Aerobic training and angiogenesis activation in patients with stable chronic heart failure: a preliminary report.

The pathophysiology of chronic heart failure (CHF) involves multiple hystologic and molecular alterations. To determine the effects of physical training on circulating endothelial progenitor cells (EPCs), angiogenesis (angiogenin, angiopoietin-1 and -2, VEGF, Tie-2, SDF-1α) and inflammation (IL-6, CRP), we compared data obtained from 11 CHF pts before and after 3 months aerobic exercise training, to those from 10 non trained CHF pts (CHF-C group, age 64 + 2 years, NYHA 2). At the end of the study, EPCs count and AP-2 serum levels significantly increased in the CHF-TR group. These preliminary data suggest a significant effect of even a short program of physical training on angiogenic activation and endothelial dysfunction

Heat shock proteins levels and expression in chronic obstructive pulmonary disease and vernal keratoconjunctivitis

Inflammatory response in different organs share many similarities, but site-specific signs. Symptoms can be related to mucosal structure changes. The aim of the study was to compare heat shock proteins (HSPs) levels and expression in chronic obstructive pulmonary disease (COPD) to other inflammatory status of mucosa, such as vernal keratoconjunctivitis (VKC), a recurrent ocular inflammatory disease in which autoimune aggression may have a pathogenetic role. We examined bronchial mucosal biopsies from COPD patients (moderate to severe stage) and conjunctival biopsies from VKC patients; age-matched controls were selected for each group. We evaluated levels (by immunohistochemistry) and expression (by RT-PCR) of a panel of HSPs, among which Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and of the main heat shock transcription factor (both HSF-1 and pHSF-1). Hsp10 levels and expression increased in all pathological conditions, Hsp27 in VKC, Hsp40 in COPD and VKC, Hsp60 in COPD, Hsp70 and Hsp90 in VKC, as compared to their appropriate controls. Transcription factor pHSF-1 positive cells were significantly increased in COPD compared to controls, while was unaltered in VKC. Moreover, all pathological tissues showed increased levels of macrophages (CD68 positive) in lamina propria, COPD showed increased levels of neutrophils (elastase positive) and VKC increased levels of eosinophils (EG2 positive). Finally, Hsp60 colocalize with elastase positive cells in COPD. These results indicate that HSPs levels and expression change during development of different types of inflammation. Further studies will prove their active involvement and functions in triggering and/or maintaining the inflammatory status

Phospho-p38 MAPK expression in COPD bronchi and in oxidative and inflammatory challenged bronchial epithelium

The role of MAPK kinases in inducing the inflammatory response in the airways of chronic obstructive pulmonary diseases (COPD) patients is incompletely studied. Objectives: To investigate the expression of activated MAPK kinases in bronchial biopsies of COPD patients and the MAPK kinase bronchial epithelial response to oxidative and inflammatory stimuli related to COPD. Expression of phospho(p)-p38, p-JNK1 and p-ERK1/2 was measured in the bronchial mucosa using immunohistochemistry in patients with mild/moderate (n=17), severe/very severe (n=16) stable COPD, control smokers (n=16), control non smokers (n=9) and in a group with mild asthma (n=9). 16HBE cells, challenged with oxidative and inflammatory stimuli, were also studied for IL-8 and MAPK kinases mRNA production. P-p38 was the most expressed MAPK kinase in the bronchial mucosa of all subjects. No significant differences were observed for immune-expression of p-p38, p-JNK and p-ERK1/2 between COPD and control subjects. 16HBE cells treated with H2O2, cytomix (TNFα+IL- 1β+IFNγ) and Lipopolysaccharide (LPS) up-regulated IL-8 mRNA production at 1h or 2h after treatments. P38α mRNA was significantly increased after H2O2 and LPS. JNK1 and ERK1 mRNA were not significantly increased after H2O2, cytomix or LPS treatments. Blocking p38α activity IL-8 mRNA production was not changed at 1h, 2h and 4h after H2O2 or LPS challenge. P-p38 immune-positivity is prevalent in the bronchial mucosa of COPD and asthmatic patients and p38 mRNA is increased after bronchial epithelial challenges suggesting a relevant role for this MAPK kinase in the induction of bronchial inflammation in COPD and asthma

Notulae to the Italian flora of algae, bryophytes, fungi and lichens: 12

In this contribution, new data concerning bryophytes, fungi and lichens of the Italian flora are presented. It includes new records, confirmations or exclusions for the bryophyte genera Acaulon, Campylopus, Entosthodon, Homomallium, Pseudohygrohypnum, and Thuidium, the fungal genera Entoloma, Cortinarius, Mycenella, Oxyporus, and Psathyrella and the lichen genera Anaptychia, Athallia, Baeomyces, Bagliettoa, Calicium, Nephroma, Pectenia, Phaeophyscia, Polyblastia, Protoparmeliopsis, Pyrenula, Ramalina, and Sanguineodiscus

Notulae to the Italian flora of algae, bryophytes, fungi and lichens: 7

In this contribution, new data concerning algae, bryophytes, fungi, and lichens of the Italian flora are presented. It includes new records and confirmations for the algae genus Chara, the bryophyte genera Cephalozia, Conardia, Conocephalum, Didymodon, Sphagnum, Tetraplodon, and Tortula, the fungal genera Endophyllum, Gymnosporangium, Microbotryum, Phragmidium, and Pluteus, and the lichen genera Candelariella, Cladonia, Flavoplaca, Lichenothelia, Peltigera, Placolecis, Rinodina, Scytinium, and Solenopsora

Notulae to the Italian flora of algae, bryophytes, fungi and lichens: 11

In this contribution, new data concerning bryophytes, fungi, and lichens of the Italian flora are presented. It includes new records and confirmations for the bryophyte genera Aneura, Aulacomnium, Dumortiera, Fossombronia, Hennediella, Hygrohypnella, Pohlia, Porella, Riccardia, Tortella, and Tortula, the fungal genera Cortinarius, Mycena, Naucoria, Trichoglossum, and Tubaria and the lichen genera Agonimia, Blastenia, Chaenotheca, Cladonia, Endocarpon, Gyalecta, Lecanographa, Parmeliella, Porpidia, Stenhammarella, and Thelidium

A family of archaea-like carboxylesterases preferentially expressed in the symbiotic phase of the mychorrizal fungus Tuber melanosporum

An increasing number of esterases is being revealed by (meta) genomic sequencing projects, but few of them are functionally/structurally characterized, especially enzymes of fungal origin. Starting from a three-member gene family of secreted putative "lipases/esterases" preferentially expressed in the symbiotic phase of the mycorrhizal fungus Tuber melanosporum ("black truffle"), we show here that these enzymes (TmelEST1-3) are dimeric, heat-resistant carboxylesterases capable of hydrolyzing various short/medium chain p-nitrophenyl esters. TmelEST2 was the most active (kcat = 2302 s -1 for p-nitrophenyl-butyrate) and thermally stable (T 50 = 68.3 \ub0C), while TmelEST3 was the only one displaying some activity on tertiary alcohol esters. X-ray diffraction analysis of TmelEST2 revealed a classical \u3b1/\u3b2 hydrolase-fold structure, with a network of dimer-stabilizing intermolecular interactions typical of archaea esterases. The predicted structures of TmelEST1 and 3 are overall quite similar to that of TmelEST2 but with some important differences. Most notably, the much smaller volume of the substrate-binding pocket and the more acidic electrostatic surface profile of TmelEST1. This was also the only TmelEST capable of hydrolyzing feruloyl-esters, suggestinng a possible role in root cell-wall deconstruction during symbiosis establishment. In addition to their potential biotechnological interest, TmelESTs raise important questions regarding the evolutionary recruitment of archaea-like enzymes into mesophilic subterranean fungi such as truffles

Bronchial inflammation and bacterial load in stable COPD is associated with TLR4 overexpression

Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial mucosa of subjects with stable COPD of different severity (n=34), control smokers (n=12) and nonsmokers (n=12). The bronchial bacterial load of Pseudomonas aeruginosa, Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pneumoniae was measured by quantitative real-time PCR.TLR4 and NOD1 expression was increased in the bronchial mucosa of patients with severe/very severe stable COPD compared with control subjects. TLR4 bronchial epithelial expression correlated positively with CD4+ and CD8+ cells and airflow obstruction. NOD1 expression correlated with CD8+ cells. The bronchial load of P. aeruginosa was directly correlated, but H. influenzae inversely correlated, with the degree of airflow obstruction. Bacterial load did not correlate with inflammatory cells.Bronchial epithelial overexpression of TLR4 and NOD1 in severe/very severe stable COPD, associated with increased bronchial inflammation and P. aeruginosa bacterial load, may play a role in the pathogenesis of COPD