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Dong-Zhu Li Qing-Xiang Zhang Xiao-Xian Dong Huai-Dong Li Xin Ma 《Journal of bone and mineral metabolism》2014,32(5):494-504
The bone protective effects of the hydrogen molecule (H2) have been demonstrated in several osteoporosis models while the underlying molecular mechanism has remained unclear. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. In this work, we evaluated the effects of incubation with H2 on receptor activator of NFκB ligand (RANKL)-induced osteoclast differentiation. We found that treatment with H2 prevented RANKL-induced osteoclast differentiation in RAW264.7 cells and BMMs. Treatment with H2 inhibits the ability to form resorption pits of BMMs stimulated by RANKL. Treatment with H2 reduced mRNA levels of osteoclast-specific markers including tartrate resistant acid phosphatase, calcitonin receptor, cathepsin K, metalloproteinase-9, carbonic anhydrase typeII, and vacuolar-type H+-ATPase. Treatment with H2 decreased intracellular reactive oxygen species (ROS) formation, suppressed NADPH oxidase activity, down-regulated Rac1 activity and Nox1 expression, reduced mitochondrial ROS formation, and enhanced nuclear factor E2-related factor 2 nuclear translocation and heme oxygenase-1 activity. In addition, treatment with H2 suppressed RANKL-induced expression of nuclear factor of activated T cells c1 and c-Fos. Furthermore, treatment with H2 suppressed NF-κB activation and reduced phosphorylation of p38, extracellular signal-regulated kinase, c-Jun-N-terminal kinase, and protein kinases B (AKT) stimulated with RANKL. In conclusion, hydrogen molecules prevented RANKL-induced osteoclast differentiation associated with inhibition of reactive oxygen species formation and inactivation of NF-κB, mitogen-activated protein kinase and AKT pathways. 相似文献
3.
Astrid Drenckhan Tobias Grob Anna Dupree Thorsten Dohrmann Oliver Mann Jakob R. Izbicki Stephanie J. Gros 《Langenbeck's archives of surgery / Deutsche Gesellschaft fur Chirurgie》2014,399(7):879-888
Purpose
It has previously been shown that gefitinib-treated patients with epidermal growth factor receptor (EGFR) gene amplification or high polysomy had a statistically significant improvement in response, time to progression, and survival in non-small cell lung cancer (NSCLC). Only few studies utilizing anti-EGFR treatment in advanced esophageal adenocarcinomas have been performed and the results have been heterogeneous. The aim of this study was to evaluate EGFR-targeted therapy with gefitinib in esophageal adenocarcinoma with a high EGFR polysomy.Methods
Novel esophageal cell lines PT6216 and LN6216c were established from primary tumor and lymph node metastasis of a patient with highly aggressive and metastatic adenocarcinoma. Pathological examination including tumor differentiation and prognostic marker analysis, immunohistochemical EGFR expression analysis, EGFR fluorescence in situ hybridization, and mutation analysis were performed. Response of novel cell lines to gefitinib treatment was evaluated by cell proliferation and vitality assays. Fifty-four esophageal adenocarcinoma specimens were evaluated for EGFR gene copy gain.Results
The primary tumor cell line PT6216 and the lymph node cell line LN6216c show a homogenously high polysomy for EGFR determined by FISH analysis. Cell proliferation and vitality are highly sensitive to the tyrosine kinase inhibitor gefitinib compared to esophageal control cells without a high polysomy for EGFR. High polysomy for EGFR was found in 35 % of patients.Conclusion
We show for the first time a significant treatment response to the EGFR tyrosine kinase inhibitor gefitinib in esophageal tumor cells with a high polysomy for EGFR, suggesting a future role of anti-EGFR therapy for esophageal adenocarcinoma patients with a high EGFR polysomy. 相似文献4.
Nisreen Elsayegh MS Henry M. Kuerer MD Heather Lin MD PhD Angelica M. Gutierrez Barrera MS Michelle Jackson MS Kimberly I. Muse MS Jennifer K. Litton MD Constance Albarracin MD PhD Aimaz Afrough MD Gabriel N. Hortobagyi MD Banu K. Arun MD 《Annals of surgical oncology》2014,21(11):3466-3472
Background
Patients with ductal carcinoma in situ (DCIS) are at increased risk for developing contralateral breast cancer (CBC). Consequently, more women with DCIS are electing to undergo contralateral prophylactic mastectomy (CPM). We evaluated factors associated with CPM in patients with DCIS who underwent genetic counseling for BRCA testing.Methods
This retrospective study involved 165 women with DCIS referred for genetic counseling between 2003 and 2011. Patient characteristics were age, marital and educational status, tumor markers, nuclear grade, family history of breast cancer (BC) and ovarian cancer (OC), race, Ashkenazi Jewish ancestry, and BRCA results. Univariate and multivariate logistic regression analyses were used to determine predictive factors associated with CPM election.Results
Of 165 patients, 44 (27 %) underwent CPM. Patients <45 years of age were more likely to elect CPM (p = 0.0098). A BRCA+ mutation was found in 17 patients (10.3 %), and BRCA+ women were more likely to elect CPM than BRCA or untested women (p = 0.0001). Patients who had a family history of OC (57.7 %) were more likely to choose CPM than those with no family history (p = 0.0004). Younger age, BRCA+, and an OC family history remained significant in the multivariate model (p < 0.008).Conclusion
The CPM rate among patients with DCIS who undergo genetic counseling is high. Factors associated with increased likelihood of CPM among this group were age, BRCA+, and a family history of OC. Further studies are needed to evaluate patients’ perceptions of CBC risk and their role in the likelihood of CPM choice. 相似文献5.
Mechanisms of graft versus host disease have been studied in Lew x BN animals transplanted with a Lew small bowel. Grafted mesenteric lymph nodes but not host mesenteric lymph nodes or host spleen, in small bowel transplanted rats undergoing lethal GVHD, provide a source of CTL with specific anti-recipient cytotoxic activity. Host MLN and host spleen display anti-recipient CTL activity only when GVHD is provoked by intraperitoneal lymphocyte injection. These data demonstrate that lethal GVHD after SBTx may occur in the absence of detectable cytotoxic activity in host lymphoid tissues, suggesting that other mechanisms are involved in the pathogenesis of GVHD after SBTx. GVHD after SBTx or lymphocyte transfer is associated with the appearance of TNF in the serum. The intensity and reversibility of this phenomenon correlate with both the clinical severity and the lethality of GVHD. Taken together these data highly suggest that TNF is directly involved in the pathogenesis of GVHD after SBTx. 相似文献
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Noboru Saeki Saya Mochizuki Teruhisa Fujii Masashi Kawamoto 《Journal of anesthesia》2014,28(4):621-624
Perioperative hemostatic management in patients with hemophilia A who develop the coagulation factor VIII (FVIII) inhibitor is challenging, because exogenous FVIII is neutralized, which boosts the inhibitor to provoke postoperative coagulopathy. Recombinant activated factor VII (rFVIIa) has become available for this type of patient, although FVIII is sometimes required. We treated a 56-year-old male patient with hemophilia A with FVIII inhibitor scheduled for total hip arthroplasty (THA) and total knee arthroplasty (TKA). We used rFVIIa for THA; however, the amount of bleeding was 2,500 ml and blood transfusion was required, which boosted FVIII inhibitor after surgery. The TKA was then scheduled for 19 months later, after the level of the inhibitor had reduced to the preoperative level. Unfortunately, rFVIIa failed to improve PT/APTT, and thus we used recombinant factor VIII (rFVIII). The amount of bleeding during TKA was 1,340 ml, while the level of the inhibitor increased to a greater level than that after THA, provoking uncontrollable bleeding. For anesthetic management in hemophilia A patients with FVIII inhibitor, anesthesiologists must pay attention to postoperative coagulopathy, and every effort should be used to minimize exposure to FVIII. Furthermore, when rFVIIa is ineffective, postponement of surgery until rFVIIa regains its efficacy may be beneficial as compared to an operation with FVIII. 相似文献
7.
Shahrbanoo F. Noori MD Alexandra Gangi MD Maria E. Nelson MD Michael Choi MD Parisa Mirzadehgan MPH Alison K. Bonk ACNP-BC James Mirocha MS Farin Amersi MD Armando E. Giuliano MD 《Annals of surgical oncology》2014,21(10):3324-3329
Objective
This study evaluates whether nodal status differs between breast cancer patients with BRCA mutations and those confirmed not to harbor mutations.Methods
A prospective database identified patients with breast cancer who underwent genetic testing and axillary staging. Comparative variables included age, as well as tumor characteristics such as size, grade, lymphovascular invasion (LVI), estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2 (HER2-neu), and nodal status.Results
Overall, 235 patients with breast cancer underwent genetic testing for BRCA mutations from June 2000 to May 2012. Of these patients, 74 (31.4 %) were found to express BRCA 1 and/or 2 mutations, and 161 (68.5 %) patients were verified to have no detectable BRCA mutation. Among the entire 235 patients tested, 92 (39.1 %) were found to have nodal disease. In univariable analysis, only LVI and tumor size correlated with presence of nodal metastasis. Of the 74 BRCA mutation carriers, 34 (45.9 %) had nodal metastasis compared with 58 of the 161 (36 %; p = 0.15) patients without a BRCA mutation. BRCA mutation carriers with nodal disease were more likely to have poorly differentiated tumors than those without mutations who had nodal disease (24/33 [72.7 %] vs. 27/57 [47.4 %]; p = 0.027).Conclusion
BRCA mutations are not themselves predictive of nodal metastasis. Patients with BRCA mutations did not have a statistically significant higher prevalence of nodal metastasis than those without mutations. 相似文献8.
Erum A. Hartung Matthew Matheson Marc B. Lande Katherine M. Dell Lisa M. Guay-Woodford Arlene C. Gerson Bradley A. Warady Stephen R. Hooper Susan L. Furth 《Pediatric nephrology (Berlin, Germany)》2014,29(10):1957-1965
Background
Autosomal recessive polycystic kidney disease (ARPKD) is an inherited disorder characterized by enlarged, cystic kidneys with progressive chronic kidney disease (CKD), systemic hypertension, and congenital hepatic fibrosis. Children with ARPKD can have early onset CKD and severe hypertension, both of which are known to have adverse neurocognitive effects. The objectives of this study were (1) to determine whether ARPKD patients have greater neurocognitive deficits compared to that of children with other causes of CKD, and (2) to examine the relative prevalence of hypertension in ARPKD, a known risk factor for neurocognitive dysfunction.Methods
We performed a cross-sectional, control-matched analysis of 22 ARPKD patients with mild-to-moderate CKD in the Chronic Kidney Disease in Children (CKiD) cohort study, compared with a control group of 44 children with other causes of CKD, matched based on glomerular filtration rate, age at study entry, and age at diagnosis.Results
Children with ARPKD in this cohort had neurocognitive functioning comparable to children with other causes of CKD in domains of intellectual functioning, academic achievement, attention regulation, executive functioning, and behavior. Blood pressure parameters were similar between the two groups; however, ARPKD patients required a significantly greater number of antihypertensive medications to achieve similar BP levels.Conclusions
ARPKD patients are potentially at risk for neurocognitive dysfunction due to early onset CKD and more severe hypertension. However, this study of children with mild-to-moderate CKD in the CKiD cohort did not demonstrate increased risk in children with ARPKD compared to children with other causes of CKD. Further studies are needed to determine if these findings are applicable to children with more severe manifestations of ARPKD. 相似文献9.
Marina Klawitter Michiyuki Hakozaki Hiroshi Kobayashi Olga Krupkova Lilian Quero Caroline Ospelt Steffen Gay Oliver Hausmann Thomas Liebscher Ullrich Meier Miho Sekiguchi Shin-ichi Konno Norbert Boos Stephen J. Ferguson Karin Wuertz 《European spine journal》2014,23(9):1878-1891
Purpose
Although inflammatory processes play an essential role in painful intervertebral disc (IVD) degeneration, the underlying regulatory mechanisms are not well understood. This study was designed to investigate the expression, regulation and importance of specific toll-like receptors (TLRs)—which have been shown to play an essential role e.g. in osteoarthritis—during degenerative disc disease.Methods
The expression of TLRs in human IVDs was measured in isolated cells as well as in normal or degenerated IVD tissue. The role of IL-1β or TNF-α in regulating TLRs (expression/activation) as well as in regulating activity of down-stream pathways (NF-κB) and expression of inflammation-related genes (IL-6, IL-8, HSP60, HSP70, HMGB1) was analyzed.Results
Expression of TLR1/2/3/4/5/6/9/10 was detected in isolated human IVD cells, with TLR1/2/4/6 being dependent on the degree of IVD degeneration. Stimulation with IL-1β or TNF-α moderately increased TLR1/TLR4 mRNA expression (TNF-α only), and strongly increased TLR2 mRNA expression (IL-1β/TNF-α), with the latter being confirmed on the protein level. Stimulation with IL-1β, TNF-α or Pam3CSK4 (a TLR2-ligand) stimulated IL-6 and IL-8, which was inhibited by a TLR2 neutralizing antibody for Pam3CSK4; IL-1β and TNF-α caused NF-κB activation. HSP60, HSP70 and HMGB1 did not increase IL-6 or IL-8 and were not regulated by IL-1β/TNF-α.Conclusion
We provide evidence that several TLRs are expressed in human IVD cells, with TLR2 possibly playing the most crucial role. As TLRs mediate catabolic and inflammatory processes, increased levels of TLRs may lead to aggravated disc degeneration, chronic inflammation and pain development. Especially with the identification of more endogenous TLR ligands, targeting these receptors may hold therapeutic promise. 相似文献10.
Yumi Noda 《Clinical and experimental nephrology》2014,18(4):558-570
The human body is two-thirds water. The ability of ensuring the proper amount of water inside the body is essential for the survival of mammals. The key event for maintenance of body water balance is water reabsorption in the kidney collecting ducts, which is regulated by aquaporin-2 (AQP2). AQP2 is a channel that is exclusively selective for water molecules and never allows permeation of ions or other small molecules. Under normal conditions, AQP2 is restricted within the cytoplasm of the collecting duct cells. However, when the body is dehydrated and needs to retain water, AQP2 relocates to the apical membrane, allowing water reabsorption from the urinary tubule into the cell. Its impairments result in various water balance disorders including diabetes insipidus, which is a disease characterized by a massive loss of water through the kidney, leading to severe dehydration in the body. Dysregulation of AQP2 is also a common cause of water retention and hyponatremia that exacerbate the prognosis of congestive heart failure and hepatic cirrhosis. Many studies have uncovered the regulation mechanisms of AQP2 at the single-molecule level, the whole-body level, and the clinical level. In clinical practice, urinary AQP2 is a useful marker for body water balance (hydration status). Moreover, AQP2 is now attracting considerable attention as a potential therapeutic target for water balance disorders which commonly occur in many diseases. 相似文献
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Masaki Wake Nobuyuki Takahashi Hiroyuki Yoshitomi Kazuaki Tanabe 《Journal of Echocardiography》2014,12(3):112-114
Heyde’s syndrome is the combined occurrence of acquired von Willebrand disease caused by aortic valve stenosis and gastrointestinal bleeding that occurs particularly in elderly patients. The bleeding may be linked to the intravascular shear-induced proteolysis of high-molecular-weight multimers (HMWMs) of von Willebrand factor (vWF). Hypertrophic obstructive cardiomyopathy (HOCM) in the left ventricular outflow tract generates a high shear stress condition that can induce such proteolysis. We report the case of a 70-year-old woman with HOCM who had severe anemia and loss of HMWMs. After reduction of the outflow gradient by medical treatment, vWF normalized, and her anemia alleviated. 相似文献
12.
Ferhan Candan Gürsel Yildiz Mansur Kayataş 《International urology and nephrology》2014,46(9):1815-1823
Purpose
Vascular access is vital for hemodialysis patients. A major factor that facilitates arteriovenous (AV) fistula failure is stenosis and thrombosis due to intimal hyperplasia developing in the venous segment of AV fistula. It has been reported that VEGF accelerated re-endothelialization, reduction in intimal thickening, and/or mural thrombus formed in the injured vascular structures. In this study, we aimed to identify the effect of the VEGF 936 gene polymorphism and vascular endothelial growth factor-A (VEGF-A) levels in the late period of AV fistula loss in hemodialysis patients.Methods
The study was carried out with a patient group of 42 individuals who experienced two or more fistula thrombosis in the late period after the AV fistula operation and also a control group of 38 patients who have not had any AV fistula thrombosis history for 3 years or more. All participants were assessed for VEGF-936C/T gene polymorphism and VEGF-A levels.Results
VEGF-936C/T genotypes were determined in the large proportion in the control group (31.6 %), while VEGF-936C/C genotypes were determined in a large proportion in the patient group (90.5 %). Individuals carrying the VEGF-936C/C genotype had an increased risk of 5.54 for getting AV fistula thrombosis. The VEGF-A levels of patient group (27.3 ± 43.5 pg/ml) were significantly lower than those of the control group (70.7 ± 53.1 pg/ml).Conclusion
There is an increased risk of AV fistula thrombosis in individuals carrying the VEGF-936C/C genotype. The other renal replacement modalities should be considered in patients with this genotype. As a result, it will be possible to prevent the morbidity and mortality due to fistula failure. 相似文献13.
Xiujuan Zang Feng Zheng Hai-juan Hong Yan Jiang Ying Song Yanping Xia 《International urology and nephrology》2014,46(8):1673-1679
Purpose
The aim of this study was to elucidate the role of neutrophil gelatinase-associated lipocalin (NGAL) in regulating apoptosis of tubular epithelial cells in a hypoxia–reperfusion model.Methods
A hypoxia–reperfusion model was established with NRK-52E cells to assess apoptosis and cell cycle progression after the addition of NGAL. We investigated the expression of four apoptosis factors, Bcl-2, Bax, Fas and FasL, as well as the expression level of two NGAL receptors, 24p3R and megalin, by both Western blot and real-time PCR.Results
NGAL induced cell proliferation and reduced apoptosis by regulating four apoptosis factors Bcl-2, Bax, Fas and FasL. Western blot demonstrated that the two NGAL receptors, 24p3R and megalin, were increased after hypoxia–reperfusion, which was reduced by exogenous NGAL. Moreover, overexpression of the two receptors induced the expression of the anti-apoptotic factor Bcl-2 and reduced the expression of pro-apoptotic Bax, Fas and FasL.Conclusions
These findings indicate that NGAL reduces apoptosis by regulating the four apoptosis factors Bcl-2, Bax, Fas and FasL through its two receptors 24p3R and megalin. These results also suggest that ectopic expression of NGAL in renal cells might provide a therapeutic strategy in ischemia–reperfusion by reducing apoptosis and promoting renal cell proliferation. 相似文献14.
Yongqiang Li Shuangshuang Zhu Bin Li Xiaofei Shao Xinyu Liu Aiqun Liu Bifang Wu Ying Zhang Honglei Wang Xiaohong Wang Kangping Deng Qin Liu Min Huang Hongmei Liu Harry Holthöfer Hequn Zou 《International urology and nephrology》2014,46(9):1785-1791
Purpose
The relationship between chronic kidney disease (CKD) and non-alcoholic fatty liver disease (NAFLD) in population with diabetes remains controversial. Our current study aimed to explore the association between NAFLD and CKD in population with prediabetes or diabetes.Methods
A cross-sectional study was conducted in Zhuhai city from June to October 2012. A total of 190 out of 334 participants with prediabetes or diabetes were enrolled in this study. CKD was defined as estimated GFR <60 ml/min per 1.73 m2 and/or albumin-to-creatinine ratio ≥30 mg/g. NAFLD was diagnosed on the basis of ultrasonographic and excluded fatty liver disease caused by other reasons such as drinking. The association between NAFLD and CKD was then analyzed using SPSS (version 19.0).Results
Subjects with NAFLD were more likely with a higher urinary albumin-to-creatinine ratio (P < 0.001). CKD were common among patients with NAFLD than those without NAFLD (P < 0.05). NAFLD was significantly associated with CKD (P < 0.05) in the unadjusted analyses as well as after adjustment for potential confounders. The unadjusted odd ratio and adjusted odd ratio for CKD were 2.25 (95 % CI 1.07–4.77, P = 0.034) and 2.68 (95 % CI 1.12–6.01, P = 0.016). When further adjusted for hypertension, serum high-density lipoprotein and serum fasting glucose, the association of NAFLD with CKD was still significant (OR 2.78, 95 % CI 1.03–7.52, P = 0.044).Conclusions
Our current study suggests that ultrasound-diagnosed NAFLD is associated with CKD among population with prediabetes or diabetes. 相似文献15.
James R. Mark Douglas C. Kelly Edouard J. Trabulsi Patrick J. Shenot Costas D. Lallas 《Journal of robotic surgery》2014,8(3):269-275
This study reports on the effect of fatigue on Urology residents using the daVinci surgical skills simulator (dVSS). Seven Urology residents performed a series of selected exercises on the dVSS while pre-call and post-call. Prior to dVSS performance a survey of subjective fatigue was taken and residents were tested with the Epworth Sleepiness Scale (ESS). Using the metrics available in the dVSS software, the performance of each resident was evaluated. The Urology residents slept an average of 4.07 h (range 2.5–6 h) while on call compared to an average of 5.43 h while not on call (range 3–7 h, p = 0.08). Post-call residents were significantly more likely to be identified as fatigued by the Epworth Sleepiness Score than pre-call residents (p = 0.01). Significant differences were observed in fatigued residents performing the exercises, Tubes and Match Board 2 (p = 0.05, 0.02). Additionally, there were significant differences in the total number of critical errors during the training session (9.29 vs. 3.14, p = 0.04). Fatigue in post-call Urology residents leads to poorer performance on the dVSS simulator. The dVSS may become a useful instrument in the education of fatigued residents and a tool to identify fatigue in trainees. 相似文献
16.
Michael J. Tessler Robert Hudson MaryAnne Naugler-Colville Diane R. Biehl 《Journal canadien d'anesthésie》1990,37(4):469-473
Two patients with hypertrophic obstructive cardiomyopathy (HOCM) presented for delivery. The first had a repeat Caesarean section with general anaesthesia and the second gave birth vaginally with epidural analgesia. Both patients developed pulmonary oedema in the peripartum period. These cases highlight the delicate fluid requirements of the pregnant patient with HOCM. The fluid management of the parturient is discussed with particular emphasis on the pathophysiology of HOCM. The indications for invasive monitoring are presented. 相似文献
17.
Yusuke Suzuki Keiichi Matsuzaki Hitoshi Suzuki Keiko Okazaki Hiroyuki Yanagawa Norio Ieiri Mitsuhiro Sato Toshinobu Sato Yoshio Taguma Joe Matsuoka Satoshi Horikoshi Jan Novak Osamu Hotta Yasuhiko Tomino 《Clinical and experimental nephrology》2014,18(5):770-777
Background
The primary abnormal manifestation in immunoglobulin A nephropathy (IgAN) is recurring bouts of hematuria with or without proteinuria. Although immunohistochemical analysis of renal biopsy tissue remains the gold standard not only for diagnosis but also for evaluating the activity of IgAN, new sensitive and reasonably specific noninvasive tests are emerging to guide therapeutic strategy applicable to all stages of IgAN. The present study examined serum levels of galactose-deficient IgA1 (Gd-IgA1) and its immune complex (IgA/IgG-IC) as noninvasive markers for the disease activity.Methods
We enrolled 50 IgAN patients (male 40 %, median age 37 years) showing complete or partial clinical remission after steroid pulse therapy with tonsillectomy (TSP) whose clinical data and serum could be followed up for 3–5 years.Results
Cross-sectional analysis revealed that the degree of hematuria and proteinuria were significantly associated with levels of Gd-IgA1 and levels of IgA/IgG-IC. Longitudinal analysis further showed that from the group of 44 patients with heavy hematuria before TSP, 31 patients showed complete disappearance of hematuria (group A), but the remaining patients did not (group B). Although the levels of Gd-IgA1 and IgA/IgG-IC in the two groups before TSP were similar, percentage decrease of Gd-IgA1 and IgA/IgG-IC levels in group A was significantly higher than in group B.Conclusion
Disease activity of IgAN assessed by hematuria and proteinuria correlated with serum levels and changes of Gd-IgA1 and IgA/IgG-IC. These new noninvasive disease activity markers can be useful for future activity scoring system and guiding therapeutic approaches. 相似文献18.
Futoshi Kawamata Shigenori Homma Nozomi Minagawa Hideki Kawamura Norihiko Takahashi Akinobu Taketomi 《World journal of surgery》2014,38(10):2716-2723
Background
Reduced-port laparoscopic surgery is the latest innovation in minimally invasive surgery. We performed single-incision plus one additional port laparoscopy-assisted anterior resection (SILS + 1-AR) starting in August 2010. This study aimed at evaluating the feasibility of SILS + 1-AR and comparing it with that of conventional laparoscopy-assisted anterior resection (C-AR).Methods
Patients with preoperative clinical stage 0 to stage III rectal cancer were included. Demographic, intraoperative, and pathological examination data, as well as short-term outcome data, of 20 patients who underwent SILS + 1-AR were retrospectively compared with that of 20 patients who underwent C-AR. Invasiveness of the two procedures was also evaluated through a vital signs diary and hematological examination on postoperative days (POD) 1, 3, and 7.Results
Operating time, mean estimated blood loss, the number of lymph nodes dissected, the number of lymph node metastases, and the mean distal resection margin length were not significantly different. However, postoperative neutrophil counts in the SILS + 1-AR group were lower than those in the C-AR group (P = 0.085). A significant difference in body temperature was observed in the SILS + 1-AR group on POD 1 (P = 0.028). No significant differences were observed in perioperative and overall morbidity between the two groups. Conversion to open surgery was required in 2 (10 %) of the 20 patients in the SILS + 1-AR group. The mean postoperative length of stay and recurrence rates were similar in the two groups.Conclusion
SILS + 1-AR for rectal cancer is similar to C-AR in safety, feasibility, and provision of oncological radicality. 相似文献19.
Shigetaka Yoshida Kenichi Ishizawa Nobuhiro Ayuzawa Kohei Ueda Maki Takeuchi Wakako Kawarazaki Toshiro Fujita Miki Nagase 《Clinical and experimental nephrology》2014,18(4):593-599
Background
The renin–angiotensin–aldosterone system (RAAS) plays pivotal roles in the pathogenesis of chronic kidney disease (CKD) progression. Aliskiren, a direct renin inhibitor, inhibits the rate-limiting step of the RAAS without any alternative pathway. It is proven to reduce albuminuria in CKD patients treated with angiotensin blockade. However, there are few reports which evaluate the advantage of aliskiren as the first-line drug against CKD progression in RAAS-activated hypertensive patients.Methods
Tsukuba hypertensive mice (THM), double transgenic mice carrying both the human renin and human angiotensinogen genes, were fed a high-salt diet and treated with hydraladine, ramipril and aliskiren for 10 weeks. Blood pressure and urinary albumin excretion were measured every 2 weeks during the experimental period. We evaluated renal histological changes and gene expression. Plasma angiotensin concentration was measured to evaluate the RAAS inhibitory effect.Results
High-salt-loaded THM showed severe hypertension and renal injury. All antihypertensive drugs suppressed blood pressure and prevented renal disease progression. RAAS blockade showed a higher renoprotective effect than hydraladine despite an equivalent blood pressure lowering effect. Aliskiren exhibited even stronger renoprotection than ramipril. Plasma angiotensin concentration was increased in THM fed both normal salt and high salt. Hydraladine did not alter the plasma angiotensin concentration. Ramipril significantly decreased angiotensin II concentration. Aliskiren treatment almost completely suppressed angiotensin I and resulted in lower angiotensin II concentration than ramipril treatment.Conclusion
Aliskiren prevents renal disease progression by suppressing both angiotensin I and II in RAAS-activated pathology. Our data suggest the application of a renin inhibitor for preventing kidney disease progression in CKD patients. 相似文献20.
Junhong Lin Yao Huang Xuelin Zhang Junbin Chen Haihui Sheng 《Pediatric nephrology (Berlin, Germany)》2014,29(10):1979-1986