以牙痛为首发症状的过敏性紫癜患儿10例

目的：通过对10例以牙痛为首发症状的过敏性紫癜患儿临床资料回顾,总结其临床特点及治疗经验,以期早发现早确诊。方法：对2010年1月~2015年12月于遵义医学院附属口腔医院儿童牙科就诊的10例根尖周炎并发过敏性紫癜患儿的临床资料进行分析。结果：10例全部接受牙体治疗,其中9例住院1次治愈出院,1例口腔内其余牙根尖周炎再发及入院2次。结论：过敏性紫癜可以牙痛为首发症状,但并未引起口腔科及多数儿科医生的警惕,导致误诊,因此打牢临床基本功,加强学科合作有利于早期发现及治疗。

Role of chloride channels in nitric oxide-induced rat hippocampal neuronal apoptosis in vitro

BACKGROUND：Chloride channels participate in non-neuronal apoptosis.However,it remains unclear whether chloride channels are involved in ischemic neuronal apoptosis.OBJECTIVE：To explore the effects of 4-acetamido-4＇-isothiocyanatostilbene-2,2＇-disulfonic acid （SITS） and 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS）,two chloride channel blockers,on the hippocampal neuronal apoptosis induced by 3-morpholinosydnonimine （SIN-1） based on the nitric oxide toxicity theory of neuronal apoptosis following ischemic brain injury.DESIGN,TIME AND SETTING：Comparative observation and in vitro experiments were performed at the laboratory of Zhuhai Campus of Zunyi Medical College from January to May 2009.MATERIALS：SIN-1,SITS,and DIDS were purchased from Sigma,USA.METHODS：Hippocampal neurons from Sprague-Dawley rats,aged 1 day,were cultured In vitro for 12 days and randomly assigned to control,SIN-1,or chloride channel blocker groups.SIN-1 group neurons were induced by SIN-1 for 18 hours to establish a model of ischemic neuronal apoptosis.Neurons in chloride channel blocker groups were treated with SITS or DIDS plus SIN-1 for 18 hours.The controls were cultured in DMEM/Ham＇s F12 complete medium alone.MAIN OUTCOME MEASURES：The apoptotic neurons and nuclear appearance were detected by Hoechst 33258 fluorescence staining; neuronal viability was quantitatively determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis.Caspase-3 activity was analyzed by Western blot.RESULTS：SIN-1 （1 mmol/L） dramatically induced apoptosis （50%-60%）.SITS and DIDS inhibited nitric oxide-induced neuronal injury in a dose-dependent manner,suppressed caspase-3 activation,reduced neuronal apoptosis,and improved neuronal survival.CONCLUSION：Chloride channel blockers can protect against neuronal injury induced by NO.Chloride channels might be involved in neuronal apoptosis following cerebral ischemia.

Ascorbic acid secretion in the human stomach and the effect of gastrin

AIM To investigate the changes of gastricmucosal ascorbic acid secretion in patients withnonulcer dyspepsia and the effect of gastrin onit,and to relate any observed changes to H.pylori infection and mucosal histology.METHODS Ascorbic acid secretions in patientswere examined by collecting continuouslygastric juice for one hour after having aspiratedand discarded fasting gastric juice.Using theclearance rate(mL/min)of ascorbic acid fromblood to gastric juice represented ascorbic acidsecretion in the gastric mucosa.Ascorbic acidconcentrations in plasma and juice weremeasured by ferric reduced method.RESULTS Gastric ascorbic acid secretions inH.pylori-positive patients(1.46 mL/min,range0.27-3.78)did not significantly differ fromthose in H.pylori-negative patients(1.25 mL/min,0.47-3.14)(P】0.05).There were nosignificant differences in ascorbic acidsecretions between patients with mild(1.56 mL/min,0.50-3.30),moderate(1.34 mL/min,0.27-2.93)and severe(1.36 mL/min,0.47-3.78)inflammation(P】0.05).There were nosignificant differences in ascorbic acidsecretions between patients without activity(l.45mL/min,0.27-3.14)and with mild(1.32mL/min,0.61-2.93),moderate(1.49mL/min,0.50-3.78)and severe(1.43 mL/min,0.51-3.26)activity of chronic gastritis either(P】0.05).Ascorbic acid secretions in patientswith severe atrophy(0.56 mL/min,0.27-1.20)were markedly lower than those in patientswithout atrophy(1.51 mL/min,0.59-3.30)and with mild(1.43 mL/ min,0.53-3.78)andmoderate(1.31 mL/min,0.47-3.16)atrophy(P【0.005).There was a significant negativecorrelation between ascorbic acid secretion andseverity of atrophy(correlation coefficient=-0.43,P【0.005).After administration ofpentagastrin,ascorbic acid secretions weremarkedly elevated(from 1.39 mL/min,0.36-2.96 to 3.53mL/min,0.84-5.91)(P【0.001).CONCLUSION Ascorbic acid secretion ingastric mucosa is not affected by H.pyloriinfection.Gastric ascorbic acid secretion ismarkedly related to the severity of atrophy,whereas not related to the severity ofinflammation and activity.Gastrin may stimulategastric ascorbic acid secretion.A decreasedascorbic acid secretion may be an importantfactor in the link between atrophic gastritis andgastric carcinogenesis.

Prostaglandin E1 protects hepatocytes against endoplasmic reticulum stress-induced apoptosis via protein kinase A-dependent induction of glucose-regulated protein 78 expression

AIM To investigate the protective effect of prostaglandin E1(PGE1) against endoplasmic reticulum(ER) stressinduced hepatocyte apoptosis, and to explore its underlying mechanisms.METHODS Thapsigargin(TG) was used to induce ER stress in the human hepatic cell line L02 and hepatocarcinomaderived cell line Hep G2. To evaluate the effects of PGE1 on TG-induced apoptosis, PGE1 was used an hour prior to TG treatment. Activation of unfolded protein response signaling pathways were detected by western blotting and quantitative real-time RTPCR. Apoptotic index and cell viability of L02 cells and Hep G2 cells were determined with flow cytometry and MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium] assay. RESULTS Pretreatment with 1 μmol/L PGE1 protected against TG-induced apoptosis in both L02 cells and Hep G2 cells. PGE1 enhanced the TG-induced expression of C/EBP homologous protein(CHOP), glucose-regulated protein(GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and m RNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phosphoeukaryotic initiation factor 2α and CHOP. Treatment with protein kinase A(PKA)-inhibitor H89 or KT5720 blocked PGE1-induced up-regulation of GRP78. Further, the cytoprotective effect of PGE1 on hepatocytes was not observed after blockade of GRP78 expression by H89 or small interfering RNA specifically targeted against human GRP78.CONCLUSION Our study demonstrates that PGE1 protects against ER stress-induced hepatocyte apoptosis via PKA pathwaydependent induction of GRP78 expression.

Effect of minocycline on cerebral ischemia-reperfusion injury

Minocylcine, a tetracycline derivate, has been shown to cross the blood-brain barrier and enter the central nervous system. In this study, cerebral ischemia-reperfusion injury models were established using the suture method, and minocycline was immediately injected intraperitoneally after cerebral ischemia-repeffusion （22.5 mg/kg, initially 45 mg/kg） at a 12-hour interval. Results showed that after minocycline treatment, the volume of cerebral infarction was significantly reduced, the number of surviving cell in the hippocampal CA1 region increased, the number of apoptotic cells decreased, the expression of caspase-3 and poly（adenosine diphosphate-ribose） polymerase-1 protein was down-regulated, and the escape latency in the water maze test was significantly shortened compared with the ischemia-reperfusion group. Our experimental findings indicate that minocycline can protect against neuronal injury induced by focal ischemia-reperfusion, which may be mediated by the inhibition of caspase-3 and poly（adenosine diphosphate-ribose） polymerase-1 protein expression.

Immunogenicity and immunoprotection of recombinant PEB1 in Campylobacter-jejuni-infected mice

AIM： To construct a prokaryotic expression vector carrying Campylobacterjejuni peblA gene and express it in Escherichia coli. Immunoreactivity and antigenicity of rPEB1 were evaluated. The ability of rPEB1 to induce antibody responses and protective efficacy was identified. METHODS： peblA gene was amplified by PCR, target gene and prokaryotic expression ptasmid pET28a （＋） was digested with BamHI and XhoI, respectively. DNA was ligated with T4 DNA ligase to construct recombinant plasmid pET28a（＋）-peblA. The rPEB1 was expressed in E. coli BL21 （DE3） and identified by SDS-PAGE. BALB/c mice were immunized with rPEBI. ELISA was used to detect the specific antibody titer and MTT method was used to measure the stimulation index of spleen lymphocyte transformation. RESULTS： The recombinant plasmid pET28a （＋）-peblA was correctly constructed. The expression output of PEB1 protein in pET28a （＋）-peblA system was approximately 33% of total proteins in E. coil The specific IgG antibody was detected in serum of BALB/c mice immunized with rPEB1 protein. Effective immunological protection with a lower sickness incidence and mortality was seen in the mice suffering from massive C. jejuni infection. CONCLUSION： rPEB1 protein is a valuable candidate for C. jejuni subunit vaccine.

罗汉果对雄性小鼠骨髓微核和精子形态的影响

背景:对罗汉果的遗传毒性进行研究,可为其安全使用提供实验依据。目的:观察罗汉果水提液对雄性小鼠骨髓细胞微核率和附睾精子畸形率的影响,了解其是否有遗传毒性。方法:按罗汉果水提液最大使用剂量(3g/mL)和最大灌胃容量(20mL/kg)灌胃小鼠,观察罗汉果水提液的急性毒性。将雄性昆明小鼠随机分为5组,分别灌胃给予30,15,7.5g/kg的罗汉果水煎液、蒸馏水,连续5d;或腹腔注射40mg/kg环磷酰胺。于灌胃第5天,采用骨髓嗜多染红细胞微核试验计算小鼠的骨髓微核率。于首次灌胃后第35天,观察小鼠精子畸形率。结果与结论:罗汉果水提液对昆明小鼠的经口急性毒性最大耐受剂量大于120g/kg。罗汉果水提液30,15,7.5g/kg灌胃后,小鼠的骨髓微核率、精子畸形率与正常小鼠无差异(P>0.05),均明显低于环磷酰胺诱发的骨髓微核率和精子畸形率(P<0.05)。说明罗汉果水提液对成年雄性小鼠无明显遗传毒性。

ClC-3 chloride channel in hippocampal neuronal apoptosis

Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol- lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was es- tablished by 0.5 mmol/L 3-morpholinosyndnomine （SIN-l）, a nitric oxide donor. The models were then cultured with 0.1 mmol/L of 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS; the chloride channel blocker）for 18 hours. Neuronal survival was detected using the 3-（4,5-dimethylthiazol- 2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay, and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining. Western blot analysis and immunochemilumi- nescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins. Real-time PCR was used to detect the mRNA expression of CIC-3. The results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted CIC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-I. Our findings indicate that the increased activities of the CIC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.

Expression of P450 and nuclear receptors in normal and end-stage Chinese livers

AIM: To investigate the expression of P450 enzyme genes by using end-stage liver disease samples and trimmed normal Chinese donor livers.

Roles of Na^+/Ca^(2+) exchanger 1 in digestive system physiology and pathophysiology

The Na^+/Ca^(2+) exchanger(NCX) protein family is a part of the cation/Ca^(2+) exchanger superfamily and participates in the regulation of cellular Ca^(2+) homeostasis. NCX1, the most important subtype in the NCX family, is expressed widely in various organs and tissues in mammals and plays an especially important role in the physiological and pathological processes of nerves and the cardiovascular system. In the past few years, the function of NCX1 in the digestive system has received increasing attention; NCX1 not only participates in the healing process of gastric ulcer and gastric mucosal injury but also mediates the development of digestive cancer, acute pancreatitis, and intestinal absorption.This review aims to explore the roles of NCX1 in digestive system physiology and pathophysiology in order to guide clinical treatments.

Neurofibromatosis type 1-associated multiple rectal neuroendocrine tumors: A case report and review of the literature

Neurofibromatosis type 1(NF-1) is commonly associated with benign or malignant tumors in both the central and peripheral nervous systems. However, rare cases of NF-1-associated multiplerectal neuroendocrine tumors have been reported. This report describes a case of a 39 year old female with NF-1 and intermittent hematochezia as a primary symptom. Physical examination showed multiple subcutaneous nodules and café au lait spots with obvious scoliosis of the back. Imaging examinations and colonoscopy found malformation of the left external iliac vein and multiple gray-yellow nodules with varying sizes and shapes in the rectal submucosal layer. Histological and immunohistochemical results suggested multiple rectal neuroendocrine tumors, a rare disease with few appreciable symptoms and a particularly poor prognosis. The patient with NF-1 presented here had not only multiple rectal neuroendocrine neoplasms but also vascular malformations, scoliosis and other multiple system lesions. This case therefore contributes to improving clinical understanding, diagnosis and treatment of related complications for patients with NF-1 who present with associated medical conditions.

Correlation between TAMs and proliferation and invasion of type endometrial carcinoma

Objective: To explore the correlation between tumor-associated macrophages and the proliferation and invasion of type endometrial carcinoma. Methods: Immunohistochemistry was used to investigate the infiltration of macrophages in normal and different types of hyperplastic endometrial lesions. The proliferation and invasion ability of type endometrial carcinoma cell line RL95-2 influenced by mononuclear macrophage cell line THP-1(constructed M2 type macrophages) was detected by CCK8 and transwell technologies respectively. Transwell was used to evaluate the recruiting ability of RL95-2 on THP-1 cells. Otherwise, the western blot was also used to detect the expression of Cyclin D1 and MMP-2 in RL95-2 with the influence of THP-1. Results: Immunohistochemistry result showed a positive correlation between the number of infiltrating macrophages and the progression of endometrial hyperplasia.THP-1 recruited by RL95-2 could promote its proliferation and invasion and enhance the expression of the Cyclin D1 and MMP-2 protein in a time dependent manner(P<0.05). Conclusions: Increase of the number of infiltrating macrophages and its contribution to the tumor inflammatory microenvironment may result in the development of the type endometrial carcinoma.

Cornel iridoid glycoside induces autophagy to protect against tau oligomer neurotoxicity induced by activation of glycogen synthase kinase-3β

Tau oligomers are the etiologic molecules of Alzheimer disease(AD), and correlate strongly with neuronal loss and exhibit neurotoxicity. Recent evidence indicates that small tau oligomers are the most relevant toxic aggregate species. The aim of the present study was to investigate the mechanisms of cornel iridoid glycoside(CIG) on tau oligomers and cognitive functions. We injected wortmannin and GF-109203 X(WM/GFX, 200 μmol·L-1 each) into the lateral ventricles to induce tau oligomer and memory impairment in rats. When oral y administered with CIG at 60 and 120 mg·kg-1 per day for 14 d, CIG decreased the escape latency in Morris water maze test. We also found that CIG restored the expression of presynaptic p-synapsin, synaptophysin, and postsynaptic density-95(PSD-95) decreased by WM/GFX in rat cortex. CIG reduced the accumulation of tau oligomers in the brain of WM/GFX rats and in cells transfected with wild type glycogen synthase kinase-3β(wt GSK-3β). In addition, CIG up-regulated the levels of ATG7, ATG12, Beclin-1, and LC3 II in vivo and in vitro, suggesting the restoration of autophagy function. These results suggest that CIG could ameliorate memory deficits and regulate memory-associated synaptic proteins through the clearance of tau oligomers accumulation. Moreover, CIG clears tau oligomers by restoring autophagy function.

Anti-inflammatory properties of lipoxin A4 protect against diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury

Lipoxin A4 can alleviate cerebral ischemia/reperfusion injury by reducing the inflammatory reaction,but it is currently unclear whether it has a protective effect on diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury.In this study,we established rat models of diabetes mellitus using an intraperitoneal injection of streptozotocin.We then induced focal cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery for 2 hours and reperfusion for 24 hours.After administration of lipoxin A4 via the lateral ventricle,infarction volume was reduced,the expression levels of pro-inflammatory factors tumor necrosis factor alpha and nuclear factor-kappa B in the cerebral cortex were decreased,and neurological functioning was improved.These findings suggest that lipoxin A4 has strong neuroprotective effects in diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury and that the underlying mechanism is related to the anti-inflammatory action of lipoxin A4.

Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons

Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2＇-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor.

Neural stem cell transplantation in the hippocampus of rats with cerebral ischemia/reperfusion injury Activation of the phosphatidylinositol-3 kinase/Akt pathway and increased brain-derived neurotrophic factor expression

The phosphatidylinositol-3 kinase （PI3K）/Akt pathway and brain-derived neurotrophic factor （BDNF） are involved in neurological functional recovery following cerebral ischemia. Therefore, we hypothesized that mechanisms of neuroprotection by transplantation of neural stem cells （NSCs） on cerebral ischemia contributed to activation of the PI3K/Akt pathway and enhanced BDNF expression. In the present study, Wortmannin （a specific, covalent inhibitor of PI3K） was administered adjacent to ischemic hippocampus by stereotactic transplantation to further confirm the neuroprotective mechanisms of NSC transplantation following cerebral ischemia. Results showed that focal infarct volume was significantly smaller in the NSCs group, but the neurological behavior score in the NSC group was significantly greater than the middle cerebral artery occlusion model group, Wortmannin treatment group, and NSCs ＋ Wortmannin treatment group. Protein expression of BDNF was significantly greater in the NSC group compared with the Wortmannin treatment group and NSCs ＋ Wortmannin treatment group. These results suggest that the neuroprotective role of NSC transplantation in the cerebral ischemia activated the PI3K/Akt pathway and upregulated BDNF expression in lesioned brains.

Role of TGF-β1/Smads pathway in carotid artery remodeling in renovascular hypertensive rats and prevention by Enalapril and Amlodipine

Objective To investigate the role of transforming growth factor-β1 （TGF-β1）, Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapril and Amlodipine. Methods The renovascular hypertensive rat （RHR） models with ＂two-kidney and one-clip＂ were established, including model group （n = 6）, sham-operated group （n = 6）, Enalapril group （10 mg/kg per day, n = 6）, Amlodipine group （5 mg/kg per day, n = 6） and combination group （Amlodipine 2.5 mg/kg per day ＋ Enalapril 5mg/kg per day, n = 6）. The medication were continuous administrated for six weeks. Carotid artery morphological and structural changes in the media were observed by HE staining, Masson staining and immuno histochemical staining. Media thickness （MT）, MT and lumen diameter ratio （MT/LD）, and the expression levels of media a-smooth muscle actin （α-actin）, proliferating cell nuclear antigen （PCNA）, TGF-β1, phosphorylated Smad2/3 （p-Smad2/3） and Smad7 in carotid arteries were measured. Results The media of carotid arteries in RHR model group was significantly thickened, the volume of smooth muscle cell was increased, and the array was in disorder; MT, MT/LD, the proliferation index of smooth muscle cell and collagen fiber area percentage of carotid arteries in the model group were significantly higher than those in the sham-operated group （P 〈 0.01）. Compared to sham-operated group, the model group had significantly higher expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05） and lower Smad7 expression. Both Enalapril and Amlodipine improved smooth muscle hypertrophy and collagen deposition, reduced RHR carotid MT, MT/LD, proliferation index of smooth muscle cell, collagen fiber area percentage and the expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05）, increased Smad7 expression （P 〈 0.05）. Moreover, the combination treatment of Enalapril and Amlodipine had significantly better effects than single Amlodipine group （P 〈 0.05）, but not single Enalapril group. Conclusions TGF-β1/Smads pathway may participate in the mechanism of carotid artery remodeling in RHR; the role of Amlodipine and Enalapril in inversing carotid artery remodeling may be related to the change of TGF-β1/Smads pathway, the combination treatment of Amlodipine and Enalapril had better effects than single administration of Amlodipine.

Unexplained abdominal pain due to a fish bone penetrating the gastric antrum and migrating into the neck of the pancreas: A case report

BACKGROUND Ingestion of foreign bodies results in gastrointestinal perforation in approximately 1% of patients,and fish bones are the objects that most commonly lead to bowel perforation. When it does occur,the terminal ileum is the most common site of perforation,followed by the duodenal C-loop. However,involvement of the pancreas is very rare. Because clinical symptoms are nonspecific and gastrointestinal perforation may present as only odynophagia or abdominal pain,a definite preoperative diagnosis and clinical intervention may be delayed.CASE SUMMARY We report the case of a 32-year-old man who presented to our hospital because of abdominal pain that had worsened over 5 d. He had no significant past history except that he had eaten fish 1 wk previously. Upper endoscopy revealed an irregular submucosal tumor on the front wall of the gastric antrum. Endoscopic ultrasonography and computed tomography showed a fish bone penetrating the gastric antrum and migratingin to the neck of the pancreas. The patient underwent laparoscopic surgery and had no complications one week after the operation.CONCLUSION A recent history of foreign body ingestion and imaging examinations are helpful for diagnosis of unexplained abdominal pain caused by foreign bodies.

Effects of minocycline on learning and memory of mice following ischemic-hypoxic cerebral injuries

An ischemic-hypoxic animal model was established using right common carotid artery occlusions and inhalation of low concentrations of oxygen in mice. At 10 days after the ischemic-hypoxic injuries, saline-treated mice exhibited significantly prolonged escape latencies in water-maze tests and significantly shorter memory latencies and more mistakes in step-down tests. In contrast, mice treated with 5 mg/kg minocycline exhibited significant reversals of each of these effects compared with the saline-treated control mice. Moreover, we found that minocycline can relieve brain water content and morphological changes in mice following ischemic-hypoxic cerebral injuries. Accordingly, our findings indicate that minocycline provides some protections against the deleterious effects of these injuries in mice.

Primary Breast Lymphoma （PBL）： A Literature Review

Primary breast lymphoma is a rare disease. It is mainly found in female patients, the right breast in more frequently involved. The majority of PBL are diagnosed by biopsy or post- operative pathological findings. The combined therapy regimen, the main part of which is CHOP chemotherapy, is the main stream. Radical surgery is to be avoided.