Pancreatic pseudotumor in pancreas divisum: CT characteristics

We report a case in which a focally spared area of pancreatic tissue in a gland otherwise replaced by fat created a "pseudomass" mimicking neoplasm on sonography and CT. The "pseudomass" appearance was related to the anomalous ductal anatomy in pancreas divisum. The spared area of pancreas creating a "pseudomass" was drained by the dorsal duct and the remainder of the pancreas that had undergone relative fatty replacement was drained by the ventral duct.     

Occlusion and the solution to the aperture problem for motion

The "aperture problem" indicates that a local reading of the velocity of an oriented contour is inherently ambiguous, insufficient by itself to recover the velocity of image points. In Wallach's "barber pole" display consisting of moving diagonal lines within an elongated rectangular aperture, it has been suggested that the unambiguous motion of edge-terminators along the longer edges of the aperture propagates towards the motion-ambiguous center part of drifting stripes. This results in the perception of a surface moving in the direction of the longer axis of the aperture. By manipulating the stereoscopic disparity of a striped pattern relative to the aperture plane, we found that the disambiguating effects of terminators could be abolished if the striped pattern was in uncrossed disparity relative to the aperture plane. Also, the motion in 3 separate horizontally oriented, and vertically aligned apertures which would otherwise be seen as moving horizontally, was seen as "linked" together and moving vertically. This occurred only when the horizontally oriented segments separating these apertures were stereoscopically coded so that they appeared as occluders in front. These findings suggest that accidental or "extrinsic" terminators created by occluding edges are treated differently from real or "intrinsic" terminators, and that the real-world constraint of occlusion is thus implemented in the ambiguity-solving processes for motion.     

Measuring maternal mortality: An overview of opportunities and options for developing countries

Background  

There is currently an unprecedented expressed need and demand for estimates of maternal mortality in developing countries. This has been stimulated in part by the creation of a Millennium Development Goal that will be judged partly on the basis of reductions in maternal mortality by 2015.     

Fine-needle aspiration cytology of the adrenal gland. Fifty biopsies in 48 patients.

Fine-needle aspiration biopsy of 50 adrenal masses from 48 patients was performed between 1984 and 1991. The series consisted of 28 males and 20 females, with an age range of 12 months to 79 years (mean age, 55 years). Clinical and/or pathologic follow-up was available in 37 patients. Fine-needle aspiration was diagnostic in all 29 malignant cases having follow-up, with no false-positive diagnoses. There were six primary malignancies (three neuroblastomas, two pheochromocytomas, and one adrenal cortical carcinoma) and 23 metastatic lesions. Of these, the lung was the most frequent primary malignancy (60%), followed by melanoma and renal cell carcinoma (8.6% each). The remaining nonmalignant fine-needle aspiration diagnoses were adrenal cortical neoplasms (most likely adenoma), adrenal cortical hyperplasia, myelolipoma, benign adrenal tissue, and abscess. Based on clinical follow-up, three other adrenal adenomas were not diagnosed by fine-needle aspiration. Six biopsy specimens (12%) were insufficient for diagnosis. Ancillary studies including electron microscopy and/or immunocytochemistry were performed on 13 malignant aspirates and provided additional confirmation of the cytology diagnosis in 12 cases. This study confirms that fine-needle aspiration is a sensitive and highly specific procedure for the evaluation of primary and metastatic malignancies involving the adrenal gland. The technique is less useful in the workup of benign processes but, in some instances, can provide specific diagnostic information.     

Autoantibody response to the Ro/La particle may predict outcome in neonatal lupus erythematosus.

This study was undertaken to determine the role of antibodies against both recombinant Ro (r-Ro) and La (r-La) proteins and polypeptides derived from the recombinant La protein in predicting fetal and neonatal outcome in children at risk to develop neonatal lupus erythematosus (NLE). All sera were obtained in the perinatal period and quantitative ELISA assays were used. We collected 41 maternal sera within 2 months of delivery of a child with NLE (21 with congenital heart disease block (CHB) and 20 with dermatologic NLE) and 19 sera from anti-Ro and/or anti-La antibody-positive mothers with systemic lupus erythematosus (SLE) who delivered a child without NLE. All sera were tested for anti-r-La and anti-r-Ro antibodies by ELISA, and most sera were tested for antibodies directed against La polypeptides by immunoblot. We found significantly higher anti-r-La antibody levels in the sera from mothers of children with NLE compared with sera from mothers of unaffected children (0.67 +/- 0.43 versus 0.14 +/- 0.30; P < 0.0001). There was a statistically significant difference in the mean anti-r-La levels between the sera of mothers of children with CHB compared with dermatologic NLE (0.51 +/- 0.45 versus 0.83 +/- 0.37 respectively; P = 0.0091). When we examined antibodies directed against the recombinant 52-kD Ro protein, there was a statistically significant elevation of titres in the sera of mothers of NLE children (0.77 +/- 0.35) compared with non-NLE mothers (0.29 +/- 0.39; P < 0.0001). There was no difference in the r-Ro levels between mothers of children with dermatologic NLE compared with CHB (0.82 +/- 0.37 versus 0.71 +/- 0.74; P = 0.32). When we examined polypeptides derived from the recombinant La protein, the mean number of polypeptides recognized by sera from mothers of children with NLE was significantly higher than the mean number of polypeptides recognized by sera from mothers of unaffected children (5.1 +/- 0.54 versus 2.3 +/- 0.54 respectively; P < 0.001). More importantly, when we examined the individual polypeptides, we found that only sera from mothers of children with NLE and not from mothers of unaffected children recognized a polypeptide designated DD (30% versus 0%, respectively). These studies indicate that the autoantibody response to the Ro/La particle can differentiate sera from mothers of children with NLE and sera from mothers of unaffected children. Furthermore, there was a difference in the anti-La autoantibody response between mothers of children with CHB and dermatologic NLE.(ABSTRACT TRUNCATED AT 400 WORDS)     

The hypothalamic magnocellular neurosecretory system of the guinea pig. II. Immunohistochemical localization of neurophysin and vasopressin in the fetus

The development of the hypothalamic magnocellular neurosecretory system of the fetal guinea pig was examined by immunohistochemistry. Neurophysin was first observed in the supraoptic nucleus (SON), median eminence (ME) and posterior pituitary (PP) on day 40 of gestation. It was not regularly present in the paraventricular nucleus (PVN) until day 47. Vasopressin was first observed in the SON, ME and PP on day 45. In the median eminence immunoreactive deposits indicative of both peptides were observed in both the fibers of the hypothalamo-hypophysial tract (H-HT) in the presumptive zona interna as well as in axons projecting to the developing primary portal plexus.     

Determination of postglomerular permselectivity to neutral dextrans in the dog

The single-pass multiple-indicator-dilution (MID) technique was used to analyze postglomerular capillary permeability. Anesthetized mongrel dogs (n = 13) during mannitol diuresis received a pulse injection of 125I-albumin (plasma reference), [14C]inulin (glomerular reference), creatinine (interstitial reference), and a homogeneous [3H]dextran molecular weight marker 6,000-12,000 dalton in the left renal artery. Simultaneous left renal venous outflow and right and left urine were rapidly sampled. Left urine recoveries of creatinine, [14C]inulin, and [3H]dextran were identical, indicating no glomerular solute flux limitation. Progressive precession of the [14C]inulin and [3H]dextran renal vein curves relative to creatinine indicated increasing postglomerular limitation to solute flux proportional to molecular size. The postglomerular solute extraction (EPG) (renal vein upslope indicator/125I-albumin) varied inversely with postglomerular renal plasma flow (F), indicating diffusion limitation. Ouabain infusion into the left renal artery significantly reduced Na reabsorption but did not alter the EPG of [14C]inulin or [3H]dextran. Permeability-surface (PS) area products calculated from EPG and F ranged from 4.86 +/- 0.89 to 0.97 +/- 0.25 (SD) cm X s-1 X 100 g-1 for indicators 5,000-12,000 dalton. [14C]Inulin PS products remained constant for F greater than or equal to 2.50 ml X s-1 X 100 g kidney-1. PS[3H]dextran/PS[14C]In (n = 20, F greater than or equal to 2.5 ml X s-1) was used to calculate an effective postglomerular capillary pore radius, r = 55.5 +/- 7.6 (SD) A.     

Association of defensin beta-1 gene polymorphisms with asthma

BACKGROUND: Defensins are antimicrobial peptides that may take part in airway inflammation and hyperresponsiveness. OBJECTIVE: We characterized the genetic diversity in the defensin beta-1 (DEFB1) locus and tested for an association between common genetic variants and asthma diagnosis. METHODS: To identify single nucleotide polymorphisms (SNPs), we resequenced this gene in 23 self-defined European Americans and 24 African Americans. To test whether DEFB1 genetic variants are associated with asthma, we genotyped 4 haplotype-tag SNPs in 517 asthmatic and 519 control samples from the Nurses' Health Study (NHS) and performed a case-control association analysis. To replicate these findings, we evaluated the DEFB1 polymorphisms in a second cohort from the Childhood Asthma Management Program. RESULTS: Within the NHS, single SNP testing suggested an association between asthma diagnosis and a 5' genomic SNP (g.-1816 T>C; P = .025) and intronic SNP (IVS+692 G>A; P = .054). A significant association between haplotype (Adenine, Cytosine, Thymine, Adenine [ACTA]) and asthma ( P = .024) was also identified. Associations between asthma diagnosis and both DEFB1 polymorphisms were observed in Childhood Asthma Management Program, a second cohort: g.-1816 T>C and IVS+692 G>A demonstrated significant transmission distortion ( P = .05 and .007, respectively). Transmission distortion was not observed in male subjects. The rare alleles (-1816C and +692A) were undertransmitted to offspring with asthma, suggesting a protective effect, contrary to the findings in the NHS cohort. Similar effects were evident at the haplotype level: ACTA was undertransmitted ( P = .04) and was more prominent in female subjects ( P = .007). CONCLUSION: Variation in DEFB1 contributes to asthma diagnosis, with apparent gender-specific effects.     

The degradation of serum amyloid A protein by activated polymorphonuclear leucocytes: participation of granulocytic elastase

To determine the role of inflammation in amyloidogenesis, we have studied the degradation of human serum amyloid A (SAA) protein by purified preparations of human blood polymorphonuclear leucocytes (PMN) and monocytes. When both PMN and monocytes were incubated in SAA-containing medium, the concentration of SAA as measured by a competitive anti-AA radioimmunoassay decreased over time. The rate of decrease of SAA was similar for both monocytes and PMN and there were no differences between four patients with amyloidosis and three normal controls. Resting PMN from normal volunteers were able to degrade SAA to smaller acid-soluble peptides within 16 hr while zymosan-activated PMN produced significant degradation within 1 hr (31%–50%). The supernatants from zymosan-treated PMN also caused marked SAA degradation within 1 hr.

The following enzyme inhibitors were able to prevent degradation of SAA by PMN supernatants; phenylmethylsulphonyl fluoride, a serine esterase inhibitor; α₁ anti-trypsin and soybean trypsin inhibitor; and acetyl-ala-ala-pro-val-chloromethyl ketone, an elastase inhibitor. The ability of a neutral lysosomal enzyme to degrade SAA was further confirmed by showing that purified PMN elastase significantly degraded ¹²⁵I-SAA.

We conclude that PMN contain one or more lysosomal enzymes capable of degrading SAA, an apoprotein of HDL₃ serum lipoproteins. Alteration in SAA proteolysis by activated PMN may contribute to the deposition of amyloid fibrils in the tissues of patients with chronic inflammatory disease.