Objective To analyze incidence of thyroid carcinoma and to explore and conclude the principle of its diagnosis and treatment.Methods One hundred and forty six patients of thyroid carcinoma in our hospital were analyzed and discussed with literature.Results 101 cases were diagnosed as thyroid carcinoma by pathological diagnosis of fast frozen sections,the positive ratio is approximately 93.5%.totle resection of affected lobe and isthmus was performed on 35 cases,total resection of affected lobe and isthmus and majority of opposite lobe was done on 37 cases.The lymph node metastasis was found by postoperative pathological diagnosis with a rate of 32.5%.Conclusions Preoperative diagnose of thyroid carcinoma is rarely available,diagnosis of thyroid carcinoma by fast frozen sections is optimal.total resection of affected lobe and isthmus or total resection of affected lobe and isthmus and majority of opposite lobe are the main operation patterns.

Objective To investigate the effect of daurinoline on basilar artery vascular smooth muscle. Methods The tension of isolated basilar artery ring of rabbit was measured. The effects of daurinoline on the basilar artery contracted by methoxamine,5-hydroxytryptamine(5-HT),KCl and Histamine( His)were also examined. Dose-response curves of 5-HT and KCl were observed as well. Results Daurinoline exerted obvious relaxation effect on the basilar artery vascular ring contracted by methoxamine,5-HT,KCl and His in a concentration-dependent manner. IC50 of daurinoline in methoxamine,5-HT,KCl and His-treated rabbits was 8.67×10-5,1.78×10-6,6.79×10-7 and 4.98×10-4 mol·L-1,respectively. The change of concentration-response curves of methoxamine,5-HT,KCl and His showed that daurinoline was a non-competitive antagonist. Conclusion Daurinoline exerts marked relaxation effect on basilar artery of rabbits through non-competitive antagonism. The mechanism of relaxation action may be related to blockage of voltage-dependent or receptor-dependent calcium channels.

Objective To investigate the changes in morphology and senescence-associated markers of the marrow-derived cardiac stem cells (MCSCs) from rats at different ages and to explore the impacts of age on proliferation, survival and differentiation of MCSCs. Methods With single-cell cloning culture, MCSCs were selected from the bone marrow of young, adult and aged male SD rats respectively. Ultrastructural changes of the cells were viewed under a transmission electron microscope.The senescence-associated changes were examined with SA-β-galactosidase staining and reactive oxygen species(ROS) staining. Distribution of cell cycle of MCSCs from different age groups was evaluated with flow cytometric analysis. Rates of the survived and apoptotic cells were determined by Annexin V/PI double-labeled flow cytometric analysis and Hochest33342 staining. Differentiation of the MCSCs toward cardiomyocytes was induced with BMP-2. Expression of cardiac transcription factors and cardiac specific genes of the cells after induction were examined with RT-PCR. CTnT expression of the cells also be examined with immunocytochemistry. Results The nucleus/plasma ratio of the cells from aged rats decrease and there are some myelin bodies in the cells of aged group. With increasing of age, the MCSCs in S+G2/M phase reduce, while β-galactosidase-positive cells and ROS-positive cells increase. Survival rate of the cells from aged rats is lower than that of the cells from young rats. At four week after induction with BMP-2, expression of Nkx2.5, GATA-4, cTnT mRNA and Cx-43 mRNA of the cells of young group increase significantly. In adult and aged group, expression of the cardiac transcription factors and cardiac specific genes is lower than that of the cells in young group. In immunocytochemical staining, cTnT expression of the cells in young group is stronger after induction with BMP-2. As compared with that of the cells in young group, cTnT expression of the cells in aged group is weak after induction. Conclusion With increasing of age, MCSCs show senescent changes, including their abilities of proliferation, survival and differentiation toward cardiomyocytes decrease.

BACKGROUND: It is indicated in a large amount of basic researches that compound danshen di wan has a certain action on removing carotid atherosclerotic plaques (CAP), but there is lack of large sample data in randomized, controlled, multi-central clinical experiment.OBJECTIVE: To observe the removing action of compound danshen di wan on CAP, compared with aspirin.DESIGN: Multi-central, randomized controlled experiment was designed.SETTING: Research Center of Traditional Chinese Medicine and Ultrasonic Department of Xinjing Hospital, Fourth Military Medical University of Chinese PLA; Department of Traditional Chinese Medicine of Second Clinical Hospital, Xi' an Jiaotong University and Department of Cardiac Internal Medicine of Xi' an Hospital of Traditional Chinese Medicine.PARTICIPANTS: Totally 162 cases were selected from the clinic of Research Center of Traditional Chinese Medicine, Fourth Military Medical University of Chinese PLA; Department of Traditional Chinese Medicine, Second Clinical Hospital, Xi' an Jiaotong University and Department of Cardiac Internal Medicine of Xi' an Hospital of Traditional Chinese Medicine from 2002 to 2004, aged varied from 40 to 80 years, the thickness of carotid internal media ≥ 1.2 mm. They were randomized into two groups, named danshen di wan group of 89 cases(cases of soft plaque and hard plaque were 49 and 40 respectively) and aspirin group of 73 cases(cases of soft plaque and hard plaque were 42 and 31 respectively).METHODS: In danshen di wan group: compound danshen di wan was administrated orally(10 pills/time, 3 times/day), in aspirin group, enteric soluble aspirin table was administrated orally(75 mg/time, once a day),continuously for 6 months. The alternations of thickness of carotid internal media were determined with ultrasonic B of high resolving power before and after treatment.MAIN OUTCOME MEASURES: Changes in thickness of carotid internal media before and after treatment.RESULTS: By practical measuring analysis, 143 cases accomplished nation of thickness of carotid internal media in the patients with soft plaque:In danshen di wan group, the thickness was remarkably decreased after treatment[ (2. 12 ± 0. 34), (2.44± 0.40) mm, t = 4. 267, P ＜ 0.01 ] . In aspirin group, it was also reduced relatively after treatment[ (2.25 ± 0. 3),of carotid internal media in the patients with hard plaque: The changes were not significant no matter in danshen di wan group or aspirin group in the comparison before and after treatment[in danshen di wan group: (2.46 ±0.42),(2.34 ± 0. 40) mm; in aspirin group: (2.42 ± 0. 44), (2. 36 ± 0. 38) mm,P＞ 0.05].CONCLUSION: Compound danshen di wan acts on removing soft atherosclerotic plaque and its effect is similar to aspirin.

Objective To observe the effects of electroacupuncture on the expressions of autophagy related protein Beclin-1 and apoptosis related protein p53 of hippocampus in rats;To explore the mechanism of electroacupuncture on Alzheimer's disease (AD).Methods The rats were randomly divided into the normal group, the sham-operation group, the model group, and the electroacupuncture treatment group. “Baihui” and “Yongquan” points were taken for electroacupuncture treatment and the treatment course was 7 days. The rats were treated once a day for 4 courses. Changes in morphology and number of Nissl positive cells were examined by Nissl staining in hippocampal CA1 regions. Expressions of Beclin-1 and p53 protein were determined by Western blot analysis.Results Number of Nissl positive cells in CA1 region of the model group was significantly less than that of normal group (P<0.01). After electroacupuncture treatment, number of pyramidal cells and expression of Nissl body significantly increased (P<0.05). Expression of Beclin-1 decreased, while expression of p53 increased in the hippocampus of the model group, compared with that in the normal group (P<0.05). However, electroacupuncture treatment could significantly upregulate the expression of Beclin-1 protein (P<0.01), but downregulate the level of p53 (P<0.05).Conclusion Electro-acupuncture treatment could fight against Aβ-induced neuronal apoptosis, and improve the morphological changes of AD’s hippocampus.

Objective To explore the protective effects of electro-acupuncture (EA) serum onβ-amyloid protein (Aβ) induced primary rat hippcampal neurons. Methods The rat models of Alzheimer's disease were established by intracerebral injection of Aβ1-40. After treated them with EA, the serum was harvested. Primary cultured hippocampal neurons were treated with Aβ25-35 to establish neuronal damage model in vitro, and divided into normal group, model group and EA serum group. The proliferation of neurons was detected by MTT test. Neuronal apoptosis was examined by TUNEL staining, and expression of cysteine aspartic acid proteases-3 (Caspase-3) was detected by immunocytochemical staining. Results MTT test showed that the cell viability was significantly decreased after treated with Aβ. While compared with the model group, cell proliferation of EA serum group was significantly enhanced (P<0.01). TUNEL staining showed that the number of apoptotic cells in EA serum group decreased significantly compared with the model group (P<0.01). After 48 h of Aβ treatment, Caspase-3 expression levels were significantly elevated. However, compared with the model group, the number of Caspase-3 positive cells in EA serum group was significantly reduced (P<0.01). Conclusion The EA serum could promote the proliferation of hippocampal neurons, reduce the expression of Caspase-3, counteract the neurotoxicity of β-amyloid protein, and reduce neuronal apoptosis.

[Objective]To summarize the experience of modern doctors in treating ulcerative colitis(UC)with"carbuncle",in order to provide more thinking for the treatment of UC by traditional Chinese medicine(TCM).[Methods]From the perspective of treating UC with"carbuncle",the etiology,pathogenesis,syndrome differentiation and treatment strategy of modern doctors treating UC with"carbuncle"were summarized by collating relevant experience articles of modern doctors.[Results]Modern doctors treat UC as"carbuncle",and believe that the cause of UC is related to exogenous evil,improper diet,mood failure,body deficiency and fatigue,the pathogenesis of which is the deficiency in origin and excess in superficiality,deficiency and excess are mixed with spleen deficiency,dampness,heat,blood stasis and poison.In the active stage of the disease,the main cause is evil and excess;in the remission stage,the main cause is spleen and kidney deficiency.Local syndrome differentiation and Yin-Yang syndrome differentiation are emphasized.In the treatment,the three methods of dispersing,promoting and tonifying are applied flexibly,dysentery and carbuncle are treated together,both inside and outside should be treated.[Conclusion]Treating UC as"carbuncle"is an effective TCM diagnosis and treatment idea,and provides a reference for exploring TCM treatment strategies.

Objective:To investigate the characteristics of clinical, muscle pathology and gene mutation in patients with nemaline myopathy caused by NEB gene mutation.Methods:The clinical and pathological data of patients with nemaline myopathy caused by NEB gene were collected from Neuromuscular Center of Jiaozuo People′s Hospital from January 1997 to January 2020. The next generation sequencing was preformed to detect NEB gene in all patients, and characteristics of gene mutation were analyzed.Results:Among the 11 patients, there were 8 males and 3 females, and 6 of them came from 2 families. The age of seeing a doctor ranged from 11 to 52 years, the age of onset was from 6 to 23 years, and the course of disease ranged from 5 to 35 years. Neurological examination showed that among the 11 patients, 8 patients had high palatal arch and long face. The muscle tone of both upperlimbs was normal, the tendon reflex was depressed, the proximal muscle strength was grade Ⅲ-Ⅴ, and the distal muscle strength was grade Ⅴ. The muscle tone of both lower extremities was reduced and the tendon reflex was absent. The proximal muscle strength was grade Ⅱ-Ⅳ and the distal muscle strength was grade Ⅲ-Ⅴ. No dysphagia or respiratory muscle involvement was found. Muscle biopsies were performed in 7 of the 11 patients, the pathological changes were muscle fibers of different sizes, circular atrophic muscle fibers and compensatory hypertrophic fibers, and occasionally denatured and necrotic muscle fibers were found. Different degrees of rod aggregation could be seen in all the 7 patients. Electron microscopic examination of 5 patients showed that there was rod aggregation between myofibrils, and most of them were located near the Z band, but no intranuclear rod was found. NEB gene was found in all 11 patients, and a total of 9 different mutation sites were detected, including 8 in exon region and 1 in intron region. Among them, c.21522+3A>G was found in 10 cases, c.1623delT was found in 3 cases and c.17611C>T was found in 3 cases. There was 1 case of c.4417C>T, c.2549delA, c.21065dupA, c.3520G>A, c.20943G>A, c.192G>A respectively.Conclusions:The clinical phenotype of nemaline myopathy caused by NEB gene has great heterogeneity. Muscle pathology shows that rod aggregation is an important basis for the diagnosis of this disease. Mutation c.21522+3A>G in intron is the most common mutation in this group of NEB gene. And the novel mutation sites of NEB gene are respectively c.17611C>T, c.2549delA, c.3520G>A, c.21065dupA, c.20943G>A and c.192G>A.

Objective:To summarize the characteristics of clinical, muscle pathology and gene mutation of late-onset reducing body myopathy caused by FHL1 gene mutation, in order to improve clinicians′ understanding of this disorder. Methods:The clinical, muscle pathology and muscle magnetic resonance imaging data of the proband from a family diagnosed as reducing body myopathy in Jiaozuo People′s Hospital in December 2021 were collected. Genetic tests and pedigree verification were conducted on the proband and her son.Results:The proband was a 59-year-old female with progressive, asymmetrical limb weakness and muscular atrophy. Her mother, sister and brother had similar symptoms. Electromyography showed myogenic and neurogenic damage. Muscle magnetic resonance imaging indicated that the lesion mainly involved the posterior muscles of the thigh and calf, as well as the gluteus maximus. The muscle pathology showed eosinophilic granular inclusion bodies and rimmed vacuoles in the muscle fibers of the lesion. The structure of myofibrils was disordered and abnormal protein deposition was observed. The gene sequencing showed the FHL1 gene p.C150S heterozygous variation. Conclusions:Late-onset reducing body myopathy is characterized by progressive asymmetric proximal limb muscle weakness, partially involving distal limb muscles and gluteus maximus. Muscle pathology shows the characteristic pathological changes of many kinds of myofibrillar myopathies. FHL1 gene mutation is an important basis for diagnosis.

Objective:To investigate the clinical characteristics and electron transfer flavoprotein dehydrogenase ( ETFDH) genetic mutations in patients with riboflavin responsive lipid storage myopathy (RR-LSM). Methods:A retrospective analysis was performed. The clinical data and muscular pathology of 26 patients with RR-LSM, admitted to our hospital from January 2009 to June 2021, were collected. Peripheral venous blood DNA was extracted, and the mutations of ETFDH gene were detected and analyzed by whole exome sequencing. Results:These 26 patients had onset of proximal limb myasthenia, 17 patients had difficulty in raising their head, 12 patients had mastication weakness, 6 had dysphagia, 5 had nausea and vomiting, and one was complicated with rhabdomyolysis and one was with reversible splenic lesion syndrome. Muscle biopsy indicated pathological deposition of lipid droplet, which type I fibers were involved mainly; degenerative necrotic muscle fibers were seen in a few cases. ETFDH gene mutations were detected in 26 patients; 23 patients had compound heterozygous mutation, two had single heterozygous mutation and one had homozygous mutation; 25 different mutation sites were found, mainly missense mutations; the C.770A>G frequency was the highest, accounting for 20% alleles (10/50); two novel mutation sites were found: c.1115A>G and c.1781T>C. Conclusion:RR-LSM is mainly characterized by proximal limb muscle weakness and fatigue intolerance, often accompanied by neck extensor and masticatory weakness; c. 770A>G is the hot site of ETFDH genetic mutations in RR-LSM patients.