Biomedical subjects
Publications and source records attributed to P Puri.
We report a case of non arteritic anterior ischemic optic neuropathy following caesarean delivery in a patient who had epidural analgesia. There was doubt as to whether it was subdural. The patient underwent caesarean section because of second stage non-progression of labor. We discuss the possible etiology of this unpleasant complication.
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OBJECTIVE: To investigate the intrinsic innervation of the upper urinary tract in congenitally hydronephrotic and normal Goettingen minipigs, using the whole-mount preparation technique. MATERIALS AND METHODS: Whole-mount preparations of hydronephrotic (two with bilateral ectopic ureters, one with left distal ureteric stenosis) and normal (three) porcine upper urinary tracts were examined by immunohistochemistry with tyrosine hydroxylase (TH) and neurofilament and by histochemical staining with NADPH-diaphorase and acetylcholinesterase. Staining results were evaluated using normal bright-field and confocal laser scanning microscopy. RESULTS: Neurofilament-, TH-immunoreactive and acetylcholinesterase-positive nerve fibres and neuronal networks were identified in the adventitial, muscle and subepithelial layers of the whole upper urinary tract. An NADPH-diaphorase-positive network was expressed in the subepithelial layer and less densely in the muscle layer. The general distribution of the identified neuronal networks was similar in hydronephrotic and normal upper urinary tracts, but the density of these neuronal networks was less in the former. The most striking observation was the absence or marked reduction of neuronal networks in the stenotic part of the ureter in the pig with left distal ureteric stenosis. CONCLUSION: Whole-mount preparations provide a method for assessing the three-dimensional topography of neuronal networks in the different layers of the porcine upper urinary tract. Although the macroscopic differences between the hydronephrotic and normal porcine upper urinary tracts were striking, changes in the innervation pattern were less obvious, except in distal ureteric stenosis.
OBJECTIVE: To evaluate retrospectively children with an antenatal diagnosis of pelvi-ureteric junction (PUJ) obstruction who required pyeloplasty for deteriorating renal function during the follow-up, specifically assessing the recovery of function after surgery. PATIENTS AND METHODS: Between 1988 and 2000, 44 consecutive patients with a prenatal diagnosis of PUJ obstruction who were initially treated by observation underwent pyeloplasty because their renal function deteriorated during the follow-up. Patients with bilateral disease, a single kidney or vesico-ureteric reflux were excluded from the study. The mean (sd) age of the patients was 13.3 (4.5) months and their mean (range) initial renal function 39.7 (30.4-45)%. In all patients the diagnostic criteria and indications for surgery were identical. The main indication for surgery was deteriorating renal function of >5%, confirmed by renal scintigraphy. Of 44 patients, 35 (77%) had severe dilatation of the renal pelvis by >3 cm. The mean (sd) deterioration in renal function during the follow-up, just before surgery, was 8.2 (2.4)%, and the mean time between the last acceptable renogram and the study showing deterioration was 8.3 (1.3) months; the mean follow-up was 5.1 (1.6) years. The results were assessed statistically using the unpaired nonparametric Mann-Whitney U-test. RESULTS: An improvement in hydronephrosis was confirmed in all patients, with renal function returning to the initial levels in 36 of 44 (81%) patients 6-12 months after surgery, although in two patients renal function did not improve after surgery. There was no significant difference between the preoperative characteristics and the degree of hydronephrosis, renal function or patient age with the level of renal functional improvement after surgery. CONCLUSION: In patients with an antenatal diagnosis of PUJ obstruction, expectant management is recommended and spares the children unnecessary surgery. Even if renal function deteriorates, delayed pyeloplasty recovers the initial functional level.
BACKGROUND/PURPOSE: Prenatal exposure to Adriamycin in a rat model (ARM) has been reported to lead to a spectrum of tracheoesophageal and associated malformations of the gastrointestinal tract, including multiple intestinal atresias. An abnormal relationship of the notochord with the foregut has been implicated in the formation of esophageal atresias. The authors hypothesised that midgut atresias arise from abnormal notochord development in the region of the midgut. This study was designed to examine the gut-notochord relationship during early embryonic development. METHODS: Timed pregnant Wistar rats were given 1.75 mg/kg of Adriamycin intraperitoneally on days 7, 8, and 9 of gestation. Embryos were recovered at 12-hour intervals from days 9.5 to 14, and at term. A control group was given saline instead of Adriamycin. Embryos were embedded in resin or wax, sectioned, and studied using light microscopy, paying particular attention to the notochord and surrounding structures. RESULTS: The notochord appeared identical in controls and experimental embryos on day 9.5. However, on day 10.5 the notochord was diffusely abnormal in ARM, distorted, and tethered to foregut as well as midgut compared with controls. This abnormality was not seen in control embryos. On day 12 the notochord abnormalities were more exaggerated in the region of the midgut in ARM embryos. Full-term ARM animals had esophageal and multiple intestinal atresias. CONCLUSIONS: The notochord is abnormal in the region of the developing midgut, and this may account for the occurrence of atresias found in this region.
PURPOSE: Vesicoureteral reflux during infancy is found mainly in males, and it is of high grade and often bilateral. The higher predominance of male infants is reported in series when the reflux is diagnosed prenatally and when it is detected after urinary tract infection. Renal parenchymal damage may already be present at birth before any episode of urinary tract infection or acquired after a febrile urinary tract infection. We evaluate the incidence of renal damage in a large series of male infants with high grade vesicoureteral reflux diagnosed after the first urinary tract infection. MATERIALS AND METHODS: We reviewed the medical and radiological records of 141 consecutive male infants 3 weeks to 1 year old (mean age 5.8 months) who were diagnosed with high grade (III to V) vesicoureteral reflux on voiding cystourethrography during 1984 to 2000 following hospitalization for the first febrile urinary tract infection. A total of 127 (90%) patients underwent technetium dimercapto-succinic acid scan to evaluate renal damage 3 to 6 months after the initial infection. RESULTS: Vesicoureteral reflux was unilateral in 46 infants and bilateral in the remaining 95, comprising 236 ureters. Reflux was grade III in 79 ureters, IV in 114 and V in 43. Renal parenchymal damage was detected in 56 (44%) of the 127 infants on dimercapto-succinic acid scan, and was bilateral in 18 and unilateral in the 38, representing 74 renal refluxing units. Renal damage was mild (greater than 40% uptake) in 47 units, moderate (less than 40% and greater than 20% uptake) in 22 U and severe (less than 20% uptake) in 5 U. CONCLUSIONS: This study shows that nearly half of the male infants with high grade reflux who present with the first febrile urinary tract infection have renal parenchymal damage. This high incidence of renal damage may be explained by the coexistence of the 3 risk factors of gender, urinary tract infection and high grade vesicoureteral reflux.
AIM: To present the results of 27 patients who had enucleation for malignant melanoma of the choroid with hydroxyapatite implant wrapped in bovine pericardium. METHOD: A retrospective study was performed on 27 patients, 12 males and 15 females, who had enucleation as a primary treatment for their choroidal melanomas. The patients were followed up at 1 week, 1 month, 3 months, and then every 6 months. A conformer was fitted at 1 week and an artificial eye at 1 month. The average follow up was 1.7 years. RESULTS: No patient had extrusion of the implant. One patient needed repair of the wound, two patients required a lateral tarsal strip, and one patient developed a conjunctival granuloma, which did not need excision. In one patient there was shallowing of the inferior fornix. The cosmetic results and ocular movement were satisfactory in all but one patient. CONCLUSION: Use of bovine pericardium as wrapping material for the hydroxyapatite implants has shown promising results with minimal extrusion rates providing an effective alternative for sclera, eliminating the potential risks of CJD.
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PURPOSE: Horseshoe kidney is the most common renal fusion anomaly. We determined the treatment and outcome of vesicoureteral reflux and ureteropelvic junction obstruction in children with horseshoe kidney. MATERIALS AND METHODS: We reviewed the medical and radiological records of 52 consecutive children, including 32 boys and 20 girls, in whom horseshoe kidney was diagnosed at 2 children's hospitals during 1990 to 1999. Patient age at diagnosis was 1 day to 12 years (mean 3.9 years). In 2 children with horseshoe kidney neuropathic bladder was secondary to spina bifida and they were excluded from study. The diagnosis was made in all cases by abdominal ultrasound and confirmed by excretory urography or (99m)technetium-dimercaptosuccinic acid scan. Voiding cystourethrography was performed in 40 cases (80%). Patients were followed for 2 to 11 years (mean 4.2). RESULTS: Associated urological anomalies were identified in 26 patients (52%) with horseshoe kidney, including primary vesicoureteral reflux in 13, ureteropelvic junction obstruction in 12 and ectopic ureter in 1. Surgical intervention to correct the anomalies in 15 of the 26 children (58%) involved pyeloplasty in 8, ureteral reimplantation in 2, endoscopic treatment for vesicoureteral reflux in 2, ureterolithotomy in 1, upper pole heminephrectomy in 1 and valve fulguration in 1. No significant complications were observed in surgically treated patients. CONCLUSIONS: More than half of the patients with a clinically symptomatic horseshoe kidney have vesicoureteral reflux or ureteropelvic junction obstruction. Many patients with horseshoe kidney require surgical intervention for associated urological anomalies with good results.
Multiple gastrointestinal atresias (MGA) have been reported to account for 6% to 32% of all intestinal atresias. Controversy exists regarding the pathogenesis. Many investigators believe MGA to be the result of multiple ischemic infarctions of the intestinal tract. However, some have suggested that MGA results from a malformative process early in fetal life. Prenatal exposure to adriamycin in a rat model has been reported to lead to a spectrum of tracheoesophageal and associated malformations of the gastrointestinal tract, including intestinal atresias, identical to these observed in humans. The aim of this study was to determine the incidence and histopathologic findings of MGA in order to understand the pathogenesis. Timed-pregnant Sprague-Dawley rats were injected with adriamycin (1.75 mg/kg) in nine different gestational-day protocols. MGA was only seen in those rats who received adriamycin on gestational days 7, 8, and 9. The litters were recovered on day 21 by cesarean section. The digestive tracts (DT) of the fetuses were harvested for macroscopic and microscopic examination. Ten rats who received adriamycin on gestational days 7, 8, and 9 produced 87 newborns; 1 was damaged during dissection. DT anomalies occurred in 80 (93%) of the 86 newborns; 94% of these demonstrated MGA. There was a very high incidence of associated anomalies in newborns with MGA. Histologically, the blind-ending atresias showed different degrees of villous hyperplasia with or without intraluminal material. This is the first report demonstrating a high rate of occurrence of MGA in the adriamycin rat model. The injection of adriamycin early in gestation, the high incidence of associated malformations, and the anatomic and histologic findings in MGA indicate that MGA is a result of a malformative rather than an ischemic process.
The n-3 and n-6 polyunsaturated fatty acids (PUFAs) are essential dietary constituents. They are potent modulators of the human immune response, and research has endeavoured to optimise the ratio of n-3 to n-6 fatty acids in the lipid emulsion component of total parenteral nutrition to harness their beneficial effects in the clinical setting. PUFAs modulate apoptosis of certain tumour cells and cell lines. Monocytes, which are major effector cells of the innate immune system, play a central role in the initiation, development, and outcome of the immune response. They are crucial in the defence against invading pathogens and are involved in the lysis of infected or malignant cells, wound healing, repair, and remodeling of tissues. In the present study we investigated whether PUFAs might evoke apoptosis in newborn monocytes. Purified cord-blood monocytes collected from uncomplicated full-term pregnancies were incubated for 24 h in complete medium in the presence or absence of one of the n-3 PUFAs docosahexaenoic acid (DHA) and eicosapentaenoic (EPA) or the n-6 PUFA arachidonic acid (AA). Following incubation, cells were triple-labelled with annexin V, CD14, and propidium iodide prior to flow-cytometric analysis to determine the degree of cell death. All experiments were performed in triplicate and data expressed as mean +/- 1 S.D. (%). In the absence of fatty acids, 30 +/- 4% of control cord monocytes underwent apoptosis or necrosis after 24 h incubation. At a concentration of 50 microM, none of the PUFAs had a significant effect on monocyte cell death, but at a dose of 100 microM, DHA resulted in 60 +/- 4% cell death (P < 0.05) while the other PUFAs had no significant effect. In contrast, at higher concentrations (200 microM), all the PUFAs significantly increased monocyte cell death (AA: 70 +/- 5%, DHA: 86 +/- 2%, EPA: 70 +/- 4%). PUFAs thus exert a potent influence on cord monocyte cell survival in vitro. Their effect is dose-dependent and DHA appears to be the most potent of the fatty acids tested. The influence of PUFAs on neonatal monocyte-cell survival suggests a novel mechanism whereby PUFAs may modulate the immune response.
Newborns with congenital diaphragmatic hernia (CDH) still have high mortality. Recently, a possible role of cardiac maldevelopment has been suggested. Human and experimental studies have demonstrated that heart weight is significantly reduced in the presence of CDH. Recent studies have suggested an important role for insulin-like growth factor-I (IGF-I) in the regulation of cardiac growth, structure, and function. Administration of IGF-I to normal rats has been shown to cause cardiac hypertrophy. Epidermal growth factor (EGF) plays an important role in cardiac differentiation and development. The aim of this study was to determine the gene-level expression of IGF-I and EGF in the hearts of rats with nitrofen-induced CDH using the reverse-transcription polymerase chain reaction technique (RT-PCR). CDH was induced in pregnant rats following administration of 100 mg nitrofen on day 9.5 of gestation (term 22 days). In control animals, the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into three groups: normal controls (n = 8), nitrofen without CDH (n = 8), and nitrofen-induced CDH (n = 8). Total RNA was extracted from the hearts in each group and measured. mRNA was extracted from total RNA. RT-PCR was performed to evaluate mRNA expressions of IGF-I and EGF. Levels of mRNA were expressed as a ratio of band density divided by that of beta-actin, a housekeeping gene known to be expressed at a constant level. IGF-I mRNA expression was significantly decreased in CDH hearts (0.177 +/- 0.109) compared to controls (0.393 +/- 0.138) (P < 0.01) and nitrofen hearts without CDH (0.321 +/- 0.088) (P < 0.05). EGF mRNA expression was significantly decreased in CDH hearts (0.218 +/- 0.118) compared to controls (0.534 +/- 0.196) (P < 0.01) and nitrofen hearts without CDH (0.383 +/- 0.136) (P < 0.05). Decreased cardiac gene expression of IGF-I and EGF in the hypoplastic heart suggests that cardiac hypoplasia in nitrofen-induced rat CDH may be due to reduced synthesis of IGF-I and EGF by myocytes in the developing heart.
Hirschsprung's disease (HD) is characterised by the absence of ganglion cells and the presence of hypertrophic nerve trunks in the distal bowel. It has been suggested that aganglionosis may be caused by failure of differentiation as a result of microenvironmental change after neuronal migration has occurred. Recently, it was reported that cell-adhesion molecules (CAMs) and fibroblast growth factors (FGFs) stimulate neurite outgrowth through activation of FGF receptors (FGFRs) in neurons. The aim of this study was to investigate the expression of CAMs FGFs, and FGFRs in ganglionic (NG) and aganglionic (AG) segments of HD in order to understand the role of CAM-FGF signalling in the pathogenesis of HD. Specimens from NG and AG segments of bowel from 11 patients with HD were obtained at the time of definitive pull-through operation, snap-frozen in OCT compound, and stored at -70 degrees C. Aganglionosis was confirmed by Haematoxylin and eosin staining and acetylcholinesterase histochemistry; 8-micron cryosections were immunostained using the standard streptavidinbiotin-immunoperoxidase method. The following antibodies were used as the first antibody; FGF2 and FGF7 for FGFs, FGFR1 and FGFR2 for FGFRs, NCAM, L1CAM, and N-cadherin for CAMs. FGF2, FGF7, and FGFR2 were expressed in neuronal tissue of NG segments as well as in hypertrophic nerves of AG segments. There was a lack of FGFRI expression in neuronal tissue of both NG and AG bowel. Immunoreactivity with all three CAMs was detected in ganglion cells in NG bowel and in hypertrophic nerve trunks in AG bowel. In contrast the numbers of CAM-positive nerve fibres in muscle layers were markedly decreased in AG bowel compared to NG bowel. The markedly decreased expression of CAMs on nerve fibres within the muscle of AG bowel suggests that CAM-FGF signalling is altered in HD, resulting in failure of enteric neuroblast migration.
Vesicoureteric reflux (VUR) is known to occur in families. In siblings of index patients with VUR, there is a much higher incidence (16% to 46%) than in the general population. The renin-angiotensin system plays an important role in renal development. Recently, it has been reported that angiotensin-converting enzyme (ACE) I/D gene polymorphism is a risk factor for renal parenchymal damage in patients with congenital urological abnormalities. The aim of this study was to investigate the ACE I/D genotype pattern in familial VUR patients. Blood samples were obtained from 86 families in which two or more members had VUR. Samples of DNA were extracted from 407 blood samples (183 affected patients and 224 non-affected family members). To detect ACE I/D polymorphism, polymerase chain reaction (PCR) amplification was performed using specific primers for the ACE gene. PCR products were electrophoresed with 2% agarose gel containing ethidium bromide. Among 224 non-affected family members the ACE genotype distribution of DD, ID, and II was 23%; 56% and 21%, respectively. The ACE genotype distribution of 183 affected patients was 28%, 47% and 25%, respectively. There was no significant difference in ACE I/D distribution between affected patients and their non-affected families. Both the ACE genotype distribution of affected patients and that of non-affected family members were not significantly different from the previously reported genotype distribution of the normal Caucasian population. This study demonstrates that ACE genotype frequencies are similar in index patients with VUR and their unaffected siblings, thus suggesting that the ACE gene is not involved in the development of familial VUR.
PURPOSE: We compared the incidence of renal scarring in infants with high grade vesicoureteral reflux in those presenting with and without urinary tract infection. METHODS AND METHODS: We reviewed the medical records of 81 male and 46 female infants (194 renal refluxing units) with a mean age of 4 months who had grade IV or V primary vesicoureteral reflux and underwent an anti-reflux procedure between 1984 and 1997. Dimercapto-succinic acid (DMSA) scans and voiding cystourethrography were performed in all cases. Patients were followed for 2 to 16 years, including 90% for greater than 3 years. Renal ultrasound and DMSA scan were done at followup. RESULTS: A total of 97 patients (76%) (148 refluxing renal units) presented clinically with urinary tract infection. The initial DMSA scan demonstrated renal scarring in 40 of the 106 grade IV (38%) and 28 of the 42 grade V (67%) refluxing renal units. There was no scarring on followup in previously normal refluxing renal units. Of the patients 30 (24%) (46 refluxing renal units) were diagnosed before a urinary tract infection developed, 16 underwent screening due to vesicoureteral reflux in a sibling and in 10 reflux was initially suspected due to hydronephrosis on prenatal ultrasound. In the remaining 4 patients vesicoureteral reflux was suspected during abdominal ultrasound to investigate abdominal pain, jaundice, associated hypospadias and fetal alcohol syndrome, respectively. DMSA scan showed evidence of scarring in 6 of 21 grade IV (29%) and 9 of 25 grade V (36%) refluxing renal units in this group. Followup revealed scarring in only 1 previously normal refluxing renal unit. CONCLUSIONS: The incidence of reflux nephropathy in primary grade V vesicoureteral reflux is lower in cases detected by screening and with treatment it remained lower than in cases of urinary tract infection that presented clinically. Early treatment of grade V vesicoureteral reflux made possible by screening may prevent renal damage.
A 59-year-old hypertensive man presented to eye casualty complaining of blurring of vision in his right eye. There was no history of any trauma or coagulation defects. Examination revealed a 4 mm hyphaema in his right eye with no evidence of rubeosis or traumatic squeal. The intraocular pressure was 32 mm Hg. The patient was managed conservatively using topical steroids and antiglaucoma medication. A number of vascular tufts were identified on slit lamp biomicroscopy and confirmed on iris angiography
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