[Clinical and imaging characteristics of patients with different types of infectious sacroiliitis].

To investigate the clinical manifestations and imaging characteristics of patients with different types of infectious sacroiliitis. Clinical data of 40 patients diagnosed with infectious sacroiliitis were retrospectively analyzed. Among the 40 patients, 16 patients were diagnosed as non-brucellar and non-tuberculous infectious sacroiliitis (ISI), 13 with tuberculous infectious sacroiliitis (TSI), and 11 with brucellar sacroiliitis (BSI). In the ISI and TSI group, female patients accounted for 11/16, 12/13, while the proportion of unilateral involvement was 15/16 and 12/13, respectively. Compared with ISI and TSI group, BSI patients were mainly male (8/11) and presented more bilateral involvement (6/11) (P<0.05). Bone erosion was more common in ISI and TSI groups than in BSI group (6/15, 7/11 and 2/10), as well as abscess formation (3/15, 4/11 and 1/10, respectively). Symptoms in all patients relieved 1-2 weeks after administration of antibiotics or anti-tuberculosis treatment, but the resolution of the magnetic resonance imaging findings delayed about 6 (3-9) months. ISI and TSI patients with infectious sacroiliitis should be differentiated from spondyloarthritis, with a characteristic of more female patients, unilateral sacroiliitis, bone erosion, soft tissue involvement and abscess formation. However, BSI patients are mainly male, more bilateral involvement and less bone destruction and abscess formation. Antibiotic therapy demonstrates significant therapeutic effects, but resolution of the magnetic resonance imaging findings responses late.

Opa interacting protein 5 promotes metastasis of nasopharyngeal carcinoma cells by promoting EMT via modulation of JAK2/STAT3 signal.

OBJECTIVE: Opa interacting protein 5 (OIP5), as a tumor promoter gene, has emerged as a regulator in several types of tumors. However, the role of OIP5 in nasopharyngeal carcinoma (NPC) has not been reported. In this study, we aimed to explore the expression and biological function of OIP5 in NPC. PATIENTS AND METHODS: The lung cancer datasets GSE12452 and GSE53819 were downloaded from the Gene Expression Omnibus (GEO) repository. Real-time-Polymerase Chain Reaction (RT-PCR) was performed to detect the expression levels of OIP5 mRNA. Cell Counting Kit-8 (CCK-8), colony-formation assay, wound healing assay and transwell assay were conducted to measure cells' proliferation, migration and invasion. Flow cytometry was used for analysis of apoptosis. Western blot assays were used to assess the effects of OIP5 on EMT and JAK2/STAT3 pathway. RESULTS: The up-regulation of OIP5 mRNA was observed in NPC tissues from both GSE12452 and GSE53819. The results of RT-PCR also showed that the expression of OIP5 mRNA was significantly up-regulated in several NPC cell lines compared to normal nasopharyngeal cells. Furthermore, lost-function assay revealed that the knockdown of OIP5 markedly suppressed NPC cells proliferation, migration and invasion, and promoted cell apoptosis. In addition, the results of Western blot showed that silencing of OIP5 suppressed the EMT in NPC cell line. Meanwhile, the knockdown of OIP5 remarkably decreased the expression of p-JAK2 and p-STAT3 protein in both CNE1 and SUNE1 cells. CONCLUSIONS: Our data indicated that OIP5 was highly expressed in NPC and promoted NPC progression by modulating JAK2/STAT3; our results shed light on utilizing OIP5 as a potential novel therapeutic target for the treatment of NPC.

MircoRNA-629 promotes proliferation, invasion and migration of nasopharyngeal carcinoma through targeting PDCD4.

OBJECTIVE: MicroRNAs (miRNA) have been demonstrated to be involved in the development and progression of several tumors, including nasopharyngeal carcinoma (NPC). However, the expression and function of miR-629 in NPC have not been elucidated before. Here, we explored the role of miR-629 in NPC cells and investigated the possible underlying mechanism. MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was first utilized to detect the expression of miR-629 in NPC tissues and adjacent normal samples, as well as NPC cell lines and normal nasopharyngeal cell line NP69. MiR-629 mimics and inhibitor was transfected in NPC cells to up-regulate or down-regulate the expression of miR-629. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry were used to explore the effects of miR-629 on the proliferation and cell circle of established NPC cells, respectively. Cell invasion and migration abilities were evaluated by transwell Matrigel assay and wound healing assay. Meanwhile, the underlying mechanism of miR-629 in NPC was detected using bioinformatics prediction and dual-luciferase analysis. In addition, Western blotting was employed to identify the expression of the miR-629 targeted protein. RESULTS: MiR-629 expression in NPC tissues was significantly higher than that of adjacent normal samples. Expression of miR-629 in NPC cells was significantly higher than that NP69 cells. Over-expressing miR-629 remarkably promoted 6-10B cell proliferation, while knocking down miR-629 significantly inhibited 5-8F cell growth compared with negative control group. Cell migration and invasion abilities were remarkably increased by miR-629 mimics transfection. However, the miR-629 inhibitor transfection in cells significantly decreased cell migration and invasion. Furthermore, dual-luciferase analysis verified that PDCD4 was a direct target gene of miR-629 in NPC cells. Knockdown of PDCD4 in cells over-expressing miR-629 restored cell proliferation and metastasis. CONCLUSIONS: In this study, the expression level of miR-629 was significantly increased in 83 NPC tissues and 4 cell lines. MiR-629 promoted NPC cell growth, migration, and invasion via repressing PDCD4 expression, which might provide a novel target for the future biotherapy for NPC.

[An analysis of the characteristics of perioperative cardiac troponin elevation in orthopaedic surgical patients].

Objective: Perioperative myocardial infarction remains a severe complication in non-cardiac surgery and is one of the major causes of death. Cardiac troponin (cTn) I elevation is associated with short-term and long-term mortality. The aim of the study was to assess the proportion rate of cTnI elevation and its clinical characteristics among patients admitted for orthopaedic surgery with or without cardiovascular events. Methods: This is a retrospective study including 27 744 patients aged 50 years or older who admitted for orthopaedic surgery from 2009-2015 in Beijing Jishuitan Hospital. Results: Two hundred and sixty-five patients [age (71.7±9.9) years] had cTnI level> 0.04 µg/L with 66% (175 patients) of them being female. Among them, 59 patients were isolated troponin rise (ITR) (n=59), 13 were preoperative acute myocardial infarction (AMI), and 193 were postoperative AMI. The proportion of postoperative AMI was 0.69%. Those patients were more likely to have a history of coronary artery disease or hypertension. Non-ST-segment elevation myocardial infarction (NSTEMI) was more common (93.3%) than ST-segment elevation myocardial infarction in these patients. Most of them did not experience ischemic symptoms. Totally 76.7% of the AMI occurred within 3 days of surgery; and the in-hospital mortality rate was 10.4%. Conclusions: Perioperative elevation of troponin is common in patients undergoing orthopaedic surgery. Most postoperative AMI were NSTEMI and with absent or atypical ischemia symptoms. Monitoring troponin levels and electrocardiograph in at-risk patients is needed to find most of the AMI.

[Effects of modified three-step procedure for anatrophic nephrolithotomy in the treatment of complex staghorn renal calculi].

Objective: To investigate the effects of modified three-step procedure for anatrophic nephrolithotomy in the treatment of complex staghorn renal calculi. Methods: A total of 22 patients with complex staghorn renal calculi between June 2013 and June 2016 at Department of Urology in Guangzhou General Hospital of Guangzhou Military Command were retrospective analyzed. There were 13 males and 9 females, ranging from 35 to 62 years old with mean age of 47 years. There were 17 patients with dull pain, and 5 patients who were found through physical examinations. Kidney calculi located in left kidney in 15 patients, right kidney in 7 patients. All patients were treated with modified three-step procedure for anatrophic nephrolithotomy. The operation time, blood loss, time of intraoperative renal ischemia, and postoperative complications were recorded. Serum creatinine (Scr), blood urea nitrogen(BUN), ß(2)-microglobulin(ß(2)-MG), diseased side glomerular filtration rate(GFR) , and renal cortical thickness of the diseased kidney in preoperative and postoperative were compared. The clinical data were compared by paired sample t test between pre-operation and post-operation. Results: The calculi were completely removed in 22 patients, the mean operation time was 84 minutes (50 to 126 minutes), the mean time of intraoperative renal ischemia was 31 minutes (20 to 56 minutes), the mean blood loss was 246 ml (150 to 360 ml). There were no secondary bleeding or urinary fistula happened, the perinephric drainage tub was removed in 3 to 7 days postoperative, the mean hospitalization time was 7 days.Compared with the preoperative, the Scr ((172.7±21.3)µmol/L vs. (146.4±22.8)µmol/L, t=7.197, P=0.000), BUN ((9.2±1.8)mmol/L vs. (8.0±0.5)mmol/L, t=3.798, P=0.001) and ß(2)-MG ((203.0±32.0)µg/L vs. (175.6±23.8)µg/L, t=5.009, P=0.000) in postoperative decreased, the diseased side GFR increased ((28.6±4.0) ml/min(31.8±3.3) ml/min, t=-3.521, P=0.002). There were no significant difference of diseased renal cortical thickness between preoperative and postoperative(t=-1.323, P=0.200). There were 12 patients with postoperative pain, 2 patients with vomiting, 3 patients with fever, and 2 patients with wound infection. The follow-up time was 6 months, no residual stones in 22 patients. Conclusion: The modified three-step procedure for anatrophic nephrolithotomy has high stone free rates with less effects on renal function and fewer complications, the method could be widely applied.

[A clinical study of single subcortical cerebral infarction of middle cerebral artery territory].

Objective: To explore the clinical characteristics of single subcortical cerebral infarction of middle cerebral artery (MCA) territory and the possible pathogenesis. Methods: A total of 344 cases diagnosed as single subcortical cerebral infarction of MCA territory were enrolled in the study and divided into the parent artery disease (PAD) group and the non-PAD group according to whether the MCA stenosis was presented or not. A total of 312 cases diagnosed as single subcortical cerebral infarction of MCA territory were divided into the BAD group and the SVD group according to the relationship between the lesion sites and MCA. Differences in the clinical and imaging feature were compared between different groups. Results: A total of 32 patients were in the PAD group. Compared with the non-PAD group, patients in the PAD group were found with higher prevalence of asymptomatic cerebral arterial atherosclerosis [93.8%(30/32) vs 57.1%(178/312), P<0.001], higher prevalence of branch atheromatous disease[75.0%(24/32) vs 58.7%(183/312), P=0.072]. A total of 183 patients were in the BAD group. Compared with the BAD group, patients in the SVD group were older[(64.7±11.2) years vs (61.7±12.2) years, P=0.031], more with hypertension [65.9%(85/129) vs 53.0%(97/183), P=0.027] and smoking [41.9%(54/129) vs 57.9%(106/183), P=0.006] and more severe leukoaraiosis. Conclusions: Single subcortical cerebral infarction of MCA territory has different etiology and pathogenesis. Evidence of systemic atherosclerosis should be carefully searched in patients with branch atheromatous disease.

Effects of different antihypertensive drugs on blood pressure variability in patients with ischemic stroke.

OBJECTIVE: Blood pressure variation is one of the factors that affects the risk of stroke recurrence and prognosis. This study investigates the effects of calcium channel blockers and beta-blockers on blood pressure variability in severe ischemic stroke patients. PATIENTS AND METHODS: The clinical data of 24 patients with ischemic stroke in our intensive care unit were analyzed, and received amlodipine or metoprolol for more than 14 days with 24-hour ambulatory blood pressure monitoring. All patients aged 61-90 years, with GCS score ≤ 8 or associated with other organ dysfunction. RESULTS: Among these 24 ischemic stroke patients, 12 received amlodipine and 12 received metoprolol. The observation period was divided into two phases: 1-6 days and 7-14 days. The decrease in blood pressure was faster in the metoprolol group than in the amlodipine group, while the average standard deviation was significantly greater and the smoothness index was less. CONCLUSIONS: Metoprolol has faster onset than amlodipine and less blood pressure variability than metoprolol.

Glycogen synthase kinase-3 reduces acetylcholine level in striatum via disturbing cellular distribution of choline acetyltransferase in cholinergic interneurons in rats.

Cholinergic interneurons, which provide the main source of acetylcholine (ACh) in the striatum, control the striatal local circuits and deeply involve in the pathogenesis of neurodegenerative diseases. Glycogen synthase kinase-3 (GSK-3) is a crucial kinase with diverse fundamental functions and accepted that deregulation of GSK-3 activity also plays important roles in diverse neurodegenerative diseases. However, up to now, there is no direct proof indicating whether GSK-3 activation is responsible for cholinergic dysfunction. In the present study, with combined intracerebroventricular injection of Wortmannin and GF-109203X, we activated GSK-3 and demonstrated the increased phosphorylation level of microtubule-associated protein tau and neurofilaments (NFs) in the rat striatum. The activated GSK-3 consequently decreased ACh level in the striatum as a result of the reduction of choline acetyltransferase (ChAT) activity. The alteration of ChAT activity was due to impaired ChAT distribution rather than its expression. Furthermore, we proved that cellular ChAT distribution was dependent on low phosphorylation level of NFs. Nevertheless, the cholinergic dysfunction in the striatum failed to induce significant neuronal number reduction. In summary, our data demonstrates the link between GSK-3 activation and cholinergic dysfunction in the striatum and provided beneficial evidence for the pathogenesis study of relevant neurodegenerative diseases.

TNIP1, SLC15A4, ETS1, RasGRP3 and IKZF1 are associated with clinical features of systemic lupus erythematosus in a Chinese Han population.

Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous clinical manifestations influenced by genetic and environmental factors. Five novel susceptibility genes (TNIP1, SLC15A4, ETS1, RasGRP3 and IKZF1) for SLE have been identified in a recent genome-wide association study of a Chinese Han population. This study investigated their relationships with disease subphenotypes, including renal nephritis, photosensitivity, antinuclear antibody (ANA), age at diagnosis, malar rash, discoid rash, immunological disorder, oral ulcer, hematological disorder, neurological disorder, serositis, arthritis and vasculitis. Significant associations were found for the single nucleotide polymorphism rs10036748 of TNIP1 with photosensitivity (odds ratio (OR) = 0.87, p = 0.01) and vasculitis (OR = 1.18, p = 0.04); rs10847697 of SLC15A4 with discoid rash (OR = 1.18, p = 0.02); rs6590330 of ETS1 with SLE of age at diagnosis <20 years (OR = 1.24, p = 8.91 x 10(-5)); rs13385731 of RasGRP3 with malar rash (OR = 1.20, p = 0.01), discoid rash (OR = 0.78, p = 0.02) and ANA (OR = 0.72, p = 0.004); rs4917014 of IKZF1 with renal nephritis (OR = 1.13, p = 0.02) and malar rash (OR = 0.83, p = 0.00038), respectively. The study suggested that these susceptibility genes might not only play important roles in the development of SLE, but also contribute to the complex phenotypes of SLE.

Reliability of the Sunnybrook Facial Grading System by novice users.

OBJECTIVES: To evaluate the intrarater and inter-rater reliability of the Sunnybrook Facial Grading System (SFGS) by novice users. DESIGN: Prospective interval study using one measurement instrument. SETTING: Tertiary teaching hospital (Sunnybrook & Women's College Health Science Centre). METHODS: Twenty-two patients with a wide spectrum of facial dysfunction recorded on videotapes were rated using the SFGS by eight novice observers independently in two different sittings separated by 3 weeks. The order of patients was randomized for the second sitting. Intraclass correlation coefficients were calculated for component scores and for total scores within and between raters. RESULTS: The intrarater reliability coefficients for the eight raters ranged from .838 to .929. This largely overlaps with the data obtained in previous studies with expert raters. The inter-rater reliability for all eight raters at time 1 was .982 and for time 2 was .970. This is higher than what was previously obtained with expert raters. CONCLUSION: The SFGS is as reliable when applied by novice users as by expert users.

KAI1/CD82 gene expression in benign prostatic hyperplasia and late-stage prostate cancer in Chinese.

AIM: To evaluate KAI1/CD82 expression in Chinese patients with benign prostatic hyperplasia (BPH) and late-stage carcinoma of prostate (CaP). METHODS: Thirty Chinese patients with benign prostatic hyperplasia and 34 with CaP (adenocarcinoma clinical stage C and D) were analyzed by means of immunohistochemical methods. RESULTS: The KAI1/CD82 expression in BPH tissue was all positive, which was uniformly located on the glandular cell membrane at the cell-to-cell borders, but KAI1/CD82 expression in metastasis CaP tissues was either significantly lower than that of BPH or negative, and the immunostaining pattern was not continuous. In late-stage CaP KAI1/CD82 expression was correlated inversely to the pathological grade ( P < 0.05), but not to clinical stage ( P > 0.05). CONCLUSION: The authors believe that decreased and negative KAI1/CD82 expression in late-stage CaP may be related to tumor progression and metastasis, and appears to be a prognostic marker.

Pediatric intracranial germinoma treated with chemotherapy alone.

BACKGROUND: Pediatric intracranial germinoma treated with radiotherapy is considered a standard treatment, but may cause significant delayed damage to the central nervous system. Chemotherapy has been shown to be effective for the treatment of an intracranial germinoma. In the past 10 years, we treated 11 cases of primary intracranial germinoma with chemotherapy alone. The purpose of this retrospective study is to review the clinical outcome of these patients. METHODS: Eleven children with newly diagnosed, previously untreated primary intracranial germinomas were treated with six courses of chemotherapy (vinblastine bleomycin, cisplatin and etoposide, VBPE). The response to chemotherapy, relapses and outcomes are reviewed and evaluated. RESULTS: All 11 assessable children achieved a complete response and are alive, with a median follow-up of 61 months. Five patients with tumors located in the midline position of the brain, including pineal, sellar, suprasellar and hypothalamic areas, had no relapse. Six patients had relapses, and all of them achieved a second complete remission after salvage focal radiotherapy. The time of onset of relapse was from nine to 24 months after chemotherapy, with an average of 16.8 months. CONCLUSIONS: VBPE chemotherapy was effective for treating newly diagnosed intracranial germinomas. Although a high rate of relapse (6/11) was observed, all of these patients survived with first or second complete remissions. It was beneficial for five children that focal radiation was eliminated and delayed post-irradiation neurologic sequelae were avoided.

Neonatal myocardial infarction: a case report.

Neonatal myocardial infarction is a rare disorder. It occurs in association with congenital heart disease or coronary artery abnormalities. In the absence of structural heart disease, perinatal asphyxia and coronary artery thromboembolism have been reported as common etiologies. Whether the Coxsackie B viral group has a causal role in adult myocardial infarction remains controversial. We report herein a case of neonatal myocardial infarction without known congenital heart disease, in whom perinatal Coxsackie B viral infection was suspected to be the underlying cause. However, definite evidence indicating a causal relationship between neonatal myocardial infarction and Coxsackie B viral infection was lacking in this case.

Interaction of transferrin with rat alveolar macrophages.

Binding of rat transferrin to isolated alveolar macrophages was investigated in the 0.125 nM to 2 microM range. Computer analysis of the data revealed two classes of binding sites, a small number (< 1000 exposed/cell) having high affinity (dissociation constant (Kd), 3.4 nM) and a large number (approximately 4 x 10(6)/cell) having low affinity (Kd 48 microM). Measurements with a monoclonal antibody to the rat transferrin (rTf) receptor yielded values in the same range as the high-affinity sites derived from studies of ligand binding. Binding to the low-affinity sites at pH 5.8 was nearly one order of magnitude stronger than that at pH 7.3. Bovine lactoferrin (12 microM), cationized bovine serum albumin (14 microM), L-arginine (50 mM), and L-lysine (50 mM) did not compete against rTf binding to the low-affinity sites. Removal of an average of 2.6 x 10(8) sialyl residues from each cell did not affect binding. Heparan sulphate proteoglycan purified from alveolar macrophages bound strongly to immobilized rTf, thus raising the possibility that the low-affinity interaction of transferrin with these cells may be mediated, at least in part, by this glycosaminoglycan.

Effect of transferrin on the degradation of glycoproteins bearing a hybrid or high-mannose glycan by alveolar macrophages.

A subfraction of hen ovalbumin and a special form of rat transferrin, possessing a hybrid glycan, were studied with respect to their binding to, and degradation by macrophages isolated from the rat lung. Both ligands were found to be degraded partly through the mannose receptor pathway and partly by another mechanism, presumably adsorptive pinocytosis. Catabolism of both proteins was markedly increased by adding standard (i.e., normally glycosylated) transferrin from various species to the medium. This increase was not diminished, or even augmented, when Ca2+ was depleted in the medium, thus implying involvement of the pinocytic pathway rather than the mannose receptor. Binding to the cell surface of both ligands was altered in the presence of transferrin. A hypothesis is advanced to suggest that when transferrin is bound to a component of macrophage plasmalemma, thought to be the glycosaminoglycan of heparan sulfate, its conformation may change in such a way that it attracts other proteins. Protein molecules temporarily captured by adsorbed transferrin would then be taken up by a "piggyback" process and degraded.

Observations with a residualizing label in use to map the catabolic sites of plasma proteins.

Rat albumin, immunoglobulin G, transferrin, and aglycotransferrin were prepared for the comparison of their sites of degradation in rats. Iodotyramine-cellobiose was used as the residualizing label and a tyrosine-iodinated portion of the corresponding protein was used as the marker of extracellular undegraded protein. Each protein yielded a distinct distribution (or map) of catabolic activity throughout the body when expressed as percent dose accumulated per gram of tissue. The maps for albumin and transferrin were broadly comparable, whereas those for immunoglobulin G and aglycotransferrin were markedly different. As a whole entity, the liver appeared to top the list of organs/tissues contributing to the degradation of albumin and transferrin. Additional experiments aimed at facilitating the interpretation of results with residualizing labels were carried out with denatured albumin, asialofetuin, and human asialotransferrin type 3. These showed that various types of cells retained the label for markedly different periods of time. We feel, therefore, that the technique is more suited for making comparative measurements than for obtaining degradation rates as absolute values in a given anatomical location.

Transport of lactoferrin from blood to bile in the rat.

The bile contains small quantities of lactoferrin, the origin of which is uncertain. For this reason, we studied the liver's capability of transferring lactoferrin from the plasma to the bile by injecting a dose (10 to 20 micrograms/100 gm) of labeled bovine lactoferrin intravenously and following its appearance in bile over 3 hr. Whether diferric or iron free, lactoferrin peaked in the bile 35 min after administration (i.e., the same time as bovine lactoperoxidase and diferric rat transferrin). However, only a small portion of the lactoferrin dose (approximately 1%) was recovered with the bile in 3 hr. On the basis of autoradiographic evidence, the excreted lactoferrin appeared intact. The biliary excretion profile of albumin, a protein thought to reach the canaliculus by paracellular diffusion, was notably devoid of a peak. This, together with competition observed between lactoferrin and lactoperoxidase on one hand and 2Fe-transferrin and lactoferrin on the other for transfer to bile, suggests that lactoferrin is routed through the hepatocyte in vesicles. The process is initiated by binding to a plasma membrane component to which lactoperoxidase and 2Fe-transferrin can also bind. Most 59Fe bound to lactoferrin accompanied the protein carrier to the bile. We conclude that under normal circumstances (i.e., when concentration of lactoferrin in the plasma is very low), lactoferrin transferred from plasma by the liver is probably not the major source of this protein in bile.

Interaction of transferrin and its iron-binding fragments with heparin.

The interaction of heparin with transferrin (Tf; bovine and rat) and the isolated iron-binding lobes of bovine Tf were investigated. Affinity chromatography of rat Tf on heparin-agarose showed that interaction depended on both the iron content of Tf and the pH of the medium. Both the iron-free and iron-saturated forms of Tf were strongly bound by the column at pH 5.6, but only the iron-free form revealed significant affinity at pH 7.4. Desialylation of Tf moderately promoted interaction, treatment with cyclohexanedione moderately reduced interaction, and succinylation abolished it altogether. In the presence of heparin, iron release from the N-terminal lobe of native bovine Tf was accelerated and from the C-terminal lobe it was slightly reduced. The heparin effect remained qualitatively the same on each lobe after their separation by tryptic digestion and DEAE-cellulose chromatography. The affinity of native bovine Tf for heparin was very close to that of its isolated N-terminal lobe, thus suggesting that it is this portion of the molecule that binds to the glycosaminoglycan. It is concluded that the consequences for iron-binding strength of the two transferrin lobes are diagonally opposite when Tf is bound to heparin as opposed to its natural cell-surface receptor.