Literature search from ms 29/4/2010

Guo, X., N. Willows, et al. (2009). "Use of vitamin and mineral supplements among Canadian adults." Canadian Journal of Public Health Revue Canadienne de Sante Publique. 100(5): 357-60.

OBJECTIVE: To estimate the prevalence and determinants of use of vitamin and mineral supplements among adult Canadians. METHODS: Data from adult respondents of the Canadian Community Health Survey Cycle (CCHS) 2.2 were used. Participants were asked about their use of vitamin and mineral supplements in the month prior to being surveyed. The prevalence of vitamin and mineral supplement use was compared across various socio-demographic and lifestyle factors. Logistic regression analysis was used to assess determinants of supplement use. RESULTS: In the month prior to the interview, 40.1% of adult Canadians took supplements. In the fully adjusted model, females of all ages were more likely to be users than males 19-30 years. Physical activity, fruit/vegetable consumption, and higher levels of household education and income were positively related to supplement use. CONCLUSIONS: A substantial proportion of adult Canadians take vitamin and mineral supplements. The use was more prevalent among those with healthier lifestyles and of socio-economically advantaged backgrounds. Further investigation is needed to reveal the impact of supplements on nutrient adequacy and health.

Gupta, R., U. Oh, et al. (2003). "Resolution of Ondine's curse after suboccipital decompression in a 72-year-old woman." NEUROLOGY 61(2): 275-6.

Gut, P., K. Huber, et al. (2005). "Lack of an adrenal cortex in Sf1 mutant mice is compatible with the generation and differentiation of chromaffin cells." DEVELOPMENT 132(20): 4611-4619.

The diversification of neural-crest-derived sympatho-adrenal (SA) progenitor cells into sympathetic neurons and neuroendocrine adrenal chromaffin cells was thought to be largely understood. In-vitro studies with isolated SA progenitor cells had suggested that chromaffin cell differentiation depends crucially on glucocorticoids provided by adrenal cortical cells. However, analysis of mice lacking the glucocorticoid receptor gene had revealed that adrenal chromaffin cells develop mostly normally in these mice. Alternative cues from the adrenal cortex that may promote chromaffin cell determination and differentiation have not been identified. We therefore investigated whether the chromaffin cell phenotype can develop in the absence of an adrenal cortex, using mice deficient for the nuclear orphan receptor steroidogenic factor-1 (SF1), which lack adrenal cortical cells and gonads. We show that in Sf1^-/- mice typical chromaffin cells assemble correctly in the suprarenal region adjacent to the suprarenal sympathetic ganglion. The cells display most features of chromaffin cells, including the typical large chromaffin granules. Sf1^-/- chromaffin cells are numerically reduced by about 50% compared with the wild type at embryonic day (E) 13.5 and E17.5. This phenotype is not accounted for by reduced survival or cell proliferation beyond E12.5. However, already at E12.5 the 'adrenal' region in Sf1^-/- mice is occupied by fewer PHOX2B⁺ and TH⁺ SA cells as well as SOX10⁺ neural crest cells. Our results suggest that cortical cues are not essential for determining chromaffin cell fate, but may be required for proper migration of SA progenitors to and/or colonization of the adrenal anlage.
Guyenet, P. G. (2008). "The 2008 Carl Ludwig Lecture: retrotrapezoid nucleus, CO2 homeostasis, and breathing automaticity." JOURNAL OF APPLIED PHYSIOLOGY 105(2): 404-16.

The retrotrapezoid nucleus (RTN) contains 2,000 glutamatergic neurons that innervate selectively the respiratory centers of the pontomedullary region. These cells are at the ventral medullary surface in a previously identified chemosensitive region. RTN neurons are highly sensitive to acid in vitro and vigorously activated by inputs from the carotid body and from the hypothalamus in vivo. Mutations of the transcription factor Phox2b cause the congenital hypoventilation syndrome (CCHS), a disease characterized by extremely reduced chemoreflexes and the loss of breathing automaticity during sleep. RTN neurons express Phox2b and develop poorly in a mouse model of CCHS, which lacks chemoreflexes. Based on these and other data, I propose that the RTN is a critical nodal point for the homeostatic regulation of arterial PCO2 and that the nucleus operates as follows. RTN always contributes a major fraction of the tonic excitatory drive to the respiratory centers. RTN neurons derive their activity from two sources: a chemosensory drive (intrinsic chemosensitivity and inputs from the carotid bodies) and synaptic inputs from higher brain centers (non-chemosensory drive). Under anesthesia or non-rapid eye movement sleep, the chemosensory drive to RTN neurons dominates, and, under these circumstances, the excitatory input from RTN to the respiratory controller is required for breathing automaticity. During waking and exercise, RTN contributes a reduced fraction of the total excitatory drive to the respiratory controller, but this fraction remains essential for CO2 homeostasis because of its exquisite chemosensitivity. The working hypothesis could explain the breathing deficits experienced by CCHS patients. [References: 114]

Guyenet, P. G., D. A. Bayliss, et al. (2009). "Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity." Respiratory Physiology and Neurobiology 168(1-2): 59-68.

Breathing automaticity and CO2 regulation are inseparable neural processes. The retrotrapezoid nucleus (RTN), a group of glutamatergic neurons that express the transcription factor Phox2b, may be a crucial nodal point through which breathing automaticity is regulated to maintain CO2 constant. This review updates the analysis presented in prior publications. Additional evidence that RTN neurons have central respiratory chemoreceptor properties is presented, but this is only one of many factors that determine their activity. The RTN is also regulated by powerful inputs from the carotid bodies and, at least in the adult, by many other synaptic inputs. We also analyze how RTN neurons may control the activity of the downstream central respiratory pattern generator. Specifically, we review the evidence which suggests that RTN neurons (a) innervate the entire ventral respiratory column and (b) control both inspiration and expiration. Finally, we argue that the RTN neurons are the adult form of the parafacial respiratory group in neonate rats. copyright 2009 Elsevier B.V. All rights reserved.

Haddad, G. G., N. M. Mazza, et al. (1978). "Congenital failure of automatic control of ventilation, gastrointestinal motility and heart rate." MEDICINE 57(6): 517-26.

A new congenital syndrome characterized by the simultaneous failure of control of ventilation (Ondine's curse) and intestinal motility (Hirschsprung's disease) is reported in three infants, all of whom died in the first few months of life; two were siblings. Detailed studies in one also revealed markedly decreased esophageal motility and abnormal control of heart rate. In one infant, minute ventilation was lower in quiet than in REM sleep and lower in both states of sleep than in wakefulness. Although the mean inspiratory flow was decreased in quiet sleep, the hypoventilation resulted primarily from a decrease in respiratory frequency. Intravenous doxapram increased ventilation but did not reverse respiratory failure. Aminophyllin, progesterone, physostigmine and chlorpromazine did not change ventilation significantly; imipramine resulted in a significant decrease. Both long and short-term variability of the heart rate were markedly decreased when compared with the normal infant. Although neuropathologic studies postmorten did not reveal an anatomic defect, we postulate that a developmental abnormality in serotonergic neurons is responsible for this new syndrome.

Hager, A., W. Koch, et al. (2007). "Effects of movement and work load in patients with congenital central hypoventilation syndrome." European journal of cardiovascular prevention & rehabilitation 14(2): 294-8.

BACKGROUND: Patients with congenital central hypoventilation syndrome lack ventilatory chemosensitivity and depend at least in part on the ergoreceptor function during exercise. In these patients a substantial increase of ventilation has been reported for passive movement during sleep as well as active movement on a treadmill. OBJECTIVES: The aim of the study was to investigate ventilatory response to an increasing work load with constant movement. METHODS AND RESULTS: Eighteen patients and 17 healthy volunteers performed a cardiopulmonary exercise test on a bicycle pedaling at a constant rate of about 60 revolutions per minute throughout the entire test. The patients were able to exercise adequately and showed normal peak oxygen uptake. There was a steep rise in minute ventilation in both groups at the start of exercise, yet there was only a minor increase in both groups during the increase of workload up to the anaerobic threshold. After the anaerobic threshold, there was again an increase in ventilation in both groups, but the increase was less prominent in the patient group. CONCLUSIONS: Ventilation in patients with congenital central hypoventilation syndrome is increased during exercise caused both by movement (mechanoreceptors) and by anaerobic workload. This facilitates a normal ventilatory drive up to the anaerobic threshold and a normal exercise capacity in these patients.

Hamilton, J. and J. N. Bodurtha (1989). "Congenital central hypoventilation syndrome and Hirschsprung's disease in half sibs." JOURNAL OF MEDICAL GENETICS 26(4): 272-4.

We report two infants with congenital central hypoventilation syndrome and Hirschsprung's disease who have the same father but different mothers. The genetic implications of these cases are discussed. [References: 11]

Hammel, M., M. Klein, et al. (2009). "Congenital Central Hypoventilation Syndrome due to PHOX2b gene defects: inheritance from asymptomatic parents." KLINISCHE PADIATRIE 221(5): 286-9.

BACKGROUND: Congenital Central Hypoventilation Syndrome (CCHS, Ondine's curse) is a rare syndrome of dysfunction of the autonomic nervous system characterized by a decreased response to hypercarbia requiring mechanical ventilation in most cases. CCHS is an autosomal-dominant disease associated with tumors of neural crest origin, segmental aganglionosis of the colon, and diffuse autonomic dysregulation symptoms. Most cases of CCHS are caused by de novo heterozygous in-frame expansions within in the PHOX2b gene. PATIENTS AND MAIN RESULTS: Here we report two families in which a PHOX2b defect was inherited from an asymptomatic parent. In family 1 an asymptomatic mother carried a mild mutation (15 bp expansion within the polyalanine repeat) also found in her daughter who was symptomatic immediately after birth but did not require mechanical ventilation. In family 2, two newborn infants with respiratory failure due to insufficient respiratory drive requiring mechanical ventilation were born to asymptomatic parents. A 39 pb expansion within the PHOX2b polyalanine repeat was found in one patient in whom DNA was available, but not in blood leukocytes from any parent. Microsatellite analyses confirmed the identity of the parents, such that a germline mosaicism has to be deduced. CONCLUSIONS: Carriers of mild PHOX2b mutations causing disease in their offspring may be asymptomatic; Modifier genes determining the clinical course may exist. Germline mosaicism may lead to CCHS in children from unaffected parents. Genetic counseling should include these variations.

Han, J. and K.-K. Ma (2002). "Fuzzy color histogram and its use in color image retrieval." IEEE Transactions of Image Processing 11(8): 944-52.

A conventional color histogram (CCH) considers neither the color similarity across different bins nor the color dissimilarity in the same bin. Therefore, it is sensitive to noisy interference such as illumination changes and quantization errors. Furthermore, CCHs large dimension or histogram bins requires large computation on histogram comparison. To address these concerns, this paper presents a new color histogram representation, called fuzzy color histogram (FCH), by considering the color similarity of each pixel's color associated to all the histogram bins through fuzzy-set membership function. A novel and fast approach for computing the membership values based on fuzzy c-means algorithm is introduced. The proposed FCH is further exploited in the application of image indexing and retrieval. Experimental results clearly show that FCH yields better retrieval results than CCH. Such computing methodology is fairly desirable for image retrieval over large image databases.

Hansen, H., K. D. Thomsen, et al. (1992). "[Ondine's syndrome (alveolar hypoventilation)]." UGESKRIFT FOR LAEGER 154(31): 2160-1.

Ondine's syndrome is a rare condition characterised by alveolar hypoventilation during sleep on account of an abnormality in the automatic control of respiration. The respiration centre does not react adequately to the carbon dioxide tension in the blood required to maintain normal ventilation. We present a description of the course in an infant with congenital Ondine's syndrome because a therapeutic possibility is now available, viz, implantation of a phrenic nerve pacemaker. The infants showed respiratory insufficiency shortly after delivery. This disappeared on tactile stimulation. The infant had generalised hypotonia with absent patellar reflexes and weak sucking reflexes and, at the age of one week, seizures developed. The infant was treated with assisted ventilation but this could be reduced to use only during the period when the infant slept. The infant was in good health with normal psychomotor development until the age of two years. Plans had been made to implant a phrenic nerve pacemaker. Unfortunately, the infant developed Syncytial-virus pneumonia complicated by bacterial superinfection and developed severe anoxic brain damage which subsequently proved fatal.

Hardy, J. D. (1989). "Aneurysm of aberrant right subclavian artery and Ondine's curse." Journal of Thoracic & Cardiovascular Surgery 97(2): 319-20.

Harper, R. M., P. M. Macey, et al. (2005). "Hypercapnic exposure in congenital central hypoventilation syndrome reveals CNS respiratory control mechanisms." JOURNAL OF NEUROPHYSIOLOGY 93(3): 1647-58.

Congenital central hypoventilation syndrome (CCHS) patients show impaired ventilatory responses and loss of breathlessness to hypercapnia, yet arouse from sleep to high CO2, suggesting intact chemoreceptor afferents. The syndrome provides a means to differentiate brain areas controlling aspects of breathing. We used functional magnetic resonance imaging to determine brain structures responding to inspired 5% CO2-95% O2 in 14 CCHS patients and 14 controls. Global signal changes induced by the challenge were removed on a voxel-by-voxel basis. A priori-defined volume-of-interest time trends (assessed with repeated measures ANOVA) and cluster analysis based on modeling each subject to a step function (individual model parameter estimates evaluated with t-test, corrected for multiple comparisons) revealed three large response clusters to hypercapnia distinguishing the two groups, extending from the 1) posterior thalamus through the medial midbrain to the dorsolateral pons, 2) right caudate nucleus, ventrolaterally through the putamen and ventral insula to the mid-hippocampus, and 3) deep cerebellar nuclei to the dorsolateral cerebellar cortex bilaterally. Smaller clusters and defined areas of group signal differences in the midline dorsal medulla, amygdala bilaterally, right dorsal-posterior temporal cortex, and left anterior insula also emerged. In most sites, early transient or sustained responses developed in controls, with little, or inverse change in CCHS subjects. Limbic and medullary structures regulating responses to hypercapnia differed from those previously shown to mediate loaded breathing ventilatory response processing. The findings show the significant roles of cerebellar and basal ganglia sites in responding to hypercapnia and the thalamic and midbrain participation in breathing control.
Harper, R. M., V. L. Schechtman, et al. (1997). "Cardiovascular and respiratory control in congenital central hypoventilation syndrome." PEDIATRIC PULMONOLOGY 23(2): 152-153.

Hartmann, H., R. Schurmann, et al. (1995). "Ventilation with negative extrathoracic pressure in a newborn girl with congenital central hypoventilation syndrome. [German]." Monatsschrift fur Kinderheilkunde 143(7): 678-680.

A female infant with congenital central hypoventilation syndrome required intubation and intermittent mandatory ventilation from the first day of lite. On day 38 she was extubated and negative extrathoracic pressure ventilation was initiated. Ventilation was adequate with a peak pressure of minus 30 cmH₂O and endexpiratory pressure of minus 6 cmH₂O and a rate of 25 per minute (inspiratory time 1 s). Upper airway obstruction occurred during respiratory tract infections and was successfully treated with additional continuous positive airway pressure via nasal mask. The infant was discharged home at an age of 7 months and is treated with nocturnal negative extrathoracic pressure ventilation at 16 months. On one occasion, hospital admission was required during a respiratory tract infection. Negative extrathoracic pressure ventilation offers a safe and noninvasive alternative to positive pressure ventilation via tracheostomy for infants with congenital central hypoventilation syndrome.
Havenith, M. N., A. Zemmar, et al. (2009). "Measuring sub-millisecond delays in spiking activity with millisecond time-bins." NEUROSCIENCE LETTERS 450(3): 296-300.

Recent evidence indicates that sub-millisecond delays in neuronal spiking activity may be relevant for neural coding. Estimates of these delays are usually made from cross-correlation histograms (CCH) binned to 1 ms. We investigated the degree to which it is possible to measure delays with sub-millisecond precision when one computes CCHs with bin sizes [greater-than or equal to]1 ms. To this end, we introduced sub-millisecond shifts into spike trains recorded from cat visual cortex. The bin sizes of 1/2 to 2 ms were the most optimal for measuring the artificial shifts, even when detecting shifts smaller than 0.5 ms. The results suggest that preferably, one should use CCHs with [similar to]1 ms binning even when investigating differences in delays considerably smaller than 1 ms. copyright 2008 Elsevier Ireland Ltd. All rights reserved.

Haxhiu, M. A., A. S. P. Jansen, et al. (1993). "CNS innervation of airway-related parasympathetic preganglionic neurons: A transneuronal labeling study using pseudorabies virus." BRAIN RESEARCH 618(1): 115-134.

The CNS cell groups that innervate the tracheal parasympathetic preganglionic neurons were identified by the viral retrograde transneuronal labeling method. Pseudorabies virus (PRV) was injected into the tracheal wall of C8 spinal rats and after 4 days survival, brain tissue sections from these animals were processed for immunohistochemical detection of PRV. Retrogradely labeled parasympathetic preganglionic neurons were seen in three sites in the medulla: the compact portion of the nucleus ambiguus, the area ventral to the nucleus ambiguus, and the rostralmost portion of the medial nucleus tractus solitarius (NTS); this labeling pattern correlated well with the retrograde cell body labeling seen following cholera toxin beta-subunit injections in the tracheal wall. PRV transneuronally labeled neurons were found throughout the CNS with the most abundant labeling concentrated in the ventral medulla oblongata. Labeled neurons were identified along the ventral medullary surface, and in nearby areas including the parapyramidal, retrotrapezoid, gigantocellular and lateral paragigantocellular reticular nuclei as well as the caudal raphe nuclei (raphe pallidus, obscurus, and magnus). Serotonin (5-HT) neurons of the caudal raphe complex (B1-B3 cell groups) and ventromedial medulla were labeled as well as a few C1 adrenergic neurons. The A5 cell group was the major noradrenergic area labeled although a small number of locus coeruleus neurons were also labeled. Several NTS regions contained labeled cells including the commissural, intermediate, medial, central, ventral, and ventrolateral subnuclei. PRV infected neurons were present in the Kolliker-Fuse and Barrington's nuclei. In the rostral mesencephalon, the precommissural nucleus of the dorsal periventricular gray matter was labeled. Labeling was present in the dorsal, lateral and paraventricular hypothalamic nuclei. In summary, the airway parasympathetic preganglionic neurons are innervated predominantly by a network of lower brainstem neurons that lie in the same regions known to be involved in respiratory and cardiovascular regulation. These findings are discussed in relationship to some of the potential CNS mechanisms that may be operative in airway disorders as well as potentially involved in certain fatal respiratory conditions such as Ondine's curse and sudden infant death syndrome (SIDS).

Hedner, J., T. Hedner, et al. (1987). "Changes in cerebrospinal fluid homovanillic acid in children with Ondine's curse." PEDIATRIC PULMONOLOGY 3(2): 131-5.

The cerebrospinal fluid (CSF) concentrations of three acid monoamine metabolites, two purines, and a group of amino acids were determined in two children with chronic central alveolar hypoventilation (Ondine's curse). The levels of all assayed neuroactive substances, metabolites, and amino acids, with one exception, were normal compared to an age-matched group of neurologically healthy children. The levels of the dopamine metabolite homovanillic acid in the children with Ondine's curse were approximately 2.4 times higher than expected for age range. The present findings may indicate a link between central nervous system dopamine activity and chronic central alveolar hypoventilation. Among other possible explanations, the changes seen might represent a primary alteration in dopamine activity or may reflect a change in dopamine turnover resulting from the chronic hypoventilation.

Heintjes Edith, M., M. Berger, et al. (2003) Exercise therapy for patellofemoral pain syndrome. Cochrane Database of Systematic Reviews Volume, DOI: 10.1002/14651858.CD003472

BACKGROUND: Patellofemoral pain syndrome (PFPS) is a common problem among adolescents and young adults, characterised by retropatellar pain (behind the kneecap) or peripatellar pain (around the kneecap) when ascending or descending stairs, squatting or sitting with flexed knees. Etiology, structures causing the pain and treatment methods are all debated in literature, but consensus has not been reached so far. Exercise therapy to strengthen the quadriceps is often prescribed, though its efficacy is still debated. OBJECTIVES: This review aims to summarise the evidence of effectiveness of exercise therapy in reducing anterior knee pain and improving knee function in patients with PFPS. SEARCH STRATEGY: We searched the Cochrane Bone, Joint and Muscle Trauma Group and Cochrane Rehabilitation and Related Therapies Field specialised registers, the Cochrane Controlled Trials Register, PEDro - The Physiotherapy Evidence Database, MEDLINE, EMBASE, CINAHL, up till December 2001 for controlled trials (randomised or not) comparing exercise therapy with control groups, or comparing different types of exercise therapy. SELECTION CRITERIA: Only trials focusing on exercise therapy in patients with PFPS were considered. Trials in patients with other diagnoses such as tendinitis, Osgood Schlatter syndrome, bursitis, traumatic injuries, osteoarthritis, plica syndrome, Sinding-Larssen-Johansson syndrome and patellar luxations were excluded. DATA COLLECTION AND ANALYSIS: From 750 publications 12 trials were selected. All included trials studied quadriceps strengthening exercises. Outcome assessments for knee pain and knee function in daily life were used in a best evidence synthesis to summarise evidence for effectiveness. MAIN RESULTS: One high and two low quality studies used a control group not receiving exercise therapy. Significantly greater pain reduction in the exercise groups was found in one high and one low quality study, though at different time points. Only one low quality study reported significantly greater functional improvement with exercise. Five studies compared exercise therapies that could be designated closed kinetic chain exercise (foot in contact with a surface) versus open kinetic chain exercise (foot not in contact with a surface). Two of these studies were of high quality, but no significant differences in improvement of function or reduction of pain were apparent between the types of exercise in any of the studies. The remaining four studies, all of which were of low quality, focused on other treatment comparisons. AUTHORS' CONCLUSIONS: The evidence that exercise therapy is more effective in treating PFPS than no exercise was limited with respect to pain reduction, and conflicting with respect to functional improvement. There is strong evidence that open and closed kinetic chain exercise are equally effective. Further research to substantiate the efficacy of exercise treatment compared to a non-exercising control group is needed, and thorough consideration should be given to methodological aspects of study design and reporting. EXERCISE THERAPY FOR PATELLOFEMORAL PAIN SYNDROME: Patellofemoral pain syndrome (PFPS) is common among adolescents and young adults. The most common symptom is pain surrounding the knee cap when sitting with bent knees (movie sign) or when performing exercises like climbing stairs or squatting. Different treatments can be tried to reduce the pain and difficulties experienced during daily activities, including drugs and massage. Exercise regimens to strengthen the muscles surrounding and supporting the knee are another option. The review of exercise therapy found some evidence that exercise therapy might help to reduce the pain of PFPS. Whether exercise reduces knee problems during daily activities is unclear however, and more trials are needed.