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Pediatr Surg Int. 2003 Aug;19(6):478-81. Epub 2003 May 13.
Plasma endothelin-1 levels in patients with biliary atresia: possible role in development of portal hypertension.

Chongsrisawat V, Chatchatee P, Samransamruajkit R, Vanapongtipagorn P, Chottivittayatarakorn P, Poovorawan Y.

Department of Pediatrics, Faculty of Medicine, Viral Hepatitis Research Unit, Chulalongkorn University and Hospital, 10330, Bangkok, Thailand.

BACKGROUND. Biliary atresia (BA) is a severe neonatal liver disease characterized by progressive extrahepatic biliary tract and intrahepatic inflammatory process. Hepatic fibrosis and portal hypertension (PH) still occur despite the disappearance of jaundice following successful hepatic portoenterostomy. Endothelin-1 (ET-1) is a potent vasoconstrictor and has been reported to stimulate hepatic collagen synthesis. The aim of this study was to demonstrate the potential role of ET-1 in the pathogenesis of the progressive inflammation, fibrosis and PH in BA. METHODS. Thirty pediatric patients with biliary atresia post-hepatic portoenterostomy and 12 healthy children were examined. The ET-1 level was determined by commercially available enzyme-linked immunosorbent assay kits. RESULTS. Endothelin-1 levels were elevated in the patients compared with those of the controls (5.45+/-3.34 vs. 2.74+/-2.17 pg/ml, P=0.01). Moreover, patients with PH also had greater levels of ET-1 than those without PH (6.73+/-3.27 vs. 3.26+/-2.2 pg/ml, P=0.004). Patients with abnormal transaminase enzymes had significantly higher ET-1 levels than those with normal enzymes (6.43+/-3.33 vs. 3.17+/-2.1 pg/ml, P=0.01). In the jaundice-free group, endothelin-1 levels were elevated in the patients with PH compared with those without PH (5.93+/-2.15 vs. 2.88+/-2.1 pg/ml, P=0.02). CONCLUSIONS. Our findings showed elevation of plasma ET-1 levels in patients with BA, especially in those with PH. ET-1 levels were also higher in patients with elevated transminase enzymes as well as in the jaundice-free group with PH. ET-1 might play a role in the pathogenesis of the progressive inflammation, fibrosis and PH in BA.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12748798&dopt=Abstract [PubMed - in process]

Ophthalmologe. 2003 May;100(5):371-7.
[Angioproliferative retinal disease caused by ischemia]

[Article in German]

Agostini HT, Hansen LL.

Universitats-Augenklinik Freiburg. agostinug.ukl.uni-freiburg.de

Ischemia is a major stimulus for angiogenesis, a biological response mechanism that describes the formation of new blood vessels from existing vessels. An ischemic cell communicates with endothelial cells by soluble factors such as VEGF (vascular endothelial growth factor) and its receptors. A major transcriptional factor for VEGF is HIF-1 (hypoxia inducible factor). Proliferation of endothelial cells alone does not result in stable vascular tubes, this is only achieved by recruiting additional cells such as pericytes. The stabilisation and destabilisation of vessels, which are important prerequisites for vascular growth, are in a dynamic equilibrium which can be modified by additional growth factors such as angiopoietins. In this review we discuss some of the molecular mechanisms leading from ischemia to proliferative retinopathy with a special focus on retinopathy of prematurity and the closely related mouse model of hyperoxia-induced retinopathy. This model is very useful when developing new antiangiogenic therapies based on the increasing understanding of the molecular pathogenesis of ischemic proliferative retinopathy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12748802&dopt=Abstract [PubMed - in process]

Parasitol Res. 2003 Aug;90(5):405-8. Epub 2003 May 14.
No evidence of Wolbachia endosymbiosis with Loa loa and Mansonella perstans.

Grobusch MP, Kombila M, Autenrieth I, Mehlhorn H, Kremsner PG.

Department of Parasitology, Institute of Tropical Medicine, University Hospital of Tubingen, Wilhelmstrasse 27, 72074, Tubingen, Germany. martin.grobuscni-tuebingen.de

Endosymbiotic Wolbachia bacteria from different filarial species, including major pathogens of humans such as Wuchereria bancrofti, Brugia malayi and Onchocerca volvulus, seem to play an important role in the development, viability and fertility of these worms. Wolbachia trigger inflammatory host responses as well as adverse reactions against standard treatment regimens and are therefore under investigation as novel treatment targets. We investigated whether Wolbachia are also endosymbiotic in Loa loa and Mansonella perstans. In both male and female adult L. loa, we found no evidence of bacteria by light or transmission electron microscopy. Furthermore, Wolbachia-specific PCR was negative in both L. loa and M. perstans microfilariae. The absence of Wolbachia in both filarial species therefore discourages the use of antibiotics as an adjunct or alternative approach to current treatment concepts for both loiasis and mansonelliasis perstans.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12748849&dopt=Abstract [PubMed - in process]

Pflugers Arch. 2003 Jul;446(4):401-9. Epub 2003 May 13.
(Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6.

Nijenhuis T, Hoenderop JG, Nilius B, Bindels RJ.

Department of Cell Physiology, Nijmegen Center for Molecular Life Sciences, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands.

The epithelial Ca(2+) channels TRPV5 and TRPV6 constitute the apical Ca(2+) entry mechanism in active Ca(2+) (re)absorption. These two members of the superfamily of transient receptor potential (TRP) channels were cloned from the vitamin-D-responsive epithelia of kidney and small intestine and subsequently identified in other tissues such as bone, pancreas and prostate. These channels are regulated by vitamin D as exemplified in animal models of vitamin-D-deficiency rickets. In addition, the epithelial Ca(2+) channels might be involved in the multifactorial pathogenesis of disorders ranging from idiopathic hypercalciuria, stone disease and postmenopausal osteoporosis. This review highlights the emerging (patho)physiological implications of these epithelial Ca(2+) channels.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12748856&dopt=Abstract [PubMed - in process]

Acta Neurochir (Wien). 2003 Apr;145(4):257-63; discussion 263-4.
Nitric oxide metabolites in cisternal CSF correlate with cerebral vasospasm in patients with a subarachnoid haemorrhage.

Woszczyk A, Deinsberger W, Boker DK.

Department of Neurosurgery, Justus-Liebig University, Giessen, Germany.

BACKGROUND: The pathogenesis of cerebral vasospasm is likely to be multifactorial. Exposure of the adventitia of large cerebral arteries to blood breakdown products initiates a cascade of changes in both morphology and vasomotor regulation of the exposed vessels. The role of nitric oxide (NO) in development of cerebral vasospasm process is controversial. Basal cerebral vascular tone requires the continuous release of NO, nevertheless NO is involved in free radical mediated injury of endothelial cell membrane. Concentrations of nitrate/nitrite (stabile endproducts of NO metabolism) were studied in cisternal cerebrospinal fluid (cCSF) in patients suffering from aneurysmal subarachnoid haemorrhage (SAH). METHOD: 21 patients suffering from aneurysmal SAH were investigated. Treatment included aneurysm clipping, cisternal drainage of CSF and intravenous nimodipine in all patients as well as tripple H therapy when indicated. TCDS was performed on a daily basis. A mean flow velocity of more than 150 cm/sec and the development a delayed neurological deficit was defined as vasospasm. CSF samples were collected on the day of surgery and for the 7 days following. NO-M (nitrite and nitrate) were measured using a commercially available test kit. FINDINGS: 5 of 21 patients developed clinically symptomatic vasospasm. There was a significant difference in NO levels between the groups. Patients with cerebral vasospasm showed significantly higher levels of NO-M in CSF than patients with a uncomplicated follow-up between day 2 and 8. INTERPRETATION: Our preliminary results indicate that SAH leads to an increase in NO-M in CSF. This increase of NO-M significantly correlates with the flow velocities in TCDS measurement suggesting that NO plays an important role in the pathogenesis of cerebral vasospasm.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12748885&dopt=Abstract [PubMed - in process]

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