The repeating dislodgement of an ASO device

Transcatheter closure with an Amplatzer Septal Occluder (ASO) has become the standard treatment for secundum atrial septal defect (ASD). However, this procedure is associated with complications, such as device dislodgement. A 52-year-old woman was admitted with exertional dyspnea. Transesophageal echocardiography showed an ASD involving a 29 mm defect. Calculated Qp/Qs was 5.6 and all the rims were > 5 mm, with the exception of the posterior rim, which was 3 mm. Transcatheter ASD closure with an ASO was performed under general anesthesia. During emergence from anesthesia, tachycardia developed and the ASO device became dislodged. Hemodynamic changes associated with the end of anesthetic administration were believed to have led to device dislodgement. In a second transcatheter ASD closure, a low dose of propofol and remifentanil was maintained during emergence from anesthesia to reduce hemodynamic changes. However, device dislodgement occurred with nonsustained ventricular tachycardia. Finally, surgical ASD closure was performed. The large defect size, high Qp/Qs, and rim deficiency may have predisposed to device dislodgement after transcatheter ASD closure with ASO. The risk of device dislodgement should be considered in advance of surgery and, in high-risk cases, the patient's cardiovascular status should be closely monitored

Degradation of Aroclor 1221 by microbial populations of the Lagos lagoon

Samples obtained from three locations in the Lagos lagoon were studied for the effect of Aroclor 1221 on their population dynamics. In all three cases, both control and experimental microcosms showedslight increases between day 5 and day 10 with the highest value of 4 × 1010 cfu/ml in control and 1.2 ×1011, 8 × 1010 and 9 × 1010 cfu/ml for Iddo, Apapa and Tin Can samples respectively. Three isolatesnamely, Bacillus subtilis, Alcaligenes eutrophus and Pseudomona aeruginosa were obtained from the microcosms after successive enrichment. All the isolates grew readily on 100 ppm of Aroclor 1221concomitant with production of yellow metabolites in mineral salts medium. Whereas maximal growth was observed at day 12 on biphenyl, that of the polychlorinated biphenyl (PCB) mixture was on day 15.Generally, growth dynamics were similar irrespective of the substrate while typical generation times, with the exception of B. subtilis on Aroclor 1221, ranged insignificantly (P < 0.05) from 6.86 to 8.35 day,thus, suggesting that chlorine substitution has little or no effect on catabolic potentials of the organisms. The degradative capability of these strains suggest that they contribute immensely to theself-purification processes occurring in the lagoon, and this could be exploited for decontamination of PCB polluted aquatic ecosystems

Two cases of possible neuro-Sweet disease with meningoencephalitis as the initial manifestation

We report 2 cases that were considered to be neuro-Sweet disease. They initially manifested with meningoencephalitis and no skin lesions, and rapidly improved with corticosteroid therapy. In both cases, patients complained of meningitic symptoms such as fever and headache, and HLA-B54 and -Cw1 turned out to be positive over the clinical course. Cerebrospinal fluid analysis showed increased levels of lymphocytes and protein. In case #1, fluid-attenuated inversion recovery (FLAIR), magnetic resonance imaging (MRI) and diffusion-weighted images (DWI) showed high-intensity signals in the right dorsal medulla oblongata, bilateral dorsal midbrain, and left thalamus. In case #2, FLAIR and DWI showed high-intensity signals in the bilateral cerebellar cortex and left caudate nucleus. Symptoms and MRI images were markedly improved in both cases after corticosteroid pulse therapy. According to published diagnostic criteria, these 2 cases were considered possible neuro-Sweet disease. These cases suggest that the combination of meningoencephalitis and HLA specificity is important to consider the possibility of neuro-Sweet disease, even without skin lesions

Mite antigen and allergen contents of house dust samples.

The house dust mite (Dermatophagoides pteronyssinus) antigen and allergen contents were measured by enzyme-linked immunosorbent assay (ELISA) with enzyme-labelled anti-human IgE and anti-mite rabbit IgG antibodies. Antigen content was high in dust samples from homes of patients with allergy but not in samples from homes of patients with Kawasaki disease or of normal control subjects. Allergen content was high in dust samples from homes of Kawasaki disease patients. However, the values overlapped, and we considered these differences to be of little ecological significance, although the assay method itself is useful.</p

cytokine profile of PFAPA

Objective : An attempt was made to identify characteristic cytokine profiles to distinguish periodic fever with aphthous stomatitis, pharyngitis and cervical adenitis syndrome (PFAPAS) from recurrent tonsillitis, of which clinical manifestations are similar to those of PFAPAS in children. Methods : Serum concentrations of IL-6, IL-4 and IFN-γ were measured during febrile episodes in pediatric patients. Results : The levels of IL-6 during febrile episodes were markedly increased above the upper limit of normal ranges in patients with both PFAPAS and recurrent tonsillitis, but there were no significant differences between groups. The levels of IL-4 during febrile episodes in PFAPAS patients were significantly lower than those in recurrent tonsillitis patients. The levels of IFN-γ during febrile episodes in PFAPAS patients were significantly higher than those in recurrent tonsillitis patients. Conclusion : In pediatric patients with PFAPAS, despite an increase of IL-6, IL-4 was suppressed with a marked increase of IFN-γ during febrile episodes. On the contrary, in febrile pediatric patients with recurrent tonsillitis, both IL-6 and IL-4, but not IFN-γ were increased. The characteristic cytokine profiles of IL-6, IL-4 and IFN-γ can be used for differential diagnosis of PFAPAS from recurrent tonsillitis in children in clinical ear, nose and throat (ENT) settings

When does facial synkinesis develop?

The objective of this study is to clarify when facial palsy patients with lower value of Electroneurography (ENoG) should begin the rehabilitation to prevent the development of facial synkinesis. For this purpose, we examined the relationship between the value of ENoG measured 10-14 days after facial palsy onset and the onset day of the development of oral-ocular synkinesis. Sixteen patients with facial palsy including 11 with Bell’s palsy and 5 with Ramsay Hunt syndrome (7 men and 9 women ; 15-73 years old ; mean age, 41.6 years) were enrolled in this study. There was no correlation between ENoG value and the onset day of the development of oral-ocular synkinesis (ρ = .09, p = .73). Oral-ocular synkinesis began to develop in 4.0 ± 0.7 months (mean ± SD ; range : 3.1-5.0 months) after facial palsy onset regardless of ENoG value. In conclusion, ENoG value cannot predict when facial synkinesis develops in patients with facial palsy. We recommend that facial palsy patients with a high risk for the development of synkinesis begin the biofeedback rehabilitation with mirror to prevent the development of facial synkinesis 3 months after facial palsy onset

Risk factors of first bite syndrome

Objective : First bite syndrome is a complication of surgical resection of parapharyngeal space tumors and the development of cramping pain in the parotid region with the first bite of a meal. The present study aimed to identify the potential risk factors for the development of first bite syndrome. Methods : We retrospectively reviewed 30 consecutive patients with parapharyngeal space tumors who had been surgically treated between August 2003 and December 2015 at our department. Results : The tumor site (prestyloid or retrostyloid) and surgical approach (transcervical-parotid, transparotid, or transcervical) were not correlated with the development of first bite syndrome. Ligation and mobilization of the external carotid artery was significantly correlated with the development of first bite syndrome. Moreover, patients with complete resection of the parotid gland did not experience first bite syndrome. Discussion : The present findings suggest that concomitant surgical settings of 1) sympathetic denervation of the parotid gland with ligation of the external carotid artery or injury of the sympathetic nerve plexus around the external carotid artery during its mobilization, and 2) residual parotid gland tissue are risk factors for the development of first bite syndrome after surgical resection of parapharyngeal space tumors

アーノルド・ファイン作品集

Urinary type IV collagen (U-Col4) and albumin excretion is evaluated to monitor the development of diabetic kidney disease. However, U-Col4 excretion in the general population without diabetes has not yet been fully elucidated. In this study, 1067 participants without diabetes and with urinary albumin-creatinine ratio <300 mg/gCr (normo- or microalbuminuria) who underwent an annual health examination in 2004 were enrolled and observed for 5 years. They were divided according to the amount of U-Col4 or urinary albumin excreted. The decline in estimated glomerular filtration rate (eGFR) was calculated. In participants with eGFR ≥80 mL/min, abnormal U-Col4 excretion was indicated as a significant independent risk factor for 10% eGFR change per year, which is one of the prognostic factors for the development of end-stage kidney disease. Moreover, in contrast to urinary albumin excretion, U-Col4 excretion was not related to age or kidney function, suggesting that some individuals with abnormal U-Col4 excretion can have an independent hidden risk for the development of kidney dysfunction. In conclusion, it is important to measure U-Col4 excretion in the general population without diabetes to determine changes in renal features in every individual and help detect future complications such as diabetic kidney disease. If U-Col4 excretion is abnormal, kidney manifestation should be carefully followed up, even if the kidney function and urinalysis findings are normal

ラムゼイ・ハント症候群症例の前庭蝸牛神経MRI造影効果と前庭蝸牛機能障害との関係

Objective: The correlation between enhancement of the vestibulocochlear nerves on gadolinium-enhanced magnetic resonance imaging (MRI) and vestibulocochlear functional deficits was examined in patients with Ramsay Hunt syndrome (RHS). Methods: Nineteen patients with RHS who showed herpes zoster oticus, peripheral facial palsy, and vertigo were enrolled. Canal paresis (CP) in the caloric test, abnormal response to ocular and cervical vestibular myogenic potentials (oVEMP and cVEMP), and refractory sensorineural hearing loss were evaluated. MRI images perpendicular to the internal auditory canal were reconstructed to identify the superior (SVN) and inferior vestibular nerves (IVN) and the cochlear nerve (CV). The signal intensity increase (SIinc) of the four-nerve enhancement was calculated as an index. Results: Among RHS patients, 79%, 53%, 17% and 26% showed CP in the caloric test, abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, respectively. SIinc rates of the SVN were significantly increased in RHS patients with CP in the caloric test, and with abnormal responses to oVEMP and cVEMP. SIinc rates of the SVN tended to increase in RHS patients with refractory sensorineural hearing loss ( p = 0.052). SIinc rates of the IVN were significantly increased in RHS patients with abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, but not in those with CP in the caloric test. SIinc rates of the CN were significantly increased in RHS patients with CP in the caloric test, abnormal response to oVEMP and refractory sensorineural hearing loss, but not in those with abnormal response to cVEMP. Conclusion: In patients with RHS, the origin of vertigo may be superior vestibular neuritis, which is affected by reactive varicella-zoster virus from the geniculate ganglion of the facial nerve through the faciovestibular anastomosis. The results also suggested that in some RHS patients, inferior vestibular neuritis contributes to the development of vertigo and that the origin of refractory sensorineural hearing loss is cochlear neuritis