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Efferent inhibition of low and medium speontaneous-rate fiber activity in response to characteristic frequency (CF) tones is greater at levels between 50 and 75 dB SPL than at lower levels, and even occurs at levels of 100 dB SPL [Guinan and Stankovic, J. Acoust. Soc. Am. 100, 1680–1690 (1996)]. The self-mixing effect of a laser diode was used to measure tone-evoked, basilar membrane (BM) displacements in the basal turn of the guinea pig cochlea during electrical stimulation of the medial efferent system. Efferent stimulation suppresses BM displacement and, for frequencies close to the CF of the measurement site and above, attenuation of tone-evoked displacements appears to be greatest for levels between 50 and 75 dB SPL, and efferent attenuation could exceed 10 dB SPL for tones at 90 dB SPL. By comparison, the attenuation of the BM vibrations caused by tones at frequencies below CF was found to be greatest for low sound pressure levels. The findings of Guinan and Stankovic therefore have their origin in events present in the vibrations of the BM.

A retrospective study of all children who had undergone renal transplantation at the National University Hospital was undertaken in order to investigate the types and frequency of infections in paediatric renal transplant recipients. A total of 13 children ranging in age from 3 to 17 years were transplanted over a 7-year period from 1989 to 1996. The mean follow-up period was 40.5 months. Ten patients (77%) had at least one episode of infection post-transplant, 70% of which occurred within the first 6 months post-transplant. These infections included urinary infections (8), disseminated cytomegalovirus (CMV) disease (4), Pneumocystis carinii pneumonia (1) and mycoplasma pneumonia (1). Urinary tract infections were significantly associated with the presence of ureteral stents. CMV disease was significantly associated with the use of mycophenolic acid in the early post-transplant period. Infection therefore continues to be a major cause of morbidity in paediatric renal transplant recipients.

The masquerade (mas) locus encodes an extracellular molecule with a striking similarity to serine proteases. The serine residue, which is essential for enzymatic activity, has been substituted by glycine, suggesting that MAS could serve to antogonize serine protease activity [Murugasu-Oei et al. (1995), Genes Dev. 9, 139–154]. We describe the expression pattern of mas mRNA and protein in the developing embryonic, larval and pupal nervous system and in the epidermis. Total loss of mas function is lethal and results in aberrations in the embryonic central and peripheral nervous systems, consistent with a role in axonal guidance. The possibility that the observed deficits in taste behavior, exhibited by animals with partial loss of mas function, are a result of defects in the adult brain are discussed.

A retrospective cohort study was undertaken to evaluate the diagnostic value of the renal medulla in acute renal allograft rejection (ARAR). One hundred and ninety-five biopsies from 98 patients were randomly selected out of 565 transplant biopsies. Biopsies were graded blindly from Grade 0 (no rejection) to Grade 3 (severe rejection) using standard criteria ; ARAR was confirmed by a fall in all cases of mean serum creatinine concentration from 0.331±0.182 to 0.184±0.079 mmol/l, with antirejection therapy. In the 43 biopsies which contained both cortex and medulla, the ARAR grades and the intensities of mononuclear cell, plasma cell, polymorphonuclear cell and eosinophil infiltrates, and of interstitial oedema and haemorrhage, were similar in cortex and medulla (Spearman's Rank Correlation r=0.55-0.81, P 0.05), except for more cortical biopsies with plasma cells ( 29%) than medullary biopsies with plasma cells (10% ; P

A retrospective cohort study was undertaken to evaluate the diagnostic value of the renal medulla in acute renal allograft rejection (ARAR). One hundred and ninety-five biopsies from 98 patients were randomly selected out of 565 transplant biopsies. Biopsies were graded blindly from Grade 0 (no rejection) to Grade 3 (severe rejection) using standard criteria; ARAR was confirmed by a fall in all cases of mean serum creatinine concentration from 0.331 +/- 0.182 to 0.184 +/- 0.079 mmol/l, with anti-rejection therapy. In the 43 biopsies which contained both cortex and medulla, the ARAR grades and the intensities of mononuclear cell, plasma cell, polymorphonuclear cell and eosinophil infiltrates, and of interstitial oedema and haemorrhage, were similar in cortex and medulla (Spearman's Rank Correlation r = 0.55-0.81, P0.001). The sensitivity, specificity and overall accuracy of medullary changes in predicting ARAR changes in the cortex were 77%, 100% and 38%, respectively. Acute vascular rejection changes could not be compared between renal cortex and renal medulla because of the anatomical differences between cortex and medulla. Further evaluation of ARAR in the all 195 biopsies, of which 188 had cortical tissue and 50 had medullary tissue, showed no significant differences in histological features (P0.05), except for more cortical biopsies with plasma cells (29%) than medullary biopsies with plasma cells (10%; P0.02). It is concluded that: (1) ARAR histological changes are similar in cortex and medulla; (2) the predictive value of ARAR medullary changes for cortical rejection changes has low sensitivity (77%) and high specificity (100%).(ABSTRACT TRUNCATED AT 250 WORDS)

This report describes a patient with acute renal failure that resulted from the ingestion of djenkol beans. Features of acute djenkolism include nausea, vomiting, bilateral loin pain, gross hematuria, and oliguria. The blood urea level was 16.2 mmol/L and the serum creatinine was 460 mumol/L. Phase contrast microscopy of the urinary sediment indicated that the hematuria was nonglomerular. Ultrasound of the kidneys showed slightly enlarged kidneys with no features of obstruction. Renal biopsy showed acute tubular necrosis similar to the single animal study reported in the literature. With conservative therapy, which included rehydration with normal saline and alkalinization of the urine with sodium bicarbonate, the acute renal failure resolved. Based on its chemistry, djenkol bean-associated acute renal failure may be analogous to acute uric acid nephropathy.

Background Patients with cirrhosis due to hepatitis B and C are at risk of developing hepatocellular carcinoma (HCC). These patients are periodically screened by imaging studies and alpha-fetoprotein (AFP) levels. Case report We present a case of a 58-year-old male with established, biopsy proven cirrhosis due to hepatitis C. He remained clinically stable for 11 years. One year prior to death, his AFP levels started to rise, reaching 300 000 IU/mL before death. Ultrasound, triple phase CT and MRI of the liver confirmed cirrhosis but failed to find any definite tumour. No tumour was seen elsewhere. He died of liver failure and the question asked by clinicians at autopsy was ‘Where is the tumour?’. At autopsy, the liver was enlarged and cirrhotic, weighing 3985 g. No obvious discrete mass lesion, suggestive of HCC, was seen on gross examination. No other mass lesions were identified elsewhere. Microscopic examination revealed extensive infiltration of liver by nodules of moderately differentiated HCC interspersed amongst cirrhotic nodules. Conclusion This case is a very rare variant of HCC which diffusely involves the liver without forming a discrete dominant mass and macroscopically mimics cirrhosis. Diagnosing this variant of HCC on a background of cirrhosis is therefore a clinical and radiological challenge. This pattern of HCC has been described in some case series, predominantly as an incidental finding in cirrhotic explanted livers with mild or no rise in AFP levels. Our case is unique as there was a high clinical suspicion of HCC, given the alarming rise in AFP levels, but radiologically no such lesion was detected.

The risk of renal papillary necrosis and renal dysfunction due to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) is unknown. In a prospective study of 259 heavy analgesic users seen in a general medical hospital over an 11-year period beginning in January 1982, 69 new cases of analgesic nephropathy with renal papillary necrosis were confirmed by intravenous urogram (26.6%), ultrasonography (30.4%), and/or computed tomography (43%). Twentynine of these patients (42%) had consumed excessive quantities of NSAIDs alone; an additional nine patients (13%) had consumed NSAIDs predominantly in combinations with paracetamol, aspirin, phenacetin, caffeine, and/or traditional herbal medications. Of those patients who consumed NSAIDs alone, 17 had consumed only a single type of NSAID and the remaining 12 had consumed multiple types of NSAIDs. The amount of NSAIDs administered ranged from 1,000 to 26,600 capsules or tablets over a 2- to 25-year period. Renal impairment (serum creatinine, 126 to 778 μmol/L) was noted in 26 of these 38 patients (64.8%). The reasons given for consuming NSAIDs include gouty arthritis (18 patients), osteoarthritis (seven patients), rheumatoid arthritis (six patients), chronic headache (three patients), gouty arthritis plus chronic headache (three patients), and chronic backache (one patient). All patients were prescribed these drugs and were followed medically. The occurrence of analgesic nephropathy was predominantly in males (male to female ratio, 1.9:1). Most of the patients did not have the characteristic psychological profile attributed previously to analgesic abuse nephropathy. Associated addictive habits, such as the use of psychotropic drugs and sleeping tablets, purgative abuse, and alcoholism, were absent. We conclude that excessive consumption of NSAIDs can lead to analgesic nephropathy with chronic renal impairment. The frequency of this problem related to the size of the population chronically receiving prescribed and nonprescribed NSAIDs needs to be carefully discerned by controlled prospective studies as part of any public health strategy to prevent end-stage renal disease.

Despite the tremendous health-care advances in recent years, external compression of the tracheobronchial tree by cardiovascular anomalies still remains a significant cause of morbidity and potential mortality in neonates and infants. As the initial presenting symptoms can be deceivingly mild, the diagnosis is easily missed without a high index of suspicion by the investigating clinician utilising the appropriate investigations. Four case studies are presented, (i) illustrating the importance of tracheobronchoscopy in assessing any neonate or infant with suspected airway obstruction; (ii) reviewing the current literature, and (iii) suggesting a comprehensive diagnostic approach by way of relevant investigations.

Background: Presacral lesions often present late because of non-specific presenting symptoms and imaging findings that are difficult to interpret. We present the clinical scenario and review of the literature. Methods: A plexiform neurofibroma presenting as a presacral mass is described, with the difficulties in diagnosis and investigation explored. Results: CT and MRI are useful imaging modalities in the diagnosis of an undifferentiated presacral mass and certainly contribute to eliminating some differential diagnoses and exploring characteristics of the lesion, but ultimately the need for a histological diagnosis and surgical excision is highlighted. Conclusion: Presacral masses are difficult to diagnose, assess and treat. Adequate imaging and histological confirmation are essential in their treatment.

Dieulafoy's disease is a submucous arterial malformation of the stomach, and is a known cause of massive upper gastrointestinal bleeding. To date, 125 cases have been reported in the literature. Fatality is high if the condition remains undiagnosed. Endoscopy is difficult but important in the diagnosis of Dieulafoy's disease. Dieulafoy's disease in two Asian women are reported here. Both required large amount of blood transfusions as the diagnosis was not recognised early. Greater awareness of the condition will enable earlier diagnosis and reduced mortality from this condition.

Renal dysplasia and agenesis as isolated findings are usually considered sporadic, noninherited abnormalities. We report three kindreds with familial renal adysplasia. Two or more children were affected in each of the families and at least one member--whether proband, sibling, or parent--had a clinically silent anomaly. Normal kidneys in the parents did not preclude the occurrence of renal adysplasia in more than one child. The empiric risks for offspring and first-degree relatives were 50% and 25%, respectively, suggesting a strong genetic factor such as a major dominant gene with variable expression. Because the disease appears to be genetic in some cases of renal adysplasia, careful screening of the proband's family, subsequent children, and pregnancies is important for the purpose of accurate genetic counseling.

A comparative study was made on two groups of children comprising 20 patients with renal hypoplasia/dysplasia in one group and 12 patients with chronic glomerulonephritis (GN) in the other, presenting with chronic renal failure (CRF) in the Department of Paediatrics, Singapore General Hospital and National University Hospital between 1975 and 1989. The age of onset of CRF, the progression of renal failure and the presence of various clinical complications were analysed and compared. The mean age of onset of CRF was earlier in patients with renal hypoplasia/dysplasia (p less than 0.001) but the progression of renal failure in these patients were slower (p less than 0.005). Hypertension occurred more frequently in the chronic GN group (p less than 0.001) while urinary tract infection (UTI) occurred more frequently in the renal hypoplasia/dysplasia group (p less than 0.004). With the early onset of renal failure and slow deterioration of renal function in patients with renal hypoplasia/dysplasia, the provision of good conservative treatment for renal failure is most important in the management of these patients. In the chronic GN patients however, with the rapidity of deterioration of renal function, early preparation for replacement therapy becomes more imminent. However, renal replacement therapy in end-stage renal failure (ESRF) is costly and not readily available, it is more prudent to delay the onset of ESRF by providing effective conservative treatment of renal failure which includes the early recognition and treatment of hypertension in chronic GN and UTI in renal hypoplasia/dysplasia.

A series of Chinese newborns of consecutive normal vaginal deliveries were investigated for the distribution of serum transferrin subtypes by polyacrylamide gel iso-electric focusing at pH 3.5-9.5. Newborns whose mothers had a history of previous spontaneous abortion (n = 189) had a significantly higher frequency of the C2 variant and the C2 gene compared to those (n = 864) without a history of spontaneous abortion. There was no significant difference in the frequency of transferrin alleles between newborns with normal and low birth weight (n = 147).

Complications of chemotherapy for a synovial sarcoma in an eight-year old boy included cisplatinum nephrotoxicity and adriamycin cardiotoxicity. The resultant renal failure and fluid overload necessitated peritoneal dialysis. Intractable hypomagnesemia was also a prominent feature.

It has been suggested that the negative charge on the surface of red blood cells (RBC) may reflect the charge on the glomerular capillaries. Measurements were made of RBC charge in patients with steroid-responsive nephrotic syndrome (SRNS) based on the binding of a cationic dye, alcian blue. There was no difference found between patients in relapse and in normal controls. We conclude that RBC charge measurements are not a reliable indicator of the glomerular charge barrier and a more specific method is required.