Transforming growth factor-beta and sonic hedgehog signaling in palatal epithelium regulate tenascin-C expression in palatal mesenchyme during soft palate development.

福岡歯科大学2020年

Management of esophageal stricture after complete circular endoscopic submucosal dissection for superficial esophageal squamous cell carcinoma

<p>Abstract</p> <p>Background</p> <p>Endoscopic submucosal dissection (ESD) permits removal of esophageal epithelial neoplasms <it>en bloc</it>, but is associated with esophageal stenosis, particularly when ESD involves the entire circumference of the esophageal lumen. We examined the effectiveness of systemic steroid administration for control of postprocedural esophageal stricture after complete circular ESD.</p> <p>Methods</p> <p>Seven patients who underwent wholly circumferential ESD for superficially extended esophageal squamous cell carcinoma were enrolled in this study. In 3 patients, prophylactic endoscopic balloon dilatation (EBD) was started on the third post-ESD day and was performed twice a week for 8 weeks. In 4 patients, oral prednisolone was started with 30 mg daily on the third post-ESD day, tapered gradually (daily 30, 30, 25, 25, 20, 15, 10, 5 mg for 7 days each), and then discontinued at 8 weeks. EBD was used as needed whenever patients complained of dysphagia.</p> <p>Results</p> <p><it>En bloc </it>ESD with tumor-free margins was safely achieved in all cases. Patients in the prophylactic EBD group required a mean of 32.7 EBD sessions; the postprocedural stricture was dilated up to 18 mm in diameter in these patients. On the other hand, systemic steroid administration substantially reduced or eliminated the need for EBD. Corticosteroid therapy was not associated with any adverse events. Post-ESD esophageal stricture after complete circular ESD was persistent, requiring multiple EBD sessions.</p> <p>Conclusions</p> <p>Use of oral prednisolone administration may be an effective treatment strategy for reducing post-ESD esophageal stricture after complete circular ESD.</p

A Postnatal Critical Period for Orientation Plasticity in the Cat Visual Cortex

Orientation selectivity of primary visual cortical neurons is an important requisite for shape perception. Although numerous studies have been previously devoted to a question of how orientation selectivity is established and elaborated in early life, how the susceptibility of orientation plasticity to visual experience changes in time remains unclear. In the present study, we showed a postnatal sensitive period profile for the modifiability of orientation selectivity in the visual cortex of kittens reared with head-mounted goggles for stable single-orientation exposure. When goggle rearing (GR) started at P16-P30, 2 weeks of GR induced a marked over-representation of the exposed orientation, and 2 more weeks of GR consolidated the altered orientation maps. GR that started later than P50, in turn, induced the under-representation of the exposed orientation. Orientation plasticity in the most sensitive period was markedly suppressed by cortical infusion of NMDAR antagonist. The present study reveals that the plasticity and consolidation of orientation selectivity in an early life are dynamically regulated in an experience-dependent manner

Attempts to retreat from a dead-ended long capillary by backward swimming in Paramecium

We have observed how the ciliate Paramecium attempts to retreat from the dead-end of a long capillary that is too narrow for turning. After many trial-and-error episodes of short-term backward swimming (SBS), which is the conventional avoidance behavior exhibited in free swimming when an obstacle is faced, long-term backward swimming (LBS) that lasted five to ten times longer was developed. LBS may have a beneficial effect for complete withdrawal from the capillary space, although in our experiment it was impossible for the organism to do so due to the capillary length. In order to identify a physically possible mechanism for LBS, we propose model equations for the membrane potential of Hodgkin–Huxley type, which describe the control of ciliary movement. The physiological implications and physical mechanism of the development of LBS are discussed

Apocrine Adenoma of the External Auditory Canal with Pseudoepitheliomatous Hyperplasia

The tumors derived of the ceruminous gland in the external auditory canal are rare. Here, we report a case of a ceruminous adenoma (apocrine adenoma) with refractory chronic inflammation in the external auditory canal. A 46-year-old man presented with otorrhea, itching, and a foreign body sensation in his right ear. A soft reddish protruding lesion was revealed at the posterosuperior portion of the entry to the right external auditory canal by otoscopy. The skin lesion was endaurally resected; histopathology showed luminal structures in the middle to deep layer of the epidermis and inflammatory granulation below pseudoepitheliomatous hyperplasia. The walls of the luminal structures consisted of inner luminal secretory cells featuring apical decapitation secretion and outer myoepithelial cells. The patient was diagnosed with an apocrine adenoma. Three years after surgery, there has been no evidence of recurrence. Complete resection, including the deep layer of the epidermis, is necessary

Dysphagia due to systemic light chain amyloidosis revealed by videoendoscopic and videofluorographic swallowing examinations

Purpose: Pharyngeal symptoms related to amyloidosis are quite rare, and there are no reports demonstrating videoendoscopic (VE) or videofluorographic (VF) swallowing examinations. We report a case of systemic light chain amyloidosis with dysphagia at the pharyngeal phase of swallowing revealed by VE and VF, and discuss the causative mechanisms. Case: A 77-year-old man presented with a 6-month history of dysphagia. An oral cavity examination revealed normal findings. Laryngofiberscopy did not show space-occupying lesions or laryngeal nerve palsy. VE revealed a crystal violet-pigmented bolus that flowed into the pharynx toward the glottis before laryngeal elevation, and then pooled in the piriform recess of the hypopharynx and was aspirated into the trachea. VF using barium sulfate showed delayed onset and poor laryngeal elevation, aspiration during swallowing, poor pharyngeal contraction, and bolus residue in the piriform recess of the hypopharynx. Opening of the upper esophageal sphincter was adequate. Flow in the esophagus was normal. The number of swallowings was increased to clear the bolus from the pharynx. VE and VF indicated impairment during the pharyngeal phase of swallowing. Histopathological analysis of the lower lip demonstrated degeneration of the minor salivary glands and hypertrophic basal membranes due to amyloid deposits; the acini and ducts had been replaced by amyloid deposits of λ light chain (AL) amyloidosis. Discussion: The possible mechanisms of pharyngeal phase impairment are peripheral neuropathy of the swallowing-related nerves and amyloid myopathy. Conclusion: Systemic amyloidosis may cause pharyngeal phase dysphagia