Objective To study the effects of allogeneic blood transfusion on expression of CD40L on peripheral blood monocytes (PBMCs) in patients undergoing radical gastrectomy for gastric carcinoma. Methods Thirty patients classified as ASA physical status Ⅰ- Ⅱ undergoing radical gastrectomy for gastric carcinoma were randomly divided into three groups with 10 patients in each group : group A received no allogeneic blood; group B received leukodepleted blood; group C received allogeneic whole blood during operation or within 12 h after operation. The patients were premedicated with intramuscular phenobarbital sodium 0.1 g and atropine 0.5 mg. Anesthesia was induced with midazolam 0.06 mg ? kg-1 , fentanyl 2 ?g ?kg-1 , propofol 1.5 mg ?kg-1 and vecuronium 8mg and maintained with continuous infusion of propofol (100?g?kg-1?min-1) and vecuronium (5?g ?kg-1?min-1) and intermittent inhalation of 1l%-2% isoflurane. The patients were mechanically ventilated after tracheal intubation. Blood samples were taken before operation and 2, 5 and 10 days after operation. The PBMCs and plasma were separated from peripheral blood by Ficoll-Hypaque centrifugation. The PBMCs were washed and incubated with the patients own plasma (final-concentration 10% ) and PHA (final concentration 20 ?g?ml-1 ) at 37℃ in a 5% CO2 atmosphere for 48h. CD40Lexpression on PBMCs was quantified by flow-cytometry.Results The demographic data including sex, age, bodyweight and duration of operation and intraoperative blood loss were comparable among the three groups. There was no significant difference in the CD40L expression before operation among the 3 groups. In group A there was no change in CD40L expression after operation. In group B CD40L expression on PBMCs increased significantly on the 2nd postoperative day, but returned to preoperative level on the 5th postoperative day. In group C the CD40L expression on PBMCs kept increasing on the 2nd and 5th postoperative day and did not return to preoperative level on the 10th day. The increase in CD40L expression was significantly larger in group C than that in group B ( P

Objective To study the clinicopathological features of syringomatous adenoma of the nipple (SAN).Methods The clinical,histopathological and immunohistochemical findings of four cases of SAN were described,with a review of the literature.The diagnosis and differential diagnosis of SAN were also discussed.Results Among the four patients,three were female,and one was male.The mean age at onset was 42 years,and clinical course ranged from 3 months to 10 years.Clinically,SAN was manifested as an asymptomatic subcutaneous nodule,which was located in the areola of breast of female patients and in the right armpit of the male patient.Histopathologically,the tumor was located in the dermis and subcutaneous tissue,composed of nests and cords of epithelial cells forming tubular structures and infiltrating the indurated stroma between smooth muscle bundles.These tubules were lined by two layers of cells and displayed a comma or tadpole shape.Keratotic microcysts were seen.Immunohistochemically,the tumor cells stained positive for cytokeratin,cytokeratin 5/6,Ki67 (1％),but negative for estrogen receptor,progesterone receptor,CerbB2,cytokeratin 8/18,P53 and gross cystic disease fluid protein-15 (GCDFP-15).The peritubular myoepithelial cells expressed P63 and smooth muscle actin (SMA).Conclusions SAN is a rare benign tumor,which is often confused with some benign and malignant carcinomas of the breast.

Objective To investigate the diagnostic value of combining carotid intima-media thickness (cIMT) with serum Galectin-3 (Gal-3) and Pentraxin 3 (PTX3) in patients with psoriasis complicated with cardiovascular disease (CVD). Methods Thirty-eight patients with psoriasis complicated with CVD were included in CVD group, 51 patients with psoriasis alone were included in psoriasis group, and 60 healthy subjects were selected as control group. Clinical data were collected from each group. The cIMT was measured using carotid ultrasound, and serum Gal-3, PTX3, and inflammatory markers[high sensitivity C-reactive protein (hs-CRP), procalcitonin (PCT), tumor necrosis factor-α (TNF-α)]were detected using enzyme-linked immunosorbent assay. Multivariate Logistic regression analysis was used to identify the influencing factors of CVD in patients with psoriasis. The receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of serum Gal-3, PTX3, and cIMT for CVD. Results The cIMT was greater in the CVD group and the psoriasis group than in the control group, and the CVD group was greater than the psoriasis group (P < 0.05). The serum levels of Gal-3, PTX3, hs-CRP, PCT, and TNF-α were higher in the CVD group and the psoriasis group than in the control group, and their levels were higher in the CVD group than in the psoriasis group (P < 0.05). The psoriasis area and severity index (PASI) score was higher in the CVD group than in the psoriasis group (P < 0.05). Pearson's correlation analysis showed that cIMT, Gal-3, and PTX3 were separately positively correlated with hs-CRP, PCT, and TNF-α (P < 0.05). Multivariate Logistic regression analysis showed that PASI score, cIMT, Gal-3, PTX3, hs-CRP, and TNF-α were independent influencing factors for CVD in patients with psoriasis (OR=1.250, 1.451, 1.432, 1.365, 1.413, 1.465; P < 0.05). The diagnostic model based on cIMT combined with serum Gal-3 and PTX3 had higher diagnostic value for CVD in patients with psoriasis than single diagnosis. The area under the curve was 0.922, with sensitivity and specificity of 0.91 and 0.85, respectively. Conclusion The cIMT, serum Gal-3, and serum PTX3 are independent influencing factors for CVD in patients with psoriasis. The combination of the three indicators has higher diagnostic value for CVD in patients with psoriasis.

ObjectiveTo investigate the pharmacodynamic effects of Houshihei San （HSHS） recorded with the effects of treating wind and limb heaviness on muscle tissue injury after middle cerebral artery occlusion （MCAO） in rats through the ferroptosis pathway. MethodsThirty SD male rats were selected and randomly grouped as follows： sham， MCAO， deferoxamine mesylate， high-dose HSHS （HSHS-H， 0.54 g·kg^-1）， and low-dose HSHS （HSHS-L， 0.27 g·kg^-1）， with 6 rats in each group. A laser scattering system was used to evaluate the stability of the MCAO model， and rats were administrated with corresponding agents by gavage for 7 days. During the administration period， behavioral， imaging and other methods were used to systematically evaluate the skeletal muscle tissue injury after MCAO and the therapeutic effect in each administration group. Hematoxylin-eosin staining was employed to evaluate the cross-section of muscle cells. Subsequently， immunohistochemistry was used to detect tumor suppressor p53 and glutathione peroxidase 4 （GPX4） in the soleus tissue. Western blot was employed to determine the protein levels of p53， GPX4， myogenic differentiation 1 （MyoD1）， nuclear factor E₂-related factor 2 （Nrf2）， Myostatin， solute carrier family 7 member 11 （SLC7A11）， muscle ring-finger protein-1 （MuRF1）， and muscle atrophy F-box protein （MAFbx） to verify the therapeutic effect in each group. ResultsCompared with the MCAO group， HSHS enhanced the locomotor ability and promoted muscle regeneration， which suggested that the pharmacological effects of HSHS were related to the inhibition of muscle tissue ferroptosis to reduce the expression of muscle atrophy factors. Behavioral and imaging results suggested that compared with the MCAO group， HSHS ameliorated neurological impairments in rats on day 7 （P<0.01）， enhanced 5-min locomotor distance and postural control （P<0.01）， strengthened grasping power and promoted muscle growth （P<0.01）， stabilized skeletal muscle length and weight （P<0.01）， and increased the cross-section of muscle cells （P<0.01）. Compared with the MCAO group， HSHS promoted the increases in glutathione and superoxide dismutase content and inhibited the increase in malondialdehyde content （P<0.05，P<0.01）. Ferroptosis pathway-related assays suggested that HSHS reduced the p53-positive cells and increased the GPX4-positive cells （P<0.01）. HSHS ameliorated muscle function decline after stroke by promoting the expression of GPX4， Nrf2， SLC7A11， and MyoD1 and inhibiting the expression of p53， Myostatin， MurRF1， and MAFbx to reduce ferroptosis in the muscle （P<0.01）. ConclusionHSHS， prepared with reference to the method in the Synopsis of Golden Chamber， can simultaneously reduce the myolysis and increase the protein synthesis in the skeletal muscle tissue after ischemic stroke by regulating the ferroptosis pathway.