Analysis of Etiology,Diagnosis,and Treatment Strategy and Efficacy of Pulsatile Tinnitus Caused by Abnormal Vascular Anatomy

Objective To investigate the etiology,clinical characteristics,diagnosis,and treatment strategies and efficacy of pulsatile tinnitus(PT)caused by vascular anatomy abnormality.Methods The clinical data of 45 patients with PT in our hospital from 2012 to 2019 were collected and retrospectively analyzed.Results All 45 patients had vascular anatomical abnormalities.The patients were divided into 10 categories according to the different locations of vascular abnormalities:sigmoid sinus diverticulum(SSD),sigmoid sinus wall dehiscence(SSWD),SSWD with high jugular bulb,pure dilated mastoid emissary vein,aberrant internal carotid artery(ICA)in the middle ear,transverse-sigmoid sinus(TSS)transition stenosis,TSS transition stenosis with SSD,persistent occipital sinus stenosis,petrous segment stenosis of ICA,and dural arteriovenous fistula.All patients complained of PT synchronous with heartbeat rhythm.Endovascular interventional therapy and extravascular open surgery were used according to the location of the vascular lesions.Tinnitus disappeared in 41 patients,was significantly relieved in 3 patients,and was unchanged in 1 patient postoperatively.Except for one patient with transient headache postoperatively,no obvious complications occurred.Conclusion PT caused by vascular anatomy abnormalities can be identified by detailed medical history and physical and imaging examination.PT can be relieved or even completely alleviated after appropriate surgical treatments.

Abnormality of thermal structure and current in the upper western tropical Pacific Ocean and its effect on subtropical high

-Mainly on the basis of the data obtained during PRC/US bilateral TOGA cruises, abnormal variation occurred during the 1986/1987 El Nino is shown in this paper about the thermal structure and circulation of the upper western tropical Pacific Ocean. The effects of the abmormal variation on the subtropical high over the Northwest Pacific Ocean are discussed. During the El Nino: (1) In the east part of the western tropical Pacific Ocean (the subsurface temperature data on the 165° E section are taken as an example), the water wanner than 29 C in the upper layer spread on the longitudinal section and positive temperature anormalies appeared in a large area of the sea surface. (2) In the west part of the western tropical Pacific Ocean (the subsurface temperature data on the 137°E section are representative ), the cross section occupied by the upper layer warmer water ( T >28 ℃ ) became shrunk, and the sea surface temperature showed negative amomalies. (3) The eastward flows in the upper layer of the 165°E section strengthened. (4)The northward flow volume of warm water from the origin area of Kuroshio, i. e. , the tropical oceanic area south of 18?0' N and from the west of 130?E to the Philippine coast, decreased. When those kinds of abnomal variation occurred, air divergence on the low level (1 000 hPa) over the Northwest Pacific Ocean was intensified, favourable to the strengthening of subtropical high over the Northwest Pacific Ocean.

Regional brain structural abnormality in ischemic stroke patients:a voxel-based morphometry study

Our previous study used regional homogeneity analysis and found that activity in some brain areas of patients with ischemic stroke changed significantly. In the current study, we examined structural changes in these brain regions by taking structural magnetic resonance imaging scans of 11 ischemic stroke patients and 15 healthy participants, and analyzing the data using voxel-based morphometry. Compared with healthy participants, patients exhibited higher gray matter density in the left inferior occipital gyrus and right anterior white matter tract. In contrast, gray matter density in the right cerebellum, left precentral gyrus, right middle frontal gyrus, and left middle temporal gyrus was less in ischemic stroke patients. The changes of gray matter density in the middle frontal gyrus were negatively associated with the clin- ical rating scales of the Fugl-Meyer Motor Assessment （r = -0.609, P = 0.047） and the left middle temporal gyrus was negatively correlated with the clinical rating scales of the nervous functional deficiency scale （r = -0.737, P = 0.010）. Our findings call objectively identify the functional abnormality in some brain regions of ischemic stroke patients.

Lipocalin-2-induced proliferative endoplasmic reticulum stress participates in Kawasaki disease-related pulmonary arterial abnormalities

Clinical cases have reported pulmonary arterial structural and functional abnormalities in patients with Kawasaki disease(KD);however,the underlying mechanisms are unclear.In this study,a KD rat model was established via the intraperitoneal injection of Lactobacillus casei cell wall extract(LCWE).The results showed that pulmonary arterial functional and structural abnormalities were observed in KD rats.Furthermore,proliferative endoplasmic reticulum stress(ER stress)was observed in the pulmonary arteries of KD rats.Notably,the level of lipocalin-2(Lcn 2),a trigger factor of inflammation,was remarkably elevated in the plasma and lung tissues of KD rats;increased Lcn 2 levels following LCWE stimulation may result from polymorphonuclear neutrophils(PMNs).Correspondingly,in cultured pulmonary artery smooth muscle cells(PASMCs),Lcn 2 markedly augmented the cleavage and nuclear localization of activating transcription factor-6(ATF6),upregulated the transcription of glucose regulated protein 78(GRP78)and neurite outgrowth inhibitor(NOGO),and promoted PASMCs proliferation.However,proapoptotic C/EBP homologous protein(CHOP)and caspase 12 levels were not elevated.Treatment with 4-phenyl butyric acid(4-PBA,a specific inhibitor of ER stress)inhibited PASMCs proliferation induced by Lcn 2 and attenuated pulmonary arterial abnormalities and right ventricular hypertrophy and reduced right ventricular systolic pressure in KD rats.In conclusion,Lcn 2 remarkably facilitates proliferative ER stress in PASMCs,which probably accounts for KD-related pulmonary arterial abnormalities.