On January 27, 1991, Dr. Dre encountered Barnes at a record release party in Hollywood. According to Barnes, he picked her up by her hair and "began slamming her head and the right side of her body repeatedly against a brick wall near the stairway" as his bodyguard held off the crowd with a gun. After Dr. Dre tried to throw her down the stairs and failed, he began kicking her in the ribs and hands. She escaped and ran into the women's restroom. Dr. Dre followed her and "grabbed her from behind by the hair again and proceeded to punch her in the back of the head". Finally, Dre and his bodyguard ran from the building.[6]
Embryonal carcinoma (EC) cells are pluripotent stem cells extensively used for studies of cell differentiation. Although retinoic acid (RA) is a powerful inducer of neurogenesis in EC cells, it is not clear what specific neuronal subtypes are generated and whether different RAR isotypes may contribute to such neuronal diversification. Here we show that RA treatment during EC embryoid body formation is a highly robust protocol for generation of striatal-like GABAergic neurons which display molecular characteristics of striatopallidal medium spiny neurons (MSNs), including expression of functional dopamine D2 receptor. By using RARα, β and γ selective agonists we show that RARγ is the functionally dominant RAR in mediating RA control of early molecular determinants of MSNs leading to formation of striatopallidal-like neurons. In contrast, activation of RARα is less efficient in generation of this class of neurons, but is essential for differentiation of functional dopaminergic neurons, which may correspond to a subpopulation of inhibitory dopaminergic neurons expressing glutamic acid decarboxylase in vivo.
Body Pump 88.rar
Cells were collected by mild trypsinization in FACS buffer (PBS supplemented with 2% FCS), fixed by 1% PFA and permeabilized by 1% saponin, followed by indirect immunostaining with primary antibody detected by a secondary antibody coupled with fluorophore (see Table 1). Only single intracellular staining was performed. Cells were washed in FACS buffer and analysed by FACS Calibur. Cell populations were assessed by FlowJo software.
GERD, especially nocturnal GERD, can have a negative impact on productivity and health-related quality of life [1, 6, 16, 17]. Emotion, sleep, eating/drinking, and physical/social functioning are all significantly affected by GERD, although the most significant impact is on sleep [17]. Effective management of GERD symptoms is important to improve quality of life. Treatment is aimed towards alleviating the symptoms caused by the acid reflux. Some guidelines suggest diet/lifestyle modifications and the use of medications to treat GERD symptoms [8, 18]. These include pharmacological agents such as antacids or alkali mixtures, H2 receptor antagonists (H2RA) or proton pump inhibitors (PPI) [8]. However, evidence-based recommendations on use of pharmacological agents during pregnancy and lactation have been lacking [9, 10].
An electronic search through online databases was conducted for relevant articles published in English between 2009 and 2020. The keywords used for the search engine to obtain relevant papers were: GERD, pregnancy, breastfeeding, lactation, treatment, antacid, alginate, proton pump inhibitor, PPI, histamine-2 receptor antagonist, H2RA, mucosal protectant, potassium-competitive acid blocker, P-CAB, promotility, prokinetic. Potential articles of interest were read through and then selected for inclusion in this review. Bibliographies of relevant articles were also checked to obtain additional articles. Studies of interventions in pregnant and breastfeeding females with GERD symptoms, dyspepsia, reflux, epigastric pain, and hyperemesis gravidarum, were included in this review.
During a sleep study, a person sleeps while measurements of various physical functions are collected using sensors attached to the head, chest, and body parts. Bodily functions that may be measured during a sleep study include:
Carotenoids are a class of more than 750 naturally occurring pigments synthesized by plants, algae, and photosynthetic bacteria (1). These richly colored molecules are the sources of the yellow, orange, and red colors of many plants. Fruit and vegetables provide most of the 40 to 50 carotenoids found in the human diet. α-Carotene, β-carotene, β-cryptoxanthin, lutein, zeaxanthin, and lycopene are the most common dietary carotenoids (1). α-Carotene, β-carotene and β-cryptoxanthin are provitamin A carotenoids, meaning they can be converted by the body to retinol (Figure 1). Lutein, zeaxanthin, and lycopene are nonprovitamin A carotenoids because they cannot be converted to retinol (Figure 2).
The most recent international standard of measure for vitamin A is retinol activity equivalent (RAE), which represents vitamin A activity as retinol. It has been determined that 2 micrograms (µg) of β-carotene in oil provided as a supplement could be converted by the body to 1 µg of retinol, giving it an RAE ratio of 2:1. However, 12 µg of β-carotene from food are required to provide the body with 1 µg of retinol, giving dietary β-carotene an RAE ratio of 12:1. Other provitamin A carotenoids in food are less easily absorbed than β-carotene, resulting in RAE ratios of 24:1. RAE ratios are shown in Table 1.
Although β-carotene can be converted to vitamin A, the conversion of β-carotene to vitamin A decreases when body stores of vitamin A are high (see Absorption, Metabolism, and Bioavailability). This may explain why high doses of β-carotene have never been found to cause vitamin A toxicity. High doses of β-carotene (up to 180 mg/day) have been used to treat erythropoietic protoporphyria, a photosensitivity disorder, without toxic side effects (8).
The cholesterol-lowering agents, cholestyramine (Questran) and colestipol (Colestid), can reduce absorption of fat-soluble vitamins and carotenoids, as can mineral oil and Orlistat (Xenical), a drug used to treat obesity (150). Colchicine, a drug used to treat gout, can cause intestinal malabsorption. However, long-term use of 1 to 2 mg/day of colchicine did not affect serum β-carotene concentrations in one study (154). Increasing gastric pH through the use of proton-pump inhibitors (Omeprazole, Lansoprazole) may decrease the absorption of a single dose of a β-carotene supplement, but the effect is unlikely to be clinically significant (155).
Consistent with the idea that the SCN serves as the master clock, the selective disruption of SCN timing, either through tissue lesioning-based approaches, or through the genetically-based abrogation of the core clock transcriptional feedback loop, leads to a loss of clock timing properties (i.e., circadian arrythmia), which manifests at the level of both basic systems-level physiology, including melatonin release, adrenal corticosterone output and core body temperature as well as behavioral processes, including locomotor activity, and sleep [19,20,21,22,23,24,25]. Together, these observations support the long-standing idea that the SCN functions as the master pacemaker.
Another key feature of AD is the dysregulation of the circadian timing system, which is best embodied by a disruption in the sleep/wake cycle (e.g., highly fragmented and shifted sleep patterns: [118,119,120,121]), which has been reported in the preclinical phase of AD and is a well-characterized component of mid- and late stage AD [122,123,124]. Additionally, alterations in the clock-regulation of core body temperature rhythms, activity rhythms, the phasing of the pineal melatonin rhythm are also comorbid features of AD [125, 126]. 2ff7e9595c
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