 participants: 53% female, age 61.2(10.7) years provided valid urine collections, with no difference in the mean urinary salt excretion between 2011: 7.9 (7.6, 8.2) (95% CI) g/salt/day and 2014: 7.8 (7.5, 8.1) g/salt/day (p = 0.589), and no difference in discretionary salt use: 35% (2011) and 36% (2014) reported adding salt sometimes or often/always at the table (p = 0.76). Those that sometimes or often/always added salt at the table and when cooking had 0.7 (0.7, 0.8) g/salt/day (p = 0.0016) higher salt excretion. There is no indication over this 3-year period that national salt reduction initiatives targeting the food supply have resulted in a population reduction in salt intake. More concerted efforts are required to reduce the salt content of manufactured foods, together with a consumer education campaign targeting the use of discretionary salt.     

Health-related quality of life in Iranian women with polycystic ovary syndrome: a qualitative study

Background

Polycystic ovary syndrome (PCOS) is associated with a range of challenging symptoms which impact patient’s lives. Iranian women with PCOS are likely to face a number of unique difficulties given particular societal and cultural norms for women. Understanding health-related quality of life (HRQoL) from a patients’perspective is critical to developing the appropriate support interventions. The present study aimed to generate an in-depthunderstanding of HRQoL Iranian women with PCOS.

Methods

Twenty Iranian women were interviewed and data was subjected to thematic analysis.

Results

Women reported substantial effects of PCOS on their quality of life, Themes generated from the data related to sexual - physical problems (An unsexualised self: loss, change and pain; and Being pained and painful); exposure and nvasion: the rejecting and invading social world (Concealing and Avoiding and Public property: public scrutiny), diminished self and diminished life (Infertile as inferior and Exhausted mind andbody) respectively.

Conclusion

PCOS is a physical - sexual, psychological and social syndrome; therefore, it is necessary to taking a more holistic approach to patient care beyond treating physical symptoms.

     

Preparation,characterization and storage of human ferritin for use as a standard for the assay of serum ferritin

Summary. This paper describes studies on the source, preparation, characterization and storage of human ferritin for use as a standard for the immunoassay of serum ferritin. Ferritin was prepared from the liver or spleen by methods including either ultracentrifugation or cadmium sulphate crystallization. Preparations were characterized by polyacrylamide gel electrophoresis in dissociating and non-dissociating buffers, iso-electric focusing, analysis of amino acid composition and measurement of protein content. The protein content of solutions of liver or spleen ferritin may be determined by the method of Lowry with bovine serum albumin as standard. Lyophilization under carefully controlled conditions in buffer containing high concentrations of albumin provides a stable preparation of ferritin. Accelerated degradation and collaborative immunological studies of two lyophilized preparations of ferritin, one from liver and one from spleen, indicate that either is an acceptable reference material.     

COVID-19 infection causes a reduction in neutrophil counts in patients taking clozapine

BackgroundMonitoring of white cell counts during clozapine treatment leads to cessation of therapy if levels fall below pre-determined values. Reductions in white cell counts, driven by lower levels of lymphocytes, have been observed with coronavirus disease 2019 (COVID-19). Neutropenia during COVID-19 has not been reported. We present data for 56 patients who were taking clozapine and had COVID-19.MethodsWe included patients who were taking clozapine at the time they tested positive for COVID-19. We compared absolute neutrophil counts, lymphocyte counts and white cell counts between baseline and the first week of infection, and baseline and the second week of infection.ResultsWe observed reductions in absolute neutrophil counts (p = 0.005), lymphocyte counts (p = 0.003) and white cell counts (p < 0.001) between baseline and the first 7 days of COVID-19. All cell counts had returned to baseline levels by days 8 to 14. Six patients experienced neutropenia (absolute neutrophil counts < 2.0 × 10⁹/L) and of those, 4 underwent mandatory cessation of clozapine. For 3 patients, clozapine treatment had been established for more than 6 months with no previous neutropenia, neutrophil levels returned to baseline within 2 weeks and no further neutropenia was observed on restarting treatment.LimitationsThis was a retrospective chart review; larger cohorts are required. Clozapine plasma levels were largely not measured by clinicians.ConclusionThese data strongly suggest that mild neutropenia in the acute phase of COVID-19 in patients who are well established on clozapine is more likely to be a consequence of the virus than of clozapine treatment.     

Measurement of transmission of vibration through the human spine using skin-mounted inertial sensors

The purpose of this study was to examine the feasibility of measuring the transmission of vibration using skin mounted inertial sensors and to assess the dynamic properties of the human spine during activities of daily living. Two inertial sensors were attached to skin overlying the first thoracic vertebra (T1) and another one over the first sacral vertebra (S1) with double sided adhesive tape. Subjects walked along a straight line, and up and down stairs at a self selected, comfortable speed. Transmissibility of vertical vibration was calculated as the ratio of the power spectral density of the acceleration signal at T1 over that at S1, over the frequency range of 0.5–12 Hz. Cross correlation and coherence of the acceleration signals between the two T1 sensors were performed to evaluate the similarity of the data after correction. Cross correlation of signals between trials was also performed to examine the repeatability of the signals. Cross correlation coefficients were found to be very high (>0.9). Inter-trial consistency of the signals of all sensors was also high (>0.9). It is concluded that skin measurement of transmission of vertical vibration is feasible with the inertial sensors and correction method presented. Different physical activities seem to elicit different frequency characteristics of vibration.     

Fibroblast growth factor-23 mutants causing familial tumoral calcinosis are differentially processed

Familial tumoral calcinosis (TC, OMIM 211900) is a heritable disorder characterized by hyperphosphatemia, normal or elevated serum 1,25-dihydroxyvitamin D, and often severe ectopic calcifications. Two recessive mutations in fibroblast growth factor-23 (FGF23), serine 71/glycine (S71G) and serine 129/phenylalanine (S129F), were identified as causing TC. Herein, we undertook comprehensive biochemical analyses of an extended TC family carrying the S71G FGF23 mutation, which revealed that heterozygous (serine/glycine, S/G) individuals had elevated serum FGF23 C-terminal fragments compared with wild-type (serine/serine, S/S) family members (P < 0.025). To understand the differential processing of FGF23 in TC patients, we transiently expressed S71G as well as S129F FGF23. FGF23 ELISA in tandem with Western analyses revealed increased proteolytic cleavage of mutant FGF23 and a limited secretion of intact protein. Furthermore, S71G and S129F FGF23 carrying mutations that disrupt the furin-like protease RXXR motif in FGF23 rescued the secretion of the intact protein, and both TC mutant proteins harboring the R176Q mutation revealed no altered sensitivity to trypsin compared with the native (R176Q)FGF23. Finally, S71G, but not S129F mutant FGF23, is rescued by temperature. In summary, FGF23 mutations causing TC lead to increased intracellular proteolysis of FGF23, most likely by furin-like proteases, due to conformational changes of the mutant protein. The destabilizing nature of these mutations provides new insight into the pathophysiology of TC and exemplifies the physiological importance of FGF23 in phosphate and vitamin D metabolism.     

A novel recessive mutation in fibroblast growth factor-23 causes familial tumoral calcinosis

Gain-of-function mutations in fibroblast growth factor-23 (FGF23) are responsible for autosomal dominant hypophosphatemic rickets, a disorder of isolated renal phosphate wasting. Patients with the disorder display hypophosphatemia with normocalcemia as well as inappropriately normal 1,25-dihydroxyvitamin D [1,25(OH)2D3] concentrations. Reciprocally tumoral calcinosis (TC) patients are often hyperphosphatemic with inappropriately normal or elevated serum 1,25(OH)2D3 levels and have ectopic and vascular calcifications, a phenotype similar to that of Fgf23 null mice. Therefore, the goal of the present studies was to test whether FGF23 was a candidate gene for TC. Two sisters in a consanguineous TC family had hyperphosphatemia and normal 1,25(OH)2D3 levels with characteristic ectopic and vascular calcifications. Interestingly, these patients had low-normal intact serum FGF23 levels but demonstrated FGF23 concentrations approximately 40 times normal when assessed with a C-terminal FGF23 serum assay. Mutational analyses identified a homozygous S71G mutation in FGF23 in the TC patients, which was not found in control alleles. Finally, modeling demonstrated that the S71G mutation most likely destabilizes full-length FGF23. In summary, recessive FGF23 mutations can lead to TC. Additionally, our findings indicate that FGF23 may adopt an unstable conformation in some TC patients, possibly leading to nonfunctional FGF23 protein.