The purpose of our studies was to investigate the relation between the condition of the adrenal and the growth of Sarcoma 180 (S_(180)) in mice. The hybrid Swiss mice were used and divided into four groups: (1) the normal mice for control, male and female, each one half, (2) testectomized mice, (3) female mice with natural resistance to S_(180), (4) S_(180)-bearing mice. The tissue slices of adrenal were stained with H. E. method. The adranal cortex was subdivided into eight zones according as I. C. Jones' opinion. The area of each zone in the cortex was measured by microscope and the weight of each adrenal was obtained with the 10~(-4) scales. The results of our studies are explained as follows:1. When the body weight of the normal adult mice increased, the adrenal weight did not increase. But there was obvious difference of adrenal weights between the normal adult male and female, the former was smaller and the later was larger.2. After S_(180) was implanted into the mice, the adrenal weight rapidly and markedly increased with the growth of S_(180) (P

Gene Rearrangement ; Humans ; RNA-Binding Protein EWS ; genetics ; Soft Tissue Neoplasms ; genetics

Objective To investigate the relationship between monocyte chemoattractant protein-1 (MCP-1) A-2518G single nucleotide polymorphism (SNPs) and susceptibility of epithelial ovarian cancer(EOC) in Chinese Han population of Hunan region.Methods MCP-1 A-2518G SNPs of the EOC were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 92 patients with EOC and 38 healthy women as control.Results MCP-1 A-2518G SNPs had AA,AG,and GG genotypes in cancer and control groups.The frequencies of AA,AG,and GG genotypes were not significantly different between cancer and control groups (AA:17.40％ and 15.79％ ; AG:44.56％ and 52.63％ ; and GG:38.04％ and 31.58％ ; P ＞0.05).Multivariate logistic regression analysis showed that there was no significant correlation between MCP-1 A-2518G polymorphism and EOC (P ＞0.05).Conclusions This present study suggested that MCP-1 A-2518G polymorphism should not be related to susceptibility of EOC in the Chinese Han population of Hunan region.

AIM:To evaluate the effect of curcumin on impaired learning-memory ability and the expression of high mobility group box protein 1 ( HMGB1 ) and c-Jun N-terminal kinase ( JNK ) in a rat model of Alzheimer disease (AD).METHODS:Male Sprague-Dawley rats, weighing 250~270 g, were randomly divided into 4 groups (n=9):blank control group (group A), model group (group B), curcumin treatment group (group C, curcumin injected intraper-itoneally at 100 mg· kg-1· d-1 for 6 consecutive days) and solvent control group (group D).The rats of AD model were induced by injection of ibotenic acid into the nucleus basalis of Meynert ( NBM) bilaterally.All rats were trained in Morris maze to assess the ability of learning and memory .The expression of HMGB1 and JNK in the hippocampus was detected by the methods of immunohistochemistry and Western blotting .RESULTS:Compared with group A , the average escape laten-cy (AEL) in groups B and D were obviously longer (P<0.05), while AEL in group C in the 5th and 6th days were signif-icantly shorter (P<0.05).The releases of HMGB1 in the CA1 and CA3 areas in groups B and D from the nucleus were a-bundant.Compared with groups B and D , HMGB1 in hippocampal CA1 and CA3 areas in group C secreted out of the nu-cleus decreased obviously (P<0.05).No significant difference of the release of HMGB1 between group A and group C was observed (P>0.05).No significant difference in the expression of HMGB1 in the hippocampus among the 4 groups was found (P>0.05).However, compared with groups B and D , the expression of JNK in group C was decreased obvi-ously (P<0.05).CONCLUSION: Curcumin significantly improves the learning and memory ability of AD rats .The probable mechanisms may be related to inhibiting the release of HMGB 1 from the nucleus of hippocampal neurons and de-creasing the expression of JNK in the hippocampus .

Objective To investigate changes in serum levels of Th22 cell ? related cytokines and complements in patients with drug eruption before and after treatment, and to explore their possible roles in the occurrence and development of drug eruption. Methods This study included 35 patients with drug eruption, and 35 sex?and age?matched healthy controls. Five milliliters of peripheral blood samples were collected from the controls and patients before and after treatment. Enzyme?linked immunosorbent assay(ELISA)was performed to measure serum levels of interleukin 22(IL?22)and IL?13, and the cytometric bead array(CBA)system was used to determine serum levels of tumor necrosis factor?α(TNF?α) and complement components C3a, C4a and C5a. Results Before treatment, the patients with drug eruption showed significantly higher serum levels of IL?22(40.85 ± 14.56 vs. 29.09 ± 8.66 ng/L, t=5.549, P<0.05), IL?13(869.94 ± 463.39 vs. 372.92 ± 151.75 ng/L, t=6.071, P<0.05), TNF?α(1.03 ± 0.64 vs. 0.44 ± 0.31 ng/L, t=4.321, P<0.05), complement C3a(55.21 ± 32.98 vs. 42.44 ± 14.26 ng/L, t=2.832, P<0.05), C4a(285.11 ± 123.91 vs. 237.00 ± 63.57 ng/L, t=2.257, P<0.05), and C5a(279.68 ± 127.72 vs. 215.98 ± 65.38 ng/L, t=2.495, P<0.05)compared with the controls. After treatment, the serum levels of IL?22, IL?13, TNF?α, complement C3a, C4a and C5a in patients decreased to(32.72 ± 11.77)ng/L,(456.21 ± 123.22)ng/L,(0.64 ± 0.39)ng/L,(45.47 ± 21.11)ng/L,(241.86 ± 84.12)ng/L and(239.61 ± 103.51)ng/L respectively, with a significant difference between the pretreatment and posttreatment values of these proteins(t = 4.443, 5.197, 3.572, 3.213, 2.728 and 4.772, respectively, all P ≤ 0.01). Additionally, the serum levels of IL?22 and IL?13 were still significantly higher in the patients than in the controls(both P < 0.05), while there were no significant differences in the serum levels of TNF?α, complement C3a, C4a or C5a between the patients and controls after treatment(all P > 0.05). Correlation analysis showed positive correlations between complement C3a and C4a serum levels(r = 0.660, P < 0.05), between C3a and C5a serum levels(r = 0.404, P < 0.05), between C4a and C5a serum levels(r = 0.501, P < 0.05), and between IL ? 22 and TNF ? α serum levels(r = 0.573, P = 0.005), but negative correlations between IL ? 22 and complement C3a serum levels(r = -0.490, P = 0.005), in patients before treatment. Conclusion The activation of Th22 cell?related cytokines and complements may play important roles in the occurrence and development of drug eruption, and IL?22 may participate in the regulation of complements.

Objective To evaluate the clinical characteristics and pathological features of Meckel's diverticulum(MD) in children.Methods 244 MD cases admitted between January 2010 and December 2014 were retropectively analyzed.Results In fifty patients,MD was an incidental finding at laparotomy or laparoscopy for unrelated entities.Among the remaining 194 symptomatic patients,there were 76 patients presenting GI bleeding,forty eight patients were identified with perforated Meckel's diverticulum,thirty six patients suffered from intestinal obstruction.34 patients had MD caused severe complications such as volvulus and intestinal necrosis,diverticular perforation and peritonitis.61 out of 76 GI bleeding patients underwent a 99mTc scan,and positive tracer was found in 42 patients.Among the 19 negative 99mTc scan patients,8 received capsule endoscopy and only 3 patients were suspected of diverticulum.242 patients underwent one stage resection of the diverticulum.Histology revealed ectopic gastric mucosa or ectopic pancreatic tissue in 128 patients.One patient died of volvulus and intestinal necrosis postoperatively,and two suffered from adhesive intestinal obstruction during one to five year's follow up.Conclusions It is necessary to maintain a high suspicion of MD in the pediatric age group with symptoms of abdominal pain,gastrointestinal hemorrhage or intestinal obstruction.Ectopic mucosa assumes the ultimate responsibility for major complications of MD.

Objective To study the changes of trans-diaphragmatic pressure (Ptra) and its correlation with esophageal pressure (Peso) through ARDS piglet model.Methods Five piglets were enrolled in the study.Peso,gastric pressure (Pgas) and intra-thoracic pressure (Pint) was monitored through balloon inserted.The data before ARDS serve as control.ARDS was produced in the piglets through saline lavage.The pressure were observed and the Ptra were calculated.The pressure changes and correlation between Ptra and Peso were analyzed as well.Linear regression with the coefficient of determination and t-test were used as appropriate.Significance was assumed for P ＜ 0.05.Results Peso,Pgas and Pint before ARDS were 7.3 ± 1.9,25.5 ± 2.4,- 1.23 ± 0.21 cmH2O,Ptra was 18.2 ± 1.6 cmH2O.While after ARDS,the data were 4.7 ± 1.4,31.1 ± 3.1 and - 1.79 ± 0.28 cmH2O,and Ptra was 26.4 ± 2.1 cmH2 O,and all these changes were obviously ( P ＜ 0.05 ).The correlation between Pint and Peso,Pint and Ptra (A) and Ptra ( B ) were 0.93 ± 0.025,0.88 ± 0.023 and 0.87 ± 0.37 before ARDS.After ARDS,the correlation changed to be 0.82 ±0.21,0.81 ±0.20 and 0.78 ±0.31.Although a bit decreased,the correlation was still positive (P ＜ 0.01 ).Conclusions There existed good correlations between Peso and Ptra as well as between Pint and Peso before or after ARDS.Ptra was increased obviously after ARDS,which could lead to respiratory muscle fatigue.

Objective: To study clinicopathologic features, diagnosis and differential diagnosis of myxoid variant of angiomatoid fibrous histiocytoma (AFH). Methods: Three cases of myxoid variant of AFHs were collected from First Affiliated Hospital of Nanjing Medical University during 2008 and 2017. EnVision method and fluorescence in situ hybridization(FISH) were used to detect immunophenotype and EWSR1 gene rearrangement, respectively. Results: There were 2 males and l female with age at 13, 31, and 42 years, respectively. The patients presented with a painless mass located superficially (subcutaneous or submucosal) in two cases or deep-seated (retroperitoneum) in one case. Grossly, the diameters of tumors were 1, 7, and 2 cm, respectively. The cut surface was solid and firm, tan to gray in colour. Histologically, the circumscribed tumor had fibrous pseudocapsule and peritumoal lymphoplasmacytic infiltrates. The tumor cells arranged in vaguely nodular growth pattern, with prominent myxoid stroma (present in 60% to 100% of the entire tumor). In hypocellular myxoid areas, the spindle to stellate tumor cells arranged in cords or reticular pattern, or in a haphazard manner. However, histiocytoid cells arranged in fascicular, sheet-like, or whorled growth pattern, as in classical AFH, were also identified in hypercelluar areas. Mild to moderate atypia was observed with low mitotic rate of (0-2)/10 HPF. Tumor necrosis was not seen. One case presented with slit-like hemorrhage and sclerosing collagen intermingled with myxoid matrix was identified in 1 case. Immunohistochemically, all cases were positive for CD68 and CD163. Two of three were positive for desmin, EMA, CD99 and one for Calponin, SMA. All cases were negative for S-100 protein, CD34, CD31, CD35, CD21 and CKpan. FISH detection was positive for EWSRl gene in all cases. Available clinical follow-up was obtained in 2 cases, revealing no evidence of disease in 6 and 89 months, respectively. Conclusions Myxoid variant of AFH is a histological subtype of AFH, with clinical features, immunophenotypes, genomic profiles and biological behavior similar to typical AFH. Their unusual morphology is easily confused with a variety of other myxoid mesenchymal neoplasms, including myoepithelioma and nerve sheath tumors.

Objective: To study the clinicopathologic features, diagnosis and differential diagnosis of pulmonary microcystic fibromyxoma. Methods: In March 2014, at the First Affiliated Hospital to Nanjing Medical University a 58-year-old female patient of pulmonary microcystic fibromyxoma was collected. The clinicopathologic, immunohistochemical and genetic profile of a case of pulmonary microcystic fibromyxoma were studied, and the relevant literature reviewed. Results: The patient was a 58-year-old female who presented with cough and sputum for 1 month. CT scan disclosed a 15 mm nodule in her right middle lobe of lung. The patient underwent a wedge resection with negative margin. Grossly, a well-demarcated peripheral lung nodule was detected, measuring 1.5 cm×1.5 cm×1.0 cm, with myxoid tan-white cut surface containing microcysts. Microscopically, the tumor was composed of bland spindled to stellate-shaped cells widely spaced within prominent fibromyxoid stroma with prominent cystic change. No mitosis or necrosis was present. There were inconspicuous slim curvilinear capillaries and occasional collection of stromal lymphocytes and plasma cells. Immunohistochemically, the tumor cells were positive for vimentin, but negative for CD34, SMA, desmin, S-100 protein, ALK, CKpan, EMA, calretinin and TTF1. Fluorescence in situ hybridization did not show chromosomal translocation involving EWSR1, DDIT3 or FUS genes. The patient was recurrence or metastasis free after follow-up for 38 months. Conclusion Pulmonary microcystic fibromyxoma is a rare benign lesion that should be differentiated from other lung tumors with myxoid characteristics.

Objective To study the clinicopathologic features , diagnosis and differential diagnosis of succinate dehydrogenase ( SDH ) deficient gastrointestinal stromal tumors ( GISTs ) as a unique tumor subtype.Methods SDHB and SDHA immunohistochemistry was performed in 120 gastric GISTs, in addition to CD117, DOG-1, CD34, smooth muscle actin (SMA), desmin,S-100 protein, cytokeratin (CK) and Ki-67.Subset of the cases was further evaluated for the presence of mutations in CKIT exons 9, 11, 13 and 17 mutations and platelet derived growth factor receptor alpha ( PDGFRA) exons 12 and 18.Results Eight of 120 (6.6%) GIST cases were found SDH-deficient including 3 male and 5 female patients (median age of 36.2 years;ranging 16 to 65 years of age).The tumors involved antrum (6 cases), lesser curvature (1 case) and fundus (1 case).Macroscopically, the dominant tumor masses varied from 3 to 10 cm in diameter with a multinodular or plexiform pattern involving the gastric wall .Microscopically ,tumor cells had predominantly epithelioid morphology , with occasional mixed spindle cell nodules .Lymphovascular invasion was identified in 5 cases.Immunohistochemistry for SDHB was negative in all 8 cases, and SDHA was negative in 5 cases.All 8 SDHB negative cases also expressed CD 117, DOG-1 and CD34, but were negative for SMA, desmin, S-100 and CK.All 8 cases were found to have wild-type CKIT and PDGFRA genes. Available clinical follow-up were obtained in 7 cases, ranging from 2 to 60 months ( median follow-up 23.3 months) , and all patient were alive .Three cases were found to have liver metastases at their first diagnosis , and one developed omental and mesenteric metastases in 17 months.Conclusions SDH-deficient GIST is a distinct subtype of GIST , with a predilection to occur in young and female patients .Characteristic pathological findings include multinodular gastric wall involvement , epithelioid cell morphology , frequently lymphovascular invasion with occasional lymph node and liver metastases , but an overall indolent clinical behavior.Immunohistochemistry for SDHB is required for the diagnosis .