Child Health in Elementary School Following California’s Paid Family Leave Program.

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Child Health in Elementary School Following California’s Paid Family Leave Program.

J Policy Anal Manage. 2017;36(4):790-827

Authors: Lichtman-Sadot S, Bell NP

Abstract
We evaluate changes in elementary school children health outcomes following the introduction of California’s Paid Family Leave (PFL) program, which provided parents with paid time off following the birth of a child. Our health outcomes--overweight, ADHD, and hearing-related problems--are characterized by diagnosis rates that only pick up during early elementary school. Moreover, our health outcomes have been found to be negatively linked with many potential implications of extended maternity leave--increased breastfeeding, prompt medical checkups at infancy, reduced prenatal stress, and reduced non-parental care during infancy. Using the Early Childhood Longitudinal Studies (ECLS) within a difference-in-differences framework, our results suggest improvements in health outcomes among California elementary school children following PFL’s introduction. Furthermore, the improvements are driven by children from less advantaged backgrounds, which is consistent with the notion that California’s PFL had the greatest effect on leave-taking duration after childbirth mostly for less advantaged mothers who previously could not afford to take unpaid leave.

PMID: 28991423 [PubMed - indexed for MEDLINE]

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Genetic counseling in CHARGE syndrome: Diagnostic evaluation through follow up.

Genetic counseling in CHARGE syndrome: Diagnostic evaluation through follow up.

Am J Med Genet C Semin Med Genet. 2017 Oct 31;:

Authors: Hefner MA, Fassi E

Abstract
CHARGE syndrome (CS) is a complex genetic disorder causing multiple birth defects and sensory deficits (hearing, vision, balance, smell). Genetic counseling in CS must include not only the provision of factual information about CS, its cause, and inheritance, but also information about the developmental implications of CS features, referral to appropriate resources, and assistance with psychosocial adaptation to this information. CS should be considered in patients with any of the major diagnostic features: coloboma, choanal atresia, semicircular canal anomalies, or cranial nerve anomalies. The prime candidates in the differential are 22q11.2 deletion and Kabuki syndromes. Evaluation of features of CS, dysmorphology examination, and genetic testing can usually distinguish between the three conditions. Genetic counseling is important from early on, to help the family understand the process of genetic diagnosis, to interpret information coming from other specialists and to provide support and resources. Parents can easily be overwhelmed with the complexity of issues facing their child at diagnosis and in the future. CS is a substantial burden on a child, with high early mortality, multiple illnesses, hospitalizations and surgeries, and apparent medical fragility throughout life. The medical complexity of CS disrupts family life and contributes to delayed development. Multiple sensory deficits (impaired vision, hearing, and balance) further contribute to delayed motor and language development despite many individuals with CS having normal intelligence. Early referral to specialists in deafblindness and sensory deficits is essential. Resources are available to assist genetic counselors in diagnosis, follow-up, and management of patients with CS.

PMID: 29088501 [PubMed - as supplied by publisher]

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Ribeye protein is intrinsically dynamic but is stabilized in the context of the ribbon synapse.

Ribeye protein is intrinsically dynamic but is stabilized in the context of the ribbon synapse.

J Physiol. 2017 Oct 31;:

Authors: Chen Z, Chou SW, McDermott BM

Abstract
Ribeye protein is a major constituent of the synaptic ribbon, an organelle that coordinates rapid and sustained vesicle release to enable hearing and balance. The ribbon is considered to be a stable structure. However, under certain physiological conditions such as acoustic overexposure that results in temporary noise-induced hearing loss or perturbations of ion channels, ribbons may change shape or vanish altogether, suggesting greater plasticity than previously appreciated. The dynamic properties of ribeye proteins are unknown. Here we use transgenesis and imaging to explore the behaviours of ribeye proteins within the ribbon and also their intrinsic properties outside the context of the ribbon synapse in a control cell type, the skin cell. By fluorescence recovery after photobleaching (FRAP) on transgenic zebrafish larvae, we test whether ribeye proteins are dynamic in vivo in real time. In the skin, a cell type devoid of synaptic contacts, Ribeye a-mCherry exchanges with ribbon-like structures on a minute timescale (t1/2  = 3.2 min). In contrast, Ribeye a of the ear and lateral line and Ribeye b of the lateral line each exchange at ribbons of hair cells an order of magnitude slower (t1/2 of 125.6 min, 107.0 min, and 95.3 min, respectively) than Ribeye a of the skin. These basal exchange rates suggest that long-term ribbon presence may require ribeye renewal. Our studies demonstrate that ribeye proteins are inherently dynamic but are stabilized at the ribbons of sensory cells in vivo. This article is protected by copyright. All rights reserved.

PMID: 29086422 [PubMed - as supplied by publisher]

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CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival.

CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival.

EMBO Mol Med. 2017 Oct 30;:

Authors: Michel V, Booth KT, Patni P, Cortese M, Azaiez H, Bahloul A, Kahrizi K, Labbé M, Emptoz A, Lelli A, Dégardin J, Dupont T, Aghaie A, Oficjalska-Pham D, Picaud S, Najmabadi H, Smith RJ, Bowl MR, Brown SD, Avan P, Petit C, El-Amraoui A

Abstract
Defects of CIB2, calcium- and integrin-binding protein 2, have been reported to cause isolated deafness, DFNB48 and Usher syndrome type-IJ, characterized by congenital profound deafness, balance defects and blindness. We report here two new nonsense mutations (pGln12* and pTyr110*) in CIB2 patients displaying nonsyndromic profound hearing loss, with no evidence of vestibular or retinal dysfunction. Also, the generated CIB2(-/-) mice display an early onset profound deafness and have normal balance and retinal functions. In these mice, the mechanoelectrical transduction currents are totally abolished in the auditory hair cells, whilst they remain unchanged in the vestibular hair cells. The hair bundle morphological abnormalities of CIB2(-/-) mice, unlike those of mice defective for the other five known USH1 proteins, begin only after birth and lead to regression of the stereocilia and rapid hair-cell death. This essential role of CIB2 in mechanotransduction and cell survival that, we show, is restricted to the cochlea, probably accounts for the presence in CIB2(-/-) mice and CIB2 patients, unlike in Usher syndrome, of isolated hearing loss without balance and vision deficits.

PMID: 29084757 [PubMed - as supplied by publisher]

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Genetic counseling in CHARGE syndrome: Diagnostic evaluation through follow up.

Genetic counseling in CHARGE syndrome: Diagnostic evaluation through follow up.

Am J Med Genet C Semin Med Genet. 2017 Oct 31;:

Authors: Hefner MA, Fassi E

Abstract
CHARGE syndrome (CS) is a complex genetic disorder causing multiple birth defects and sensory deficits (hearing, vision, balance, smell). Genetic counseling in CS must include not only the provision of factual information about CS, its cause, and inheritance, but also information about the developmental implications of CS features, referral to appropriate resources, and assistance with psychosocial adaptation to this information. CS should be considered in patients with any of the major diagnostic features: coloboma, choanal atresia, semicircular canal anomalies, or cranial nerve anomalies. The prime candidates in the differential are 22q11.2 deletion and Kabuki syndromes. Evaluation of features of CS, dysmorphology examination, and genetic testing can usually distinguish between the three conditions. Genetic counseling is important from early on, to help the family understand the process of genetic diagnosis, to interpret information coming from other specialists and to provide support and resources. Parents can easily be overwhelmed with the complexity of issues facing their child at diagnosis and in the future. CS is a substantial burden on a child, with high early mortality, multiple illnesses, hospitalizations and surgeries, and apparent medical fragility throughout life. The medical complexity of CS disrupts family life and contributes to delayed development. Multiple sensory deficits (impaired vision, hearing, and balance) further contribute to delayed motor and language development despite many individuals with CS having normal intelligence. Early referral to specialists in deafblindness and sensory deficits is essential. Resources are available to assist genetic counselors in diagnosis, follow-up, and management of patients with CS.

PMID: 29088501 [PubMed - as supplied by publisher]

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Ribeye protein is intrinsically dynamic but is stabilized in the context of the ribbon synapse.

Ribeye protein is intrinsically dynamic but is stabilized in the context of the ribbon synapse.

J Physiol. 2017 Oct 31;:

Authors: Chen Z, Chou SW, McDermott BM

Abstract
Ribeye protein is a major constituent of the synaptic ribbon, an organelle that coordinates rapid and sustained vesicle release to enable hearing and balance. The ribbon is considered to be a stable structure. However, under certain physiological conditions such as acoustic overexposure that results in temporary noise-induced hearing loss or perturbations of ion channels, ribbons may change shape or vanish altogether, suggesting greater plasticity than previously appreciated. The dynamic properties of ribeye proteins are unknown. Here we use transgenesis and imaging to explore the behaviours of ribeye proteins within the ribbon and also their intrinsic properties outside the context of the ribbon synapse in a control cell type, the skin cell. By fluorescence recovery after photobleaching (FRAP) on transgenic zebrafish larvae, we test whether ribeye proteins are dynamic in vivo in real time. In the skin, a cell type devoid of synaptic contacts, Ribeye a-mCherry exchanges with ribbon-like structures on a minute timescale (t1/2  = 3.2 min). In contrast, Ribeye a of the ear and lateral line and Ribeye b of the lateral line each exchange at ribbons of hair cells an order of magnitude slower (t1/2 of 125.6 min, 107.0 min, and 95.3 min, respectively) than Ribeye a of the skin. These basal exchange rates suggest that long-term ribbon presence may require ribeye renewal. Our studies demonstrate that ribeye proteins are inherently dynamic but are stabilized at the ribbons of sensory cells in vivo. This article is protected by copyright. All rights reserved.

PMID: 29086422 [PubMed - as supplied by publisher]

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CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival.

CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival.

EMBO Mol Med. 2017 Oct 30;:

Authors: Michel V, Booth KT, Patni P, Cortese M, Azaiez H, Bahloul A, Kahrizi K, Labbé M, Emptoz A, Lelli A, Dégardin J, Dupont T, Aghaie A, Oficjalska-Pham D, Picaud S, Najmabadi H, Smith RJ, Bowl MR, Brown SD, Avan P, Petit C, El-Amraoui A

Abstract
Defects of CIB2, calcium- and integrin-binding protein 2, have been reported to cause isolated deafness, DFNB48 and Usher syndrome type-IJ, characterized by congenital profound deafness, balance defects and blindness. We report here two new nonsense mutations (pGln12* and pTyr110*) in CIB2 patients displaying nonsyndromic profound hearing loss, with no evidence of vestibular or retinal dysfunction. Also, the generated CIB2(-/-) mice display an early onset profound deafness and have normal balance and retinal functions. In these mice, the mechanoelectrical transduction currents are totally abolished in the auditory hair cells, whilst they remain unchanged in the vestibular hair cells. The hair bundle morphological abnormalities of CIB2(-/-) mice, unlike those of mice defective for the other five known USH1 proteins, begin only after birth and lead to regression of the stereocilia and rapid hair-cell death. This essential role of CIB2 in mechanotransduction and cell survival that, we show, is restricted to the cochlea, probably accounts for the presence in CIB2(-/-) mice and CIB2 patients, unlike in Usher syndrome, of isolated hearing loss without balance and vision deficits.

PMID: 29084757 [PubMed - as supplied by publisher]

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