A trial in the Karelian Republic of oral rehydration and Lactobacillus GG for treatment of acute diarrhoea

In a controlled trial in Petrozavodsk, Karelia, the effects of oral rehydration and Lactobacillus strain GG (LGG) on recovery from acute diarrhoea (27% rotavirus, 21% bacterial aetiology) were studied in 123 children aged between 1 and 36 months of age. On admission to hospital, the patients were first randomized to receive either isotonic oral rehydration solution (ORS) with osmolality 311mosmol/l and sodium 90mmol/l (WHO-ORS), or a hypotonic ORS with osmolality 224mosmol/l and sodium 60mmol/l (Light-ORS), and thereafter randomized to receive either 5 × 10⁹ colony forming units of LGG or a matching placebo. The two ORS performed equally for acute rehydration, and oral rehydration with either ORS was associated with a shorter duration of diarrhoea than intravenous rehydration ( p = 0.036). Patients receiving LGG had a significantly shorter duration of watery diarrhoea [mean (SD) 2.7 (2.2) days] than those receiving the placebo [3.7 (2.8) days, p = 0.03]. LGG significantly shortened the duration of rotavirus diarrhoea but not diarrhoea with confirmed bacterial aetiology.     

Creatine kinase isoenzyme BB concentrations in cerebrospinal fluid in asphyxiated preterm neonates

Creatine kinase isoenzyme BB was determined in cerebrospinal fluid (CSF) in 79 preterm neonates using an original enzyme-linked immunosorbent assay. The criterion for inclusion was an Apgar score of 7 or less at 5 min of life. Neurological examination was performed on day 2 and day 5 of life. CSF was obtained on the same days. Lumbar puncture was performed on 41 of these babies on day 2 and in 39 on day 5 of life (one baby underwent lumbar puncture twice). All babies had clinical features of hypoxic-ischemic encephalopathy (HIF) which was classified according to Sarnat and Sarnat. The control group consisted of 90 asphyxiated term babies and 30 adults without CNS pathology. The concentration of CK-BB in cerebrospinal fluid (meanSD) was significantly higher ( p < 0.0005) in preterm (168.0 2) than in term babies (29.0 3.1) and healthy adults (5.3 1.2). Our results demonstrate the possibility of using the classification system of Sarnat and Sarnat for assessment of the severity of brain damage not only in term, but also in preterm babies. Neonates with HIE stages II and III showed markedly higher CK-BB values than those with HIE I on day 2 ( p < 0.025) and day 5 ( p < 0.05) of life. CK-BB values were markedly higher in preterm babies with none of some primitive responses (head turning, Babkin's reflex, palmar grasp). The mean concentration of CK-BB was higher in neonates with retarded psychomotor development compared with those with normal development ( p < 0.05) on day 3, and after 6 and 9 months. At 12 months of age no significant difference in median CK-BB concentration was detected between neonates with normal and developmental disturbances. Asphyxia, cerebrospinal fluid, creatine kinase BB isoenzyme, hypoxic-ischemic encephalopathy, neonates     

Coupling of astrocyte connexins Cx26, Cx30, Cx43 to oligodendrocyte Cx29, Cx32, Cx47: Implications from normal and connexin32 knockout mice

Oligodendrocytes in vivo form heterologous gap junctions with astrocytes. These oligodendrocyte/astrocyte (A/O) gap junctions contain multiple connexins (Cx), including Cx26, Cx30, and Cx43 on the astrocyte side, and Cx32, Cx29, and Cx47 on the oligodendrocyte side. We investigated connexin associations at A/O gap junctions on oligodendrocytes in normal and Cx32 knockout (KO) mice. Immunoblotting and immunolabeling by several different antibodies indicated the presence of Cx32 in liver and brain of normal mice, but the absence of Cx32 in liver and brain of Cx32 KO mice, confirming the specificity and efficacy of the antibodies, as well as allowing the demonstration of Cx32 expression by oligodendrocytes. Oligodendrocytes throughout brain were decorated with numerous Cx30-positive puncta, which also were immunolabeled for both Cx32 and Cx43. In Cx32 KO mice, astrocytic Cx30 association with oligodendrocyte somata was nearly absent, Cx26 was partially reduced, and Cx43 was present in abundance. In normal and Cx32 KO mice, oligodendrocyte Cx29 was sparsely distributed, whereas Cx47-positive puncta were densely localized on oligodendrocyte somata. These results demonstrate that astrocyte Cx30 and oligodendrocyte Cx47 are widely present at A/O gap junctions. Immunolabeling patterns for these six connexins in Cx32 KO brain have implications for deciphering the organization of heterotypic connexin coupling partners at A/O junctions. The persistence and abundance of Cx43 and Cx47 at these junctions after Cx32 deletion, together with the paucity of Cx29 normally present at these junctions, suggests Cx43/Cx47 coupling at A/O junctions. Reductions in Cx30 and Cx26 after Cx32 deletion suggest that these astrocytic connexins likely form junctions with Cx32 and that their incorporation into A/O gap junctions is dependent on the presence of oligodendrocytic Cx32.     

A prospective epidemiological study of new incident GISTs during two consecutive years in Rh?ne Alpes region: incidence and molecular distribution of GIST in a European region

Background:

Preliminary data indicate that the molecular epidemiology of localised gastrointestinal stromal tumour (GIST) may be different from that of advanced GIST. We sought to investigate the molecular epidemiology of sarcomas, including GIST, in the Rhone-Alpes region in France.

Patients and methods:

A prospective and exhaustive study in the Rhone-Alpes Region in France to assess the precise incidence of primary sarcomas with systematic centralised pathological review and molecular analysis was conducted for 2 consecutive years.

Results:

Among 760 patients with a confirmed diagnosis of sarcoma, 131 (17%) had a GIST. The majority of patients had gastric primaries (61%). Mutational analysis could be performed in 106 tumour samples (74%), and 71 (67%) had exon 11 mutations. PDGFRA mutations were found in 16% of cases, which is twice as high as previously reported for advanced GIST.

Conclusion:

Data indicate that PDGFRA mutations in localised GIST may be twice as high as what was previously reported in patients with advanced disease. This finding may have important consequences for patients offered adjuvant imatinib, although most of these tumours are in the low-risk group.     

Osteoclastic acidification pathways during bone resorption

Osteoclasts resorb bone by attaching to the surface and then secreting protons into an extracellular compartment formed between osteoclast and bone surface. This secretion is necessary for bone mineral solubilization and the digestion of organic bone matrix by acid proteases. This study summarizes the characterization and role of each type of ion transport and defines the main biochemical mechanisms involved in the dissolution of bone mineral during bone resorption. The primary mechanism responsible for acidification of the osteoclast-bone interface is vacuolar H+-adenosine triphosphatase (ATPase) coupled with Cl- conductance localized to the ruffled membrane. Carbonic anhydrase II (CAII) provides the proton source for extracellular acidification by H+-ATPase and the HCO3- source for the HCO3-/Cl- exchanger. Whereas some transporters are responsible for the bone resorption process, others are essential for pH regulation in the osteoclast. The HCO3-/Cl- exchanger, in association with CAII, is the major transporter for maintenance of normal intracellular pH. An Na+/H+ antiporter may also contribute to the recovery of intracellular pH during early osteoclast activation. Once this mechanism has been rendered inoperative, another conductive pathway translocates the protons and modulates cytoplasmic pH. Inward-rectifying K+ channels may also be involved by compensating for the external acidification due to H+ transport. These different effects of transport processes, either on bone resorption or pH homeostasis, increase the number of possible sites for pharmacological intervention in the treatment of metabolic bone diseases.     

Congenital dilatation of extrahepatic bile ducts in children. Experience in the central hospital of Hue, Vietnam.

BACKGROUND/PURPOSE: The authors present a study of a series of cases in children with congenital dilatation of the extrahepatic bile ducts (CDEBD). METHODS: Between November 1998 and October 2002, 38 children aged between 50 days and 15 years suffering from CDEBD, admitted to the Central Hospital in Hue, Vietnam, were treated surgically with a minimum follow-up of one year. RESULTS: Diagnosis was based only on ultrasonography which was 100% accurate. According to Miyano's classification, 26 cases presented as cystic dilatation of the main bile duct (MBD) associated with dilatation of the intrahepatic bile ducts, while in the other 12 cases the dilatation of the MBD was of the fusiform type. The surgical treatment of choice was extensive excision of the dilatated extrahepatic bile ducts and biliary drainage according to the Roux-en-Y method in 36/38 patients. The other two patients underwent surgery for internal biliary drainage without removing the cysts. During follow-up we observed one case of pancreatitis out of the 36 patients who underwent excision of the dilatated extrahepatic bile ducts, while the two patients who had internal biliary drainage without removal of the cysts suffered from numerous attacks of cholangitis. CONCLUSIONS: The reflux of bile in the dilated biliary tree plays an important role in the etiopathogenesis of CDEBD. Excision of the extrahepatic bile ducts and internal biliary drainage by Roux-en-Y has proved a satisfactory surgical method.     

Electron Microscopic Study of Left Ventricular Cardiomyocyte Mitochondriom in Rats Subjected to Head-Down Tilt

The mitochondriom of left-ventricular cardiomyocytes in rats subjected to head-down tilt was studied at the electron microscopic level. The ultrastructure of individual mitochondria was disturbed and the number of intermitochondrial contacts in the perinuclear zone increased after 30-day head-down tilt. These parameters did not return to normal over 30 days after 30-day tilt. Repeated 14-day head-down tilt led to a more pronounced increase in the number of intermitochondrial contacts, mitochondria with abnormal ultrastructure were still observed.