Humans ; Sciatic Neuropathy/etiology* ; Arthroplasty, Replacement, Hip/adverse effects* ; Peripheral Nerve Injuries/etiology* ; Sciatic Nerve/injuries*

Objective To investigate the effects of high spermatic vessel dissection on testicular morphological alteration of SD rats in prepuberty,puberty and sexual maturity phases.Methods Thirty-day-old SD rats were divided into 2 groups underwent sham operation and left high spermatic vessel dissection as a simulation of Palomo′s maneuver.Detailed morphological investigations were made at 3 different postoperative intervals among the 3rd day,30th day and 56th day.Results High spermatic vessel dissection in prepubertal rats induced acute testicular ischemia in the operated testes on the 3rd day.Most of the operated testes on the 30th day showed testicular atrophy.And all the operated testes showed testicular atrophy and sperm disappearance in epididymis on the 56th day.Conclusion High dissection of spermatic vessel in prepubertal rats induced testicular ischemia in prepuberty and testicular growth failure in puberty,testicular atrophy completely and sperm production losing in sexual maturity phase.

BACKGROUNDPercutaneous transluminal renal angioplasty with stent is an effective procedure for atherosclerotic renal artery stenosis. However, the decision to perform this procedure has recently raised considerable debate. The aim of this study was to assess the effects of percutaneous transluminal renal angioplasty with stent in atherosclerotic renal artery stenosis patients, especially as it relates to blood pressure control and renal function improvement.

METHODSA retrospective analysis was made of the clinical data from 125 atherosclerotic renal artery stenosis patients who underwent percutaneous transluminal renal angioplasty from July 2004 to June 2008 in the Department of Vascular Surgery of Beijing Chaoyang Hospital. We compared blood pressure, number of oral antihypertensive medications, and renal function changes pre and post-procedure at 24 months follow-up.

RESULTSA total of 125 atherosclerotic renal artery stenosis patients underwent percutaneous transluminal renal angioplasty and 143 stents were placed. At 24 months follow-up, both systolic and diastolic blood pressure and the number of oral antihypertensive medications were significantly reduced (P < 0.05). Overall, the estimated glomerular filtration rate did not change significantly (P > 0.05); however, a significant increase in estimated glomerular filtration rate was observed in the subgroup of patients with a lower baseline estimated glomerular filtration rate and in the subgroup of patients with bilateral renal artery stenosis (P < 0.05).

CONCLUSIONPercutaneous transluminal renal angioplasty is a safe procedure for atherosclerotic renal artery stenosis patients, providing a significant improvement in blood pressure control and reduction in the number of oral antihypertensive medications.

Aged ; Angioplasty, Balloon ; adverse effects ; methods ; Antihypertensive Agents ; therapeutic use ; Atherosclerosis ; complications ; Blood Pressure ; Female ; Glomerular Filtration Rate ; Humans ; Male ; Middle Aged ; Renal Artery Obstruction ; etiology ; mortality ; physiopathology ; therapy ; Retrospective Studies ; Stents ; adverse effects

Objective: To evaluate the feasibility, safety, and effectiveness of CT-guided microcoil localization of solitary pulmonary nodules (SPNs) for guiding video-assisted thoracoscopic surgery (VATS). Materials and Methods: Between June 2016 and October 2019, 454 consecutive patients with 501 SPNs who received CTguided microcoil localization before VATS in our institution were enrolled. The diameter of the nodules was 0.93 ± 0.49 cm, and the shortest distance from the nodules to the pleura was 1.41 ± 0.95 cm. The distal end of the microcoil was placed less than 1 cm away from the nodule, and the proximal end was placed outside the visceral pleura. VATS was performed under the guidance of implanted microcoils without the aid of intraoperative fluoroscopy. Results: All 501 nodules were marked with microcoils. The time required for microcoil localization was 12.8 ± 5.2 minutes. Microcoil localization-related complications occurred in 179 cases (39.4%). None of the complications required treatment. A total of 463 nodules were successfully resected under the guidance of implanted microcoils. VATS revealed 38 patients with dislocated microcoils, of which 28 underwent wedge resection (21 cases under the guidance of the bleeding points of pleural puncture, 7 cases through palpation), 5 underwent direct lobectomy, and the remaining 5 underwent a conversion to thoracotomy. In 4 cases, a portion of the microcoil remained in the lung parenchyma. Conclusion CT-guided microcoil localization of SPNs is safe and reliable. Marking the nodule and pleura simultaneously with microcoils can effectively guide the resection of SPNs using VATS without the aid of intraoperative fluoroscopy.

Objective: To evaluate the feasibility, safety, and effectiveness of CT-guided microcoil localization of solitary pulmonary nodules (SPNs) for guiding video-assisted thoracoscopic surgery (VATS). Materials and Methods: Between June 2016 and October 2019, 454 consecutive patients with 501 SPNs who received CTguided microcoil localization before VATS in our institution were enrolled. The diameter of the nodules was 0.93 ± 0.49 cm, and the shortest distance from the nodules to the pleura was 1.41 ± 0.95 cm. The distal end of the microcoil was placed less than 1 cm away from the nodule, and the proximal end was placed outside the visceral pleura. VATS was performed under the guidance of implanted microcoils without the aid of intraoperative fluoroscopy. Results: All 501 nodules were marked with microcoils. The time required for microcoil localization was 12.8 ± 5.2 minutes. Microcoil localization-related complications occurred in 179 cases (39.4%). None of the complications required treatment. A total of 463 nodules were successfully resected under the guidance of implanted microcoils. VATS revealed 38 patients with dislocated microcoils, of which 28 underwent wedge resection (21 cases under the guidance of the bleeding points of pleural puncture, 7 cases through palpation), 5 underwent direct lobectomy, and the remaining 5 underwent a conversion to thoracotomy. In 4 cases, a portion of the microcoil remained in the lung parenchyma. Conclusion CT-guided microcoil localization of SPNs is safe and reliable. Marking the nodule and pleura simultaneously with microcoils can effectively guide the resection of SPNs using VATS without the aid of intraoperative fluoroscopy.

OBJECTIVETo study the effects of benzo(a)pyrene (BaP) on the cell cycle distribution and activities of mitogen-activated protein kinase (MAPK) signal molecules (ERK1/2, JNK1/2 and p38) in human embryo lung cells (HELF), and to investigate the relationship between alterations of MAPK protein phosphorylation and the cell cycle distributions.

METHODSThe phosphorylation of MAPK were induced by exposing HELF cells to BaP at 0.1, 0.5, 2.5 and 12.5 micromol/L. The phosphorylation and protein expression levels of ERK1/2, JNK1/2 and p38 were determined through western-blotting assay. And the flow cytometry assay was used to measure the cell cycle effects in HELF cells after treatment with 2.5 micromol/L BaP for 24 h.

RESULTSThe phosphorylation levels of ERK1/2, JNK1/2 and p38 were significantly increased through BaP exposure. In addition, the phosphorylation of these three MAPKs has similar alteration pattern. We found that exposure of cells to 2.5 microM of BaP for 24 h resulted in a decrease of G(0) and G(1) population by 11.9% (F = 41.38, P < 0.01) and an increase of S population by 17.2% (F = 68.13, P < 0.01). Three chemical inhibitors of MAPK (AG126, SP600125 and SB203580) could significantly inhibit the cell cycle alteration because of BaP treatment.

CONCLUSIONERK1/2, JNK1/2 and p38 could positively regulate the BaP independently induced cell cycle alterations.

Benzo(a)pyrene ; toxicity ; Cell Cycle ; drug effects ; Cells, Cultured ; Fibroblasts ; drug effects ; metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Lung ; cytology ; embryology ; MAP Kinase Kinase 4 ; metabolism ; MAP Kinase Signaling System ; drug effects ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitogen-Activated Protein Kinase 8 ; metabolism ; Mitogen-Activated Protein Kinase 9 ; metabolism ; Signal Transduction ; drug effects ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo study the role of E2F1/4 pathway in vitamin C reversing benzo (a) pyrene [B (a) P]-induced changes of cell cycle in human embryo lung fibroblasts (HELF) and the relationship between E2F1 and cyclin D1/CDK4.

METHODSThe stable transfectants, HELF transfected with antisense cyclin D1 and antisense CDK4, were established to detect the relationship of signaling pathway. Cells were cultured and pretreated with vitamin C before stimulation with B (a) P for 24 hours. The expression levels of cyclin D1, CDK4, E2F1 and E2F4 were determined by Western blot and the band intensity was analysed as the relative value to control by using the Gel-Pro 3.0 software. Flow Cytometric Analysis was employed to detect the distributions of cell cycle.

RESULTSB (a) P significantly elevated the expression levels of cyclin D1, CDK4, E2F1 and E2F4 in HELF cells. Vitamin C decreased the expression levels of above proteins in B (a) P-stimulated HELF cells. The expression levels of these proteins in B (a) P-treated above transfectants were lower than those in B (a) P-treated HELF cells. The expression levels of above proteins with vitamin C combined with antisense cyclin D1 were decreased as compared to those with antisense cyclin D1 alone. B (a) P increased the percentage of S phase as compared to the controls [(41.1 +/- 0.2)% vs (33.5 +/- 3.2)%, P < 0.05]. Both vitamin C [(33.2 +/- 0.6)% vs (41.1 +/- 0.2)%, P < 0.05] and antisense cyclin D1 [(31.2 +/- 1.3)% vs (41.1 +/- 0.2)%, P < 0.05] suppressed the changes of cell cycle induced by B (a) P. Vitamin C combined with antisense CDK4 markedly suppressed B (a) P-induced changes of cell cycle as compared to those with antisense CDK4 alone.

CONCLUSIONVitamin C might reserve the B (a) P-induced changes of cell cycle via intracellular signaling pathway of cyclin D1-CDK4/E2F-1/4.

Ascorbic Acid ; pharmacology ; Benzo(a)pyrene ; antagonists & inhibitors ; toxicity ; Cell Cycle ; drug effects ; Cyclin D1 ; metabolism ; E2F1 Transcription Factor ; metabolism ; E2F4 Transcription Factor ; metabolism ; Humans ; Lung ; cytology ; embryology ; Signal Transduction

OBJECTIVETo study the role of mitogen activated protein kinase (MAPK)/activator protein-1 (AP-1) pathway in benzo(a)pyrene (B(a)P)-induced changes of cell cycle in human embryo lung fibroblasts (HELF).

METHODSAP-1 luciferase activity was determined by the Luciferase reporter gene assay using a luminometer. The expression levels and activity of extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal kinase (JNK) and p38 were determined by Western blot. Flow cytometric analysis was employed to detect the distributions of cell cycle. The dominant negative mutant of ERK2, JNK1 and p38 were applied to detect the upstream or downstream relationship of signaling pathways.

RESULTSB(a)P treatment resulted in a marked activation of AP-1 and its upstream MAPK, including ERK, JNK and p38 in human embryo lung fibroblasts (HELF). B(a)P exposure also led to increase the population of cells at S phase compared to control (P < 0.01) with a concomitant decline of cells at G(1) phase. B(a)P-induced cell cycle alternation was markedly impaired by stable expression of a dominant negative mutant of ERK2 or JNK1, but not p38. B(a)P-induced AP-1 transactivation was inhibited by the overexpression of dominant-negative mutant of ERK2 or JNK1, but not p38. Inhibition of the activation of AP-1 by curcumin, a chemical inhibitor of AP-1, significantly inhibited the cell cycle changes in response to B(a)P treatment.

CONCLUSIONERK and JNK, but not p38, mediated benzo(a)pyrene-induced cell cycle changes by AP-1 transactivation in HELF.

Benzo(a)pyrene ; pharmacology ; Blotting, Western ; Cell Cycle ; drug effects ; Cells, Cultured ; Fibroblasts ; cytology ; drug effects ; metabolism ; Flow Cytometry ; Humans ; Lung ; cytology ; embryology ; Mitogen-Activated Protein Kinase 1 ; metabolism ; physiology ; Mitogen-Activated Protein Kinase 8 ; metabolism ; physiology ; Phosphorylation ; Transcription Factor AP-1 ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

BACKGROUNDEndovascular therapy is a treatment option for localized occlusion of the subclavian artery. In this report the long-term experience with 59 patients is presented.

METHODSBetween June 1998 and September 2008, we used endovascular therapy to treat 61 subclavian arterial obstructive lesions in 59 patients (46 males and 13 females, 34 - 82 years of age with a mean age (61.9 + or - 11.0) years). Twenty patients (34%) had clinical symptoms due to vertebrobasilar insufficiency, 26 (44%) had disabling arm ischemia, and 13 (22%) had both symptoms. We performed all procedures under local anesthesia. The approaches were from the femoral artery (n = 47), brachial artery (n = 1, involving bilateral subclavian disease) or both (n = 11). Sixty stents were implanted. All patients were followed-up at 1, 3, 6, and 12 months post-procedure, and annually thereafter.

RESULTSWe achieved technical success in 58 (95.1%) arteries, all of which were stented. There were three technical failures; two were due to the inability to cross over an occlusion, necessitating the switch to an axillo-axillary bypass, and the third was due to shock after digital subtraction angiography and prior to stenting. Arterial stenosis pre- and post-stenting was (83.6 + or - 10.8)% and (2.5 + or - 12.5)% (P < 0.01). Clinical success was achieved in 55 of the 59 patients (93.4%). Of the four clinical failures, three were technical and the remaining patient had a stent thrombosis. Systolic blood pressure difference between the two brachial arteries was (44.7 + or - 18.5) vs. (2.2 + or - 3.9) mmHg (P < 0.01). Primary patency was 98% at 12 months, 93% at 24 months, and 82% at 5 years. Five patients were lost to follow-up by 12 months post-stenting. Significant recurrent obstruction developed in five patients with resumption of clinical symptoms. The overall survival rate was 98.2% at 12 months, 89.5% at 24 months, and 84.5% at 5 years.

CONCLUSIONSEndovascular therapy for proximal subclavian arterial obstructive lesions is effective and successful. This minimally invasive treatment may be the first choice of treatment for proximal subclavical arterial obstructive lesions.

Adult ; Aged ; Aged, 80 and over ; Arterial Occlusive Diseases ; pathology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Stents ; Subclavian Artery ; pathology ; Subclavian Steal Syndrome ; pathology ; therapy ; Vertebrobasilar Insufficiency ; pathology ; therapy

OBJECTIVETo study the molecular mechanism of the inhibitory effects of vitamin C on benzo[a]pyrene (B[a]P)-induced changes of cell cycle in human embryo lung fibroblast (HELF) cells.

METHODSThe stable transfectants, HELF transfected with antisense cyclin D1 and antisense CDK4, were established. Cells were cultured and pretreated with vitamin C before stimulation with B[a]P for 24 h. The expression levels of cyclin D1, CDK4, E2F1, and E2F4 were determined by Western blot. Flow cytometric analysis was employed to detect the distributions of cell cycle.

RESULTSB[a]P significantly elevated the expression levels of cyclin D1, E2F1, and E2F4 in HELF cells. Vitamin C decreased the expression levels of cyclin D1, E2F1, and E2F4 in B[a]P-stimulated HELF cells. Dose-dependent relationships were not found between the different concentrations of vitamin C (10, 100, 500, 1000, and 5000 micromol/L) and the expression levels of cyclin D1, E2F1, and E2F4 in HELF cells. The expression levels of cyclin D1, E2F1, and E2F4 in B[a]P-treated transfectants were lower than those in B[a]P-treated HELF cells. The expression levels of cyclin D1 and E2F4 treated with vitamin C and antisense cyclin D1 were decreased compared with those treated with antisense cyclin D1 alone. The effects of vitamin C combined with antisense CDK4 on the expression levels of cyclin D1 and E2F1/E2F4 were similar to those of antisense CDK4 alone. B[a]P progressed HELF cells from G1 to S phase. Both vitamin C and antisense cyclin D1 suppressed the changes of cell cycle progressed by B[a]P. However, antisense CDK4 did not attenuate the above changes. Vitamin C combined with antisense CDK4 markedly suppressed B[a]P-induced changes of cell cycle as compared with antisense CDK4. But the inhibitory effects of vitamin C combined with antisense cyclin D1 on B[a]P-induced changes of cell cycle were similar to those of vitamin C alone or antisense cyclin D1 alone.

CONCLUSIONSB[a]P progressed HELF cells from G1 to S phase via intracellular signaling pathway of cyclin D1/E2F. Vitamin C may modulate this signaling pathway to protect cells from injury caused by B[a]P.

Ascorbic Acid ; pharmacology ; Benzo(a)pyrene ; Blotting, Western ; methods ; Cell Cycle ; drug effects ; physiology ; Cells, Cultured ; Cyclin D1 ; metabolism ; Cyclin-Dependent Kinase 4 ; metabolism ; Dose-Response Relationship, Drug ; E2F1 Transcription Factor ; metabolism ; Fibroblasts ; cytology ; drug effects ; metabolism ; G1 Phase ; drug effects ; physiology ; Humans ; Lung ; cytology ; embryology ; RNA, Antisense ; genetics ; S Phase ; drug effects ; physiology ; Transfection ; methods