Complete Genome Sequence of Clostridium innocuum Strain LC-LUMC-CI-001, Isolated from a Patient with Recurrent Antibiotic-Associated Diarrhea.

Here, we report the complete genome sequence of Clostridium innocuum strain LC-LUMC-CI-001. As recently as 2018, C. innocuum was generally considered a benign gastrointestinal microorganism. This strain was isolated from the stool of a patient with recurrent Clostridioides difficile infection-like illnesses.

Complete Genome Sequence of Clostridium innocuum Strain ATCC 14501.

We report the complete genome sequence of Clostridium innocuum ATCC 14501, which was isolated in 1962 from an appendiceal abscess. At that time, the isolated strain was designated C. innocuum, given its suspected lack of virulence, but recent reports suggest that C. innocuum is an emerging pathogen.

Acro-cardio-facial syndrome associated with neuroepithelial cyst: a case report.

Acro-cardio-facial syndrome (ACFS) is a very rare genetic syndrome. Only 5 patients have been reported in the literature so far. A female neonate presented with limb abnormalities, cleft palate and congenital heart disease was diagnosed as ACFS. Her cranial magnetic resonance imaging revealed a huge cerebral neuroepithelial cyst. To our knowledge, this is the first case of ACFS in the literature associated with a neuroepithelial cyst in the brain.

Inhibition of vascular endothelial growth factor-induced retinal neovascularization by retinoic acid in experimental retinopathy of prematurity.

Vascular endothelial growth factor (VEGF) has an important role in the pathogenesis of retinopathy of prematurity (ROP) and inhibition of VEGF expression in the neovascular phase might prevent destructive neovascularization in ROP. It is suggested that retinoids exert a highly potent antiangiogenic activity by inhibiting VEGF expression. The aim of this study was to demonstrate the preventive effect of retinoic acid (RA) on the VEGF-induced retinal neovascularization in a rat model of ROP. Wistar albino rats were placed into incubators at birth and exposed to an atmosphere alternating between 50 % and 10 % O(2) every 24 hours. After 14 days, the animals were removed to room air and received either an intraperitoneal injection of RA (5 mg/kg/day) (n=9) or saline (n=4) daily for six days, and sacrificed at 21 days. Other rats (n=4) were raised in room air and served as age-matched controls. The globe of each eye was cut through the cornea and embedded in paraffin. Serial sections were stained with hematoxylin-eosin for quantification of neovascular nuclei. The avidin-biotin peroxidase method was performed for evaluation of VEGF expression. The average number of neovascular nuclei was significantly lower in the control group compared to that in the ROP groups. In addition, it significantly decreased in the RA-treated ROP group compared to that of the saline-administrated ROP group. VEGF immunostaining was overall negative in room air-exposed rats. The VEGF immunostaining score significantly decreased in the RA-treated ROP group compared to that in the saline-administered ROP group. RA treatment might be beneficial in preventing neovascularization resulting from oxygen-induced retinopathy by downregulation of VEGF expression.

Heat shock protein 70 expression in neonatal rats after hypoxic stress.

OBJECTIVES: The tissue damage due to hypoxia in newborns is to some extent age-dependent; organs of premature babies are more vulnerable to hypoxic insult than full-term neonates. The aim of this immunohistochemical study was to investigate the role of heat shock protein 70 (HSP70), a stress-inducible protein, in developing the response to hypoxia in premature newborns. METHODS: Postnatal day-7 rats (corresponding to a human fetus of 32-34 weeks' gestation) and day-12 rats (corresponding to a full-term newborn infant) (n = 7) were subjected to mild hypoxia at 33 degrees C. Control rats (n = 7) for each group breathed room air for 4 h. After 4 h of recovery, the animals were killed, and brains, hearts and kidneys were removed for immunohistochemical staining. RESULTS: Immunohistochemically, HSP70 expression was found to be induced in the hippocampus and myocardium after exposure to hypoxia. The level of HSP70 expression in the hippocampus after hypoxic stress was significantly higher in the 12-day rats than in the 7-day rats (p = 0.03). However, HSP70 expression in the myocardium did not show any significant difference between the two groups. In addition, no significant induction of HSP70 expression was apparent in the kidney of rats exposed to hypoxia or in any organ of the control animals. CONCLUSIONS: We conclude that diminished HSP70 expression in the hippocampus of premature newborns may play a critical role in developing the response to hypoxic stress. However, HSP70 expression in the heart and the kidney after exposure to hypoxia did not appear to be related to fetal maturity.

Involuntary movements in infantile cobalamin deficiency appearing after treatment.

Involuntary movements may be a symptom in most infants who present with neurologic syndrome of infantile cobalamin (vitamin B12) deficiency. In this report, two infants with cobalamin deficiency are presented. These patients also developed a striking movement disorder that appeared a few days after treatment with intramuscular cobalamin. The movement disorder was characterized by severe involuntary movements, which were a combination of tremor and myoclonus particularly involving tongue, face, pharynx, and legs. The neurologic symptoms improved within a few days after the administration of clonazepam. In each patient the mother was also cobalamin deficient and the infant was solely breast-fed. The cause of involuntary movements that can appear rarely after treatment in infantile cobalamin deficiency is not known. Besides initial neurologic presenting symptoms of cobalamin deficiency, the occurrence of involuntary movements after treatment should also receive attention. This movement disorder may disappear spontaneously, or an additional treatment may be an alternative approach if the symptoms are severe.

Oral cyclic megadose methylprednisolone therapy for chronic immune thrombocytopenic purpura in childhood.

The objectives of this study were to investigate the effectiveness of oral megadose methylprednisolone (OMMP) therapy in children with chronic immune thrombocytopenic purpura (ITP). Twenty-two patients were given oral methylprednisolone daily for 7 d (30 mg/kg for 3 d and then 20 mg/kg for 4 d). OMMP therapy was repeated once per month if the platelet count was less than 20,000/mm3 at the 30th day of therapy, for up to six courses. The number of platelets of all patients increased gradually during the OMMP therapy, with a peak number at the 7th day, then decreased until the 14th day, and remained relatively stable until 12 months. During the study no patient had a platelet count less than 20,000/mm3 at the 3rd day and 50,000/mm3 at the 7th day. Although the number of platelets was gradually decreased between the 7th and 14th days, it remained above 100,000/mm3 for at least 12 months in the nine patients, and above 20,000/mm3 in the four patients. None of these 13 patients required hospitalization or therapy during the follow-up period. All of the patients tolerated the medication well. None of them reported side-effects that were severe enough to discontinue therapy. We conclude that OMMP therapy is a safe, easy and effective therapy in children with refractory chronic ITP, and it may provide long-term remission in about two thirds of the patients.