A non-recurrent inferior laryngeal nerve in a man undergoing thyroidectomy: a case report

<p>Abstract</p> <p>Introduction</p> <p>A non-recurrent variant of the inferior laryngeal nerve has been seldom reported. These reports are mostly based on cadaveric dissection studies or large chart review studies in which the emphasis is placed on the determination of the frequency of the variation, and not on the clinical appearance of this variant. We graphically describe the intraoperative identification of a non-recurrent inferior laryngeal nerve.</p> <p>Case Presentation</p> <p>A 44-year old Caucasian man was referred to the Head and Neck Surgery Outpatient Clinic with the diagnosis of a nodular mass in his left thyroid lobe that had been growing for one year. A fine needle aspiration puncture was compatible with thyroid papillary cancer. It was decided that the patient should undergo total thyroidectomy. During surgery, a non-recurrent right inferior laryngeal nerve was noted. This nerve emanated from the right vagus nerve, entering the larynx 3 cm after its origin. The nerve did not show a recurrent course. The nerve on the left side had a normal configuration. The surgery and post-operative period were uneventful, and the patient had no change in his voice.</p> <p>Conclusion</p> <p>This paper allows those interested to become acquainted with the normal intraoperative appearance of a non-recurrent inferior laryngeal nerve. This will undoubtedly be of significance for all of those performing invasive diagnostic and surgical procedures in the neck and upper thoracic regions, in order to minimize the risk of iatrogenic injury to this nerve. This is of extreme importance, since a unilateral lesion of this nerve may result in permanent hoarseness, and a bilateral lesion may lead to aphonia and life-threatening dyspnea.</p

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Opiate receptors are expressed in mouse podocytes.

<p>Paraffin sections were prepared from 2-month-old mice kidneys, and immunofluorescence staining was performed to detect the expression of opiate receptors. Nephrin was used as a marker of podocytes.</p

Inhibition of AKT, p38, and JNK attenuates morphine-induced decrease of SD molecules expression.

<p><b>A.</b> Human podocytes were pretreated with of LY294002 (LY), SB203580 (SB), or SP600125 (SP) for 1 h before 10⁻⁶ M morphine was added. After another 24 h incubation at 37°C, the cell lysate were collected for Western blot. <b>B–E.</b> Quantification of the expression of nephrin (<b>B</b>), synaptopodin (<b>C</b>), CD2AP (<b>D</b>), and podocin (<b>E</b>) in <b>A</b>, and the results (mean ± SD) represent three independent samples. * p<0.05 compared with blank control, while # p<0.05 compared with morphine treatment alone.</p

Morphine activates AKT, p38 and JNK.

<p>Human podocytes were starved in serum free medium for 12 h, and then 10⁻⁶ M morphine was added. Cell lysates were collected at different time points for Western blot.</p

Morphine increases ROS generation in podocyte.

<p><b>A.</b> Human podocytes were treated with 10⁻¹⁰ to 10⁻⁶ M morphine for 12 h, and were labeled with DCFH for 30 min. After washing with PBS, the cells were incubated at room temperature for 2 h, and the ROS generation was determined. * p<0.001 compared with control (0 M). <b>B.</b> Kinetics of ROS generation for 10⁻⁶ M morphine treatment. <b>C.</b> Paraffin sections were prepared from control or morphine-receiving mice, and immunofluorescent staining was performed to detect the nuclear expression of 8-OHdG, a molecular marker of oxidative damage to DNA. WT1 was used as a marker of podocytes.</p

Opiate receptors are expressed in human podocytes.

<p>Total RNAs were prepared from human podocytes (labeled as P1, P2), and were used for RT-PCR to detect the expression of delta opiate receptor (DOR), kappa opiate receptor (KOR), and mu opiate receptor (MOR). RNAs from human fetal brain (B) were used as positive control. GAPDH was used as internal control.</p