Sequential Pulses of Apical Epithelial Secretion and Endocytosis Drive Airway Maturation in Drosophila

Kinetics of hydrophilic solute entry into endolymph (EL), perilymph (PL), and cerebrospinal fluid (CSF) were studied after intravenous administration (sodium, urea, glycerol, mannitol, sucrose) and cerebral lateral ventricle injection (urea, sucrose) of tracers in anesthetized rats. Samples of cochlear EL, PL of scala vestibuli (PLV), PL of scala tympani (PLT), and cisternal CSF were obtained. The data showed slow entry of tracers in PLV, PLT, and CSF as follows: Na greater than urea greater than mannitol approximately sucrose; slower entry of mannitol and sucrose in PLT and CSF than in PLV; 1 h delayed peak of radioactivity in PLV compared with the immediate peaks in PLT and CSF after CSF injection, and the value of PLV peak was 13% that in CSF; extremely slow entry of nonelectrolytes in EL. These results indicate that PLV originates mainly from plasma across a blood-perilymph barrier that restricts the entry of small hydrophilic solutes. The blood-perilymph barrier is most likely composed of an endothelial barrier associated with an epithelial secretion. The latter could be located at the vasculo-epithelial zone of the spiral limbus.

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Anterior Cervical Corpectomy and Fusion with excision of recurrent long segmental midline anterior cervical arachnoid cyst

Nepal Journal of Neuroscience ◽

10.3126/njn.v17i2.30168 ◽

2020 ◽

Vol 17 (2) ◽

pp. 60-64

Author(s):

Ashish Jung Thapa ◽

Asheesh Tandon ◽

Alok Agrawal

Keyword(s):

Arachnoid Cyst ◽

Posterior Approach ◽

Complete Removal ◽

Complete Excision ◽

Cervical Corpectomy ◽

Cyst Excision ◽

Anterior Midline ◽

Epithelial Secretion ◽

Anterior Cervical Corpectomy ◽

The Ideal

Anterior midline cervical arachnoid cysts are very rare, common in the thoracic region. The treatment of midline ventrally lying arachnoid cyst may be challenging via a posterior approach because of a lack of direct visualization of the entire cyst, in particular, its attachment to the cord, complete excision of the cyst wall through a posterior approach is not always possible. Incomplete excision at the first operation and the reaction caused by the epithelial secretion from the marsupialized cyst makes surgery for recurrence very difficult. So, Anterior cervical corpectomy and fusion (ACCF) with cyst excision may be the ideal approach for the anterior midline arachnoid cyst with complete removal and fewer chances of recurrence. Here we report a case of long segmental recurrent midline anterior arachnoid cyst which is completely excised using an anterior cervical corpectomy and fusion and the patient improved drastically neurologically.

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Inflammation and cell-cell interactions in airway hyperresponsiveness

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1991.260.4.l189 ◽

1991 ◽

Vol 260 (4) ◽

pp. L189-L206 ◽

Cited By ~ 9

Author(s):

A. R. Leff ◽

K. J. Hamann ◽

C. D. Wegner

Keyword(s):

Smooth Muscle ◽

Airway Smooth Muscle ◽

Airway Hyperresponsiveness ◽

Difficult Problem ◽

Experimental Models ◽

Cytotoxic Effects ◽

Epithelial Secretion ◽

Eosinophil Granule ◽

Conducting Airways ◽

Reactive Airways

Airway hyperresponsiveness results from the conversion of normally reactive airways to a state of augmented responsiveness to constrictor stimuli. Although the mechanism accounting for the induction of airway hyperresponsiveness remains elusive, recent investigations have suggested that inflammation may be a sine qua non for human asthma. Numerous experimental models have demonstrated the necessity of circulating granulocytes as mediators of augmented bronchoconstriction during immune challenge. It is not known how granulocytes are targeted for selective migration to the conducting airways of the lung during hyperresponsive states; however, recent evidence implicates the upregulation of granulocyte adhesion molecules on both the endothelial and epithelial surfaces of the airway. There is evidence that during migration diapedesis, granulocytes interact with epithelial and endothelial cells to produce regionally secreted mediators that upregulate the responsiveness of adjacent airway smooth muscle and/or cause lumenal edema, thus augmenting the effect of constrictor stimuli. Most evidence suggests that the eosinophil is the most important granulocyte in these responses and that eosinophilic infiltration and activation may account for the unique, spasmodic, and cyclic nature of hyperreactive airways. The molecular biology of the eosinophil granule proteins has characterized four distinct substances, each of which exerts potential cytotoxic effects on airway epithelium by different mechanism. In addition, at least one of these proteins, the major basic protein, appears to cause direct, noncytotoxic stimulation of epithelial secretion that upregulates nonspecifically the response of airway smooth muscle to contractile stimuli. The recognition of inflammation as the essential component to airway hyperresponsiveness provides a fresh approach to a difficult problem and suggests a host of novel therapies for human asthma.

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Emerging neuropeptide targets in inflammation: NPY and VIP

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00493.2012 ◽

2013 ◽

Vol 304 (11) ◽

pp. G949-G957 ◽

Cited By ~ 67

Author(s):

Bindu Chandrasekharan ◽

Behtash Ghazi Nezami ◽

Shanthi Srinivasan

Keyword(s):

Nervous System ◽

Immune System ◽

Enteric Nervous System ◽

Intracellular Signaling ◽

Enteric Neurons ◽

Vast Number ◽

Paracrine Effects ◽

Intracellular Signaling Pathways ◽

Inflammatory Processes ◽

Epithelial Secretion

The enteric nervous system (ENS), referred to as the “second brain,” comprises a vast number of neurons that form an elegant network throughout the gastrointestinal tract. Neuropeptides produced by the ENS play a crucial role in the regulation of inflammatory processes via cross talk with the enteric immune system. In addition, neuropeptides have paracrine effects on epithelial secretion, thus regulating epithelial barrier functions and thereby susceptibility to inflammation. Ultimately the inflammatory response damages the enteric neurons themselves, resulting in deregulations in circuitry and gut motility. In this review, we have emphasized the concept of neurogenic inflammation and the interaction between the enteric immune system and enteric nervous system, focusing on neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). The alterations in the expression of NPY and VIP in inflammation and their significant roles in immunomodulation are discussed. We highlight the mechanism of action of these neuropeptides on immune cells, focusing on the key receptors as well as the intracellular signaling pathways that are activated to regulate the release of cytokines. In addition, we also examine the direct and indirect mechanisms of neuropeptide regulation of epithelial tight junctions and permeability, which are a crucial determinant of susceptibility to inflammation. Finally, we also discuss the potential of emerging neuropeptide-based therapies that utilize peptide agonists, antagonists, siRNA, oligonucleotides, and lentiviral vectors.

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