Total laryngectomy is a crucial surgical intervention for patients with advanced malignant tumors of the larynx and nasopharynx. Despite its effectiveness, this procedure permanently severs the connection between the nasal cavity and the lower respiratory tract, leading to the cessation of nasal airflow. This disruption significantly impairs the patient's sense of smell and adversely affects their quality of life. Although olfactory loss is common in these patients, the assessment and rehabilitation of their olfactory function are often overlooked. This article reviews relevant literature on evaluating olfactory function and rehabilitation methods following total laryngectomy, with the aim of providing a theoretical foundation to enhance olfactory rehabilitation and overall quality of life for these patients.
Humans ; Laryngectomy/rehabilitation* ; Quality of Life ; Smell ; Laryngeal Neoplasms/surgery* ; Olfaction Disorders/etiology*

In recent years,significant breakthroughs have been achieved in the immunotherapy for Alzheimer's disease.In line with global advancements,two anti-amyloid-β monoclonal antibodies have been approved and successfully launched in China for clinical use.Lecanemab and Donanemab were officially used in June 2024 and April 2025 in China,respectively.In order to standardize the rational and safe application of anti-amyloid-β monoclonal antibodies for Alzheimer's disease in China,this article integrates recom-mendations from the clinical trials and real-world experience from the author's team and domestic peers to further update the recom-mendations for the clinical use of anti-amyloid-β monoclonal antibody based on the 2024 version.It includes indications for therapy,pre-treatment evaluation and preparation,administration protocols and safety measures during treatment,and post-treatment monitor-ing strategies.

This paper summarized Professor ZHOU Zhongying's experience in differentiating and treating hepatitis and liver cirrhosis from deficiency and excess. It is considered that the pathogenesis of hepatitis and liver cirrhosis belongs to deficiency in root and excess in branch， with depletion of liver， spleen and kidney as the root， and constraint and bind of damp-heat and stasis toxin as the branch. Moreover， mutual cause and promotion between deficiency and excess leads to the disease. For general principle of treatment， it is recommended to clear and transform pathogenic excess， supplement deficiency and rectify the healthy qi. In the early stage of hepatitis and cirrhosis， excess pathogen hyperactivity is the main manifestation， which can be treated by clearing and transforming damp-heat and stasis toxin， supplemented by regulating spleen and stomach， with modified Yinchenhao Decoction （茵陈蒿汤） and Biejiajian Pill （鳖甲煎丸）. In the middle and late stages， cases with deficiency-excess complex were more common， which should be treated by clearing damp-heat and stasis toxin， regulating and supplementing liver-spleen-kidney， using medicinals with the function of clearing heat and dispelling damp， dissolving stasis and resolving toxins to treat the branch. Moreover， Liujunzi Decoction （六君子汤）， Yiguan Decoction （一贯煎）plus Erzhi Pill （二至丸） and Buzhong Yiqi Decoction （补中益气汤） modifications are suggested respectively in correspondence to the different kinds of root deficiency including irregular liver and spleen， liver and kidney yin deficiency， and liver-spleen-kidney deficiency.

Emaciation is a common physical condition in clinical practice,often accompanied by symptoms related to"excessive fire in thin people".Insufficient yin-qi is the main physiological and pathological basis of emaciation,and excessive dryness-heat is the secondary manifestation.The disease involves five viscera,with the spleen as the core.The principle of treatment is to nourish yin-qi as the main method,and to dissipate stagnant heat as the auxiliary method.Specifically,it includes two aspects:treating the root cause and treating the symptoms.Treating the root cause should nourish yin-qi to improve the"emaciation"constitution,and treating the symptoms should dissipate stagnant heat to eliminate the"excessive fire"state.The importance of the two should be determined ac-cording to the severity and urgency of the excessive fire.Clinically,the addition and subtraction of medicinal ingredients are made ac-cording to factors such as the urgency of the root cause and symptoms,the state of emaciation and the ability to eat,the degree of defi-ciency or excess of fire-heat,the pathogenesis of the disease,and the season.

Objective To investigate the effect of ischemic postconditioning on autophagy and learning and memory impairment in rats with ischemia-reperfusion injury by P38MAPK.Methods Ninty-six rats were randomly divided into sham group ( Sham group), cerebral ischemia reperfusion group ( CIR group),cerebral ischemic postconditioning group ( CIP group) and cerebral ischemic postconditioning com-bined with SB203580 group (CIP + SB203580 group),and 24 rats in each group. The rat model of cerebral ischemia was established by Pulsinelli four-vessel occlusion. The learning and memory abilities of rats were measured by Morris water maze. HE staining were used to detect the morphological changes of hippocampal neurons. The phosphorylation of P38MAPK and Beclin-1,LC3-Ⅱexpression were observed by immunohisto-chemistry. Results Compared with the Sham group,the number of crossing the platform decreased(24 h: (3.04±0.20)times),and the escape latency was longer in CIR group(24 h:(58.38±1.52) s) (all P＜0.05). The number of survival neurons reduced (24 h:70.93±1.86),and the expression of P38MAPK,LC3-Ⅱ,Bec-lin-1 in immunohistochemistry were increased in CIR group(all P＜0.05). Compared with CIR group,the number of crossing the platform at each time point increased (24 h:(5.46±0.50)times),the escape latency was shorter (24 h:(52.42±1.53)s),the number of survival neurons increased at each time point(24 h:(83.07±5.30)) and the expression level of P38MAPK decreased in the CIP group,while the expression lev-el of LC3-II,Beclin-1 increased (all P＜0.05).Compared with the CIP group,the number of crossing the plat-form((24 h:(7.13±0.33)times),the escape latency was shorter (24 h:(48.04±1.39)s),the number of survival neurons increased at each time point(24 h:(91.40±1.74)),and the expression of P38MAPK was down-regulated,while the expression of LC3-II,Beclin-1 were up-regulated in CIP +SB203580 group(all P＜0.05). Conclusion Ischemic postconditioning can improve learning and memory impairment in rats with is-chemia-reperfusion injury by P38MAPK regulating autophagy.

Objective To study polymorphism of phosphatase and tensinhomologue (PTEN)-induced kinase 1(PINK1) gene of exon 5 in Parkinson patients who located in Guangxi ,and its relationship with Parkinson disease (PD) .Methods PCR ,single strand conformation polymorphism (SSCP) and sequencing analyze were conducted to analyze the PINK 1 gene′s exon 5 polymorphism in 28 cases of early-onset PD patients ,22 cases of late-onset PD patients(early-onset PD patients + late-onset PD patients = PD group) and 55 of control group .Results The intronic intervening sequence 5-5G-A (IVS5-5G-A ) polymorphism and G12164A polymer-phism which were located on PINK1 gene of exon 5 were chain relation .The G/A ,A /A genotype frequency was significantly higher in PD group (42 .0% ) than that in control group (23 .6% ) (χ2 = 4 .034 ,P= 0 .045) .The frequency was also significantly higher in late-onset PD patients (45 .5% )than that of 38 cases who were older than 50 years old in control group(21 .1% )(χ2 = 3 .951 ,P=0 .047) .There were no significant differences in alleles .Conclusion This research suggests that chain relation polymerphism at IVS5-5G-A and G12164A in PINK1 gene may be a susceptible factor for PD patients in Guangxi .