Correlation between serum leptin level and sleep monitoring indexes in patients with obstructive sleep apnea hypopnea syndrome and its predictive value: a cross-sectional analysis.

Objective: To investigate the association between serum leptin (LP) level and polysomnography (PSG) parameters in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). Methods: A cross-sectional study was conducted. The data of subjects who underwent PSG at hospital between January 2021 and December 2022 were collected retrospectively, 220 participants were included. The subjects were categorized into simple snoring group (n = 45), mild OSAHS group (n = 63), moderate OSAHS group (n = 52), and severe OSAHS group (n = 60). The general characteristics, PSG indices, and serological indices were collected retrospectively. Pearson correlation analysis was used to observe the correlation between serum LP level and PSG parameters. The value of serum LP level in predicting OSAHS was analyzed by receiver operating characteristic curve. Results: The serum LP level was positively correlated with micro-arousal count, micro-arousal index (MAI), high apnea hypopnea index, times of blood oxygen decreased by≥3% and time in saturation lower 90%, and negatively correlated with lowest nocturnal oxygen saturation and mean oxygen saturation (p < 0.05). The area under the curve (AUC) of serum LP level in predicting the occurrence of OSAHS was 0.8276 (95% CI: 0.7713-0.8839), and when the Youden index was 0.587, the sensitivity was 72.00%, and the specificity was 86.67% (p < 0.0001). In the population with high MAI, the AUC of serum LP level in predicting the occurrence of OSAHS was 0.8825 (95% CI: 0.7833-0.9817), and when the Youden index was 0.690, the sensitivity was 79.00% and the specificity was 90.00% (p < 0.0001). Conclusion: Serum LP level is associated with the severity of OSAHS. Serum LP level demonstrates a strong predictive value for the occurrence of OSAHS, particularly in population with high MAI.

Oxygen desaturation index, lowest arterial oxygen saturation and time spent below 90% oxygen saturation as diagnostic markers for obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) syndrome is associated with a high mortality, and blood oxygen indexes play an important role in evaluating this disease. The objective of this study was to explore the value of blood oxygen indexes, including minimum oxygen saturation (LSpO2), oxygen reduction index (ODI) and time spent with oxygen saturation below 90% (TS 90%), as diagnostic markers for OSA syndrome. METHODS: In this retrospective study, 320 patients with OSA treated in Ningbo First Hospital from June 2018 to June 2021 were included and divided into mild, moderate, and severe groups according to the severity of the condition (n = 104, 92, and 124, respectively). The blood oxygen indexes as well as the apnea-hypopnea index (AHI) were compared. The Spearman correlation analysis was performed to explore the relationship between the parameters. Receiver operating characteristic curves were generated to evaluate the diagnostic value of the blood oxygen indexes for OSA syndrome. RESULTS: There were significant differences in body weight, body mass index, and blood pressure before and after sleep among the groups (P < 0.05). LSpO2 levels followed a pattern with the severe group showing the lowest values, followed by the moderate group, and then the mild group, whereas ODI and TS 90% levels showed the opposite (P < 0.05). Spearman correlation analysis showed that AHI, ODI, TS 90% were positively correlated with severity of OSA, whereas LSpO2 was negatively correlated with severity of OSA. ODI showed a high diagnostic value for OSA (area under curve (AUC) = 0.823, 95% CI: 0.730-0.917). TS 90% showed a high diagnostic value for OSA (AUC = 0.872, 95% CI: 0.794-0.950). LSpO2 showed high accuracy in diagnostic value for OSA (AUC = 0.716, 95% CI: 0.596-0.835). The combination of the 3 indexes demonstrated a high diagnostic value for OSA (AUC = 0.939, 95% CI: 0.890-0.989). The diagnostic value of the combined signature was found to be significantly higher compared to the value of individual indexes (P < 0.05). CONCLUSION: The evaluation of the severity of OSA should not rely solely on a single observation index, but rather on a combination of ODI, LSpO2 and TS 90%. This combined diagnostic signature can provide a more comprehensive assessment of the patient's condition and serve as an alternative diagnostic basis to ensure timely diagnosis and appropriate clinical treatment for OSA.

Application of the Mimic Valsalva Maneuver with the Help of a Saccule in Cerebrospinal Fluid Rhinorrhea Reconstruction Surgery.

OBJECTIVE: To explore the mimic Valsalva maneuver with the help of a saccule handled by an anesthesiologist in order to locate the leakage channel and repair the fistula during intranasal endoscopic reconstruction surgery of cerebrospinal fluid rhinorrhea. METHODS: From 2012 to 2014, 8 patients were diagnosed with cerebrospinal fluid rhinorrhea by medical histories, physical and biochemical examination. All patients were treated with intranasal endoscopic reconstruction surgery of cerebrospinal fluid rhinorrhea. During the surgery, the mimic Valsalva maneuver with the help of a saccule was carried out once or twice by an anesthetist during the operation. Intranasal endoscopy was used to accurately locate the leakage site as shown by the exact fistula. Temporal fascia, fascia lata, middle turbinate mucosa and nasal septum mucosa were all used to repair the fistula. RESULTS: After the surrounding mucosa was removed, the exact leakage sites were accurately found. Fascia materials were used in all 8 patients. All patients were successfully treated after their first operation, and 1 patient was successfully treated by two operations with no complications and recurrences. All the patients were followed up for 1 month to 2 years. CONCLUSION: The convenient method of the mimic Valsalva maneuver with the help of a saccule handled by an anesthesiologist has a good prospect in cerebrospinal fluid rhinorrhea reconstruction surgery.

The neurovascular protective effects of huperzine A on D-galactose-induced inflammatory damage in the rat hippocampus.

BACKGROUND: Chronic administration of D-galactose (D-gal) results in oxidative stress and chronic inflammatory aging. Age-related changes in the brain result in neurovascular damage and blood-brain barrier (BBB) dysfunction. However, little is known regarding D-gal-induced neurovascular damage, as well as the protective effects of huperzine A. OBJECTIVE: The purpose of this study was to utilize a D-gal-induced rat model to investigate the activation of neurovascular inflammatory damage and apoptosis in the rat hippocampus and to understand whether huperzine A alleviates D-gal-induced neuronal and vascular inflammatory injury. METHODS: Aging rats were treated with D-gal (300 mg/kg s.c. for 8 weeks), were coadministered D-gal and huperzine A (D-gal 300 mg/kg and huperzine A 0.1 mg/kg s.c. for 8 weeks) or served as the saline-treated control group rats (same volume of saline given subcutaneously for 8 weeks). Changes in hippocampal morphology and biomarkers of inflammatory damage were analyzed. RESULTS: Our study revealed that chronic administration of D-gal resulted in the activation of glia and vascular endothelial cells and upregulation of mRNA and protein levels of cell-associated adhesion molecules and inflammatory cytokines via nuclear factor (NF)-κB inhibitor degradation and NF-κB nuclear translocation. The inflammatory injury caused significant BBB dysfunction, decreased density of tight junctions (TJs) and apoptosis in the rat hippocampus. Coadministration of huperzine A not only markedly inhibited the D-gal-induced increase in acetylcholinesterase (AChE) activity, but also alleviated D-gal-induced neurovascular damage by inhibiting D-gal-induced NF-κB activation, improving cerebrovascular function and suppressing the D-gal-induced decrease in the density and protein levels of TJs and cell apoptosis. CONCLUSIONS: Our findings provided evidence that D-gal induced a proinflammatory phenotype mediated by NF-κB in the rat hippocampus. Moreover, huperzine A suppressed D-gal-induced neurovascular damage and BBB dysfunction, partly by preventing NF-κB nuclear translocation. The inhibiting effect of huperzine A on AChE activity might play an important role in attenuating D-gal-induced inflammatory damage.

The anti-inflamm-aging and hepatoprotective effects of huperzine A in D-galactose-treated rats.

Oxidative stress contributes to a chronic inflammatory process referred to as "inflamm-aging". Acetylcholinesterase inhibitors (AChEI) can enhance cholinergic transmission and act as anti-inflammatory agents via immunocompetent cells expressing α-7 acetylcholine receptors (AChR). The present study explores the possible role of huperzine A, a reversible and selective AChEI, against D-gal-induced oxidative damage, cell toxicity and inflamm-aging in rat livers. In two-month-old rats with normal liver function, an 8-week administration of D-gal (300 mg/kg subcutaneously (s.c.) injected), significantly increased hepatic impairment, ROS generation and oxidative damage, hepatic senescence, nuclear factor-kappa B (NF-κB) activation and inflammatory responses. An 8-week co-administration of both D-gal (300 mg/kg s.c.) and huperzine A (0.1 mg/kg s.c.) not only significantly decreased hepatic function impairment, ROS generation, oxidative damage, but also suppressed inflamm-aging by inhibiting hepatic replicative senescence, AChE activity, IκBα degradation, NF-κB p65 nuclear translocation and inflammatory responses. The expression levels of pro-inflammatory cytokine mRNA and proteins, such as TNFα, IL-1ß and IL-6 decrease significantly, and the protein levels of the anti-inflammatory cytokine IL-10 display an obvious increase. These findings indicated that D-gal-induced hepatic injury and inflamm-aging in the rat liver was associated with the development of a pro-inflammatory phenotype in this organ. D-gal induced damage-associated molecular patterns (DAMPs) because oxidative damages might play an important role in D-gal-induced hepatic sterile inflammation. Huperzine A exhibited protective effects against D-gal-induced hepatotoxicity and inflamm-aging by inhibiting AChE activity and via the activation of the cholinergic anti-inflammatory pathway. The huperzine A mechanism might be involved in the inhibition of DAMPs-mediated NF-κB nuclear localization and activation.

[Preparation of ethosomes encapsulated with 5-fluorouracil and the effect of local administered 5-FU ethosome on laryngotracheal stenosis of rabbit].

OBJECTIVE: To evaluate the efficacy of Ethosomes encapsulated with 5-FU in treatment of laryngotracheal stenosis in rabbit models. METHOD: The 5-FU ethosome was prepared by the thin film hydration method, and the size distribution and the encapsulation efficiency was investigated. The tracheal mucosa was scraped about 0.5 cm in width with a nylon brush to induce the scar formation in the airway,then animals were divided into three groups: 5-FU ethosome group,5-FU group and saline group. Drugs were injected into scar by paracentesis under endoscope in each group respectively. The severity of stenosis was observed under laryngofiberoscope immediately, 7, 14, 21 days after administration. RESULT: Airway stenosis of 5-FU ethosome group was not significantly different compared with 5-FU group at 7 days after administration, but 5-FU ethosome significantly reduced the airway stenosis at 21 days after administration when compared with 5-FU group and no restenosis was noticed during the observation period. CONCLUSION: Ethosomes encapsulated with 5-FU was effective for laryngotracheal stenosis. It is a potentially new method for ameliorating airway stenosis originated from granulation tissue.