OBJECTIVETo study the effect of rutin on body weight and obesity-induced reproductive impairment in male mice.

METHODSTwenty-four male mice were randomized equally into normal control group, high-fat diet group (HFD group), and HFD + rutin intervention group (HRU group). After 28 days of treatments, the testes and epididymis of the mice were collected for detection of total cholesterol (TC) and triglycerides (TG) levels and for pathological examinations with HE staining. The expressions of related genes was detected with real-time PCR, and Western blotting was used to detect the expression of Ucp1 protein in the samples.

RESULTSAfter 28 days of treatments, the mean body weight was lower in mice with rutin intervention than in those in HFD group. The mice in HFD group showed significantly higher TG levels in the testis and epididymis and higher TC levels in the epididymis than those in the control and HRU groups. In HFD group, the testis and the epididymis displayed loosened structures with abnormalcell structure, and the number ofmature spermatozoa in the lumen was decreased and the mobility of the sperms was reduced; all these changes were significantly alleviated in HRU group. The expression levels of Ucp1 mRNA and protein increased (P<0.05) and the expressions of Mcp1 and TNF-α decreased significantly in the mice after rutin treatment (P<0.05).

CONCLUSIONRutin can effectively inhibit rapid increase of body weight and protect against obesity-induced reproductive impairment in obese mice.

Purpose To investigate the clinicopathologic characteristics, diagnosis, differential diagnosis and prognosis of malignant solitary fibrous tumor/hemangiopericytoma ( SFT/HPC). Methods Sixteen cases of intracranial malignant SFT/HPC were retrospectively studied. The clinical data, imaging features, histopathological and immunohistochemical characteris-tics were analyzed. Results The 8 male and 8 female patients were between 31 and 71 years of age ( mean 51). The median age was 51 years (range, 31-71 years). 16 malignant SFT/HPC cases were originated from intracalvarium. The imaging features showed intracranial neoplasms with relatively clear surrounding boundaries. Microscopically spindle shaped cells were hypercel-lular, and exhibited≥5 mitoses per 10 HPF. Cytological atypia was mild. The clinicopathologic characteristics included pattern-less growth pattern, storiform or fascicular growth pattern, solita-ry fibrous tumor-like regions and hemangiopericytoma-like re-gions. Tnere were 2 cases with abundant papillary structure and 2 with sarcomatous structure, 2 with focal necrosis, 2 with inva-ded cerebral tissues, and 10 with invaded meninges. Immuno-histochemically, 93. 75% ( 15/16 ) cases were positive for STAT6, with 15/16 showing diffuse staining. 87. 5% (14/16) cases were positive for CD34, with 37. 5% (6/16) showing dif-fuse staining. 81. 25% (13/16) cases were positive for BCL-2. 68. 75% (11/16) cases were positive for CD99. The Ki-67 in-dex ranged from 5% to 40% . Sixteen patients were followed up for 1-64 months, and 7 patients ( 43. 75% ) had recurrences. Conclusion Malignant SFT/HPC shares malignant behaviours. STAT6 is a specific marker for the diagnosis of this tumor. The prognosis of malignant SFT/HPC is related to the extent of tumor excision and long-term follow-up.

OBJECTIVETo detect 22q11 microdeletion in the children and fetuses affected by congenital heart defects.

METHODMLPA P250 kit was used to detect 22q11 microdeletion in 100 cases of sporadic congenital heart defects including 40 fetuses and 60 patients diagnosed by ultrasound.

RESULTTwo cases from the fetuses and 1 case from the patients were found to have 22q11 microdeletion.

CONCLUSIONThree cases had 22q11 microdeletion in the congenital heart defects.

Child ; Child, Preschool ; Chromosome Deletion ; Chromosomes, Human, Pair 22 ; Female ; Heart Defects, Congenital ; diagnosis ; genetics ; Humans ; Infant ; Male ; Nucleic Acid Amplification Techniques ; methods

OBJECTIVETo explore the preliminary clinical evaluation of hepatectomy with total hemi-hepatic vascular exclusion.

METHODSTwenty-eight patients with primary liver cancer were divided into two groups of hepatectomy with total hemi-hepatic vascular exclusion (group A) and total hepatic inflow occlusion (group B). The time of hepatic vascular control, intraoperative blood loss, volume of removed liver, postoperative liver function recovery and complications were compared between the two groups.

RESULTSThe intraoperative blood loss in group A was (296 +/- 240) ml, which was less significantly than that in group B [(582 +/- 497) ml] (P<0.05). The serum pre-albumin levels on the day 1, 3 and 7 after operation in group A were (164 +/- 39) mg/L, (111 +/- 17) mg/L and (104 +/- 23) mg/L, which were higher significantly than that in group B [(134 +/- 34) mg/L, (90 +/- 22) mg/L and (82 +/- 35) mg/L] (P<0.05). While the time of hepatic vascular control and volume of lost liver were no difference between the groups (P>0.05). There were no significant difference in other items between the groups.

CONCLUSIONSIntraoperative blood loss and liver damage of hepatectomy under the total hemi-hepatic vascular exclusion could be less than that under the other methods of vascular occlusion. It could be worth improving and applying further.

Adult ; Aged ; Blood Loss, Surgical ; prevention & control ; Carcinoma, Hepatocellular ; surgery ; Female ; Hepatectomy ; adverse effects ; methods ; Humans ; Liver ; blood supply ; surgery ; Liver Neoplasms ; surgery ; Male ; Middle Aged ; Regional Blood Flow ; Retrospective Studies

OBJECTIVE: To determine the diagnostic value and efficacy for risk stratification of myeloperoxidase (MPO) levels in patients with acute coronary syndrome (ACS). METHODS: One hundred and sixty-two patients were enrolled in this study. All patients underwent coronary angiography. They were divided into 3 groups: ACS group (n=54), SAP group (n=54) and control group (n=54). Blood samples were taken from the artery before angiography in all patients and the concentrations of MPO, hsCRP and cTnI were measured. Each subject was asked details of history of hypertension, hyperlipidemia, diabetes and smoking habits. The efficacy of therapy, the cardiovascular events (myocardial infarction, the need for revascularization, or death) were recorded after 6 months of follow-up. RESULTS: The plasma MPO level in ACS group (30.98 ng/mL) was significantly higher than those in the SAP group (14.67 ng/mL) and the control group(14.23 ng/mL)(P<0.01), and the plasma MPO levels in patients of the SAP group and the control group were not significantly different (P=0.74). There was no obvious correlation between the levels of plasma MPO and the serum levels of cTnI, hsCRP,the prevalence of the 4 major risk factors for CHD. Multivariate logistic regression analysis showed that plasma MPO level, free plasma glucose and sex were the significant variables. The risk for subsequent cardiovascular events was higher in the patients with elevated level of MPO. CONCLUSION Plasma MPO may be a new risk biomarker for ACS and may predict the incidence of subsequent cardiovascular events.
Acute Coronary Syndrome ; blood ; enzymology ; Aged ; Biomarkers ; blood ; Case-Control Studies ; Female ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Peroxidase ; blood

Aldosterone-producing adrenocortical carcinoma (ACC) is a rare endocrine malignancy. Only a few cases are reported in China. This systematic review investigated the diagnosis and treatment strategy of aldosterone-producing ACC through a recent case of the disease. A case of a 49-year-old female who diagnosed with aldosterone-producing ACC by hormonal assays, medical imaging and pathology. Her condition has been alleviated after surgery. Aldosterone-producing ACC is a rare malignancy with limited treatment options and surgery is the primary treatment strategy.

OBJECTIVETo investigate the clinical and pathological features, diagnosis and treatment of Castleman disease (CD).

METHODSClinical features and related information on diagnosis and treatment of eight cases of CD were retrospectively analyzed. The size of involved lymph nodes ranged from (2 cm x 2 cm x 3 cm) - (4 cm x 3 cm x 2 cm). The lymph nodes were found in level I (1 case), level II (3 cases), level III (3 cases) and level IV (1 case). CT examination in eight patients showed the lesions manifested as ellipse soft masses. Dynamic contrast CT scan in four patients showed ring-enhanced area around the masses. Blood routine examination in eight patients were generally normal, with six patients had mild anemia.

RESULTSBased on the clinical classification, all lesions in this group were localized CD. Histopathology indicated that all lesions were of hyaline-vascular type. After surgery, there was no recurrence during the follow-up period.

CONCLUSIONSPatients with localized CD mainly have lymphadenectasis in a single location. The CT scan can give some evidence. Surgery should be given first priority.

Adolescent ; Adult ; Aged ; Castleman Disease ; diagnosis ; pathology ; Female ; Humans ; Lymph Nodes ; pathology ; Male ; Middle Aged ; Neck ; pathology ; Retrospective Studies ; Young Adult

ObjectiveTo investigate the diagnosis and treatment of familial hypokalemic periodic paralysis with acidosis. MethodsThe proband's medical history， clinical manifestations， laboratory examinations and imaging characteristics were retrospectively analyzed， and prevalence situation of family members was investigated in detail. Next generation sequencing technology was used to detect the pathogenic gene loci related to periodic paralysis， and the relevant literatures were summarized. ResultsThe proband was definitely diagnosed as familial hypokalemic periodic paralysis. There was a heterozygous mutation in the SCN4A gene of the proband， which was c.2006G>A， resulting in amino acid changes R669H.The proband's grandfather， father and uncle shared the same variation. ConclusionsFamilial hypokalemic periodic paralysis with paroxysmal acidosis is rare， which is easily misdiagnosed as renal tubular acidosis. c 2006G>A mutation in SCN4A gene is the molecular basis of the disease in this family. The clinical phenotypes of different gene mutations are different， and gene screening is helpful for diagnosis and treatment.