Cerebral cortical arterioles in focal neocortical areas develop increased permeability to plasma proteins and protein tracers in experimental hypertensive encephalopathy. The mechanism underlying this increased permeability has been the subject of several studies. In our previous studies of angiotensin-induced acute hypertension, pinocytosis appeared to be the principal mechanism for the increased blood-brain barrier (BBB) permeability observed. In the present study pinocytotic activity was assessed quantitatively to determine whether enhanced pinocytosis was confined to the permeable arteriolar segments of hypertensive animals. In addition, the effect of horseradish peroxidase (HRP) itself on the pinocytotic activity of normal cerebral cortical arteriolar endothelium was determined. In 12 rats following administration of HRP, hypertension was induced by an infusion of angiotensin. The animals were perfusion-fixed 90 s after the onset of the infusion. Control animals received saline only or HRP only. The area of arteriolar endothelium in cross section was determined by a planimeter from overlapping electron micrographs taken at a constant magnification around the circumference of the vessel wall. Results indicate a significant (P less than 0.001) increase in the number of pinocytotic vesicles in the permeable arteriolar segments of hypertensive animals as compared with nonpermeable arteriolar segments of the same animals and comparable segments of normotensive rats. In addition, eight times as many vesicles appear to be transporting tracer in the permeable arteriolar segments of hypertensive animals as compared to the nonpermeable segments of the same animals and normotensive animals. HRP alone did not affect the pinocytotic index, there being no difference (P greater than 0.05) in the number of vesicles in normotensive animals receiving saline only and those receiving HRP only. Our previous observation that disruption of endothelial cells or their tight junctions did not occur was confirmed.

The objective of this study was to evaluate the treatment outcomes and risk factors of women with surgical stage I endometrial adenocarcinoma who were initially treated with surgery alone and subsequently developed isolated vaginal recurrences. Patients with surgical stage I endometrial adenocarcinoma diagnosed from 1975 to 2002 were identified from tumor registry databases at seven institutions. All patients were treated with surgery alone including a total hysterectomy, bilateral salpingo-oophorectomy, pelvic (+/- para-aortic) lymph node dissection, and peritoneal cytology and did not receive postoperative radiation therapy. Vaginal recurrences were documented histologically. Metastatic disease in the chest and abdomen was excluded by radiologic studies. Overall survival was calculated by the Kaplan-Meier method. Sixty-nine women with surgical stage I endometrial cancer with isolated vaginal recurrences were identified. Of the 69 patients, 10 (15%) were diagnosed with stage IA disease, 43 (62%) were diagnosed with stage IB disease, and 16 (23%) were diagnosed with stage IC disease. Patients diagnosed with grade 1 disease were 22 (32%), grade 2 disease were 26 (38%), and grade 3 disease were 21 (30%). Among women, 81% with isolated vaginal recurrences were salvaged with radiation therapy. The mean time to recurrence was 24 months, and the mean follow-up was 63 months. Among women, 18% died from subsequent recurrent disease. The 5-year overall survival was 75%. The majority of isolated vaginal recurrences in women with surgical stage I endometrial cancer can be successfully salvaged with radiation therapy, further questioning the role of adjuvant therapy for patients with uterine-confined endometrial cancer at the time of initial diagnosis.

Background:Reduction of bone mineral density (BMD) is a known and established phenomenon in chronic obstructive pulmonary disease (COPD). However, there have been no data regarding osteoporosis/osteopenia in COPD patients in India.Aim:To look for the degree and frequency of osteoporosis/osteopenia in our OPD patients being diagnosed as COPD.Materials and Methods:Thirty-seven randomly selected patients with COPD were assessed for BMD with commercially available ultrasound bone densitometer (HOLOGIC SAHARA) in a pulmonary OPD. Some cofactors for reduced BMD were also noted.Results:Out of the 37 COPD (all belonging to the GOLD III/IV category) patients studied, the BMD was found to be normal in 10 (27%) patients, while 27 (73%) patients were found to have osteopenia/osteoporosis [19 (51.35%) and 8 (21.62%) patients having osteopenia and osteoporosis, respectively].Conclusion:Frequency of osteoporosis and osteopenia was found to be very high (73%) in our population of advanced COPD. The data suggest a need for further in-depth study regarding the issue.

Oligosaccharide residues on the endothelial luminal plasma membrane of rat cerebral cortical vessels were localized using biotinylated lectins. In addition, the effect of pretreatment of brain slices with neuraminidase prior to the binding of cationized ferritin (CF) and certain lectins was studied. Conjugates of biotinylated lectins and avidin-D horseradish peroxidase reaction product were evenly distributed on the endothelium of arterioles, capillaries, and venules. Lectin binding sites were observed on the plasma membrane of pinocytotic vesicles open onto the vascular lumen and at the luminal end of the interendothelial space only. The following sugar residues were localized: alpha-D-mannosyl, alpha-D-glucosyl, beta-N-acetylglucosaminyl, sialyl, D-galactosyl, alpha-L-fucosyl, and alpha-N-acetyl-D-galactosaminyl. Following pretreatment of brain slices with neuraminidase beta-D-gal-(1-3)-D-galN-acetyl groups were demonstrated on endothelium. In this respect, cerebral endothelium differs from noncerebral endothelium which is reported to have peanut agglutinin binding sites without neuraminidase pretreatment. Anionic groups on cerebral endothelium were demonstrated at the same locations as the lectin binding sites. Following neuraminidase pretreatment there was reduction, but not absence, of CF binding supporting the observation that surface charge is not wholly due to sialyl groups. The role of monosaccharide residues in states of altered cerebrovascular permeability remains to be determined.