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Gunter Bentsen posted an update 21 hours, 38 minutes ago
Therefore, the interference of circadian genes by cisplatin can have multiple, opposing effects on apoptosis and cell proliferation, which may have unintended pro-cancer effects. Melatonin and intracellular Ca2+ also have a dual-effect on cell proliferation and apoptosis and can disrupt circadian rhythms.Recently, it has been suggested that sleep problems in autism spectrum disorder (ASD) not only are associated symptoms, but may be deeply related to ASD pathogenesis. Common clinical practice relating to developmental disorders, has shown that parents of children with ASD have often stated that it is more difficult to raise children in the neonatal period because these children exhibit sleep problems. This study investigated the possibility that abnormal neonatal sleep-wake rhythms are related to future ASD development. We administered questionnaires to assess parent(s) of children with ASD and controls. A retrospective analysis was conducted among 121 children with ASD (94 male and 27 female children) recruited from the K-Development Support Center for Children (K-ASD), 56 children with ASD (40 male and 16 female children) recruited from the H-Children’s Sleep and Development Medical Research Center (H-ASD) and 203 children (104 male and 99 female children) recruited from four nursery schools in T-city (control). Irritable/over-reactive types of sleep-wake rhythms that cause difficulty in raising children, such as 1) frequently waking up, 2) difficulty falling asleep, 3) short sleep hours, and 4) continuous crying and grumpiness, were observed more often in ASD groups than in the control group. Additionally, the number of the mothers who went to bed after midnight during pregnancy was higher in the ASD groups than in the control group. Sleep-wake rhythm abnormalities in neonates may be considerable precursors to future development of ASD. Formation of ultradian and postnatal circadian rhythms should be given more attention when considering ASD development. Although this is a retrospective study, the results suggest that a prospective study regarding this issue may be important in understanding and discovering intervention areas that may contribute to preventing and/or properly treating ASD.Sleep deprivation (SD) and fatigue have detrimental effects on performance in operational settings. Few studies have investigated the cumulative effects of SD and fatigue on performance under heavy workload demands. Therefore, we investigated the efficacy of multiple repeated doses of caffeine as a countermeasure to SD and fatigue during 77 h total SD (TSD) during the early morning hours. Twenty-three males and females, 18 – 35 years of age, who identified as moderate caffeine consumers completed the Psychomotor Vigilance Task (PVT) 141 times during the experimental test period. Caffeine was administered in a multi-dose paradigm over three nights without sleep. Participants received either caffeine (200 mg) or placebo at the beginning of each 2-h test block from 0100 – 0900 (800 mg total per night). β-Nicotinamide clinical trial While PVT speed declined for both groups across all 3 nights, the caffeine group consistently out-performed the placebo group. Caffeine maintained attentiveness (1-5 s lapses) on night 1, but this advantage was lost on nights 2 and 3. Caffeine outperformed placebo for responsive lapses (5-9 s lapses) across all three nights, but caffeine performance was still notably worse than at baseline. Prolonged non-responsive lapses (beyond 10 s) were only reduced by caffeine on night 2. Caffeine was more effective than placebo across all nights at sustaining completion speed of a complex motor sequence task and a manual coordination task. Essentially, caffeine is an effective countermeasure for SD, as it mitigates declines in speed and failures to respond, and sustains motor planning and coordination. However, caffeine does not restore normal functioning during SD and cannot be considered as a replacement for sleep.
Examine the use of systemic phosphodiesterase inhibition (sildenafil) to clear central serous chorioretinopathy (CSCR).
In a long-standing CSCR patient, sildenafil produced a rapid resolution. When discontinued (dechallenge) the CSCR returned. When rechallenged, the CSCR again rapidly disappeared and did not recur in 5 months of continued therapy.
AND IMPORTANCE Systemic sildenafil can cause rapid clearance of CSCR and can augment or replace other treatments.
AND IMPORTANCE Systemic sildenafil can cause rapid clearance of CSCR and can augment or replace other treatments.
To report a case in which the axial length (AL) shortened and the choroid thickened due to the use of violet light-transmitting eyeglasses.
A 4-year-old boy with high myopia was referred to Keio University Hospital. He was prescribed standard eyeglasses. Six months after the first visit, his best-corrected visual acuities were 1.2 and 0.4 in the right and left eyes, respectively, with the standard eyeglasses, and he was diagnosed with anisometropic amblyopia. The right eye then was patched for 6 hours daily during the daytime. Because of the availability of violet light-transmitting eyeglasses, we changed the eyeglasses and instructed his parents to have him engage in outdoor activities for over 2 hours daily to be exposed to sufficient violet light. As a result, the violet light entered his left eye and minimal violet light entered his right eye. The changes in the ALs, choroidal thicknesses, and cycloplegic objective refractions in the right and left eyes during 2 years of wearing violet light-transmitting eyeglasses were +0.85 and -0.20 mm, +4.9 and+115.7 μm, and -1.02 and+1.88 D, respectively.
We successfully described a case in which the myopia improved, the AL shortened, and the choroid thickened after using violet light-transmitting eyeglasses.
We successfully described a case in which the myopia improved, the AL shortened, and the choroid thickened after using violet light-transmitting eyeglasses.
To report a rare case of optic neuritis with spine demyelination following H1N1 virus infection.
A 66-year-old female presented with decreased vision in both eyes (left>right) following a recent episode of fever and flu. She was diagnosed as H1N1 infection confirmed by viral antigen analysis of throat swab. On examination, she had a profound vision drop in the left eye with optic disc edema. MRI brain and orbit revealed bilateral optic nerve and frontal dural thickening with a ring-enhancing lesion in the right frontal lobe. MRI spine showed long cord signals at T1-T7 suggestive of demyelination. The patient had a complete recovery of vision and visual fields after intravenous and oral steroids.
Influenza A virus can manifest with a wide range of symptoms including flu-like illness to neurological complications. This case highlights optic neuritis as a presenting feature of H1N1 infection.
Influenza A virus can manifest with a wide range of symptoms including flu-like illness to neurological complications.