Serotonin content of normal and inflamed appendix: a possible role of serotonin in acute appendicitisVASEI, MOHAMMAD; ZAKERI, ZEINAB; AZARPIRA, NEGAR; HOSSEINI, SEYED VAHID; SOLAYMANI‐DODARAN, MASOUD
doi: 10.1111/j.1600-0463.2008.00916.xpmid: 19132991
The appendix is lined by a mucosa which has many neuroendocrine cells containing serotonin. Local release of serotonin can act as a mediator of inflammation. In this study we explored the serotonin content of the neuroendocrine cells of the appendixes removed for clinical diagnosis of appendicitis. Appendix specimens were divided into three groups: Acute appendicitis (AA), non‐appendicitis (NA), and follicular hyperplasia (FH). Normal appendix specimens from patients undergoing elective abdominal surgery were used as the control group (NL). All sections were exposed to proteinase K, incubated with anti‐serotonin, chromogranin A, and synaptophysin antibodies, and treated with the LSAB kit. Polygonal cells were seen within the crypt epithelium (enterochromaffin cell, EC) and within the lamina propria (subepithelial neuroendocrine cell, SNC). In AA, only 16 cases (64%) showed serotonin staining in non‐destructed glands. There was a significant reduction in the number of ECs in AA compared to the FH (96%), NA (100%) and NL (100%) groups (P<0.001). Chromogranin and synaptophysin immunostaining also showed a significant reduction in the number of ECs in AA compared with the other three groups (P<0.001). SNC serotonin reactivity was lower in the AA group compared with the other groups (p<0.001). The inflamed appendix is markedly depleted of serotonin in the epithelium and lamina propria. Local serotonin release from ECs and SNCs in the appendix may act as an inflammatory mediator in appendicitis and is likely to be the source of raised blood serotonin in AA.
Staphylococcus aureus as source of catheter‐related bloodstream infection evaluated by PFGE and rep‐PCR typing in a Brazilian hospitalSADOYAMA, GERALDO; SANTOS, KÁTIA REGINA NETTO DOS; BRILHANTE, ANIKE PEREIRA; FILHO, PAULO PINTO GONTIJO
doi: 10.1111/j.1600-0463.2008.01053.xpmid: 19132992
Staphylococci are a common cause of catheter‐related bloodstream infection (CR‐BSI), and epidemiological typing is an important tool for effective infection control. This study evaluated by PFGE and rep‐PCR whether Staphylococcus aureus strains isolated from skin and catheter tips were related to specimens isolated from blood. A prospective observational study, carried out in a clinical surgical ward at a Brazilian hospital between September 2000 and November 2002, investigated non‐tunneled central venous catheters from 179 patients. S. aureus isolates were mainly obtained from blood (41.4%), while coagulase‐negative staphylococci strains were more often isolated from the skin at the catheter insertion site (49.7%) and from the catheter tip (57.5%). Among the 21 strains isolated from 9 patients at 2 or 3 sites simultaneously, 9 were methicillin‐resistant S. aureus (MRSA) and 12 were methicillin‐susceptible S. aureus (MSSA). Seven patients harbored the same S. aureus strain isolated from the skin, blood and/or catheter tip cultures. MRSA isolates belonged to one PFGE pattern (type A‐ subtypes A1, A2 and A3), and to two rep‐PCR patterns (a and b). MSSA isolates were distinguished in five PFGE (B to F) and in three rep‐PCR (c, d and e) patterns. Both PFGE and rep‐PCR methods indicated that the skin at the catheter insertion site was the origin of CR‐BSI caused by S. aureus.
pS2 (TFF1) expression in prostate carcinoma: correlation with steroid receptor statusABDOU, ASMAA GABER; AIAD, HAYAM ABDEL SAMIE; SULTAN, SULTAN MOHAMED
doi: 10.1111/j.1600-0463.2008.01009.xpmid: 19132993
pS2 or TFF1 is a member of the trefoil factor family, which is distributed throughout the gastrointestinal tract in both normal and diseased tissues. It is also considered to be one of the major estrogen‐regulated proteins and an indicator of estrogen receptor (ER) functionality. pS2 has previously been investigated in benign and malignant prostate lesions with little information about its relationship to steroid receptor status. Our purpose was to correlate pS2 expression with steroid receptor status (ER alpha and progesterone receptor (PR)) and other pathologic variables in prostate carcinoma. 15 benign prostate hyperplasia (BPH) and 47 prostate carcinoma cases were investigated by means of immunohistochemistry for pS2, ER and PR expression. 80% of BPH showed pS2 cytoplasmic immunoreactivity in hyperplastic acini and about half of these cases also exhibited nuclear staining decorating basal or both basal and luminal nuclei. pS2 was highly expressed in prostate carcinoma (91.4%) with both cytoplasmic and nuclear patterns of staining. The latter pattern was significantly associated with carcinoma having a low Gleason score (p=0.02). pS2 lacked any significant correlation with steroid receptor status, stage or grade. Univariate survival analysis revealed a significant impact of stage (p=0.03) and nodal status (p<0.0001) on patient outcome. The diagnostic value of pS2 expression in prostate carcinoma validated 74.19% accuracy, 91.48% sensitivity and 78.18% positive predictive value. The high sensitivity of pS2 expression in prostate carcinoma could make it a suitable marker for diagnosis of prostate carcinoma, especially in metastatic cases of unknown origin. The absence of correlation and dissimilarity in immunolocalization between pS2 and ER alpha leads to the assumption that ER alpha could not be the regulatory protein for pS2 and may raise questions about the functionality of ER alpha in prostate. The nuclear pattern of pS2 immunoreactivity either in benign or malignant prostatic lesions is similar to the published data on ER beta distribution and could also identify a subset of carcinoma patients with a favorable prognosis.
Pathological findings in rats with experimental allergic encephalomyelitisDONG, MEI; LIU, RUICHUN; GUO, LI; LI, CHUNYAN; TAN, GUOJUN
doi: 10.1111/j.1600-0463.2008.00726.xpmid: 19132994
The aim of this study was to establish an animal model of experimental allergic encephalomyelitis (EAE) and examine the basic pathological changes, as well as expression and distribution of MMP‐2 and MMP‐9, in Wistar rats. Tissue sections were processed for HE staining, Weil myelin staining, and modified Bielschowsky staining. Expression and distribution of glial fibrillary acidic protein (GFAP), matrix metalloproteinase‐2 (MMP‐2) and matrix metalloproteinase‐9 (MMP‐9) were detected with immunohistochemistry. We divided the EAE into five types, depending on pathological characteristics and clinical manifestations: acute EAE, relapsing‐remitting EAE, progressive EAE, benign EAE, and asymptomatic EAE. Rats with acute EAE suffered from quick, severe attacks with widespread inflammatory cells and axonal loss. No demyelination or astrocytic hyperplasia was found around the lesions. Rats with relapsing‐remitting EAE broke down twice, with many perivascular cuffs and demyelinating plaques in lesions; hyperplastic and hypertrophic astrocytes characterized old lesions and axonal loss was evident. Rats suffering from progressive EAE exhibited continuous aggravation without improvement, accompanied by perivascular cuffs, demyelination, increased gliocytes and axonal damage. Rats with benign EAE recovered to a normal state with obviously decreased inflammatory cells and almost entirely unaffected myelin and axons. Rats with asymptomatic EAE also had various pathological changes that were not coincident with their clinical manifestations. Elevated expression of MMP‐2 and MMP‐9 was concordant in different types of EAE, but the extent differed in each type of EAE. MMP‐2 and MMP‐9 can be expressed in the form of vascular endothelial cells, meninges, or accumulated inflammatory cells. Multiple clinical courses of disease were demonstrated in Wistar rat EAE, with attributes similar to multiple sclerosis (MS) in clinical and pathological characteristics. Elevated expression of MMP‐2 and MMP‐9 may play a role in some aspects of pathological changes in EAE, for example, destroying the blood‐brain barrier, degrading the myelin sheath, and damaging axons.
Feeding of mice with Arabidopsis thaliana expressing the HIV‐1 subtype C p24 antigen gives rise to systemic immune responsesLINDH, INGRID; KALBINA, IRINA; THULIN, SARA; SCHERBAK, NIKOLAI; SÄVENSTRAND, HELENA; BRÅVE, ANDREAS; HINKULA, JORMA; STRID, ÅKE; ANDERSSON, SÖREN
doi: 10.1111/j.1600-0463.2008.00900.xpmid: 19132995
Development of transgenic edible plants, to be used as production, storage and delivery systems for recombinant vaccine antigens, is a promising strategy to obtain cost effective vaccines against infectious diseases, not least for use in developing countries. Therefore, we used Agrobacterium tumefaciens‐mediated gene transfer to introduce the p24 gag gene encoding the nucleocapsid protein from HIV‐1 subtype C into the Arabidopsis thaliana plant genome. Eighteen plant lines were confirmed positive for the p24 gene by PCR; four of these lines showed an apparent homozygous phenotype when grown on selective medium and these lines also showed transcription of the p24 gene into its corresponding mRNA. The mRNA in all four cases generated the p24 protein in plants, as verified by Western blot analysis. The plants were shown to contain between 0.2 μg and 0.5 μg p24 protein per g of fresh tissue. Analysis of the localisation of the p24 protein showed that stem tissue contained the largest amount of protein, more than twice as much as leaf tissue, whereas no p24 protein was detected in roots. By using Southern blotting, we found that 4, 2–3, 2 and 1 T‐DNA insertion events took place in the four lines 1, 2, 7, and 10, respectively. The genetic insertions of line 1 were stable from the T2 to the T5 generation and gave rise to the p24 protein in all cases, as verified by Western blotting. In mice fed with fresh transgenic A. thaliana (line 10), anti‐gag IgG was obtained in serum after a booster injection with recombinant p37Gag. No immune response was observed after equal booster injection of untreated mice or mice fed with A. thaliana WT plants.
Expression of caspase‐3‐dependent apoptosis in mural thrombi leukocytesCHU, PAO‐HSIEN; JUNG, SHIH‐MING; YEH, CHI‐HSIAO; WU, HSUEH‐HUA; SHIU, TZU‐FANG; SHE, HUNG‐CHUNG; TSENG, NGAN‐MING
doi: 10.1111/j.1600-0463.2008.00971.xpmid: 19132996
Failure of arteriovenous access is mostly due to graft thrombosis and multifactorial, with medical and surgical etiologies. Apoptosis of blood cells, such as macrophages, lymphocytes and eosinophils, may play an important role in thrombus formation. We also investigated caspase‐3‐dependent apoptosis in thrombi. We recorded clinical parameters in 43 consecutive patients with vascular access failure (13 men, 30 women; mean age±SD, 64.6±14.2 years) who underwent surgical thrombectomy. Major presentations included absent (92%) and/or near near‐absent (16%) flow through the access during hemodialysis. Cardiovascular risk factors were hypertension (70%), hyperlipidemia (47%), diabetes mellitus (47%), chronic obstructive pulmonary disease (12%), heart failure (12%), coronary artery disease (21%), and stroke (16%). Laboratory data included hemoglobin level of 100±17 g/L, total white blood cell count of 7.65±2.14×109/L, and platelet count of 205.6±57.9 1000/ìL. Abnormal biochemistry data included elevated blood urea nitrogen level of 63.5±24.4 mg/dL and creatinine level of 8.6±4.0 mg/dL (normal <1.4 mg/dL). Thrombi were characterized by apoptosis (32%) in a caspase‐dependent pathway in all types of leukocytes. Thrombi in arteriovenous access failure demonstrate apoptosis by means of the caspase‐3 pathway in white blood cells.