Ulnar nerve sonography in leprosy neuropathy.

A 23-year-old woman presented with a half-year history of right forearm sensory and motor dysfunction. Ultrasound imaging revealed definite thickening of the right ulnar nerve trunk and inner epineurium, along with heterogeneous hypoechogenicity and unclear nerve fiber bundle. Color Doppler exhibited a rich blood supply, which was clearly different from the normal ulnar nerve presentation with a scarce blood supply. The patient subsequently underwent needle aspiration of the right ulnar nerve, and histopathological examination confirmed that granulomatous nodules had formed with a large number of infiltrating lymphocytes and a plurality of epithelioid cells in the fibrous connective tissues, with visible atypical foam cells and proliferous vascularization, consistent with leprosy. Our report will familiarize readers with the characteristic sonographic features of the ulnar nerve in leprosy, particularly because of the decreasing incidence of leprosy in recent years.

Tracing type 1 diabetic Tibet miniature pig's bone marrow mesenchymal stem cells in vitro by magnetic resonance imaging (1).

BACKGROUND: Traditional cell-tracking methods fail to meet the needs of preclinical or clinical research. Thus, the aim of the present study was to establish a new method of double labeling bone marrow mesenchymal stem cells (BMSCs) from type 1 diabetic (T1D) minipigs with super-paramagnetic iron oxide (SPIO) and enhanced green fluorescent protein (eGFP) and tracing them using MRI in vitro. METHODS: Isolated BMSCs from T1D minipigs were labeled with eGFP and different concentrations of SPIO. The effects of lentivirus (LV)-eGFP transfection and SPIO on the viability and growth curves of BMSCs were determined by Trypan blue exclusion, the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay and flow cytometry. Cellular ultrastructure was evaluated by transmission electron microscopy. Magnetic resonance imaging was used to evaluate BMSCs labeled with SPIO-eGFP complexes 6 weeks after labeling. RESULTS: Expression of eGFP in BMSCs peaked 96 h after transfection with LV-eGFP. Prussian blue staining revealed scattered blue granules in the cytoplasm of SPIO-labeled cells. Transmission electron microscopy revealed that the dense granules aggregated mainly in secondary lysosomes. On MRI, T2* -weighted imaging was far more sensitive for SPIO-labeled BMSCs than other image sequences 3 and 6 weeks after the cells had been labeled with SPIO-eGFP. CONCLUSIONS: We have developed a relatively simple and safe method for double labeling of BMSCs from T1D minipigs using SPIO and LV-eGFP and tracing them in vitro by MRI for 6 weeks.

Elevation of serum procalcitonin in patients after chemical pleurodesis with intrapleural injection of OK-432.

INTRODUCTION: In patients with refractory pleural effusion or pneumothorax, fever and elevated level of white blood cell count (WBC) are frequently observed after chemical pleurodesis with intrapleural injection of OK-432, which make it difficult to differentiate whether it was from the side effects of OK-432 or concurrent bacterial infection. OBJECTIVE: Procalcitonin (PCT) levels were measured before and after pleurodesis so as to discuss whether PCT is useful for distinguishing between the side effects of OK-432 and concurrent bacterial infection. METHOD: Twenty-six patients with refractory pleural effusion or pneumothorax who underwent chemical pleurodesis with intrapleural injection of OK-432 at the First Affiliated Hospital of Sun Yat-sen University between August 2010 and August 2012 were included in our study. Levels of PCT and WBC were measured before and after pleurodesis. RESULT: Of all 26 patients, 22 patients were with refractory pleural effusion, and the other four were with pneumothorax. The median serum levels of PCT and WBC elevated from 0.155 to 1.470 ng/mL (P = 0.009) and from 5.920 to 10.475 × 10(9) /L (P = 0.000), respectively. No patient was given antibiotics and fever subsided. CONCLUSION: Intrapleural injection of OK-432 could increase the serum level of PCT and WBC with no bacterial infection. The serum PCT level may not be useful to distinguish whether fever was caused by the side effects of OK-432 or concurrent bacterial infection.

Intensive statin therapy: a favorable adjunct to the improvement of small-diameter vascular grafts.

To assess the effect of intensive statins therapy on the outcome of small-diameter vascular prosthesis, we investigated whether atorvastatin treatment (30 mg/d) could accelerate the re-endothelialization process and improve the patency rate in a canine infrarenal abdominal aorta-expanded polytetrafluoroethylene (ePTFE) bypass model. Furthermore, we also evaluated the effect of atorvastatin on the migratory and adherent capacity of circulating endothelial progenitor cells (EPCs) in vitro. Improved patency was confirmed by Doppler sonography and arteriography. Histological and scanning electron microscopy illustrated enhanced re-endothelialization process. Treatment with atorvastatin enhanced the circulating pool of EPCs with fortified migratory and adherent capacity. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that atorvastatin treatment increased endothelial nitric oxide synthase (eNOS) and kinase insert domain receptor (KDR) messenger RNA (mRNA) expression in cultured EPCs and neointima. In conclusion, intensive statin therapy could be considered a favorable option to improve small-diameter vascular graft patency.

[The value of regulated upon activation normal T cell expressed and secreted in the pathogenesis of varicose ulcer of lower limbs].

OBJECTIVE: To study the effectiveness of RANTES in the pathogenesis of venous ulceration. METHODS: 40 Chronic venous insufficiency (CVI) individuals were enrolled in the study and separated into the ulceration group (n=20) and non-ulceration group (n=20), according to CVI with or without ulceration, 10 healthy individuals were enrolled as control group. The expression of RANTES mRNA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in blood. Immunohistochemical staining of RANTES were carried in normal skin, in the tissue at the brim of ulceration and in the tissue of cured or curing ulceration. RESULTS: In ulceration group, the expression of RANTES mRNA in blood increased obviously. Compared with the other two groups, they were significant different (P < 0.05). The difference was also significance in the other two groups (P < 0.05). The average number of RANTES positive expression in normal skin is 28 +/- 13, in the tissue at the brim of ulceration is 107 +/- 44, and in the tissue of cured or curing ulceration is 35 +/- 20. There are significant difference between normal skin and the tissue at the brim of ulceration (P < 0.05). The average number of RANTES positive expression in the tissue of cured or curing ulceration is lower than that's in the tissue at the brim of ulceration. CONCLUSION: The high expression of RANTES may be one of the important mechanisms of varicose ulcer.

Static pressure promotes rat aortic smooth muscle cell proliferation via upregulation of volume-regulated chloride channel.

Arterial smooth muscle cell proliferation is a key event in the development of hypertension associated vascular disease. Although previous studies have found that pressure itself can promote cell proliferation and DNA synthesis in vascular smooth muscle cells, the mechanisms are not clear. Recent accumulating evidence indicate that volume-regulated chloride channel plays an important role in the regulation of cell proliferation induced by numerous mitogenic factors. However, whether volume-regulated chloride channel is involved in hypertension-induced vascular smooth muscle cell proliferation remains to be determined. In this study, we found that static pressure promoted rat aortic smooth muscle cell proliferation and cell cycle progression. Static pressure treatment increased volume-regulated chloride currents and ClC-3 expression. Inhibition of chloride channel with pharmacological blockers or knockdown of ClC-3 with ClC-3 antisense transfection attenuated pressure-evoked cell proliferation and cell cycle progression. Static pressure enhanced the production of reactive oxygen species (ROS) in aortic smooth muscle cells. Diphenyleneiodonium (DPI) or apocynin pretreatment inhibited pressure-induced ROS production as well as cell proliferation. Furthermore, DPI or apocynin attenuated the pressure-induced upregulation of ClC-3 protein and hypoosmolarity-activated chloride current. Our data suggest that volume-regulated chloride channel plays a critical role in static pressure-induced cell proliferation and cell cycle progression, suggesting the therapeutic importance of volume-regulated chloride channel for treatment of hypertension attendant vascular complications.

[Static pressure induces vascular smooth muscle cells proliferation and apoptosis].

OBJECTIVE: To study the role of static pressure on proliferation and apoptosis of the vascular smooth muscle cells. METHODS: Vascular smooth muscle cell line A10 were cultured at normal atmosphere, 80 mmHg, 100 mmHg, 200 mmHg static pressure respectively. Cell viability was determined by MTT assay, cell cycle and apoptosis rate were analyzed by flow cytometer. RESULTS: After exposure to lower static pressure (100 mmHg) for 48 hour, cell viability and proliferation index (PI) of A10 cell significantly increased, the percentage of A10 cell in G(0)/G(1) phase decreased significantly and the apoptosis rate showed no difference as compared with those exposed to atmospheric pressures. However after exposure of A10 cell to higher static pressure (200 mmHg) for 48 hours, cell viability and proliferation index (PI) significantly decreased, the percentage of A10 cell in G(0)/G(1) phase increased significantly, apoptosis rate significantly increased, as compared with cells exposed to atmospheric pressure. CONCLUSION: Lower static pressure can facilitate vascular smooth muscle cells proliferation, while higher pressure can induce cell apoptosis.