This study aimed to investigate whether the administration of mononuclear cells derived from human umbilical cord blood cells (UCBCs) could ameliorate hypoxic-ischemic brain injury in a neonatal rat model. The left carotid arteries of 7-day-old rats were ligated, and the rats were then exposed to 8% oxygen for 60 min. Mononuclear cells derived from UCBCs using the Ficoll-Hypaque technique were injected intraperitoneally 6 h after the insult (1.0 × 10⁷ cells). Twenty-four hours after the insult, the number of cells positive for the oxidative stress markers 4-hydroxy-2-nonenal and nitrotyrosine, in the dentate gyrus of the hippocampus in the UCBC-treated group, decreased by 36 and 42%, respectively, compared with those in the control group. In addition, the number of cells positive for the apoptosis markers active caspase-3 and apoptosis-inducing factor decreased by 53 and 58%, respectively. The number of activated microglia (ED1-positive cells) was 51% lower in the UCBC group compared with the control group. In a gait analysis performed 2 weeks after the insult, there were no significant differences among the sham-operated, control and UCBC groups. An active avoidance test using a shuttle box the following week also revealed no significant differences among the groups. Neither the volumes of the hippocampi, corpus callosum and cortices nor the numbers of neurons in the hippocampus were different between the UCBC and control groups. In summary, a single intraperitoneal injection of UCBC-derived mononuclear cells 6 h after an ischemic insult was associated with a transient reduction in numbers of apoptosis and oxidative stress marker-positive cells, but it did not induce long-term morphological or functional protection. Repeated administration or a combination treatment may be required to achieve sustained protection.

LT4 is widely used for infants, including VLBW infants, and no major complications have been reported. However, our study revealed that more than a few cases of LCC were associated with the administration of LT4 in VLBW infants. In conclusion, careful attention is necessary when initiating the administration of LT4 to VLBW infants.

Infants with trisomy 18 (T18) previously had a poor prognosis; however, the intensive care of these patients has markedly diversified the prognosis. We investigated the current situation of patients with T18, clarified factors for survival discharge, and surveyed actual home healthcare. A total of 117 patients with T18 admitted to nine institutions between 2000 and 2015 were retrospectively investigated. After excluding four patients whose outcomes were unclear, we divided 113 patients into two groups—the survival discharge group (n = 52) and the death discharge group (n = 61)—and compared maternal factors, perinatal factors, neonatal factors, and therapeutic factors between the groups. In addition, home healthcare, readmission, utilization of respite care and home nursing, and cause of death among the survival group were surveyed. Fifty‐two (44%) patients with T18 survived at discharge and their 1‐year survival rate was 29%. The survival group had a longer gestation period, larger physique, and longer survival time, compared to the death group. Independent factors associated with survival discharge were the absence of an extremely low birthweight infant (ELBWI), the absence of esophageal atresia and patent ductus arteriosus, and cardiovascular surgery. All surviving patients required some home healthcare. The most frequent cause of death was a respiratory disorder. We recommend discussing the treatment strategy with families in the presence of neonatologists or pediatric surgeons, who can explain differences in prognosis, based on the gestation period, birthweight, severity of cardiovascular disease, and cardiovascular surgery.

Riding giant roller coasters may increase the risk of subdural hematomas. There have been three recent case reports on the topic. 1-3 A 26-year-old man developed bilateral subdural hematomas after riding a double-loop, corkscrew-type roller coaster. 1 A 64-year-old hypertensive man had headaches after his first rollercoaster ride and developed a left-sided chronic subdural hematoma after 11 more rides. These two cases had successful surgical evacuation. 1-2 A fatal outcome was reported in a 73-year-old man being treated with warfarin. 3 This patient developed a left-sided subdural hematoma and a parenchymal temporal hematoma 5 days after a roller-coaster ride. Despite surgery, he died 13 days later.We report the new case of a previously healthy woman who developed headaches and bilateral chronic subdural hematomas after a series of roller-coaster rides.Case report. A 24-year-old Japanese woman visited our hospital with a headache of 4 days duration. She was otherwise in good health and did not previously have headaches. She drank alcohol only on social occasions and did not smoke. She visited amusement parks three or four times per year. The headache developed as the woman was on her way home from Fujikyu Highland Park, Yamanashi Pref., Japan, where she had ridden three different roller coasters, each twice. One of these, the Fujiyama, is the world's highest roller coaster at 259 feet. It has a drop of 230 feet at an angle of 65°and has the world's fastest speed of 81 mph (http://www.rollercoaster.com/statistics accessed March 1, 1999). There was no direct trauma to her head or loss of consciousness during the rides. In the first interview, she did not mention rollercoaster rides but stressed how hard her visual display terminal (VDT) work had been over the past 2 months.The woman's headache was constant, mainly suboccipital, worse in the evening, and partially relieved by rest. Upon examination, her temperature was 36.8°C, blood pressure 84/50 mm Hg, and heart rate 72 beats per minute. She was alert, cooperative, and well oriented. There was no evidence of head trauma, and her tympanic membranes were normal. Her neck was supple, but her shoulders were stiff and tender. Neurologic examination results were normal. Her pupils were equal and reactive to light, and there was no papilledema or retinal hemorrhages. Routine laboratory tests for blood and urine all were normal. Tension-type headache was initially diagnosed, and muscle relaxants were prescribed for 4 weeks with some benefit; the headaches fluctuated but were unrelieved.Two months later, MRI of the head ruled out an organic problem and showed bilateral subdural hematomas with neomembranes (figure). At this time, coagulation tests gave a platelet count of 189,000/mm 3 , a bleeding time of 4 minutes, a whole-blood clotting time of 6 minutes, a prothrombin time of 12.2 sec, an activated partial thromboplastin time of 40 seconds, and an AT-III of 111%. Fibrinogen and fibrin degradation product (FDP) serum levels were normal. We evacuated both hematomas, which ...

Neonatal hypoxic-ischemic (HI) encephalopathy (HIE) remains a major cause of mortality and persistent neurological disabilities in affected individuals. At present, hypothermia is considered to be the only applicable treatment option, although growing evidence suggests that cell-based therapy might achieve better outcomes. Dedifferentiated fat (DFAT) cells are derived from mature adipocytes via a dedifferentiation strategy called ceiling culture. Their abundance and ready availability might make them an ideal therapeutic tool for the treatment of HIE. In the present study, we aimed to determine whether the outcome of HIE can be improved by DFAT cell treatment. HI injury was achieved by ligating the left common carotid artery in 7-day-old rat pups, followed by 1-h exposure to 8% O₂. Subsequently, the severity of damage was assessed by diffusion-weighted magnetic resonance imaging to assign animals to equivalent groups. 24 h after hypoxia, DFAT cells were injected at 10⁵ cells/pup into the right external jugular vein. To evaluate brain damage in the acute phase, a group of animals was sacrificed 48 h after the insult, and paraffin sections of the brain were stained to assess several acute injury markers. In the chronic phase, the behavioral outcome was measured by performing a series of behavioral tests. From the 24th day of age, the sensorimotor function was examined by evaluating the initial forepaw placement on a cylinder wall and the latency to falling from a rotarod treadmill. The cognitive function was tested with the novel object recognition (NOR) test. In vitro conditioned medium (CM) prepared from cultured DFAT cells was added at various concentrations to neuronal cell cultures, which were then exposed to oxygen-glucose deprivation (OGD). The number of cells that stained positive for the apoptosis marker active caspase-3 decreased by 73 and 52% in the hippocampus and temporal cortex areas of the brain, respectively, in the DFAT-treated pups. Similarly, the numbers of ED-1-positive cells (activated microglia) decreased by 66 and 44%, respectively, in the same areas in the DFAT-treated group. The number of cells positive for the oxidative stress marker 4-hydroxyl-2-nonenal decreased by 68 and 50% in the hippocampus and the parietal cortex areas, respectively, in the DFAT-treated group. The HI insult led to a motor deficit according to the rotarod treadmill and cylinder test, where it significantly affected the vehicle group, whereas no difference was confirmed between the DFAT and sham groups. However, the NOR test indicated no significant differences between any of the groups. DFAT treatment did not reduce the infarct volume, which was confirmed immunohistochemically. According to in vitro experiments, the cell death rates in the DFAT-CM-treated cells were significantly lower than those in the controls when DFAT-CM was added 48 h prior to OGD. The treatment effect of adding DFAT-CM 24 h prior to OGD was also significant. Our results indicate that intravenous injection with DFAT cells i...

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Many children with trisomy 18 have apneas from the neonatal period. It has been reported that some children with trisomy 18 have epilepsy, including epileptic apneas. However, no previous report has described epileptic apneas in trisomy 18 neonates. We retrospectively reviewed the clinical records of neonates with trisomy 18 who were born at Anjo Kosei Hospital between July 2004 and October 2013 and investigated whether they had epileptic apneas during the neonatal period and whether antiepileptic drugs (AEDs) were effective for treating them. We identified 16 patients with trisomy 18. Nine patients who died within 3 days of birth were excluded. Five of the remaining seven patients had apneas. All five patients underwent electroencephalograms (EEGs) to assess whether they suffered epileptic apneas. Three of the five patients had EEG-confirmed seizures. In two patients, the apneas corresponded to ictal discharges. In one patient, ictal discharges were recorded when she was under mechanical ventilation, but no ictal discharges that corresponded to apneas were recorded after she was extubated. AEDs were effective for treating the apneas and stabilizing the SpO2 in all three patients. Among neonates with trisomy 18 who lived longer than 3 days, three of seven patients had EEG-confirmed seizures. AEDs were useful for treating their epileptic apneas and stabilizing their SpO2. Physicians should keep epileptic apneas in mind when treating apneas in neonates with trisomy 18.

We concluded that it might therefore be important to centralize infants with CDH, especially those with isolated CDH with a prenatal diagnosis, to tertiary centers in Japan in order to improve the survival rates.