A case of eosinophilic lymphoid granuloma(ELG)was reported and the related literatures were reviewed.ELG is rare in clinic. The etiology and pathogenesis of ELG was unclear.The clinical feature includes enlarged lymph nodes which were always predilected for the head and neck regions,eosinophilic granulocytes and serum IgE rising.Lymphoid tissue hyperplasis formation of lymphoid follicles with active germinal centres are common in pathological examination.There is diffuse infiltration of eosinophils in interfollicular and perivascular zones. Surgery,drug therapy and radiotherapy are all effective for the treatment,but recurrence is often.

Objective To evaluate the role of mitochondrial fission in anoxia-reoxygenation injury to rat hippocampal neurons.Methods Neurons were enzymatically isolated from hippocampi of newborn Sprague-Dawley rats (less than 24 h old).The primary hippocampal neurons were cultured and seeded in 25 mm × 25 mm culture flasks at a density of 7 × 105/ml.The cultured neurons were randomly assigned into 3 groups (n =18 each) using a random number table:control group (C group),anoxia-reoxygenation group (I/R group),and mitochondrial fission inhibitor mdivi-1 group (M group).In group I/R,the vehicle dimethyl sulfoxide (DMSO,final concentration ＜ 0.1％) was added prior to anoxia and the cells were then incubated for 40 min.In group M,mdivi-1 (dissolved in DMSO,final concentration of DMSO ＜ 0.1％) was added prior to anoxia and the cells were then incubated for 40 min.The hippocampal neurons were subjected to oxygen-glucose deprivation (OGD) for 6 h followed by restoration of O2 supply for 20 h.After 20 h of reoxygenation,the level of reactive oxygen species (ROS) (by ELISA),cell apoptosis (using flow cytometry),and expression of mitochondrial fission protein Drp1,Bcl-2 and Bax (by Western blot) were measured.The apoptosis rate and the ratio of Bcl-2 to Bax were calculated.Results Compared with C group,ROS content and apoptosis rate were significantly increased,the expression of Drp1 and Bax was up-regulated,the expression of Bcl-2 was down-regulated,and the ratio of Bcl-2 to Bax was decreased in I/R group (P ＜ 0.05).Compared with I/R group,ROS content and apoptosis rate were significantly decreased,the expression of Drp1 and Bax was down-regulated,the expression of Bcl-2 was up-regulated,and the ratio of Bcl-2 to Bax was increased in M group (P ＜ 0.05).Conclusion Mitochondrial fission is involved in anoxia-reoxygenation injury to rat hippocampal neurons via mitochondria-mediated apoptotic pathway.

Objective To evaluate the reliability of lactate clearance rate in evaluating the efficacy of early fluid resuscitation in the patients with severe sepsis.Methods One hundred and forty-two patients with severe sepsis,aged 28-87 yr,were enrolled in the study.Isotonic crystalloid fluid was infused after admission to ICU to maintain central venous pressure ≥ 8 mmHg,mean arterial pressure ≥ 65 mmHg,central venous oxygen saturation (ScvO2) ≥ 70％,and urine output ≥ 0.5 ml·kg 1 ·h-1 within 6 h.The patients were divided into 2 groups according to the treatment outcome:survival group and death group.Immediately before fluid resuscitation and at 6,12 and 24 h after fluid resuscitation,blood samples were collected from the central vein for blood gas analysis and ScvO2 was recorded.Blood samples were collected from the peripheral vein for determination of the concentration of lactate and lactate clearance rate was calculated.Results Compared with survival group,the lactate clearance rate was significantly decreased at 6,12 and 24 h after fluid resuscitation,and no significant change in ScvO2 was found in death group.Conclusion Lactate clearance rate can evaluate the efficacy of early fluid resuscitation in the patients with severe sepsis.

Objective To evaluate effect of dexmedetomidine on mitochondrion-dependent apoptosis during hypoxia-reoxygenation (H/R) injury to hippocampal neurons of rats.Methods The primarily cultured hippocampal neurons of Sprague-Dawley rats were divided into 4 groups (n =40 each) using a random number table method:control group (C group),vehicle group (V group),H/R group and dexmedetomidine group (D group).Hippocampal neurons were subjected to oxygen-glucose deprivation followed by restoration of oxygen supply to establish the model of H/R injury.Dexmedetomidine 1 μmol/L was added at 6 h of reoxygenation in D group.The viability of neurons was measured by methyl thiazolyl tetrazolium assay at 20 h of reoxygenation.The ultrastructure of mitochondria was observed by transmission electron microscopy.The expression of cytochrome c (Cyt c),caspase-3,Fis1 and Drp1 was detected by Western blot.The neuronal apoptosis was detected by flow cytometry,and apoptosis rate was calculated.Results Compared with C group,no significant change was found in the viability of neurons in group V (P＞0.05),and the viability of neurons was significantly decreased,the apoptosis rate was increased,the expression of Cyt c,caspase-3,Fis1 and Drp1 was up-regulated (P＜0.05),and the damage to mitochondrial ultrastructure was accentuated in H/R and D groups.Compared with H/R group,the viability of neurons was significantly increased,the apoptosis rate was decreased,the expression of Cyt c,caspase-3,Fis1 and Drp1 was down-regulated (P＜0.05),and the damage to mitochondrial ultrastructure was significantly attenuated in D group.Conclusion The nechanism by which dexmedetomidine reduces the H/R injury to hippocampal neurons is related to inhibiting mitochondrion-dependent apoptosis in rats.