Experimental model for investigating trans-mucosal gas exchanges in the middle ear of the rat

OBJECTIVE: The total pressure in the middle ear depends on the air composition of this gas pocket, i.e. on gas exchanges occurring through either the Eustachian tube (ET) or mucosa. The aim of this study was to develop an experimental model to investigate the exclusive role of trans-mucosal gas exchanges in the middle ear (ME). MATERIAL AND METHODS: Both tympanic membranes of 20 Sprague-Dawley rats were punctured under general anesthesia. Rats were divided into two equal groups. Group 1 had no ET obstruction. In Group 2, the ET was blocked, after velar incision, by cauterization and application of cyanoacrylate glue into the lumen. One open transparent glass tube containing a droplet of colored water was placed horizontally and connected hermetically to each ear canal. The ME was then flushed with room air through the tube. Variations in ME gas volume were measured by reading the displacement of the liquid droplet in the horizontal tube. The kinetics of variations in gas volume between groups were displayed and statistically compared using a two-sided t-test. RESULTS: The pattern of variations in ME gas volume with time was similar in the two groups. Both were characterized by a decrease with three phases and an elimination rate of approximately 0.152 +/- 0.026 microl/min. There was no significant difference in the mean rate of ME volume changes between the two groups. CONCLUSION: This experimental model allows investigation of trans-mucosal gas exchanges. These exchanges exhibit an absorptive function resulting in a negative pressure that must be compensated, under physiological conditions, by air flow through the ET.     

Nonimmune fetal ascites: a series of 79 cases

OBJECTIVE: The purpose of this study was to analyze the precision of ultrasonography in defining the cause and prognosis in fetal ascites. STUDY DESIGN: We conducted a retrospective study of 79 cases of fetal ascites. RESULTS: The mortality rate was 57% overall and ranged from 100% (7/7 cases) for metabolic storage disease to 0% (0/3 cases) in chylous ascites. Ascites before 24 weeks of gestation or combined with fetal hydrops indicates poor prognosis (respectively, 78.6% vs 45% mortality rate after 24 weeks; P<.01; and 77% vs 50.8% without hydrops; P<.02). Ascites was organic in 45 cases, infectious in 13 cases, idiopathic in 12 cases, and genetic in 9 cases. The cause was defined ultrasonographically in 28 of the 45 organic ascites and in 8 of the 25 isolated ascites. Urinary cause was the most frequent and the most successfully specified cause (14/15 cases). CONCLUSION: Routine ultrasonography detects fetal ascites, but the cause is extremely variable and difficult to specify. When associated with fetal hydrops, the prognosis is poor.     

Imaging of early stages of osteonecrosis of the knee

Osteonecrosis of the knee can present as a spontaneous and primary or a secondary clinical entity. The natural history of osteonecrosis follows a course of several sequential stages, and the later stages of both entities seem to be irreversible. Early diagnosis of osteonecrosis is crucial: the earlier the stage of the lesion at the time of diagnosis, the better the prognosis.Clinically, early diagnosis and treatment of osteonecrosis might prevent unnecessary surgery in cases with a concomitant degenerative meniscal tear. Early-stage osteonecrosis should be ruled out before surgery, because arthroscopy has lately been associated with osteonecrosis. Not every imaging method is equally suitable for detecting pathognomonic changes in each stage of osteonecrosis. Early-stage osteonecrosis is difficult to diagnose,because various differential diagnoses must be kept in mind. Moreover, there is a diagnostic window between the onset of symptoms and the appearance of pathognomonic changes on plain radiographs and MRI.     

Further characterisation of particulate neuronal nitric oxide synthase in rat small intestine

Neuronal NO-synthase (nNOS) was investigated in rat longitudinal muscle/myenteric plexus (LM/MP) tissue at the cellular and subcellular level. Using preparations and double immune staining and light and electron microscopy, we concluded that, in these preparations, nNOS is only present in neuronal cells. However, in spite of numerous attempts to morphologically identify the NOS-containing subcellular structure, no firm conclusions were possible. Consequently, the problem was approached by biochemical methods including gradient centrifugation followed by analysis of the fractions. Using a protocol involving gentle homogenisation of the tissue, we found that about 10% of the nNOS immune reactivity was particle-bound confirming previous results (Biochem. Pharmacol. 60 (2000) 145). However, applying a different protocol including strong homogenisation, we now demonstrated that about 50% of the immune reactive nNOS was sedimentable. The results suggested that particulate nNOS is associated with one single subcellular structure, which is different from the plasma membrane, rough and smooth endoplasmic reticulum, mitochondria and lysosomes. The equilibrium sedimentation characteristics of the nNOS containing particles corresponded partly to those containing vasoactive intestinal polypeptide (VIP) or synaptobrevin. Application of non-equilibrium centrifugation conditions, however, demonstrated that almost no co-localisation occurred. We conclude that, in the LM/MP tissue, nNOS is about 50% particle-bound in a subcellular structure, which is different from the VIP-containing particle and from synaptobrevin-containing exocytotic particles.     

Massive ovarian edema revealing gastric carcinoma: a case report

Tumor-like enlargement of the ovaries due to accumulation of edema fluid within the ovarian stroma is referred to as massive ovarian edema (MOE). The pathogenesis of MOE is thought to be intermittent torsion of the ovary on its pedicle, causing partial obstruction of venous and lymphatic drainage. The diagnosis of MOE is based on imaging techniques. The case described here due to ovarian lymphatic vessel obstruction by carcinoma cells shows that metastatic disease may be a cause of MOE.     

Measurement of nuchal translucency as a single strategy in trisomy 21 screening: should we use any other marker?

OBJECTIVE: To evaluate the role of nuchal translucency thickness as a single marker in screening for trisomy 21 at 10-16 weeks' gestation. METHODS: From December 1996 to October 2001, nuchal translucency was measured in 11,281 consecutive early second trimester fetuses referred to our unit for prenatal care and delivery. Scans were performed by eight experienced ultrasonographers, under strict methodological criteria. RESULTS: Chromosomal abnormalities were found in 118 cases (52 trisomy 21). Using nuchal translucency greater than the 95th centile as a cut-off, the overall detection rate was 71.2% with a specificity of 95.4%, and a positive predictive value of 14%. In the trisomy 21 selected group, detection rate, specificity, and positive predictive value for nuchal translucency were 92.3%, 95.4%, and 8.5%, respectively. The detection rate of trisomy 21 reached 100% when nuchal translucency was measured between 10 and 14 weeks' gestation, maintaining the same specificity. CONCLUSION: Early second trimester nuchal translucency measurement can achieve prenatal detection rates of trisomy 21 greater than 95% with a 5% false-positive rate. With a detection rate so high, the benefits of using additional markers may be less than previously considered. Although maternal age, other sonographic or Doppler markers, and maternal serum biochemistry might play a role in prenatal strategies to detect fetal chromosomal abnormalities, the high detection rate of trisomy 21 fetuses using nuchal translucency as a single parameter suggests that early nuchal translucency measurement between 10 and 14 weeks' gestation can be a simple screening strategy for this condition.     

Decreased topotecan platelet toxicity with successive topotecan treatment cycles in advanced ovarian cancer patients.

The dose-limiting toxicities of the DNA topoisomerase I inhibitor topotecan are hematological. We prospectively analyzed the platelet toxicity pattern in patients receiving topotecan to optimize the clinical management of topotecan hematotoxicity. Twenty-one advanced ovarian cancer patients, all pretreated with cisplatin and paclitaxel, were treated with 1.25 mg/m2/day topotecan as a 30 min infusion for 5 days, every 3 weeks. No prophylactic granulocyte colony stimulating factor (G-CSF) was given. No topotecan dose reduction was planned according to hematologic toxicity. One hundred and thirty-three topotecan courses were administered (median per patient 6; range: 1-15). Despite no dose reduction, the mean platelet nadir values were significantly less pronounced at cycle 2 than at cycle 1 (82 versus 46 x 10(3)/mm3, p=0.0007). Similar differences were found between cycle 1 and any following cycle. The percent of patients experiencing grade 4 thrombocytopenia decreased from 43% at the first cycle, to 15 and 19% at the second and third courses, respectively (p=0.058). We conclude that the currently recommended topotecan schedule is feasible in heavily pretreated ovarian cancer patients without prophylactic G-CSF. The severity of topotecan-induced thrombocytopenia is maximal at the first cycle but significantly decreases from the second cycle in the absence of dose reduction.