Cloned mouse mast cells resemble, by ultrastructure, immature mast cells observed in vivo. These mast cell clones can be grown in the absence of any other cells, facilitating direct investigations of their biochemistry and function. We find that cloned mast cells express plasma membrane receptors (Fc~R) that bind mouse IgE with an equilibrium constant (KA) similar to that of normal mouse peritoneal mast cells. In addition, cloned mast cells do not display detectable la antigens and cannot enhance Ig secretion when added to lymphocyte cultures or mediate natural killer lysis. In the presence of I mM sodium butyrate, cloned mast cells stop dividing and acquire abundant electron-dense cytoplasmic granules similar to those of mature mast cells. Their histamine content increases concomitant with cytoplasmic granule maturation and may exceed that of untreated mast cells by 50-fold. Unlike peritoneal mast cells, cloned mast cells incorporate 35S04 into chondroitin sulfates rather than heparin. 1-hese findings demonstrate that, unlike fully differentiated mouse peritoneal mast cells, cloned immature mouse mast cells contain no heparin and low levels of histamine. In addition, they establish that high-affinity Fc, R are expressed early in mast cell maturation, well before completion of cytoplasmic granule synthesis and mediator storage.We have previously reported methods to clone mast ceils with normal karyotypes from mouse hematopoietic tissue in vitro (30). Our cloned mast cells contain less histamine than normal mouse peritoneal mast cells and resemble immature mast cells by morphology. Others have described similar findings with uncloned cells (22,32,38,42,43,51,53). Although some mast cells synthesize heparin when fully differentiated (23, 54), certain mast cell tumors are devoid of heparin and incorporate 3BSO4 into chondroitin sulfate exclusively (18). Histochemical evidence suggests that normal immature connective tissue mast cells (6) and the mast cells in the intestinal lamina propria of rodents (25, 50) also may synthesize glycosaminoglycans other than heparin, but this notion has not been confirmed directly.In this report, we show that cloned mast cells closely resemble, by ultrastructure, immature mast cells found in vivo.Cloned mast cells incorporate 35804 preferentially into chondroitin sulfates, confirming histochemical evidence that immature mast cells contain little heparin. In addition, cloned mast cell proliferation, cytoplasmic granule synthesis, and mediator storage can be modulated in vitro, permitting direct analysis of mast cell maturation. MATERIALS AND METHODS AntiseraLyt-1.2 and Lyt-2.2 antisera, prepared as described (45), were kindly donated by F. W. Shen~; monoclonal antibody against Thy-l.2 (mc-a-Thy-l.2) was donated by Ed Clark2; and mc-a-Lyt-1 and mc-a-Lyt-2 were gifts from J. Ledbetter and L Herzenberg a. Mast cells were examined for la antigens using ATH-a-ATL alloantisera (16) or mc-a-Ia (10-3.6, reference 35) generously provided by John Freed and J. M. Kupinski 4. Mast Cells...

Sleep disturbance during menopause is a common and important complaint faced by many women. There are many factors that may play a role in this problem, including vasomotor symptoms and changing hormone levels, circadian rhythm abnormalities, exacerbation of primary insomnia, mood disorders, coexistent medical conditions as well as lifestyle factors. Sleep can be measured both objectively and subjectively; however, correlation between the two measures is not high. Most of the menopause-related sleep disturbances have been reported as qualitative in nature; however, there have also been studies showing changes in objective measures. This discrepancy has implications with regard to evaluation of research in sleep and menopause, as well as application in the clinical setting. Investigations of inadequate sleep and sleep problems during the menopausal period and obtaining a thorough understanding of the factors contributing to these problems are essential in formulating treatment strategies. Such strategies can vary from hormonal treatment and medications to lifestyle and behavioural modification.

A novel all-cause diagnostic metric for identifying co-existing morbidities of clinical relevance to nocturia in patients who present across disciplines and medical specialties has been developed. TANGO has the potential to improve practice and smooth inequalities associated with a siloed approach to assessment and subsequent care of patients with nocturia.

Epilepsy is a group of neurological conditions in which there is a pathological and enduring predisposition to generate recurrent seizures. Evidence over the last few decades suggests that epilepsy may be associated with increased sleep-disordered breathing, which may contribute towards sleep fragmentation, daytime somnolence, reduced seizure control, and cardiovascular-related morbidity and mortality. Chronic sleep-disordered breathing can result in loss of gray matter and cause deficits to memory and global cognitive function. Sleep-disordered breathing is a novel and independent predictor of sudden cardiac death and, as such, may be involved in the mechanisms leading to sudden unexpected death in epilepsy. Despite this, the long-term consequences of sleep-disordered breathing in epilepsy remain unknown, and there are no guidelines for screening or treating this population. There is currently insufficient evidence to indicate continuous positive airway pressure (CPAP) for the primary or secondary prevention of cardiovascular disease, and recent evidence has failed to show any reduction of fatal or nonfatal cardiovascular endpoints. Treatment of sleep-disordered breathing may potentially improve seizure control, daytime somnolence, and neurocognitive outcomes, but few studies have examined this relationship. In this review, we examine sleep-disordered breathing in epilepsy, and discuss the potential effect of epilepsy treatments. We consider the role of CPAP and other interventions for sleep-disordered breathing and discuss their implications for epilepsy management.

In acute hypercapnic Chronic obstructive pulmonary disease (COPD) patients, the Ward model of NIV care achieved equivalent clinical outcomes, whilst being more cost-effective than HDU or ICU models.

ObjectiveTo examine the prevalence and risk factors of sleep-disordered breathing (SDB) in individuals with epilepsy and psychogenic nonepileptic seizures (PNES).MethodsWe conducted a cross-sectional study of consecutive patients admitted for inpatient video-EEG monitoring at The Royal Melbourne Hospital, Australia, between December 1, 2011, and July 31, 2017. Participants underwent routine clinical investigations during their monitoring period including polysomnography, neurocognitive testing, and screening instruments of daytime somnolence, sleep quality, and quality of life.ResultsOur study population consisted of 370 participants who received a diagnosis of epilepsy (n = 255), PNES (n = 93), or both disorders (n = 22). Moderate to severe SDB (defined by an apnea-hypopnea index ≥15) was observed in 26.5% (98/370) of individuals, and did not differ across subgroups: epilepsy 26.3% (67/255), PNES 29.0% (27/93), or both disorders 18.2% (4/22; p = 0.610). Following adjustment for confounders, pathologic daytime sleepiness predicted moderate to severe SDB in epilepsy (odds ratio [OR] 10.35, 95% confidence interval [CI] 2.09–51.39; p = 0.004). In multivariable analysis, independent predictors for moderate to severe SDB in epilepsy were older age (OR 1.07, 95% CI 1.04–1.10; p < 0.001) and higher body mass index (OR 1.06, 95% CI 1.01–1.11; p = 0.029), and in PNES older age (OR 1.10, 95% CI 1.03–1.16; p = 0.002).ConclusionPolysomnography during inpatient video-EEG monitoring identified a substantial number of patients with undiagnosed SDB. This was remarkable in the subgroup with PNES, who were often female and obese. Identification of risk factors may improve management of SDB in these populations. The association with pathologic daytime sleepiness suggests that SDB may be an important contributor to these common and disabling symptoms in patients with epilepsy.

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