Chronic HBV infection may not only cause liver damage , but also lead to renal injury . HBV-related kidney injuries mainly include ( 1 ) HBV-associated glomerulonephritis , ( 2 ) hepatorenal syndrome, and (3) kidney injuries caused by long-term nucleos(t)ide analogues therapy.This paper mainly reviews the pathogenesis and therapeutic principle of HBV-related kidney injuries , so as to provide the foundation for clinical management .

Objective To evaluate the primary result of proximal femoral nail anti-rotation(PF-NA)in treating osteoporotic intertrochanterie fractures. Methods Between March 2006 and August 2007.PFNA or Gamma nail intemal fixation were performed in 31 patients with osteoporotic intertrochan-tefie fractures.of whom were 19 males and 12 females at a mean age of 75.6 years(45-89 years).Ac-cording to AO classification,there were 8 type A1 fractures,16 type A2 fractures and 7 type A3 fractures.Aeearding to Evans-Jensen classification.18 cases were rated as Evans Ⅱ and 13 as Evans II.AIl frac-tares were closed ones and 6 patients were combined with internal diseases.PFNA was implanted throush a mini-incision without exposure of the fracture section during operation in 12 patients. Results Of all.6 patients received emergency operation,19 did operation within 3 days and 6 waited for selective op-eration(5-7 days)after controlling internal diseases.PFNA had shorter operation time,less hlool loss and shorter union time compared with Gamma nail(P＜0.05).No complications such as infection,non-union or loosening of nails were found.According to HarriS hip rate scale system,the excellence rate of PFNA was 83.4%and that of Gamma nail 73.7%. Conclusion PFNA is a good choice to treat osteo-perotie intertrochanteric fractures.owing to its advantages of stable fixation,minor trauma,eaSy opera-tion.short operation time,little bleeding,minor lOSS of selerotin and early exercise.

Objective To investigate the differences of expression and activation of natural killer (NK) cell G2D (NKG2D) in patients with different immune status of chronic hepatitis B virus (HBV) infection, and to explore the significance of NKG2D-mediated immune injury in HBV infection.Methods Fifteen chronic HBV carriers (immune tolerance),15 chronic hepatitis B (CHB, immune activation) patients, 15 HBV-related acute/subacute-on-chronic liver failure (HBV-ACLF, immune over-activation) patients were enro1led in this study from January 2010 to December 2011 in the Third Hospital of Hebei Medical University.The frequencies of NK cells and NKG2D+ NK cells in peripheral blood mononuclear cells (PBMC) were detected by flow cytometry.The NKG2D mRNA expressions were measured by real-time fluorescent quantitative polymerase chain reaction.Localization and hemi-quantitative analysis of NKG2D+ cells in liver tissue were performed by immunohistochemistry staining.Concentrations of serum interferon(IFN)-γ, tumor necrosis factor(TNF)-α, perforin and granzyme B were quantified by enzyme 1inked immunosorbent assay (ELISA).Normally distributed continuous variables were analyzed using one-way analysis of variance (ANOVA), followed by Student-Newman-Keuls q test for evaluating variances between each two groups.For non-normally distributed data or heterogeneity of variance, differences between groups were analyzed using nonparametric Kruskal-Wallis H test, followed by Nemenyi test for pairwise comparisons.Pearson chi-square test was used to analyze categorical variables.Results The percentages of NK cells in PBMC were (13.58±3.24)% in healthy controls, (5.42±2.18)% in chronic HBV carriers, (7.92±2.85)% in HBV-ACLF group and (8.43±2.92)% in CHB group.The percentage of NK cells in PBMCs was lower in each chronic HBV-infected group compared with healthy controls (F=22.04, P<0.05).The frequency of NKG2D+ NK cells in HBV-ACLF group (18.92±5.85)% was the highest, followed by CHB group (12.85±3.39)%, healthy controls (8.45±2.86)%, and chronic HBV carriers (3.36±1.05%), with the statistically significant differences between each two groups (H=46.09, P<0.01).Intrahepatic NKG2D mRNA expression and NKG2D+ cells density were highest in HBV-ACLF group (6.58±1.86 and 30.69±6.67, respectively), followed by CHB group (3.25±0.95 and 17.36±4.13, respectively) and chronic HBV carriers (0.69±0.20 and 3.16±1.24, respectively), with the statistically significant differences between each two groups (H=52.10 and 52.73 respectively, both P<0.01).The similar patterns were observed in serum IFN-γ, TNF-α, perforin and granzyme B concentrations.Conclusions NKG2D expresses variously in patients with different immune status of chronic HBV infection.Activation of NKG2D may take part in the immune pathogenesis of chronic HBV infection.

The prognosis of hepatitis B virus (HBV) infection is determined by innate immunity,adaptive immunity,and a variety of regulatory factors in the host.Controversy still exists over the role of innate immunity in the progression of HBV infection.Adaptive immunity,especially the immune response mediated by CD8+ T cells,plays an important role in HBV clearance.However,in patients with chronic infection,such CD8+ T cells are often exhausted and associated with various regulatory factors including programmed cell death 1 and T-cell immunoglobulin mucin-3.This article elaborates on the association of chronicity of HBV infection with host immune system and various regulating factors.

To summarize the case of combined heart-lung transplantation for a patient who survived for 8.5 years. On September 20, 2003, at Second Xiangya Hospital of Central South University, homologous heartlung transplantation was performed on a male patient who was diagnosed with cardiopulmonary failure secondary to congenital ventricular septal defect with severe pulmonary hypertension. Heart-lung allograft was preserved with 1500 mL modified St.Thomas solution and 3000 mL modified LPD solution. Postoperative immunosuppressive therapies included: methylprednisolone and human anti-lymphocyte globulin protein in the induction period; and combination of ciclosporin A, CellCept and prednisolone in the stable period. In 2007, the treatment was changed to CellCept mg, twice a day+FK506 4 mg, twice a day. The patient lived 8.5 years of normal life with cardiac function of NYHA I-II. Echocardiogram showed left ventricular ejection fraction of 61% to 74%. Heart-lung transplantation proved reliable therapy modality for terminal cardiopulmonary failure. Excellent donor organ preservation and proper perioperative treatment are key factors for long-term survival after heart-lung transplantation.
Eisenmenger Complex ; surgery ; Follow-Up Studies ; Graft Rejection ; Heart Septal Defects, Ventricular ; complications ; surgery ; Heart-Lung Transplantation ; methods ; Humans ; Hypertension, Pulmonary ; etiology ; surgery ; Immunosuppressive Agents ; therapeutic use ; Male ; Young Adult

Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by infection. When an infection occurs, as the first line of defense of the body's immune system, neutrophils are first recruited to the site of infection to capture and kill pathogens by releasing neutrophil elastase (NE). However, a large amount of NE release will injury the surrounding normal tissues and induce organ dysfunction or failure. NE inhibitors can inhibit NE activity and reduce inflammatory response, which may be a promising drug for the treatment of sepsis. Currently, a variety of NE inhibitors have been developed and reported, but there is no systematic overview of their characteristics, and the role and underlying mechanisms of NE and related inhibitors in sepsis have not been thoroughly discussed. This article will make a review in this regard, in order to elucidate the effect of NE and its inhibitors in sepsis.

Humans ; Benzodiazepines ; Hypnotics and Sedatives/therapeutic use* ; Intensive Care Units ; Midazolam

Determining whether patients have volume-responsiveness is one of the frequently asked questions in the intensive care unit, especially in shock patients. Evaluating the volume status and volume responsiveness can help clinical medical staff accurately grasp the patient's cardiac preload, guide reasonable volume management, and help improve patient prognosis. Therefore, many non-invasive and invasive methods have been proposed to evaluate volume responsiveness. Inferior vena cava ultrasound has been widely used to guide the fluid management of critically ill patients due to its simplicity, non-invasiveness, and good repeatability. This article reviews the clinical applications of inferior vena cava ultrasound in fluid management of critically ill patients, so as to provide a reference for circulatory management of critically ill patients.

To investigate the mutation site of pathogenic gene in patients with hypertrophic cardiomyopathy (HCM) and to analyze the relationship between the genotype and clinical phenotype. Methods: Targeted exon capture sequencing was conducted in a HCM proband for 30 coding exons related HCM gene by all exon amplification and high-throughput sequencing. Furthermore, Sanger sequencing was performed in other family member and in 200 healthy volunteers for verification. The familial investigation included in clinical presentation, physical examination, electrocardiogram and echocardiography. Results: There were 3/6 blood relatives carrying cardiac myosin-binding protein gene MyBPC3 G772A heterozygous mutation, the mutation site was at 258 amino acid of MyBPC3 as glutamic acid (Glu) was substitute to lysine (Lys), such mutation was not found in rest of family member and not in healthy volunteers. The onset of proband and her daughter was rather late, they had palpitation and chest tightness; echocardiography showed interventricular septum basal segment thickening (16-18) mm. Proband was complicating paroxysmal ventricular tachycardia, malignant arrhythmia and heart failure, the maximum pressure gradient of left ventricular outflow was 56 mmHg, which with the high risk for sudden death. Conclusion: Comprehensive gene test has been helpful for clinical stratification, early diagnosis and treatment. MYBPC3 site mutation c.G772A might be the pathogenic mutation in that specific HCM family.