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This study aimed to investigate the effect of therapy with peripheral nerve stimulation (PNS) and pulsed radiofrequency (PRF) combined or PNS and PRF separately in patients with herpes zoster ophthalmicus (HZO).This cohort study included 106 cases of HZO. Three groups were identified according to the type of treatment received: combination therapy (PNS+PRF) (n=38), PRF (n=37), and PNS (n=31). The observations at 0, 1, 2, and 4 weeks; 3 and 6 months; and 1 and 2 years after the operation were analyzed. Observations at each follow-up included baseline characteristics, Numerical Rating Scale (NRS) and the Pittsburgh Sleep Quality Index (PSQI), concomitant pain medication usage, relapse rate, and adverse events.The postoperative NRS of all 3 groups were significantly lower than preoperative scores. The PSQI of the 3 groups was significantly improved postoperatively, and the concomitant pain medication gradually decreased. Regarding long-term efficacy, the pain NRS and PSQI scores of the PNS+PRF and PNS groups were significantly lower than those of the PRF group ( P0.05), and the relapse rate of the PRF group was higher than that of the PNS+PRF and PNS groups ( P0.05). No significant difference was observed between the PNS+PRF and the PNS groups.Both PNS and PRF treatment of HZO can decrease the pain score, yielding no serious complications. The combination of PNS and PRF or PNS alone resulted in more significant pain relief than treatment with PRF alone. Thus, PNS therapy may be a better treatment option for HZO.

The COVID-19 pandemic has caused substantial losses worldwide in people's lives, health, and property. Currently, COVID-19 is still prominent worldwide without any specific drug treatment. The SARS-CoV-2 pathogen is the cause of various systemic diseases, mainly acute pneumonia. Within the pathological process, neutrophils are recruited to infected sites, especially in the lungs, for the first stage of removing invading SARS-CoV-2 through a range of mechanisms. Macroautophagy/autophagy, a conserved autodegradation process in neutrophils, plays a crucial role in the neutrophil phagocytosis of pathogens. NETosis refers to neutrophil cell death, while auto-inflammatory factors and antigens release NETs. This review summarizes the latest research progress and provides an in-depth explanation of the underlying mechanisms of autophagy and NETosis in COVID-19. Furthermore, after exploring the relationship between autophagy and NETosis, we discuss potential targets and treatment options. This review keeps up with the latest research on COVID-19 from neutrophil autophagy and NETosis with a new perspective, which can guide the urgent development of antiviral drugs and provide guidance for the clinical treatment of COVID-19.

Postoperative thoracic surgery is often accompanied by severe pain, and opioids are a cornerstone of postoperative pain management, but their use may be limited by many adverse events. Several studies have shown that the perioperative application of esketamine adjuvant therapy can reduce postoperative opioid consumption. However, whether esketamine has an opioid-sparing effect after thoracic surgery is unclear.To explore the opioid-sparing effect of different doses of esketamine infusion during thoracic surgery and its impact on patient recovery.Randomized controlled study.A single-center study with a total of 120 patients.Patients were randomly allocated to 1 or 3 groups receiving intraoperative intravenous infusions of esketamine 0.15 mg · kg-1· h-1 (group K1), esketamine 0.25 mg · kg-1· h-1(group K2), or placebo (group C). Postoperative opioid consumption, and postoperative indicators like extubation time, PACU stay time, and adverse events were recorded for each group.The consumption of hydromorphone during the first 24 and 48 postoperative hours was significantly reduced in patients of group K2 compared to those of group C and group K1. The time to extubation and post anesthesia care unit (PACU) stay were significantly shorter in group K2 than in group K1 and group C. The time to first feed and off the bed time after surgery were shorter in groups K1 and K2 than in group C. Patients in group K2 were significantly satisfied with patient controlled intravenous analgesia (PCIA) than in groups K1 and C.The sample size calculation was based mainly on the index of hydromorphone consumption.Intraoperative intravenous esketamine at 0.25 mg · kg-1 · h-1 reduced postoperative opioids consumption by 34% in postoperative 24 hours and 30% in postoperative 48 hours in patients undergoing thoracic surgery. It also improved the quality of perioperative recovery.

Percutaneous balloon compression (PBC) is a safe and effective method to treat trigeminal neuralgia. Despite it is known that intraoperative balloon volume is crucial in the prognosis of PBC patients and correlates with Meckel's cave (MC) size, it is a lack of objective and valid criteria for intraoperative balloon volume of PBC.The aim of this study was to evaluate the relationship between the size of MC and the volume of a pear-shaped balloon in improving the prognosis of patients receiving PBC.Retrospective study.Patients were divided into 3 groups according to their prognosis, and simple linear regression equations were established separately. Group A was defined as having recurrence. Group B was defined as having no recurrence and a Barrow Neurological Institute facial numbness (BNI-N) score of 2 with no recurrence. Correlation analysis was carried out to determine the association of the intraoperative balloon volume with MC size. We attempted to construct simple linear regression models after verifying that both parameters were in compliance with the requirements of this model.Until the end of the 6-months follow-up, 60 patients (93.8%) reported no pain, and 4 patients (6.3%) experienced no significant pain relief. Sixteen (25.0%) patients had severe facial numbness, 48 (75.0%) patients had no facial numbness or had only mild numbness. All 3 groups had a significant correlation between balloon volume and MC size. Group A: Balloon volume (cm3) = -0.371 + 1.883*MC size (R2 = 0.882); Group B: Balloon volume (cm3) = 0.110 + 1.274*MC size (R2 = 0.861); and Group C: Balloon volume (cm3) = 0.011 + 1.835*MC size (R2 = 0.857).The main limitation of our study is its observational retrospective nature, and we were unable to further analyze the intraoperative balloon pressure and volume, as well as validate the accuracy of the model. In additional this was a single-center study with a small sample size and a short follow-up period. These may have contributed to the bias in the final results. A multicenter, prospective study with a large sample size should be performed to further investigate the long-term effects of individualized balloon volumes and the correlation between pressures.The equation [balloon volume (cm3) = 0.110 cm3 + 1.274*MC size] yields an appropriate value at which the patient has a low recurrence rate and a low degree of facial numbness. Preoperative measurement of MC size can be used to guide the intraoperative balloon volume and to predict the patient's prognosis.

The mechanism of peripheral axon transport in neuropathic pain is still unclear. Chemokine ligand 13 (CXCL13) and its receptor (C-X-C chemokine receptor type 5, CXCR5) as well as GABA transporter 1 (GAT-1) play an important role in the development of pain. The aim of this study was to explore the axonal transport of CXCL13/CXCR5 and GAT-1 with the aid of the analgesic effect of botulinum toxin type A (BTX-A) in rats.Chronic constriction injury (CCI) rat models were established. BTX-A was administered to rats through subcutaneous injection in the hind paw. The pain behaviors in CCI rats were measured by paw withdrawal threshold and paw withdrawal latencies. The levels of CXCL13/CXCR5 and GAT-1 were measured by western blots.The subcutaneous injection of BTX-A relieved the mechanical allodynia and heat hyperalgesia induced by CCI surgery and reversed the overexpression of CXCL13/CXCR5 and GAT-1 in the spinal cord, dorsal root ganglia (DRG), sciatic nerve, and plantar skin in CCI rats. After 10 mmol/L colchicine blocked the axon transport of sciatic nerve, the inhibitory effect of BTX-A disappeared, and the levels of CXCL13/CXCR5 and GAT-1 in the spinal cord and DRG were reduced in CCI rats.BTX-A regulated the levels of CXCL13/CXCR5 and GAT-1 in the spine and DRG through axonal transport. Chemokines (such as CXCL13) may be transported from the injury site to the spine or DRG through axonal transport. Axon molecular transport may be a target to enhance pain management in neuropathic pain.

Recurrent trigeminal neuralgia (TN) after surgical operations can be quite difficult to treat, and treatment measures have not been standardized. Patients often have long-term, repeated severe pain, which may easily cause anxiety and depression and can exert a negative effect on the quality of life. Despite the known efficacy of percutaneous balloon compression (PBC) for TN, it is unclear whether PBC can be used as the preferred surgical treatment for postoperative recurrent TN and effectively improve patients' negative emotions.This study aimed to evaluate the clinical curative effect of PBC in patients with postoperative recurrent TN and analyze the improvement in conditions such as anxiety, depression, and sleep disorders.Retrospective study.Center of Pain Medicine, Department of Anesthesiology, pain, and Perioperative Medicine, the First Affiliated Hospital of Zhengzhou University.Clinical data from 121 postoperative recurrent TN patients who underwent PBC between August 2017 and June 2019 were retrospectively reviewed and analyzed. The Barrow Neurological Institute pain intensity (BNI-P) score was used to measure the severity of pain. The Hospital Anxiety and Depression Scale (HADS) and Pittsburgh Sleep Quality Index (PSQI) were used to evaluate anxiety, depression, and sleep status.On postoperative day 1, 104 patients (86.0%) reported no pain, 9 patients (7.4%) had occasional pain that did not require medication, and 8 patients (6.6%) experienced no significant pain relief. The total efficacy was 93.4%. Moreover, 3 patients (2.5%) reported significant pain relief 2 weeks postoperatively. Within a follow-up time of 12 months, 101 (83.5%) patients remained pain-free, while 5 patients (4.1%) experienced recurrence. Taking into account economic factors, the patients were tolerant to pain after taking medication and did not undergo repeated PBC. Forty-six patients (38.0%) suffered from anxiety, 70 patients (57.9%) had depression, and 62 patients (51.2%) had poor sleep quality preoperatively. There were significant improvements in anxiety, depression, and sleep status postoperatively compared with preoperatively. Postoperative side effects included facial numbness in 115 patients (95.0%), masticatory muscle weakness in 86 patients (71.1%), herpes simplex in 18 patients (14.9%), and diplopia secondary to abducens nerve palsy in 2 patients (1.7%). None of the patients had corneal anesthesia, anesthesia dolorosa, aseptic meningitis, cerebrospinal fluid leakage, subarachnoid hemorrhage, carotid cavernous fistula, or death in this study.This study was a single-center retrospective study, the sample size was small, and the follow-up time was relatively short. Therefore, the long-term efficacy of PBC for postoperative recurrent TN needs further evaluation from multiple centers with a large sample size and long-term follow-up.PBC is a minimally invasive, safe, and effective procedure. Moreover, it significantly improves the symptoms of anxiety, depression, and sleep quality caused by TN, so it appears to be regarded as an optimized choice for patients with recurrent TN after surgical procedures.

Background In children, erythromelalgia is a rare but difficult to manage condition that results in bilateral episodic pain and redness in distal extremities. It is heat intolerant and relieved by cooling. Management of erythromelalgia is difficult and requires a complex multidisciplinary approach. Case Description We present a case of successful treatment of erythromelalgia with short-term spinal cord stimulation in a 12-year-old girl. The patient had severe burning pain, having undergone trials of multiple medical therapies before presenting to our department. Dual-lead spinal cord stimulator electrodes were successfully implanted without complication, leading to excellent pain control, now 8 months postimplant. Conclusions This case spurs interest for future research in neuromodulation as part of the multimodal regimen to treat pediatric erythromelalgia.

Chemokines are important regulators of immune, inflammatory, and neuronal responses in peripheral and central pain pathway. The aim of this study was to investigate whether chemokine (C-X-C motif) ligand 13 (CXCL13) and its receptor (C-X-C chemokine receptor type 5, CXCR5) involve in the development of bone cancer pain (BCP) and the regulation of morphine analgesia in rats. The change of pain behaviors in BCP rats were measured by testing paw withdrawal threshold (PWT). The levels of CXCL13, CXCR5 and signal pathway proteins (p-p38, p-ERK and p-AKT etc.) in the spinal cord were measured via western blots. The expression of CXCL13 and CXCR5 in spinal cord was increased in BCP rats. The BCP rats showed decrease of PWTs, which was relieved by CXCR5i. Intrathecally injection of murine recombinant CXCL13 (mrCXCL13) decreased the PWTs of BCP rats and opposed morphine-induced analgesia in BCP rats. In BCP rats, the signal pathway proteins (p38, ERK and AKT) in the spinal cord were activated. CXCL13 and morphine had contrary effect on the phosphorylation of these proteins. MrCXCL13 directly increased the levels of p-p38, p-ERK and p-AKT in BCP rats. However, morphine decreased the levels of these proteins in BCP rats. While blocking the activation of p-p38, p-ERK and p-AKT, morphine analgesia was enhanced. These results suggest CXCL13 participated in bone cancer pain and opposed morphine analgesia via p38, ERK and AKT pathways. It may be a target to enhance pain management in cancer pain patients.

Botulinum toxin type A (BTX-A) was widely used to treat neuropathic pain in clinic. The underlying analgesic mechanism of BTX-A involves in axonal transport. The chemokine (C-X-C motif) ligand 13 (CXCL13) and GABA transporter 1 (GAT-1) played important roles in chronic pain. We established a chronic constriction injury (CCI) model. The pain behaviors of rats were measured by testing paw withdrawal thresholds (PWTs) and paw withdrawal latencies (PWLs). The level of proteins was measured by western blots. In our results, the CCI rats showed decrease of PWTs and PWLs, which were relieved by BTX-A. BTX-A reversed the over-expression of CXCL13 and GAT-1 in spinal cord, DRG, sciatic nerve and plantar in CCI rats and characterized in dose-dependent manner. The inhibition of BTX-A on proteins we examined didn’t show significant trend among time points. The analgesic effect of BTX-A disappeared after the axon transport of sciatic nerve blocked by the colchicine. But the PWTs of the colchicine treated CCI rats were higher than non- colchicine-treated CCI rats. Colchicine decreased the levels of CXCL13 and GAT-1 in CCI rats. What’s more, the proteins we examined peaked at the sciatic nerve in the non-colchicine group, but the phenomenon disappeared in the colchicine group. In conclusion, the BTX-A and colchicine relieve neuropathic pain and suppress the increase of CXCL13 and GAT-1. Colchicine prevents the analgesic effect of BTX-A by blocking axon transport. The axon transport may play roles in the peripheral mechanisms of neuropathic pain.

Object Ninjurin2 (nerve injury induced protein 2, NINJ2) is a molecule which mediates cell-to-cell and cell-to-extracellular matrix interactions in the nervous system. Clinical study shows NINJ2 is associated with the development of postherpetic neuralgia. However, it is lack of direct evidence that NINJ2 participated in neuropathic pain. In this study, we aim to investigate the role of NINJ2 in the development of neuropathic pain in spared sciatic nerve injury rats and the underlying mechanism. Method Spared sciatic nerve injury (SNI) models were established. The level of NINJ2 and p-p65 (a NF-κB family member) were measured in SNI rats by western blots and immunofluorescent staining. Lentivirus encoding small interfering RNA targeting NINJ2 (RNAi) was intrathecally injected into rats. Then the change of pain behavior of rats induced by NINJ2 RNAi was tested by Von-Frey hairs. The change of p-p65 in the spinal cord in rats after NINJ2 RNAi treatment was also measured by western blots. inhibitor of p-p65-induced change of TNF-α, IL-1β, and IL-6 levels were measured by ELISA. Results NINJ2 and p-p65 were increased in the spinal cord of SNI rats on the 3, 7, 14th days after modeling. NINJ2 were mainly expressed in neurons, and co-located with p-p65 in the spinal dorsal horn. When down regulating the level of NINJ2 by RNAi, the development of pain in SNI rats was partially blocked. Phosphorylation of p65 was also inhibited by NINJ2 RNAi. Blocking the phosphorylation of NF-κB pathway could inhibit the increase of TNF-α, IL-1β, and IL-6 in the spinal cord of SNI rats. Conclusion NINJ2 protein was increased in the spinal cord of SNI rats. It participated in the development of nerve injury-induced neuropathic pain by activating neuroinflammation in the spinal cord via NF-κB pathway. This study provides a new target to investigate the mechanism of neuropathic pain.

Long non-coding RNAs are novel regulators in neuropathic pain. In this study, we aimed to explore the role and the mechanism of lncRNA FIRRE in regulating the secretion of microglial cells-derived proinflammatory cytokines in neuropathic pain. The female mouse model of neuropathic pain was established by bilateral chronic constriction injury (CCI) surgery. The mouse primary microglial cells were induced by lipopolysaccharide (LPS). The interaction between FIRRE and high mobility group box 1 (HMGB1) was assessed by RNA immunoprecipitation, RNA pull-down, and ubiquitination assays. FIRRE expression was upregulated in the spinal cord tissue of female CCI mice and LPS-induced microglial cells. The concentrations of IL-1β, TNF-α, and IL-6 from LPS-induced microglial cells were reduced by FIRRE knockdown. FIRRE bound to HMGB1 and negatively regulated its protein level. The ubiquitination degradation of HMGB1 was promoted by FIRRE silence. The HMGB1 over-expression reversed the inhibitory effect of FIRRE silence on the secretion of IL-1β, TNF-α, and IL-6 from LPS-induced microglial cells. The in vivo experiment showed that FIRRE knockdown alleviated neuropathic pain of CCI female mice. Our findings indicated that lncRNA FIRRE downregulation inhibits the secretion of microglial cells-derived proinflammatory cytokines by decreasing HMGB1 expression, thereby relieving neuropathic pain of female mice.

Previous studies have demonstrated that myeloid zinc finger 1 (MZF1) in the dorsal root ganglion (DRG) participates in neuropathic pain induced by chronic-constriction injury (CCI) via regulation of voltage-gated K+ channels (Kv). Emerging evidence indicates that transient receptor potential vanilloid 1 (TRPV1) is involved in the development and maintenance of neuropathic pain. Although it is known that the transcription of TRPV1 is regulated by Kruppel-like zinc-finger transcription factor 7 (Klf7)—and that the structure of TRPV1 is similar to that of Kv—few studies have systematically investigated the relationship between MZF1 and TRPV1 in neuropathic pain. In the present study, we demonstrated that CCI induced an increase in MZF1 and TRPV1 in lumbar-level 4/5 (L4/5) DRGs at 3 days post-CCI and that this increase was persistent until at least 14 days post-CCI. DRG microinjection of rAAV5-MZF1 into the DRGs of naïve rats resulted in a decrease in paw-withdrawal threshold (PWT) and paw-withdrawal latency (PWL) compared with that of the rAAV5-EGFP group, which started at four weeks and lasted until at least eight weeks after microinjection. Additionally, prior microinjection of MZF1 siRNA clearly ameliorated CCI-induced reduction in PWT and PWL at 3 days post-CCI and lasted until at least 7 days post-CCI. Correspondingly, microinjection of MZF1 siRNA subsequent to CCI alleviated the established mechanical allodynia and thermal hyperalgesia induced by CCI, which occurred at 3 days postinjection and lasted until at least 10 days postinjection. Microinjection of rAAV5-MZF1 increased the expression of TRPV1 in DRGs. Microinjection of MZF1 siRNA diminished the CCI-induced increase of TRPV1, but not P2X7R, in DRGs. These findings suggest that MZF1 may contribute to neuropathic pain via regulation of TRPV1 expression in DRGs.

KRas mutations are frequently seen in solid tumors such as lung (~25%), colorectal (~40%) and pancreatic (~90%) cancers. The G12C mutation accounts for ~50% of all KRas mutations in lung cancer and to a lower percentage in other tumor types. Recently, selective inhibitors targeting the KRas-G12C mutation through covalent link to the cysteine of the mutated protein have been advanced to early clinical development and exhibited encouraging response in patients with lung cancer. Here, we present a novel small molecule compound that specifically inhibits KRas-G12C in vitro (cell lines) and in vivo (cell line-derived xenograft tumor models). The anti-tumor activity of D-1553 is evaluated across a panel of cancer cell lines including lung, pancreatic and colorectal cancers and shown to be active only in cancer cells with KRas-G12C mutation. In addition, D-1553 is highly potent in vivo in various cell line-derived xenograft tumor models with KRas-G12C mutation as a single agent. When D-1553 is combined with MEK inhibitor, SHP2 inhibitor or cytotoxic agents, further tumor growth inhibition or regression was observed in tumor xenograft models. These data suggest that D-1553 has anti-tumor activity in a broad spectrum of cancers and is suitable for tissue-agnostic clinical development targeting cancers with KRas-G12C mutation. D-1553 is currently in a Phase 1/2 clinical trial evaluating safety, tolerability, PK and efficacy in patients with advanced solid tumors harboring KRasG12C mutation (NCT04585035). Citation Format: Zhe Shi, Jifang Weng, Xiaochong Fan, Emma Wang, Qingqing Zhu, Liangshan Tao, Zixing Han, Zhenwu Wang, Haotao Niu, Yueheng Jiang, Ling Zhang, Xing Dai, Yaolin Wang. Discovery of D-1553, a novel and selective KRas-G12C Inhibitor with potent anti-tumor activity in a broad spectrum of tumor cell lines and xenograft models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 932.

Ras protein plays a critical role in cell growth and proliferation by transmitting signal from cell surface receptor tyrosine kinase to downstream cellular proteins such as RAF and MEK. KRas is one of the most frequently mutated oncogenes, with mutations at residues G12, G13, and Q61, found in lung, colon, pancreatic and other solid malignancies. We have developed an orally bioavailable, covalent inhibitor of KRas G12C, D-1553, with potent in vitro biochemical, cellular activity and in vivo efficacy. Here we report the efficacy of D-1553 in a large panel of patient-derived xenograft (PDX) tumor models with KRas G12C mutation. In the lung cancer PDX models, D-1553 exhibited tumor growth inhibition (TGI) from 43.6% to 124.3%, with 4 out of 8 models showing tumor regression. In the colorectal cancer PDX models, the range of TGI was from 60.9% to 105.7%, with 3 out of 9 models showing regression. Combination treatment of D-1553 with chemotherapy and targeted agents demonstrated enhanced anti-tumor activity resulting in more tumor regression compared to single agent treatment. These observations from PDX models support the combination treatment as a key to increased overall response rate to KRas G12C inhibitor in clinical trial. D-1553 is currently in a Phase 1/2 clinical trial for patients with advanced solid tumors harboring KRas G12C mutation (NCT04585035). Citation Format: Zhe Shi, Jifang Weng, Xiaochong Fan, Qingqing Zhu, Emily Robb, Alyssa Moriarty, Michael Wick, Yueheng Jiang, Ling Zhang, Xing Dai, Yaolin Wang. Potent in vivo anti-tumor activity of D-1553 as a single agent and in combination with targeted therapeutics in a broad spectrum of patient-derived xenograft tumor models with KRas G12C mutation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1056.

CD4+ T cells play an important role in the progression of type 2 diabetes mellitus (T2DM). It is known that T cell responses can be suppressed by myeloid-derived suppressor cells (MDSCs). In this study, we aimed to explore the potential role of MDSCs in the progression of T2DM, and to examine whether the underlying mechanism was associated with CD4+ T cells. Peripheral blood samples were obtained from T2DM patients and healthy controls, as well as C57BL6J db/db mice and control heterozygous (db/-) mice. The frequency of MDSCs and CD4+ T cells was analyzed using flow cytometry. Serum levels of the cytokines interleukin (IL)-4, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ were quantified using ELISA kits. Cell proliferation was assessed using carboxyfluorescein succinimidyl ester (CFSE) labeling. In addition, the severity of insulitis was assessed using H&E staining of the pancreata. The data showed an increased frequency of CD11b+/CD33+ MDSCs and CD4+ T cells in the peripheral blood of T2DM patients. In addition, there were decreased IL-4 level and increased TNF-α and IFN-γ levels in the serum from T2DM patients. In db/db mice, an increased frequency of CD11b+/Gr-1+ MDSCs and CD4+ T cells was found in splenocytes, as well as in the peripheral blood. MDSCs inhibited the proliferation and modulated the cytokine secretion of CD4+ T cells in vitro and delayed the development of diabetes in NOD/SCID mice. In conclusion, MDSCs suppress CD4+ T cell activity and prevent the development of T2DM.

Objective: To study the relationship between the target effective site concentration (Ce) of rocuronium and the degree of recovery from neuromuscular blockade in elderly patients. Methods: 50 elderly patients (ASA grade II) scheduled for selective surgical procedure under general anaesthesia were randomly divided into two groups, A and B, with 25 cases in each group. The Ce of rocuronium for intubation was 3 μg·ml-1 in both groups, and the Ce during operation were 0.8 and 1.0 μg·ml-1 in group A and B, respectively. When target controlled infusion of rocuronium was stopped, without the administration of reversal agents for neuromuscular blockade, the relationship between Ce and the first twitch height (T1) was studied by regression analysis. Results: There was a significant linear relationship between Ce and T1, and there was no statistical difference in regression coefficient and interception between group A and B (P>0.05). Conclusion: The degree of recovery from neuromuscular blockade could be judged by the target effective site concentration of rocuronium at the time of reversal from neuromuscular blockade in the elderly patients.