Ghrelin, a gastric peptide hormone, has been reported to regulate growth hormone secretion and energy homeostasis. Here we show that ghrelin promotes neural proliferation in vivo and in vitro in the rat dorsal motor nucleus of the vagus (DMNV). Ghrelin receptor mRNA and immunoreactivity were detected in tissues from DMNV. Systemic administration of ghrelin (130 nmol kg −1 ) significantly increased 5-bromo-2 -deoxyuridine (BrdU) incorporation in the DMNV in adult rats with cervical vagotomy (BrdU positive cells; from 27 ± 4 to 69 ± 14 n = 5, P < 0.05). In vitro, exposure of cultured DMNV neurones to ghrelin significantly increased the percentage of BrdU incorporation into cells in both dose-dependent (10 −9 -10and time-dependent (6 h to 48 h) manners. Ghrelin significantly increased voltage-activated calcium currents in isolated single DMNV neurones from a mean maximal change of 141 ± 26 pA to 227 ± 37 pA. Upon removal of ghrelin, calcium currents slowly returned to baseline. Blocking L-type calcium channels by diltiazem (10 µM) significantly attenuated ghrelin-mediated increments in BrdU incorporation (n = 5, P < 0.05). Ghrelin acts directly on DMNV neurones to stimulate neurogenesis.

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Background No study had directly compared the reliability, correlation with clinical symptoms, and surgical outcomes of dural sac cross-sectional area (DCSA), nerve root sedimentation sign (SedSign), and morphological grade for lumbar spinal stenosis (LSS). Methods From January 2017 to December 2020, 202 patients with LSS were retrospectively analyzed. The narrowest segments were assessed via T2-weighted cross-sectional images using DCSA, morphological grade, and SedSign by two independent observers. Three classifications’ reliabilities were evaluated. Correlations between three classifications and between each of the classifications and symptoms or surgical outcomes 12 months postoperatively were evaluated. Results There were 144 males and 58 females; 23, 52, and 127 patients had the narrowest segment in L2–3, L3–4, and L4–5, respectively. The intra-observer reliability of DCSA ranged from 0.91 to 0.93, and the inter-observer reliability was 0.90. The intra-observer reliability of SedSign ranged from 0.83 to 0.85, and the inter-observer reliability was 0.75. The intra-observer reliability of morphological grade ranged from 0.72 to 0.78, and the inter-observer reliability was 0.61. Each of these classifications was correlated with the other two (P < 0.01). For preoperative symptoms, DCSA was correlated with leg pain (LP) (r =  − 0.14), Oswestry Disability Index (ODI) (r =  − 0.17), and claudication (r =  − 0.19). Morphological grade was correlated with LP (r = 0.19) and claudication (r = 0.27). SedSign was correlated with ODI (r = 0.23). For postoperative outcomes, morphological grade was correlated with LP (r =  − 0.14), and SedSign was correlated with ODI (r = 0.17). Conclusions Substantial to almost perfect intra and inter-observer reliabilities for the three classifications were found; however, these classifications had either weak correlations with symptoms and surgical outcomes or none at all. Based on our findings, using one of them without conducting other tests for LSS will have limited or uncertain value in surgical decision-making or evaluating the prognostic value.

In order to study the role of nitric oxide (NO) in ischemic brain injury. Global cerebral ischemia was established in SD rats by modified Pulsinelli's method. The activities of constitutive nitric oxide synthase (cNOS), inducible NOS (iNOS), neuronal NOS (nNOS), nitrite (NO2) and cyclic GMP in cerebral cortex, hippocampus, striatum and cerebellum at different time intervals were measured by radioimmunoassy, NADPH‐d histochemistry and fluorometry methods. The results showed that the activities of cNOS increased at 5 min in four regions and decreased in cortex, hippocampus and striatum at 60 min, in cerebellum at 15 min iNOS increased in cortex and striatum at 15 min, in hippocampus and cerebellum at 10 min, and persisted to 60 min. The expression of nNOS increased after 5 min ischemia in cortex, striatum and hippocampus, and return to normal at 30–60 min. The NO2 and cGMP also increased after 5–15 min ischemia and returned to normal after 30–60 min ischemia. These results indicated that the NO participated in the pathogenesis of cerebral ischemia injury and different types of NOS play different role in the cerebral ischemia injuries. Selected specific NOS inhibitors to decreased the excessive production of NO at early stage may help to decrease the ischemic injury.