Incentivizing Authorization for Deceased Organ Donation With Organ Allocation Priority: The First 5 Years.

The allocation system of donor organs for transplantation may affect their scarcity. In 2008, Israel's Parliament passed the Organ Transplantation Law, which grants priority on waiting lists for transplants to candidates who are first-degree relatives of deceased organ donors or who previously registered as organ donors themselves. Several public campaigns have advertised the existence of the law since November 2010. We evaluated the effect of the law using all deceased donation requests made in Israel during the period 1998-2015. We use logistic regression to compare the authorization rates of the donors' next of kin in the periods before (1998-2010) and after (2011-2015) the public was made aware of the law. The authorization rate for donation in the period after awareness was substantially higher (55.1% vs. 45.0%, odds ratio [OR] 1.43, p = 0.0003) and reached an all-time high rate of 60.2% in 2015. This increase was mainly due to an increase in the authorization rate of next of kin of unregistered donors (51.1% vs. 42.2%). We also found that the likelihood of next-of-kin authorization for donation was approximately twice as high when the deceased relative was a registered donor rather than unregistered (89.4% vs. 44.6%, OR 14.27, p < 0.0001). We concluded that the priority law is associated with an increased authorization rate for organ donation.

Calciuria and preeclampsia.

Urinary calcium excretion has been reported to be diminished in preeclampsia. The objective of the present study was to determine urinary calcium excretion in pregnant patients with chronic arterial hypertension (CAH) and preeclampsia (PE), and in normotensive patients (N). Forty-four pregnant patients (gestational age, 20-42 weeks; 18 CAH, 17 PE, 9 N) were evaluated for calciuria, proteinuria, plasma uric acid and blood pressure. Patients with PE (82 +/- 15.1 mg/24 h) showed significantly lower calciuria (P < 0.05) than the group with CAH (147 +/- 24.9 mg/24 h) and the N group (317 +/- 86.0 mg/24 h) (P < 0.05, Student t-test). Plasma uric acid was significantly higher in the PE group (6.1 +/- 0.38 mg/dl) than the CAH group (5.0 +/- 0.33 mg/dl; P < 0.05), which also presented higher proteinuria levels, although the difference was not statistically significant. Diastolic and systolic blood pressure did not differ between the PE (164 +/- 105 mmHg) and CAH (164 +/- 107 mmHg) groups. Calciuria was significantly lower in the group with preeclampsia than in the group with chronic arterial hypertension. We conclude that calciuria can be a further factor for identifying preeclampsia.

Calciuria and preeclampsia

Urinary calcium excretion has been reported to be diminished in preeclampsia. The objective of the present study was to determine urinary calcium excretion in pregnant patients with chronic arterial hypertension (CAH) and preeclampsia (PE), and in normotensive patients (N). Forty-four pregnant patients (gestational age, 20-42 weeks; 18 CAH, 17PE, 9N) were evaluated for calciuria, proteinuria, plasma uric acid and blood pressure. Patients with PE (82 + 15.1 mg/24 h) showed significantly lower calciuria (P<0.05) than the group with CAH (147 + 24.9 mg/24 h) and the N group (317 + 86.0 mg/24 h) (P<0.05, Student t-test), Plasma uric acid was significantly higher in the PE group (6.1 + 0.38 mg/dl) than the CAH group (5.0 + 0.33 mg/dl; P<0.05), which also presented higher proteinuria levels, although the difference was not statistically significant. Diastolic and systolic blood pressure did not differ between the PE (164 + 105 mmHg) and CAH (164 + 107 mmHg) groups. Calciuria was significantly lower in the group with preeclampsia than in the group with chronic arterial hypertension. We conclude that calciuria can be a further factor for identifying preeclampsia.

Aluminum-induced neurofibrillary degeneration affects a subset of neurons in rabbit cerebral cortex, basal forebrain and upper brainstem.

Neurofibrillary tangles in Alzheimer's disease show a predilection for cortical pyramidal and subcortical projection neurons. The antigenic composition, neuronal specificity and distribution of aluminum-induced neurofibrillary degeneration were examined in regions of rabbit brain analogous to those that develop neurofibrillary tangles in Alzheimer's disease. Neurofibrillary degeneration was induced by intraventricular instillation of aluminum chloride. In aluminum-treated rabbits, intensely immunoreactive filamentous aggregates were seen in affected neuronal perikarya after staining with an antiphosphorylated neurofilament antibody (SMI 31), while in controls immunoreactivity was confined to axon-like elements. Monoclonal antibodies against Microtubule-associated protein 2 and tau, which stain human neurofibrillary tangles, did not stain aluminum-induced neurofibrillary degeneration. Pyramidal neurons exhibiting neurofibrillary degeneration formed a discrete linear pattern in layers III and V of cortex. Cortical somatostatin and nicotinamide adenine dinucleotide phosphate diaphorase-reactive neurons identified in double-stained sections were unaffected. Large perikarya in the vicinity of the globus pallidus, some of which contained acetylcholinesterase, were frequently SMI 31-immunoreactive. Among the cell groups affected in the upper brainstem were the nucleus raphe dorsalis and locus coeruleus. These findings show that aluminum-induced neurofibrillary degeneration differs antigenically from neurofibrillary tangles in Alzheimer's disease. Nevertheless, many neuronal subsets that are particularly susceptible to Alzheimer's disease, including cortical pyramidal neurons, basal forebrain cholinergic neurons and upper brainstem catecholaminergic neurons, are also affected by aluminum-induced neurofibrillary degeneration.

An immunocytochemical comparison of cytoskeletal proteins in aluminum-induced and Alzheimer-type neurofibrillary tangles.

Exposure of the central nervous system (CNS) of rabbits to aluminum salts produces a progressive encephalopathy. Examination of CNS structures discloses widespread perikaryal neurofibrillary tangle (NFTs) formation. The aluminum-induced NFTs consist of collections of normal neurofilaments, and differ ultrastructurally and in their solubility characteristics from Alzheimer-type NFTs, the latter being composed of largely insoluble paired helical filaments. The present study compares NFTs found in the rabbit to those of Alzheimer's disease, using monoclonal antibodies (SMI 31, SMI 32) that recognize phosphorylated and non-phosphorylated determinants respectively in normal neurofilaments, and an antiserum raised against purified microtubules. Paraffin-embedded sections were stained by the avidin-biotin immunocytochemical method. Intense staining of aluminum-induced NFTs was found after processing with SMI 31 and SMI 32, while no staining of non-tangled perikarya of control rabbits or of Alzheimer-type NFTs was seen. Antimicrotubule anti-serum gave weak, nonfocal staining in the aluminum-treated and control rabbits, while Alzheimer-type NFTs were stained intensely. These results show that phosphorylated and non-phosphorylated neurofilaments accumulate in aluminum-induced NFTs, thus complementing the previously demonstrated specific slowing of the axonal transport of neurofilaments in aluminum intoxication. Further, they suggest that the presence of microtubular proteins may be necessary for altered neurofilaments to take on a paired helical configuration.

Interaction of crocidolite asbestos with hamster respiratory mucosa in organ culture.

Organ cultures of hamster trachea were used to study the effects of crocidolite asbestos on the respiratroy epithelium and the uptake of asbestos by cells of the mucosa. International Union Against Cancer (U.I.C.C.) crocidolite was suspended in medium over a range of concentrations and precipitated on the epithelial surface for 1 hour. At intervals during the ensuing 4 weeks, morphologic changes were documented by light, scanning electron, and transmission electron microscopy. Cytotoxic alterations in differentiated mucosal cells appeared to relate to the amount of crocidolite added to the cultures. Necrosis and desquamation of surface cells were accompanied by basal cell hyperplasia. These proliferating cells phagocytosed the dust and incorporated it into lysosomes. Crocidolite was also found interposed between cells of the hyperplastic basal cell layer. Transport of asbestos particles to the submucosa and uptake by mesenchymal cells was apparent after 1 week.

Lesions of the islets of Langerhans in encephalomyocarditis virus-infected mice with diabetes mellitus-like disease. I. Acute lesions.

Mice infected with the M variant of the encephalomyocarditis (EMC) virus develop lesions of the islets of Langerhans associated with a diabetes mellitus-like disease. Ultrastructural alterations become evident in capillaries and beta cells at a time when large amounts of virus are present in the pancreatic tissue. Although some beta cells become necrotic, degranulation and contraction of intact cells is the prominent lesion. Changes in the capillaries appear early in the course of the infection and later are associated with interstitial fibrosis in and around the islets. During early convalescence, beta cells are degranulated and exhibit striking alterations of cytoplasmic organelles. These changes appear to be consequent to increased metabolic activity by the residual insular tissue. Interestingly enough, specific lesions of the alpha cells are not observed.