Objective To evaluate the effect of clinical pathway in pulmonary thrombus embolism (PTE) .Methods 60 cases of PTE were admitted department of respiratory from 2011 to 2012 and divided into the experimental group and the control group ,30 cases for each group .The control group was implemented with normal process of hospital management while experimental group de-veloped clinical pathways .The efficacy ,department of respiratory drug costs ,complications and patient satisfaction were recorded and computed .Results The average department of respiratory and drug costs in experimental group respectively was (17 .13 ± 2 .22)days ,(16 545 .04 ± 1 557 .44) RMB and (7 050 .83 ± 372 .74) RMB ;less than (19 .77 ± 3 .41)day ,(17 709 .45 ± 1 902 .05) RMB and (7 345 .75 ± 450 .82) RMB in control group ,there were significant difference between the two groups (P<0 .05) .The satisfaction scores of experimental group and the control group respectively were (93 .47 ± 3 .88)sores and (90 .90 ± 5 .30)scores , there was significant difference between the two groups (P<0 .05) .The therapeutic effect and complication rates between experi-mental group and control group were no significant difference (P>0 .05) .Conclusion The effect of clinical pathway in PTE have a positive role in reducing hospitalization time ,total costs ,drug costs and increasing satisfaction ,it is worth to develop in primary hos-pital .

Objective To research the clinical value of cerebrospinal fluid and peripheral blood tuberculosis infection T cell spot test(TSPOT .TB) in the diagnosis of tuberculous meningitis(TBM) .Methods 35 cases of TBM and 40 cases of non-TB intracranial infection in this hospital from September 2015 to September 2016 were selected as the observation group and control group respectively .T-SPOT .TB was adopted to detect mycobacterium tuberculosis effector T cells in cerebrospinal fluid and detect peripheral blood mononuclear cells .Results The T-SPOT .TB detection positive rates of cerebrospinal fluid and peripheral blood in the observation group were 97 .14% and 80 .00% respectively ,which were significantly higher than 2 .50% and 0 .00% in the control group ,the difference was statistically significant(P＜ 0 .05);the sensitivity and negative predictive value in cerebrospinal fluid T-SPOT .TB detection were 97 .14% and 97 .50% ,which were significantly higher than 80 .00% and 85 .11% in peripheral blood T-SPOT .TB detection ,the difference was statistically significant (P＜0 .05);the specificity and positive predictive value in the cerebrospinal fluid T-SPOT .TB detection was 97 .50% and 97 .14% respectively ,while which in peripheral blood T-SPOT .TB detection were 100 .00% and 100 .00% respectively ,but the difference between the two groups was not statistically significant ( P＞0 .05) .Conclusion The detection of cerebrospinal fluid and peripheral blood T-SPOT .TB detection can provide early diagnostic basis for TBM ,moreover cerebrospinal fluid T-SPOT .TB detection has higher sensitivity and possesses an important clinical application value .

Herpes simplex viruses type 1(HSV1)is among the most ubiquitous human pathogens that cause a wide variety of disease states.The latent infection of the central nervous system and sporadically reactivation is the central part of HSV1 pathogenesis,which also brings challenges to antiviral therapies.At present,the mechanism of establishing,maintaining and reactivation of HSV1 has not been fully clarified,whereas it has been generally accepted that the epigenetic regulation may play an important role.Accumulating researches have also indicated that the lytic and latent viral genomes exhibit the different chromatin structures,and the accumulation of diverse post-translational modifies the histones endow viral genes with transcriptional activation or repression features.In addition,the latency-associate transcripts of virus may also participate in the genome epigenetic modification.In this review,we summarize the research progress of epigenetic regulation of HSV1 and highlight the critical role of chromatin remodeling in HSV1 lytic proliferation and establishment of latent infection.

Objective : To discuss the changes of serum lipoprotein phospholipase A2 (Lp - PLA2) and c-reactive protein (CRP) levels in atorvastat in treatment for the patients with periodontitis and hyperlipidemia. Methods : 148 patients with periodontitis and hyperlipidemia were involved, and divided into basic group (foundation treatment, 82 cases) and statin group (foundation treatment plus 20 mg atorvastatin treatment, 66 cases). 40 healthy cases from the medical center health personnel were selected as the healthy group. Attachment levels (AL), bleeding index (BI), serum total cholesterol (TC), triacylglycerol (TG), Lp - PLA2, and CRP levels were checked and compared before and after 6 months of treatment. Lp - PLA2 and CRP were checked by enzyme linked immunosorbent assay (ELISA), and their relationship were analyzed by the method of Pearson. Results: When the disease group were compared with the healthy group, the statistics were as follows: AL（3.92 ± 0.51 mm vs 0.42 ± 0.06 mm）, BI（2.81 ± 0.48 vs 0.34 ± 0.05）, TC（5.27 ± 0.83 mmol/L vs 4.02 ± 0.62 mmol/L）, TG（2.67 ± 0.41 mmol/L vs 0.93 ± 0.17 mmol/L）, Lp-PLA2（243.57 ± 58.71 μg/L vs 132.24 ± 34.27 μg/L）, CRP（9.72 ± 3.27 μg/L vs 3.21 ± 0.87 μg/L）, and the statistics of disease group were significantly higher than the healthy group with a significant difference (P< 0.05). When Statin group was compared with basis group, the statistics were as follows: AL（3.70 ± 0.10 mmvs 3.78 ± 0.11 mm）, BI（1.05 ± 0.28 vs 1.43 ± 0.32）, TC（3.82 ± 0.67 mmol/L vs 4.51 ± 0.71 mmol/L）, TG（1.30 ± 0.29 mmol/L vs 1.83 ± 0.34 mmol/L）, Lp-PLA2（157.43 ± 40.18 μg/L vs 199.43 ± 47.24 μg/L）, CRP（4.21 ± 3.02 μg/L vs 6.37 ± 3.28 μg/L）, and the statistics of statin group were lower than that in basis group with a significant difference (P< 0.05). Pearson analysis showed Lp-PLA2 and CRP levels were positively correlated (r = 0.672, P< 0.05). Conclusion It shows the changes of Lp- PLA2 and CRP level were related with the clinical conditions of periodontitis combined with hyperlipidemia, and atorvastatin therapy can effectively reduce the body's blood lipid levels, and improve the treatment effects of periodontitis combined with hyperlipidemia.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Objective To observe the efficacy of microwire penetration combined with ozone intervention for fallopian tube obstructive infertility.Methods Data of 149 patients with fallopian tube obstructive infertility were retrospectively analyzed.Patients in group A(n=44)underwent conventional fallopian tube recanalization(FTR),in group B(n=51)underwent microwire penetration FTR,while those in group C(n=54)received microwire penetration FTR combined with ozone.The recalculation rate 1 month after treatment and natural pregnancy rate within 1 year after treatment were compared among groups.Results The recalculation rate 1 month after treatment of group A,B,C was 63.38%(45/71),80.22%(73/91)and 92.78%(90/97),respectively,increased in order among groups(all P＜0.05).The natural pregnancy rate within 1 year after treatment of group A,B,C was 20.45%(9/44),27.45%(14/51)and 48.15%(26/54),respectively,of group C was higher than of group A and B(both P＜0.05),not significantly different between group A and group B(P=0.427).Conclusion Microwire penetration combined with ozone intervention had better efficacy than conventional FTR and microwire penetration FTR alone for treating fallopian tube obstructive infertility.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.