Hepatic stem cells transplantation might be an important treatment strategy for patients with end stage liver diseases and related research has become a focus of recent studies.Hepatic stem cells of different sources have great therapeutic potential in clinical practice,but much research still need to be done before it can be used as a routine method in clinical practice. This review discusses the characteristics of hepatic stem cells and its role in liver regeneration after liver damage.

In the article we described a case of 61-year-old male with pharyngeal paraesthesia for 3 months. Physical examination: lean physique; vast uneven white membrane above hard palate, soft palate and pharynx mucous membrane, not easy to wipe and extend to the throat. The neck without cervical lymph node enlargement. Blood routine test: WBC 4.92 x 10(9)/L, N 64.3%, L 18.7%, EO 7.1%. RBC 4.08 x 10(12)/L, PLT 181 x 10(9)/L. No significant abnormal in the other blood biochemical indexes, tumor marker and immune indexes; blood bacteria culture: negative; blood culture: negative; sputum culture (3 times): all negative; anti-HIV screening test: positive, serum HIV testing: positive(the test done by Shanghai Pudong new area's centers for disease control and detection). The incidence of HIV/AIDS is still low at present, so the diagnosis of HIV/AIDS can be ignored easily by the otolaryngology doctor. If the patient with oral cavity and pharyngeal ulcer delayed healing, the doctor should be alert to,HIV/AIDS infection. We should check serum HIV antibody to eliminate or confirm HIV/AIDS earlier.
HIV Infections ; diagnosis ; Humans ; Male ; Middle Aged ; Otolaryngology ; methods

Abstract?AIM: To determine the relation between each of the optical coherence tomography ( OCT) patterns, etiologies and visual acuity in patients with cystoid macular edema ( CME) .?METHODS:Fifty-seven eyes with CME from 52 patients were included in our study. The data of this cross sectional study was collected rfom p atient s wtih CME assessed by OCT, who also underwent fun dus photography and visual acuity test the same day. The best corrected visual acuity ( BCVA ) was assessed by using E chart a nd converted in logarithm of the minimum angle of resolution( logMAR ) . Thevisual acuity varied from 2.3 logMAR to 0 logMAR w ith a mean of 1.11±0.57. The etiology was determined from medical history and the fundus ph otograph of the patient. Four O CT grades established according to ratio between the vertical size of largest cyst and the maximum macular thickness (<30 %,≥30% <60%,≥60% <90%and≥90%) were considered. The correlation was established by calculating the Pearson's correlatio n coefficient “r” and the statistical significance was considered when P value was inferior to 0.05.?RESULTS: OCT grade I V was the most associated with very severe visual loss with the greatest mean VA of 1.96± 0.23 logMAR and the correlation between OCT grades and visual acuity was strongly statistically significant ( r =0.729, P <0.001 ). The central retinal vein occlusion ( CRVO) was the most underlying disease associated with worsev ision, with the gre atest mean VA of 2 logMAR and the correlation was statistically significant ( r=0.375, P=0.004).Another associated OCT pattern, the disruption of bot h inner segment/outer segment ( IS/OS) and external limiting membrane ( ELM) , was inversely associated with severe visual loss ( high mean VA=1.11 ±0.57 logMAR, with statistically significant correlation, r=-0.346, P=0.008 ) . The presence of both vitreoretinal traction components and outer retinal layers disruption were significantly associated with OCT grade IV ( r=0.390, P=0.003) and CRVO (r=0.362, P=0.006).?CONCLUSION:In this study, the OCT fourth grade and CRVO seem to be more significantly associated with the worse vision in patients with CME.

Aim To explore the role of nicotinamide adenine dinucleotide phosphate ( NADPH ) oxidase in high glucose-induced injury in H9c2 cardiac cells. Methods H9 c2 cardiac cells were exposed to differ-ent concentrations of high glucose(5. 5 mmol·L-1 ,11 mmol · L-1 ,22 mmol · L-1 ,33 mmol · L-1 ,44 mmol ·L-1 , 55 mmol · L-1 ) for 24 h and different time pints of high glucose(0 h,12 h,24 h,36 h,48 h,72 h) . Cell viability was measured by MTT colorimetry, the protein expression of Bcl-2 , Bax and NADPH oxi-dase submits such as p22 phox , p47 phox and p67 phox were determined by western blotting. Results H9c2 cardi-ac cells exposure to high glucose for 24 h showed on decrease in cell survival and the Bcl-2 expression while an increase in the Bax expression ( P<0. 05 ) . Moreo-ver, high glucose could markedly up-regulate the activ-ity of NADPH oxidase characterized by the enhanced expression of p22 phox , p47 phox and p67 phox ( P<0. 05 ) . Conclusion Activating NADPH oxidase may play an important role in high glucose-induced injury in H9 c2 cells.

Apoptosis ; Gene Expression Profiling ; Hepatic Stellate Cells ; pathology ; Humans ; Liver ; metabolism ; Liver Cirrhosis ; genetics ; metabolism ; pathology ; Liver Diseases ; genetics ; metabolism ; pathology ; MicroRNAs ; metabolism ; physiology ; Transforming Growth Factor beta1 ; metabolism

Objective To study the changes of umbilical blood lactate,pH, blood sugar(BS),bilirubin, electrolyte, osmotic pressure (OP) in the newboms with fetal distress.Methods Thirty-five newborns with fetal distress (distress group) and 40 healthy new-borns (control group) were studied. Distress group were divided into distress group Ⅰ and distress group Ⅱ respectively, based on without or with neonatal asphyxia. Concentration of umbilical blood lactate was determined with enzyme method, pH, BS,serum total bilirubin (BIL), serum electrolyte (Na+ ,K+ ,Ca2+ ) and OP were analyzed respectively. Results 1. The difference of incidence of newborn asphyxia between distress groups (29.03%) and control group (2.50%) was statistically significant. 2. Compared with the controls and distress group Ⅰ, the umbilical blood lactate concentration significantly increased in distress group Ⅱ (P 0.05).The incidence of hyperglycemia was significantly elevated in distress groups than that in the control group. 4. Lactate concentration in distress I and distress fl group showed negative correlation with pH. Conclusion The concentration of umbilical blood lactate can provide the proof for diagnosis and prognosis of fetal distress.

Objective To investigate the protective effect of sevoflurane on the brain against focal ischemia-reperfusion(I/R)injury and its mechanism.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into 3 groups(n=8 each):group Ⅰ sham operation;grouop Ⅱ I/R and group Ⅲ I/R + sevoflurane.The rats were anesthetized with intraperitoneal chloral hydrate 300 mg?kg~(-1).Middle cerebral artery occlusion(MCAO)was produced by insertion of a 4-0 mono-filament nylon thread with rounded tip at bifurcation of right common carotid artery into internal carotid artery.The nylon thread was advanced cranially until resistance was felt.The depth of insertion was 18-20 mm.After 3 h MCAO the thread was withdrawn to allow reperfusion.In group Ⅲ the animals inhaled 1.0 MAC sevoflurane for 30 min at 30 min before reperfusion.The rectal temperature of the animals was kept at 36.5-37.5℃.At the end of 24 h reperfusion the animals were weighed again.The animals'neurological deficit was evaluated using Zea Longa score(0=no defcit,4=unable to walk and unconscious).The animals were then killed.The neuronal apoptosis in striatum was assessed(TUNEL)and the PKC protein expression in striatum was determined by immunocyto-chemistry.Results The body weight of the animals in I/R group was significantly reduced after 24h reperfusion as compared to the body weight before ischemia (P＜0.01),while in control group and sevoflurane group there was no significant difference in the body weight before and after sham operation or I/R.The neurological deficit scores were significantly higher in I/R group than in sevoflurane group.The number of apoptotic neurons in striatum was significantly higher in I/R group than in sevoflurane group.The PKC expression in striatum was significantly higher in sevoflurane group than in I/R group (P＜0.01).Conclusion 1.0 MAC sevoflurane inhalation has protective effect on the brain against I/R injury. Upregulation of PKC expression in striatum decreased by I/R is involved in the mechanism.

Adult ; Breast ; pathology ; Breast Neoplasms ; diagnostic imaging ; pathology ; Female ; Humans ; Lymphoma, Non-Hodgkin ; diagnostic imaging ; pathology ; Ultrasonography

Objective To evaluate the role of signal transducer and activator of transcription 3 (STAT3) signaling pathway in the reduction of myocardial ischemia-reperfusion (I/R) injury by diazoxide postconditioning in rats.Methods Sixty adult male Sprague-Dawley rats,aged 3 months,weighing 240-260 g,were randomly divided into 5 groups (n =12 each):sham operation group (S group),I/R group,vehicle group (V group),diazoxide postconditioning group (D group),and STAT3 signaling pathway inhibitor Stattic group (St group).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.In V and D groups,0.4％ dimethyl sulfoxide and 7 mg/kg diazoxide (in 1 ml of 0.4％ dimethyl sulfoxide) were injected through the femoral vein at the onset of reperfnsion,respetively.In St group,Stattic was injected through the femoral vein 10 min before reperfusion,and the other procedures were the same as those in D group.The infarct size (IS) and myocardial apoptosis were detected by TTC staining and TUNEL,respectively.Apoptotic index (AI) was calculated.STAT3 mRNA expression in myocardial tissues was detected using RT-PCR.Western blot was used to detect the phosphorylation of STAT3.Results Compared with S group,the IS and AI were significantly increased and the expression of STAT3 mRNA and phosphorylation of STAT3 were decreased in I/R group (P ＜ 0.05).Compared with I/R group,the IS and AI were significantly decreased and the expression of STAT3 mRNA and phosphorylation of STAT3 were increased in D group (P ＜ 0.05).There was no significant difference in IS,AI,expression of STAT3 mRNA and phosphorylation of STAT3 between V group and St group (P ＞0.05).Compared with group D,the IS and AI were significantly increased and the expression of STAT3 mRNA and phosphorylation of STAT3 were decreased in St group (P ＜ 0.05).Conclusion STAT3 signaling pathway is involved in the reduction of myocardial I/R injury by diazoxide postconditioning in rats.

Objective To evaluate the relationship between extracelluar signal?regulated protein kinase 1∕2 (ERK1∕2) and signal transducer and activator of transcription 3 (STAT3) signaling pathways involving in cardioprotection induced by diazoxide postconditioning in rats. Methods Sixty adult male Sprague?Dawley rats, aged 3 months, weighing 240-260 g, were randomly divided into 5 groups ( n=12 each) using a random number table: sham operation group ( SH group ) , ischemia?reperfusion ( I∕R ) group, diazoxide postconditioning group ( D group ) , ERK1∕2 inhibitor U0126 group ( U group ) , and STAT3 inhibitor Stattic group ( St group) . Myocardial I∕R was produced by occlusion of anterior descending branch of the coronary artery followed by 120 min reperfusionIn I∕R and D groups, 0?4% dimethyl sulfoxide 1 ml and 7 mg∕kg diazoxide ( in 1 ml of 0?4% dimethyl sulfoxide) was injected through the femoral vein at the onset of reperfusionIn U and St groups, U0126 100 μg∕kg and Stattic 500 μg∕kg were injected through the femoral vein at 10 min before reperfusion, and the other procedures were similar to those previously described in group DAt 120 min of reperfusion, the rats were sacrificed, and myocardial specimens were obtained from the left ventricle for determination of myocardial infarct size, cell apoptosis, and ERK1, ERK2 and STAT3 mRNA expression ( real?time PCR), and phosphorylated ERK1∕2 ( p?ERK1∕2) and phosphorylated STAT3 (p?STAT3) (using Western blot). Apoptosis index (AI) was calculated. Results Compared with group S, the myocardial infarct size and AI were significantly increased, and the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was down?regulated in group I∕R. Compared with group I∕R, the myocardial infarct size and AI were significantly decreased, and the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was up?regulated in group D. Compared with group D, the myocardial infarct size and AI were significantly increased in U and S groups, the expression of ERK1, ERK2 and STAT3 mRNA, p?ERK1∕2 and p?STAT3 was down?regulated in group U, and the expression of STAT3 mRNA and p?STAT3 was down?regulated, and no significant change was found in ERK1 and ERK2 mRNA and p?ERK1∕2 expression in group S. Conclusion STAT3 signaling pathway is located downstream of ERK1∕2 signaling pathway in the mechanism by which diazoxide postconditioning reduces myocardial I∕R injury in rats.