This paper summarizes Professor SUN Yuanzheng's academic thought and clinical experience in treating diabetic retinopathy (DR) with yuan-primary and luo-connecting meridian-regulating acupuncture. Professor SUN considers that the fundamental cause of DR lies in visceral dysfunction, with stagnation in the ocular collateral vessels and impairment of the mysterious orifices being the core pathogenesis. He proposes the treatment model of "regulating viscera, unblocking ocular collaterals, and opening mysterious orifices" based on yuan-primary and luo-connecting meridian-regulating acupuncture. Yuan-primary and luo-connecting points are used to balance qi, blood, yin, and yang of the viscera. Baihui (GV20) is stimulated with transcranial repetitive acupuncture to activate the yang qi of the governor vessel and invigorate qi in the twelve meridians, improving systemic microcirculation. Combining this with stimulation of ocular areas, Fengchi (GB20), and periocular points, the stasis in the ocular collaterals are cleared and the mysterious orifices are unblocked, addressing both the root and manifestations of DR.
Humans ; Diabetic Retinopathy/physiopathology* ; Acupuncture Therapy/history* ; Meridians ; Acupuncture Points ; Qi

Cerebral fat embolism (CFE) combined with pulmonary fat embolism (PFE) is an extremely rare and serious complication after fat injection. In order to improve the understanding of the mechanism of this complication, this article reported the diagnosis, treatment and pathological results of a patient with CFE and PFE after facial autologous fat injection. A 34-year-old female underwent an injection of autologous fat in her right cheek at another institution in March 2021 and developed into a coma. 1.5 hours later, she was taken to the Emergency Department of the Second Affiliated Hospital of Hainan Medical University. CT revealed a massive infarction in the right cerebral hemisphere and bilateral acute pneumonia. The patient was treated with dehydration, anti-infection, anticoagulation and microcirculation improvement in the intensive care unit. But the patient died due to the critical condition. Postmortem autopsy and histopathological examination, revealed ischemic stroke with hemorrhagic transformation, and pulmonary embolism with acute pneumonia. It was speculated that the fat embolus passed through the damaged main trunk or branch of the right facial artery, and then retrograde to the right external carotid artery, common carotid artery and internal carotid artery to cause middle cerebral artery occlusion. At the same time, the embolus returned to the right atrium along with the accompanying vein of the above artery, and reached the pulmonary vascular bed through the pulmonary circulation, resulting in pulmonary embolism. Plastic surgeons should have extensive knowledge with the anatomical structure of facial blood vessels, master the injection techniques, and improve the awareness of fat embolism when performing facial fat transplantation.

Cerebral fat embolism (CFE) combined with pulmonary fat embolism (PFE) is an extremely rare and serious complication after fat injection. In order to improve the understanding of the mechanism of this complication, this article reported the diagnosis, treatment and pathological results of a patient with CFE and PFE after facial autologous fat injection. A 34-year-old female underwent an injection of autologous fat in her right cheek at another institution in March 2021 and developed into a coma. 1.5 hours later, she was taken to the Emergency Department of the Second Affiliated Hospital of Hainan Medical University. CT revealed a massive infarction in the right cerebral hemisphere and bilateral acute pneumonia. The patient was treated with dehydration, anti-infection, anticoagulation and microcirculation improvement in the intensive care unit. But the patient died due to the critical condition. Postmortem autopsy and histopathological examination, revealed ischemic stroke with hemorrhagic transformation, and pulmonary embolism with acute pneumonia. It was speculated that the fat embolus passed through the damaged main trunk or branch of the right facial artery, and then retrograde to the right external carotid artery, common carotid artery and internal carotid artery to cause middle cerebral artery occlusion. At the same time, the embolus returned to the right atrium along with the accompanying vein of the above artery, and reached the pulmonary vascular bed through the pulmonary circulation, resulting in pulmonary embolism. Plastic surgeons should have extensive knowledge with the anatomical structure of facial blood vessels, master the injection techniques, and improve the awareness of fat embolism when performing facial fat transplantation.

The regulatory T cells (Treg) and helper T cells 17 (Th17) play an important role in regulation of the tumor microenvironment in hepatocellular carcinoma (HCC) because Treg/Th17 imbalance was associated with HCC cell invasion and progression. Moreover, the suppressor of cytokine signaling 1 (SOCS1), a negative regulator of the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway, regulates Treg and Th17 proliferation and differentiation. This review summarized and discussed the recent advancement and progress in control of the Treg/Th17 balance in HCC and the immunity-related mechanisms in HCC development and progression, i.e., the SOCS1 structure and functions, SOCS1 role in regulation of Treg/Th17 balance in HCC, and future research direction of the field.

The immune mechanism of chronic hepatitis B (CHB) persistent infection is closely associated with T cells, and the development of T cells requires the coordination of a variety of cytokines. The proteins of the signal transducer and activator of transcription (STAT) family are mainly involved in the signal transduction of cytokines, and STAT5a/b and STAT3 play an important role in the differentiation and development of regulatory T cells (Treg) and T helper 17 cells (Th17). This article analyzes the association of STAT3 and STAT5 with Treg/Th17 balance in CHB and investigates the chronicity of hepatitis B virus infection and the regulatory mechanism of liver inflammation.

Objective To explore the changes of dopamine D2 receptor in dopamine pathway in in-somnia patients and discuss its clinical significance. Methods From January 2016 to December 2016, 15 patients with insomnia (1 male, 14 females, age:(44.3±8.6) years) and 15 gender-/age-matched-healthy volunteers (control group;3 males, 12 females, age:(40.5±9.0) years) were included to undergo resting brain 11C-Raclopride PET/CT imaging. The D2 receptor binding potential (BPND) of the dopamine pathway was calculated by molecular imaging and kinetic analysis toolbox ( MIAKAT) software. The BP ND , Hamilton depression scale ( HAMD) , transient and graphics memory scale results were compared with two-sample t test and Mann-Whitney u test between the two groups. Pearson correlation analysis was used to evaluate the correlation between BPND(nucleus accumbens, caudate nucleus, putamen) and Pittsburgh sleep quality in-dex ( PSQI) , HAMD, course of disease, transient memory and graphical memory scale scores in the patient group. Results The BP ND in bilateral putamen, nucleus accumbens and left caudate nucleus of patients was lower than that of controls( left putamen:z=-2.717, right putamen:z=-2.883, both P<0.01;left nu-cleus accumbens:t=-2.269, right nucleus accumbens:t=-2.410, both P<0.05;left caudate nucleus:t=-2.632,P<0. 05), but the BPND level of right caudate nucleus was not significantly different(z=-0.850, P>0.05) . The scores of HAMD in the patient group were higher than those in control group ( t=10. 273, P<0. 01), while the scores of instantaneous memory (t=-4.888, P<0.01) and graphical memory scale (t=-2.624, P<0.05) were lower. There were significant negative correlations between the BP ND of bilateral nucleus ac-cumbens, caudate nucleus and putamen and the course of insomnia in the patient group ( r range:-0.761 to-0.682, all P<0.01) . Conclusion Patients with insomnia have abnormal neurotransmitter system of dopa-mine D2 and it may play a role in the pathogenesis of insomnia.

Objective To investigate the abnormal functional connectivity (FC) between the cores (including sublaterodorsal nucleus (SLD) and ventrolateral periaqueductal gray matter (vlPAG)) and the whole brain in rapid eye movement sleep behavior disorder (RBD) by resting state functional magnetic resonance imaging (rfMRI).Methods A total of 41 subjects recruited in the Department of Neurology,the People's Hospital of Zhengzhou University were enrolled in this study according to international diagnosis criteria,including 20 with idiopathic RBD (iRBD group) and 21 age,sex-matched normal controls (control group).All subjects were examined by Hoehn-Yahr Staging,cognitive tests and rfMRI.Resluts HoehnYahr staging score was 0(0,0) in the iRBD group,which showed no significant difference from that in the control group (0 (0,0),Z =-1.820,P =0.069).The scores of Rey Auditory Verbal Learning Test (AVLT) N1,AVLT N2,Symbol Digital Modalities Test,Rey-Osterrieth Complex Figure Test-Copy were 3.80 ± 1.67,5.10 ± 1.77,33.00(31.25,34.00) and 22.00(20.25,26.00) respectively in the iRBD group,which were significantly lower than that in the control group (4.95 ± 1.28,t =2.482,P =0.017;6.43±1.16,t =2.848,P=0.007;33.00(29.50,35.50),Z=-3.792,P=0.000;35.00(33.00,36.00),Z =-2.351,P =0.019) respectively.The scores of Trail Making Test 1 (86.5 (70.0,100.0))and Trail Making Test 2 (197.0(180.5,211.5)) in the iRBD group were significantly higher than that in the control group (66.0(49.0,91.5),112.0(99.5,173.0) respectively,Z=-2.373,P=0.018;Z =-3.105,P =0.002).Compared with the control group,the FC analysis showed reduced connections from the right SLD to the bilateral cingnlate gyrus (t =-4.173) and bilateral frontal gyrus (t =-2.965(left),-3.662(right)),from the vlPAG to the left precentral-postcentral gyrus(t =3.930),and from the vlPAG to the right frontal gyrus (t =4.141) in the iRBD.There was no statistically significant difference from the left SLD to the whole brain.Conclusion There were abnormal FCs from the SLD and vlPAG to cognitive and motor areas in RBD patients,perhaps leading to clinical RBD symptoms such as cognitive deterioration and movement disorder.

Objective To investigate the abnormal functional connectivity (FC) between the substantia nigra (SN) and the brain motor area in rapid eye movement sleep behavior disorder (RBD) by Unified Parkinson′s Disease Rating Scale (UPDRS), Hoehn-Yahr Scale and resting state functional magnetic resonance imaging (rfMRI).Methods A total of 34 subjects (14 with RBD (RBD group), 12 with Parkinson′s disease (PD group), and 8 age, sex-matched normal controls (control group)) recruited in the Department of Neurology, Henan Provincial People′s Hospital from 2014 to 2015 were enrolled in this study according to international diagnosis criteria.All subjects were examined by UPDRS, Hoehn-Yahr Scale and rfMRI.Results UPDRS scores and Hoehn-Yahr staging were 0.00 (0.00, 3.75) and 0.00 (0.00, 0.50) respectively in the RBD group, which were significantly different from that in the PD group (30.5 (18.75, 33.00) and 1.75 (1.50, 2.50), respectively;Z=-3.782, P<0.05 and Z=-2.963, P<0.05), whereas not significantly different from that in the control group (0.00 (0.00, 0.00),0.00 (0.00, 0.00), respectively;Z=1.16, P>0.05 and Z=1.10, P>0.05).The FC analysis showed alterations from the right SN to bilateral cerebellum respectively among the three groups (Fright cerebellum=12.975, Fleft cerebellum=6.144;P<0.05);furthermore, there were significant increases in the RBD group compared with the PD group (t=-4.602,-5.080, P<0.005).The FC analysis showed reduced correlation from the right SN to the left prefrontal cortex in the RBD and the PD groups compared with the control group (t=-4.899,-3.500, P<0.005), but there was no statistically significant difference between the RBD and the PD groups (t=2.035, P>0.05).Conclusions There was abnormal FC from the SN to motor areas in RBD patients, and partial alterations were similar as PD patients.rfMRI provided an evidence that RBD might be presymptom of PD.

Objective To observe non-displaceable binding potential (BPND) changes of striatal dopamine D2 receptors(SDDR) in patients with first-episode major depressive disorder (MDD) using 11C-Raclopride PET/CT,and to analyze the relationship between BPND and Hamilton rating scale for depression (HAM-D).Methods From December 2014 to December 2015,patients with first-episode MDD and age/gender-matched healthy controls underwent brain MRI and 11C-Raclopride PET/CT in this prospective study.BPND of bilateral SDDR was calculated by molecular imaging and kinetic analysis toolbox (MIAKAT).BPND changes of bilateral SDDR and their relationship with HAM-D score were analyzed.Paired t test,two-sample t test and Pearson correlation analysis were used.Results A total of 20 MDD patients (8 males,12 females,average age: (32.80±9.76) years) and 20 healthy controls (9 males,11 females,average age:(29.25±6.93) years) were enrolled in this study.The 11C-Raclopride uptake in brain tissue of the MDD group and control group were mainly distributed in bilateral striatum,and very few 11C-Raclopride was distributed in bilateral cerebral cortex and cerebellum.In MDD group,the BPND level of bilateral SDDR had no statistical differences(t values: 0.69,0.35,both P>0.05),and similar results were found in the control group(t values: 0.28,0.24,both P>0.05).Compared with the control group,however,the MDD group had lower BPND level of bilateral SDDR(t values: 3.13-4.41,all P<0.05).The BPND of bilateral caudate nucleus and/or putamen D2 receptors was correlated with HAM-D total score,anxiety/somatization factor score,cognitive impairment factor score,retardation factor score and sleep disturbance factor score(r values: from-0.688 to-0.453,all P<0.05).Conclusions The binding potential of SDDR in patients with first-episode MDD is declined,and the BPND level of SDDR is correlated with symptoms of depression.The abnormality of SDDR may be an important molecular mechanism of the abnormality of midbrain-striatal dopamine reward circuits in MDD patients.

BACKGROUND: Alginic sodium diester (ASD) possesses neuroprotective function because of its selective calcium antagonist effects.OBJECTIVE: To compare the influences of ASD on intraneuronal Ca2+content and nerve cell apoptosis before and after reperfusion in focal cerebral ischemic rats.DESIGN: Randomized controlled observation.SETTING: Neurological Department of Xiangya Hospital Affiliated to South China University; Laser Orthopedic Surgery of the First Hospital Affiliated to Southern China University.MATERIALS: This experiment was carried out between November 2003and April 2004 at the Neurological Department of Xiangya Hospital Affiliated to South China University. A total of 65 male SD rats were recruited and randomized into 6 groups; 17 got lost during the experiment, and the other 48 rats completed the experiment with 8 rats in each group.METHODS: In sham operation group, an incision was made on rats' cervical skin and sutured. Right cerebral middle artery was occluded in rats of ischemic group, ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group, and ASD 10 mg/kg postischemic group. After that, rats in all but ischemic group were subjected to intraperitoneal injection of various dosage of ASD or excipient 30minutes before reperfusion and 5 hours after reperfusion. FCM was used to determine intraneuronal Ca2+ content and rate of nerve cell apoptosis;meanwhile, neurological dysfunction was scored.MAIN OUTCOME MEASURES: [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia. [2]Correlation of behavioral obstacle score with intraneuronal Ca2+ fluorescence intensity and neuronal apoptosis in rats with right cerebral middle artery ischemia.RESULTS: Totally 65 rats were enrolled in this study, 17 of which got lost and the other 48 rats entered the result analysis. [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia: The score was obviously reduced in ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group and ASD 10 mg/kg postischemic group as compared with ischemic group (1.80±0.21, 2.20±0.23, 1.20±0.11, 2.00±0.22, 3.40±0.65); moreover,functional improvement was more obvious due to pre-reperfusional administration than post-reperfusional administration. Intraneuronal Ca2+ concentration was reduced after ASD administration at different degrees and lower than that of ischemic group. Decrement of intraneuronal Ca2+ concentration was found most obvious due to 10 mg/kg ASD administration 30 minutes before reperfusion, approximately reduced by 70%; moreover, neuronal apoptosis rate on the ischemic side was obviously suppressed by ASD administration, displaying time-dependent manner, with apoptotic suppression effect more obvious in pre-reperfusional group than in post-reperfusional group (5.68%, 10.03%; 4.00%, 9.91%). [2] Correlation of behavioral obstacle score of right cerebral middle artery ischemic rats with intraneuronal Ca2+ fluorescence intensity and membrane associated protein/propidium iodide apoptosis: Obvious positive correlation was found between behavioral obstacle score and intraneuronal Ca2+ fluorescence intensity and detection rate of membrane associated protein/propidium iodide apoptosis (r=0.51,0.62, P ＜ 0.05); intraneuronal Ca2+ fluorescence intensity was also positively correlated with the detection rate of membrane associated protein/propidium iodide apoptosis (r=0.84, P ＜ 0.05).CONCLUSION: [1] ASD can exert anti-apoptosis effect by suppressing the increment of intraneuronal Ca2+ concentration, thus having neuroprotective function and ultimately improving neurological dysfunction. [2] Its effect displays time-dependent manner, and neurological functional improvement is more obvious by pre-reperfusional administration than by post-operational administration.