False positive cases of elevated tetradecenoyl carnitine in newborn mass screening showed significant loss of body weight

Tryptophan depleting protocols are commonly used to study the role of serotonin in mood disorders. The present study examined the impact of a tryptophan-deficient diet and fluoxetine on the serotonergic regulation of neuroendocrine function and body weight. We hypothesized that the regulation of postsynaptic 5-HT1A receptors is dependent on the levels of 5-HT in the synapse. Rats on a control or a tryptophan-deficient diet received daily injections of saline or fluoxetine (5 or 10 mg·kg-1·day-1 ip) from day 7 to day 21. The tryptophan-deficient diet produced a 41% reduction in the level of 5-HT but no change in the density of [3H]paroxetine-labeled 5-HT transporters. Treatment with fluoxetine inhibited the gain in weight in rats maintained on the control diet. The tryptophan-deficient diet produced a significant loss in body weight that was not significantly altered by treatment with fluoxetine. Treatment with fluoxetine produced a dose-dependent desensitization of hormone responses to injection of the 5-HT1A receptor agonist (±)8-hydroxy-2-(di- n-propylamino)tetralin ((±)8-OH-DPAT). The tryptophan-deficient diet produced an increase in the basal levels of corticosterone but did not alter the basal levels of ACTH or oxytocin. Also, this diet inhibited the magnitude of 8-OH-DPAT-induced increase in plasma levels of ACTH and oxytocin but did not impair the ability of fluoxetine to desensitize the 5-HT1A receptor-mediated increase in plasma hormones. These data suggest that a reserve of 5-HT enables fluoxetine to desensitize postsynaptic 5-HT1A receptors in the hypothalamus. In conclusion, the profound physiological changes induced by tryptophan depletion may complicate the interpretation of studies using this experimental approach.

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Newborn mass screening for galactosemia

European Journal of Pediatrics ◽

10.1007/bf02143801 ◽

1995 ◽

Vol 154 (S2) ◽

pp. S37-S39 ◽

Cited By ~ 19

Author(s):

Susanne Schweitzer

Keyword(s):

Mass Screening ◽

Newborn Mass Screening

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Carotid body denervation effect on cytochrome oxidase activity in pre-Bötzinger complex of developing rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00765.2002 ◽

2003 ◽

Vol 94 (3) ◽

pp. 1115-1121 ◽

Cited By ~ 20

Author(s):

Qiuli Liu ◽

Judy Kim ◽

Jamye Cinotte ◽

Patricia Homolka ◽

Margaret T. T. Wong-Riley

Keyword(s):

Body Weight ◽

Cytochrome Oxidase ◽

Carotid Body ◽

Significant Loss ◽

Receptor Subunit ◽

Aspartate Receptor ◽

Bötzinger Complex ◽

Neurokinin 1 ◽

Maturational Process ◽

Carotid Body Denervation

Previously, we found that the rat pre-Bötzinger complex (PBC) exhibited reduced cytochrome oxidase (CO) activity on postnatal days (P) 3–4 and especially on P12, with a concomitant decrease in glutamate and N-methyl-d-aspartate receptor subunit 1, and an increase in GABA, GABAB, glycine recptor, and glutamate subunit 2. We hypothesized that the PBC would be more affected by carotid body denervation (CBD) during the two critical windows than at other times. Pairs of CBD and sham animals at each postnatal day from P2 to P14 and at P21 were operated on and survived for 3 days. Brain stems were processed for CO and neurokinin-1 receptor for the identification of PBC. Results indicate that CBD caused a significant loss in body weight in all animals and a reduction in PBC somal size when the surgery was between P2 and P7. CBD also induced a significant decrease in CO activity of the PBC in most animals and a distinct delay, as well as prolongation of the maturational process, especially when induced close to P3 and P11–P13.

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Experience and Problems of Newborn Mass Screening for Inborn Errors of Metabolism in Japan

Pediatrics International ◽

10.1111/j.1442-200x.1981.tb01242.x ◽

1981 ◽

Vol 23 (1) ◽

pp. 24-34

Author(s):

Teruo Kitagawa ◽

Misao Owada ◽

Takeshi Sakiyama ◽

Tomohiko Kojima ◽

Wakio Kondo

Keyword(s):

Mass Screening ◽

Inborn Errors Of Metabolism ◽

Inborn Errors ◽

Newborn Mass Screening

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Oxysterol changes along with cholesterol and vitamin D changes in adult phenylketonuric patients diagnosed by newborn mass-screening

Clinica Chimica Acta ◽

10.1016/j.cca.2012.10.011 ◽

2013 ◽

Vol 416 ◽

pp. 54-59 ◽

Cited By ~ 8

Author(s):

Hironori Nagasaka ◽

Yoshiyuki Okano ◽

Akihiko Kimura ◽

Tatsuki Mizuochi ◽

Yoshitami Sanayama ◽

...

Keyword(s):

Vitamin D ◽

Mass Screening ◽

Newborn Mass Screening

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Shallow Convolutional Neural Network for COVID-19 Outbreak Screening using Chest X-rays

10.36227/techrxiv.12156522.v1 ◽

2020 ◽

Cited By ~ 6

Author(s):

Himadri Mukherjee ◽

Subhankar Ghosh ◽

Ankita Dhar ◽

Sk. Md. Obaidullah ◽

KC Santosh ◽

...

Keyword(s):

Neural Network ◽

Deep Learning ◽

Convolutional Neural Network ◽

Mass Screening ◽

False Positive ◽

False Positive Rate ◽

Experimental Tests ◽

X Rays ◽

Imaging Data ◽

Learning Models

<div><div><div><p>Among radiological imaging data, chest X-rays are of great use in observing COVID-19 mani- festations. For mass screening, using chest X-rays, a computationally efficient AI-driven tool is the must to detect COVID-19 positive cases from non-COVID ones. For this purpose, we proposed a light-weight Convolutional Neural Network (CNN)-tailored shallow architecture that can automatically detect COVID-19 positive cases using chest X-rays, with no false positive. The shallow CNN-tailored architecture was designed with fewer parameters as compared to other deep learning models, which was validated using 130 COVID-19 positive chest X-rays. In this study, in addition to COVID-19 positive cases, another set of non-COVID-19 cases (exactly similar to the size of COVID-19 set) was taken into account, where MERS, SARS, Pneumonia, and healthy chest X-rays were used. In experimental tests, to avoid possible bias, 5-fold cross validation was followed. Using 260 chest X-rays, the proposed model achieved an accuracy of an accuracy of 96.92%, sensitivity of 0.942, where AUC was 0.9869. Further, the reported false positive rate was 0 for 130 COVID-19 positive cases. This stated that proposed tool could possibly be used for mass screening. Note to be confused, it does not include any clinical implications. Using the exact same set of chest X-rays collection, the current results were better than other deep learning models and state-of-the-art works.</p></div></div></div>

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Comparison of skinfold measurment and standard body weight as a method of mass screening for obesity.

Japanese journal of MHTS ◽

10.7143/jhep1985.17.397 ◽

1990 ◽

Vol 17 (4) ◽

pp. 397-407

Author(s):

Hiroyuki Imamura ◽

Kayoko Honda ◽

Masahiro Minayoshi ◽

Masaru Imai ◽

Kazuhiro Kunikata ◽

...

Keyword(s):

Body Weight ◽

Mass Screening

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Abstract 76: Ablation of Parkin Attenuates Acute Cardiotoxicity of Doxorubicin Associated with Mitophagy

Circulation Research ◽

10.1161/res.111.suppl_1.a76 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Chengqun Huang ◽

Allen Andres ◽

Jennifer Ramil ◽

Roberta Gottlieb

Keyword(s):

Body Weight ◽

Cardiac Dysfunction ◽

Mitochondrial Protein ◽

Significant Loss ◽

High Dose ◽

Male Mice ◽

Mitochondrial Content ◽

Significant Deterioration ◽

Knock Out ◽

Acute Cardiotoxicity

Parkin is an E3 ubiquitin ligase expressed in heart, skeletal muscle and brain. However, the function of Parkin in the heart is largely unknown. We previously showed in cardiomyocytes and the ischemic heart that Parkin translocates to mitochondria to selectively remove damaged mitochondria through autophagy. It has been shown that Doxorubicin (Dox) induces cardiotoxicity characterized by impaired mitochondrial respiration and energetic failure (PLoS One. 2010; 5:e12733). Here, we investigated the role of Parkin in acute Doxorubicin-induced cardiac dysfunction in mice. Acute cardiotoxicity was induced by IP injection of a single dose of 15 mg/kg Doxorubicin hydrochloride in 10-12 wk-old C57BL/6J (WT) mice and Parkin knock out (PKO) mice matched by age, sex and body weight. Analysis of histology, hemodynamics, and mitochondrial content was performed 7d after Dox. Dox induced significant loss of body weight but less in PKO mice (20% in WT vs 12% in PKO). Dox toxicity was more severe in male mice. Signs of discomfort (decreased mobility and hunched posture) were noted 4d after Dox in 90% of WT male mice vs. 20% of PKO males. Mortality at 7d was 30% in WT mice vs. 10% in PKO mice. Dox caused reduction in heart size to a greater extent (10-20%) in WT than in PKO mice. Significant deterioration of hemodynamics was seen in WT mice 7d after Dox; this was attenuated in PKO mice. Because Parkin mediates mitophagy, we examined autophagy and mitochondrial content 7d in Dox treated hearts. Dox resulted in extensive autophagy and decreased mitochondrial protein content in WT mice; this was attenuated in PKO mice. These results suggest that high-dose Dox triggers extensive Parkin-dependent mitophagy which may contribute to acute cardiac dysfunction. We suggest that therapy directed at the PINK1-Parkin mitophagy pathway may be beneficial in the setting of doxorubicin overdose.

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