Advance in Functional Restoration of Injured Nerve with Low Level Laser and its Utilization in the Dental and Maxillofacial Region

The inferior alveolar nerve and facial nerve are the two most important nerves in the dental and maxillofacial region. The injury to them is one of the major postoperative complications after alveolar surgery and orthognathic surgery. However, recovering the nerve function after injury takes a long time and the recovery effect tends to be unsatisfactory. In recent years, an intensively investigated technique, low level laser which has been applying in assisting the recovery of nerve function, has been gradually proved to be effective in clinically treating postoperative nerve injury. In this article we review in terms of the mechanisms involved in low level laser-assisted functional restoration of nerve injury and its clinical application in the recovery of nerve function in the dental and maxillofacial area as well.     

临床护理路径用于ICU重症颅脑损伤患者护理中的价值

目的 探讨临床护理路径用于ICU重症颅脑损伤患者护理中的价值。方法 选择2017年11月～2018年10月进行ICU重症颅脑损伤治疗的患者100例作为对象,随机数字表法分为对照组(n=50)和观察组(n=50)。对照组给予常规护理,观察组在其基础上应用临床护理路径,15 d护理后比较患者依从性情况、对患者护理前后心理状态进行评分,对不良并发症产生情况进行比较。结果 观察组康复锻炼依从、按时用药依从及饮食依从高于对照组(P0.05)。护理前两组SDS与SAS评分比较差异无统计学意义(P0.05),护理后,观察组SDS与SAS评分低于对照组(P0.05)。观察组出现压疮、泌尿感染、以及发热的发生率显著低于对照组(P0.05)。结论 将临床护理路径用于ICU重症颅脑损伤患者的护理中,提高了患者的护理依从性,减少了不良情绪以及不良并发症的产生,有助于患者整体治疗,值得推广应用。     

PCI和静脉溶栓治疗急性心肌梗死的疗效比较

目的探讨经皮冠状动脉介入(PCI)和静脉溶栓在急性心肌梗死患者中的应用价值。方法选择我院2013年1月至2014年9月收治的60例急性心肌梗死患者作为研究对象,随机分为实验组和对照组各30例。实验组患者采用PCI治疗,对照组患者采用静脉溶栓治疗,比较两组患者血管再通率、死亡发生率、ST段回落情况、住院时间、近远期不良事件发生率、左室舒张末径和左室射血分数变化情况。结果实验组血管再通率显著高于对照组,差异有统计学意义(P<0.05),而近期和远期不良事件发生率均低于对照组,近期不良事件发生率组间比较差异有统计学意义(P<0.05),而远期不良事件发生率比较差异无统计学意义(P>0.05)。实验组患者死亡发生率、ST段回落和住院时间均低于对照组,差异均有统计学意义(P<0.05)。实验组左室射血分数在术后1个月、3个月和6个月时均显著高于对照组,差异均有统计学意义(P<0.05)。结论急性心肌梗死患者应用PCI治疗可显著提高血管再通率、降低死亡和不良事件发生率,有效改善心功能。     

��沿ײ����������Ĥ�������ʵ���о�

??Objective    To investigate the characteristics of indirect injury of periodontal membrane caused by maxillofacial impact injury. Methods    The study was carried out at the laboratory of oral and maxillofacial trauma in Fourth Military Medical University??from November 2013 to January 2014. Totally 18 dogs were divided equally into six groups with random allocation??the right mandible of each dog was impacted by a cylindroid iron cap whose weight was 0.26kg??but teeth were not injured directly??the animals were killed 6 h??24 h??3 d??7 d??2 wk and 4 wk later??respectively??the histopathologic manifestations of periodontal membrane of the fourth premolar of right mandible??the second premolar of right mandible and the second premolar of left mandible were observed. Results    The injury of periodontal membrane of the fourth premolar of right mandible was relatively obvious??but the pathologic changes were reversible??periodontal membrane of the second premolar of right mandible was injured slightly??yet no obvious histopathologic change could be observed in periodontal membrane of the second premolar of left mandible. Conclusion    Maxillofacial impact injury can cause indirect injuries of periodontal membrane of adjacent teeth??but the pathologic changes are reversible??traumatic severity decreases as the distance of the tooth to the wound area increases.     

Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia–reperfusion injury

Systematic administration of anti-inflammatory cytokine interleukin 4 (IL-4) has been shown to improve recovery after cerebral ischemic stroke. However, whether IL-4 affects neuronal excitability and how IL-4 improves ischemic injury remain largely unknown. Here we report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia–reperfusion (I/R) injury. In multi-electrode array (MEA) recordings, IL-4 reduces spontaneous firings and network activities of mouse primary cortical neurons. IL-4 mRNA and protein expressions are upregulated after I/R injury. Genetic deletion of Il-4 gene aggravates I/R injury in vivo and exacerbates oxygen-glucose deprivation (OGD) injury in cortical neurons. Conversely, supplemental IL-4 protects Il-4^−/− cortical neurons against OGD injury. Mechanistically, cortical pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic hyperexcitability and enhanced excitatory synaptic transmissions in Il-4^−/− mice. Furthermore, upregulation of Nav1.1 channel, and downregulations of KCa3.1 channel and α6 subunit of GABA_A receptors are detected in the cortical tissues and primary cortical neurons from Il-4^−/− mice. Taken together, our findings demonstrate that IL-4 deficiency results in neural hyperexcitability and aggravates I/R injury, thus activation of IL-4 signaling may protect the brain against the development of permanent damage and help recover from ischemic injury after stroke.     

脑心通胶囊治疗脑梗死合并心肌缺血的多中心非随机临床对照试验

目的：观察脑心通胶囊（步长制药）治疗脑梗死合并心肌缺血患者的临床疗效。方法选取2013年10月至2014年12月北京21所医院神经内科收治的符合入组条件的急性脑梗死伴心肌缺血患者，非随机分为脑心通组（基础治疗基础上加用步长脑心通胶囊）和对照组（仅基础治疗）。对比分析第4周、8周、12周时2组心电图变化以及使用NIHSS和改良mRankin评估第12周时神经功能变化。结果入组544例，剔除16例（不良事件2例、自动放弃1例、违背规则1例、失访6例、其他6例），实际完成试验528例（包含测量资料缺失病例），其中脑心通组291例，对照组237例。心肌缺血改善的有效率脑心通组和对照组第4周差异无统计学意义（18．1％、14．9％， P ＝0．704）；但第8周（27．7％、14．3％， P ＝0．001）和第12周（31．3％、16．9％，P ＜0．01）差异有统计学意义（ P ＜0．05）。第12周时NIHSS减少≥2分脑心通组（77．7％）明显高于对照组（68．4％）（ P ＜0．05），mRankin 减少≥1分脑心通组（67．7％）显著高于对照组（56．1％）（ P ＜0．05）。多因素分析心电图改善的独立影响因素是脑心通（ P ＝0．005）和第12周时AST的降低（ P ＝00．47）；神经功能改善的影响因素包括脑心通治疗、基线收缩压和肌酐水平、既往心脏病或高脂血症病史。结论脑心通胶囊联合基础治疗对脑梗死合并心肌缺血临床疗效确切。     

Is dose modification or discontinuation of nilotinib necessary in nilotinib-induced hyperbilirubinemia?

Nilotinib is a specific breakpoint cluster region-Abelson leukemia virus-tyrosine kinase inhibitor that is used as an effective first- or second-line treatment in imatinib-resistant chronic myelogenous leukemia (CML) patients. Hepatotoxicity due to nilotinib is a commonly reported side effect; however, abnormal liver function test (LFT) results have been reported in asymptomatic cases. When alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are more than five-fold the upper limit of the normal (ULN) or when the serum total bilirubin level is more than three-fold the ULN, dose modification or discontinuation of nilotinib is recommended, resulting in decreased levels of hematological indicators in certain patients with CML. Nilotinib-induced hyperbilirubinemia typically manifests as indirect bilirubinemia without elevated ALT or AST levels. Such abnormal liver functioning is thus not attributed to the presence of a true histologic lesion of the liver. The underlying mechanism may be related to the inhibition of uridine diphosphate glucuronosyltransferase activity. Therefore, nilotinib dose adjustment is not recommended for this type of hyperbilirubinemia, and in the absence of elevated liver enzyme levels or presence of abnormal LFT findings, physicians should consider maintaining nilotinib dose intensity without modifications.