Effects of Crop Rotation, Cultivar, and Irrigation and Nitrogen Rate on Verticillium Wilt in Cotton.

A field experiment was conducted under center-pivot irrigation in four wedges, with one wedge in continuous cotton (CC) and three wedges in a rotation (ROT) with 2 years cotton and 1 year in sorghum. Three irrigation rates (base = 1.0B, 1.5B, and 0.5B) were applied during 2007 to 2009 on a susceptible (ST) and partially resistant (PR) cultivar. Nitrogen applied during the season was proportional to irrigation rate. In the ROT wedges, 0.5B, 1.0B, and 1.5B irrigation and nitrogen rates averaged 1, 3, and 9% incidence of wilt, respectively. Disease incidence in the CC wedge averaged 6, 18, and 34% wilt incidence for 0.5B, 1.0B, and 1.5B irrigation and nitrogen rates. In the ROT wedges, the ST cultivar returned $143/ha more than the PR cultivars at the 0.5B irrigation and nitrogen rate whereas, at the 1.0B and 1.5B rates, the PR cultivars averaged $121 and $350/ha more than the ST cultivar. There was no significant irrigation and nitrogen or cultivar effect in the CC wedge on net value; however, trends were similar to the ROT wedge. Overall, ROT returned $285/ha more than CC, PR cultivars returned $123/ha more than the ST cultivar, and 1.0B returned $271 and $296/ha more than 0.5B and 1.5B rates, respectively. Microsclerotia density of V. dahliae averaged 2/cm3 of soil in the ROT wedges and 23/cm3 of soil in the CC wedge. Crop rotation, avoiding excessive irrigation, and using a partially resistant cultivar all reduced incidence of Verticillium wilt and improved net returns.

Effect of a Terminated Cover Crop and Aldicarb on Cotton Yield and Meloidogyne incognita Population Density.

Terminated small grain cover crops are valuable in light textured soils to reduce wind and rain erosion and for protection of young cotton seedlings. A three-year study was conducted to determine the impact of terminated small grain winter cover crops, which are hosts for Meloidogyne incognita, on cotton yield, root galling and nematode midseason population density. The small plot test consisted of the cover treatment as the main plots (winter fallow, oats, rye and wheat) and rate of aldicarb applied in-furrow at-plant (0, 0.59 and 0.84 kg a.i./ha) as subplots in a split-plot design with eight replications, arranged in a randomized complete block design. Roots of 10 cotton plants per plot were examined at approximately 35 days after planting. Root galling was affected by aldicarb rate (9.1, 3.8 and 3.4 galls/root system for 0, 0.59 and 0.84 kg aldicarb/ha), but not by cover crop. Soil samples were collected in mid-July and assayed for nematodes. The winter fallow plots had a lower density of M. incognita second-stage juveniles (J2) (transformed to Log(10) (J2 + 1)/500 cm(3) soil) than any of the cover crops (0.88, 1.58, 1.67 and 1.75 Log(10)(J2 + 1)/500 cm(3) soil for winter fallow, oats, rye and wheat, respectively). There were also fewer M. incognita eggs at midseason in the winter fallow (3,512, 7,953, 8,262 and 11,392 eggs/500 cm(3) soil for winter fallow, oats, rye and wheat, respectively). Yield (kg lint per ha) was increased by application of aldicarb (1,544, 1,710 and 1,697 for 0, 0.59 and 0.84 kg aldicarb/ha), but not by any cover crop treatments. These results were consistent over three years. The soil temperature at 15 cm depth, from when soils reached 18 degrees C to termination of the grass cover crop, averaged 9,588, 7,274 and 1,639 centigrade hours (with a minimum threshold of 10 degrees C), in 2005, 2006 and 2007, respectively. Under these conditions, potential reproduction of M. incognita on the cover crop did not result in a yield penalty.

The distribution of apolipoprotein E alleles in Scottish perinatal deaths.

BACKGROUND: The apolipoprotein E (ApoE) polymorphism has been well studied in the adult human population, in part because the e4 allele is a known risk factor for Alzheimer's disease. Little is known of the distribution of ApoE alleles in newborns, and their association with perinatal brain damage has not been investigated. METHODS: ApoE genotyping was undertaken in a Scottish cohort of perinatal deaths (n = 261), some of whom had prenatal brain damage. The distribution of ApoE alleles in perinatal deaths was compared with that in healthy liveborn infants and in adults in Scotland. RESULTS: ApoE e2 was over-represented in 251 perinatal deaths (13% v 8% in healthy newborns, odds ratio (OR) = 1.63, 95% confidence interval (CI) 1.13 to 2.36 and 13% v 8% in adults, OR = 1.67, 95% CI 1.16 to 2.41), both in liveborn and stillborn perinatal deaths. In contrast, the prevalence of ApoE e4 was raised in healthy liveborn infants (19%) compared with stillbirths (13%, OR = 1.59, 95% CI 1.11 to 2.26) and with adults (15%, OR = 1.35, 95% CI 1.04 to 1.76). However, no correlation was found between ApoE genotype and the presence or absence of perinatal brain damage. CONCLUSIONS: This study shows a shift in ApoE allelic distribution in early life compared with adults. The raised prevalence of ApoE e2 associated with perinatal death suggests that this allele is detrimental to pregnancy outcome, whereas ApoE e4 may be less so. However, ApoE genotype did not appear to influence the vulnerability for perinatal hypoxic/ischaemic brain damage, in agreement with findings in adult brains and in animal models.

Brain damage and axonal injury in a Scottish cohort of neonatal deaths.

Despite the clinical and medicolegal significance attached to perinatal asphyxia, the neuropathological basis of this condition remains obscure. There are very few studies in the literature which correlate the pathological findings in neonatal brains with detailed epidemiological data, and none which are population based. In a Scotland-wide study of neonatal deaths, 70 brains have been examined. On the basis of glial and macrophage reactions, we previously identified infants with putative antepartum brain damage in this cohort and have related these reactions to signs of birth asphyxia. The present study explores the extent of neuronal/axonal injury in these infants since this is likely to be the basis for neurological deficits in surviving infants. We have also investigated these brains for beta-amyloid precursor protein (betaAPP) positivity to determine whether this is a useful marker of neuronal injury in neonates. Neuronal eosinophilia and karyorrhexes were detected in 43% and 27% of the cohort, respectively; maximally in the subiculum and ventral pons, but often present elsewhere. White matter damage was detected in 24% of cases but without classic cystic lesions of periventricular leucomalacia. betaAPP positivity was present in neuronal soma in 52% of cases and, in axons, in 27% of cases, and was seen from as early as 25-weeks gestation. Axonal bulbs were clearly delineated by betaAPP positivity and were usually located in the cerebral white matter and internal capsule, and infrequently in the brain stem. Although white matter damage and betaAPP axonal positivity were often detected in the same cases (P = 0.034), these features also occurred independently of each other. Both neuronal karyorrhexes and white matter betaAPP positivity were significantly correlated with the features of birth asphyxia, particularly a history of seizures. Immunocytochemistry for both betaAPP and glial fibrillary acidic protein proved useful in detecting neuropathological features which escaped detection on routine examination, particularly in preterm infants. The presence together of recent and older damage in individual brains suggests that there is an ongoing neuronal response to cerebral insults. We find that betaAPP is a useful marker of white matter damage in the neonatal brain. Immunopositivity for betaAPP in these circumstances is not attributable to inflicted or accidental trauma. While birth-related trauma cannot be ruled out, hypoxia/ischaemia is a likely cause in these infants. However, the exact pathogenesis of neuronal/axonal injury in the neonatal brain remains unclear.

Novel SOX9 expression during human pancreas development correlates to abnormalities in Campomelic dysplasia.

Haploinsufficiency of SOX9, which encodes a homeodomain transcription factor, results in Campomelic dysplasia. Classical features of this disorder (e.g. skeletal dysplasia and 46,XY sex reversal) are in concordance with SOX9 expression profiles during human embryonic development. We report the robust expression of SOX9 throughout the pancreas during human embryogenesis, at levels of detection equivalent to the developing skeleton and testis. In the early foetal period, SOX9 expression declines and, in particular, is not apparent within the pancreatic islets. In keeping with this profile, examination of three cases with Campomelic dysplasia revealed abnormal pancreatic morphology. Epithelial cells were less densely packed within the mesenchymal stroma and islets less clearly formed with variable expression of hormone and beta cell markers. Taken together, these data indicate a novel potential role for SOX9 in pancreas development during human embryogenesis and early foetal life.

Pattern of malformations in the axial skeleton in human trisomy 13 fetuses.

The purpose of this study was to analyse the development of the axial skeleton in human trisomy 13 fetuses and to define which fields in the axial skeleton are affected in this condition. We investigated nine human fetuses with trisomy 13 and gestational ages of 14-19 weeks. Whole body radiographs and radiographs of midsagittal tissue blocks of the cranial base and the spine were studied. In the youngest fetus, 14 w GA, no malformations were observed. In eight fetuses, 17-19 weeks GA, malformations occurred in the lumbosacral spine. In four fetuses additional malformations were observed in the thoracic spine. The study showed that there was a correspondence between the extent of malformation in the lumbosacral spine and the thoracic spine. When mild malformation occurred in the lumbosacral region, no malformation was observed in the thoracic region, whereas malformation was observed in the thoracic region when there was extensive malformation in the lumbosacral region. Malformations did not occur in the cervical spine or the basilar part of the occipital bone, but the postsphenoidal part of the sphenoid bone was small and irregular in the six cases where it could be examined. In seven fetuses there was malformation or agenesis of the nasal bone. This pattern of axial skeletal malformations in trisomy 13 fetuses was not described previously. Comparisons are made with previous studies of the fetal axial skeleton in trisomy 18 and trisomy 21, where the pattern of malformations was different. We reiterate our recommendation that axial skeletal radiography should be part of the postmortem examination of fetuses with suspected or verified chromosome abnormalities.

Pattern of malformations in the axial skeleton in human trisomy 18 fetuses.

We examined and described the development and abnormalities of the axial skeleton in 10 human trisomy 18 fetuses. Whole-body radiographs and radiographs of midsagittal tissue blocks of the cranial base and the spine were studied. In 3 fetuses no spinal radiographs were available. Seven osseous regions or fields along the body axis were analyzed, four in the spine, and three in the cranial base and nasal bones. Malformations occurred in the occipital field in all fetuses. This was a characteristic notching, either unilateral or bilateral, of the basilar part of the occipital bone. Nasal bones were abnormal in 8 cases, either absent or hypoplastic. Malformations were found in the thoracic and/or lumbosacral field in 7 fetuses. A single abnormality was found in the cervical spine in one fetus. The pattern of axial skeletal malformation in trisomy 18 fetuses recorded in the present study has not been described previously. Axial skeletal radiography should be included in autopsies of fetuses when chromosome disorders are present or suspected. The methods applied here are unaffected by autolysis.

Pattern of malformations in the axial skeleton in human trisomy 21 fetuses.

In the present study, we analyzed the development of the axial skeleton in human trisomy 21 fetuses and defined the fields in the axial skeleton affected in this form of aneuploidy. We investigated 31 human fetuses with trisomy 21, gestational ages 12-24 weeks, on the basis of radiographs of midsagittal tissue blocks of the axial skeleton, comprising the cranial base and the spine. Malformation or agenesis of the nasal bone was present in 19 of 31 fetuses. Nineteen cases had vertebral malformations. Fourteen fetuses had malformations in the cervical region, four in the thoracic and eight in the lumbosacral region. In 1 of 31 fetuses, malformation was seen in the basilar part of the occipital bone. The basisphenoid component appeared scallop-shaped in 30 cases. The pattern of axial skeletal malformations in trisomy 21 fetuses recorded here has not been described previously. Comparison is made with our recent study of trisomy 18, where the pattern of axial skeletal malformations was quite different. It is recommended that axial skeletal radiography should be part of the autopsy of fetuses where chromosome abnormalities are known or suspected.

Fraser syndrome (cryptophthalmos-syndactyly syndrome): a review of eleven cases with postmortem findings.

Detailed postmortem findings from 11 cases of probable Fraser (cryptophthalmos-syndactyly) syndrome are reported. Eight cases presented as neonatal deaths, one as a stillbirth, and there were 2 midtrimester fetuses. All of the cases had ocular, otic, digital, laryngeal, and renal abnormalities. Details of the pregnancies and sibship data are also reported. The possibility of prenatal diagnosis for this syndrome is discussed.

Pattern of malformations in the axial skeleton in human triploid fetuses.

We examined the axial skeleton in 15 human triploid fetuses (10 with XXX and 5 with XXY sex chromosomes). All fetuses 14-29 weeks of gestational age (GA), underwent whole-body radiography, permitting analysis of the nasal bone and the spine. From 9 of these, detailed radiographs were taken of midsagittal blocks of the cranial base and the spine, permitting detailed analysis of the cranial base. NASAL BONE: Of 14 fetuses, where the nasal bone was seen on lateral projection, it appeared short in 10 cases. SPINE: The spine was normal in 7 of 15 fetuses; malformations occurred in 8. These were osseous fusions between 2 or more vertebral bodies, most frequently in the cervical and thoracic regions, and disproportions in the sizes of the cervical bodies. Fusions occurred in 5 cases alone, and in one case in combination with disproportions of vertebral size. Disproportions alone occurred in 2 cases. CRANIAL BASE: Malformation of the basilar part of the occipital bone was found in 5 of the 9 fetuses investigated. Of 9 fetuses, bilateral ossification centers of the postsphenoid bone occurred in 7, and shell-like ossification centers in 2. There was no difference in the type of malformations in the different axial fields related to genotype (XXX and XXY). CONCLUSION: The most remarkable findings in the axial skeleton of triploid fetuses are vertebral fusions in 6 of 15 cases; clefts of vertebral bodies, previously reported as common findings in trisomy fetuses, are not demonstrated.

Skeletal malformations in fetuses with Meckel syndrome.

In six fetuses with Meckel syndrome (gestational age 16-23 weeks, crown-rump length 130-170 mm) the skeleton was examined as part of the autopsy procedure using whole body radiography and special radiographic techniques. In the upper and lower limbs we found similar types of polydactyly. We noted four types, based on the number and morphology of metacarpals and metatarsals. In the individual fetus there was more often similarity in the pattern of malformation in the two hands or in the two feet than there was between the pattern of malformation seen in the hands and that seen in the feet. Only one foot was normal. Malformations of the cranial base (the basilar part of the occipital bone or the postsphenoid bone) occurred in five cases, and the vertebral bodies in the lumbar region of the spine were malformed (cleft) in three cases. It is proposed that a skeletal analysis be included in the future evaluation of phenotypes in Meckel syndrome.

Pituitary gland and sella turcica in human trisomy 18 fetuses.

The purpose of this study was to elucidate the phenotypic conditions in the sella turcica/pituitary gland complex in human trisomy 18 fetuses. Fourteen human fetuses with gestational ages from 12 to 39 weeks were included in the study. Normal fetuses at corresponding ages were used as controls. Whole body and special radiographic examination was undertaken before the midsagittal cranial base block, including the pituitary gland, was excised and analyzed histologically and immunohistochemically (keratin wide spectrum [KWS], thyroid-stimulating hormone [TSH], and neurophysin [Nph]). In all trisomy 18 fetuses, TSH-positive adenopituitary tissue was present in the sella and in greater or lesser amounts pharyngeally. The neurohypophysis was Nph-positive and located normally in the sella turcica. The adenohypophyseal tissue reacted either KWS-faint or KWS-negative, whereas KWS-positive reaction occurs in normal fetuses. This circumstance might suggest an altered cytoskeletal structure of the surface ectoderm in the pituitary placode in trisomy 18. The sella turcica was malformed in all the fetuses. Very broad craniopharyngeal canals were observed in some of the fetuses. Because endocrine disorders occur in many congenital malformations, it is essential in future studies to chart the sella turcica/pituitary gland region systematically in different genotypes.

Pituitary gland and sella turcica in human trisomy 21 fetuses related to axial skeletal development.

The purpose of the present investigation was to study the sella turcica/pituitary gland region in trisomy 21 fetuses and to relate the findings in the region to the ossification pattern in the axial skeleton formed by the cranial base and spine. Material from 22 human fetuses with trisomy 21, CRL 80 mm to CRL 190 mm, corresponding to gestational ages from 14 to 21 weeks, was examined and compared with material from gestation-matched normal controls. After radiography, tissue blocks from the cranial base, including the pituitary gland, were examined and compared with those of normal fetuses. Four different types of sella turcica/ pituitary gland morphology were observed. Thirteen fetuses (Type I) were morphologically normal. Minor abnormalities occurred in the sella turcica and pituitary gland (adenopituitary gland tissue pharyngeally) in six fetuses (Types II and III). There was agreement between the histologically recorded deviations in the sella turcica and the radiographic observations of the basisphenoid bone. In three cases (Type IV) out of 22, more pronounced structural abnormalities occurred in the sella turcica, and radiographically the basisphenoid bone appeared cleft. All sella turcica changes observed in trisomy 21 were situated anteriorly in the base of the sella. In all cases the basilar part of the occipital bone was normal. Minor changes in the sella turcica region were mainly accompanied by cervical vertebral abnormalities, while the most severe abnormalities occurred in association with malformations in the lumbar vertebrae. There was no association between sella turcica malformations and the absence or presence of the nasal bone.

Hand development in trisomy 21.

The purpose of the present study was to evaluate hand size and maturity in fetuses with trisomy 21 (Down syndrome). Twenty-five fetuses, crown-rump length (CRL) 55-222 mm, foot length (FL) 8-42 mm, were included in the study. After whole-body radiography (Hewlett Packard Faxitron), special radiographs of the hand and foot were taken. Hand length was measured as the length of the third finger from the distal tip of the distal phalanx to the proximal tip of the metacarpal bone, the digital-metacarpal length (DML). The lengths of the proximal phalangeal bone (PPL) and the metacarpal bone (MCL) of the third finger were also measured. The DML, PPL, and MCL values of each fetus were related to CRL and FL. The individual hand bones were evaluated with regard to time of appearance on radiographs, sequence in comparison with the normal sequence of appearance, and morphology. The hand length is normal during the first half of the fetal period, whereas the length of individual bones in the third finger is reduced. The normal sequence of ossification, with the middle phalanx of the fifth finger last to ossify, also occurred in Down syndrome; however, this bone appeared later in Down syndrome. In four of the fetuses it did not appear.

Clinical phenotype of desmosterolosis.

We describe a child with lethal multiple malformations and generalised accumulation of desmosterol. The infant had macrocephaly, a hypoplastic nasal bridge, thick alveolar ridges, gingival nodules, cleft palate, total anomalous pulmonary venous drainage, ambiguous genitalia, short limbs, and generalised osteosclerosis. Gas chromatography-mass spectrometry demonstrated an abnormal accumulation of desmosterol in kidney, liver. and brain. Higher than normal levels of the same sterol were detected in plasma samples obtained from both parents. The biochemical phenotype in this infant is highly suggestive of a novel inborn error of cholesterol biosynthesis caused by an autosomal recessive deficiency of 3betahydroxysterol-delta24-reductase. A phenotypic overlap of this case with Raine syndrome was noted; however, desmosterol accumulation was not found on postmortem tissue samples from a previously reported case of this disorder.

Prenatal malformed lumbar vertebral corpora in trisomies 21, 18, and 13, evaluated radiographically and histologically.

The aim of the present study was to compare, both radiographically and histologically, malformed vertebral lumbar corpora in trisomies 21, 18 and 13 with earlier reported normal corporal development in the axial lumbar region. Axial skeletons of human fetuses (GA 15-22 wk) derived from therapeutically induced abortion were investigated in connection with requested autopsy. The number of lumbar vertebral corpora examined for each genotype was as follows: 20 from trisomy 21, 10 from trisomy 18, and 10 from trisomy 13. After radiography in frontal, lateral and axial projections, the individual vertebral corpora were decalcified and horizontally embedded in paraffin. The blocks were serially sectioned and stained with toluidine blue and alcian blue/van Gieson. The radiographic characteristics of the vertebral corpora varied from an almost normal appearance of the corporal bone to complete clefting of the bony corpora. Histological examination showed accumulations of cartilage centrally, in some cases associated with amorphous material. Pronounced metachromatic differences were observed in the cartilaginous ground substance. The study showed identical phenotypic characteristics in the corpora from trisomy 21, trisomy 18, and trisomy 13. It is characteristic of all three genotypes that there are central anomalies, corresponding to the location of the notochord in normal corpora, and marked regional differences in metachromasia in the ground substance of the cartilage.

Malformations of cranial base structures and pituitary gland in prenatal Meckel syndrome.

The sella turcica region, including the clivus and the pituitary gland, was studied histologically in five human fetuses with Meckel syndrome (MS). All cases had malformed sella turcica and malformed clivus with irregularly shaped notochordal remnants. We consider that these three characteristics are constant phenotypic traits in MS. The adenohypophysis was present in three cases. In one of these, ectopia of the gland occurred with adenopituitary tissue overlying the dorsum sella, and in another remnants were found in the pharyngeal submucosa. In two fetuses the neurohypophysis was not found. The findings in the region were compared to normal findings and to findings in trisomy 18, where cranial base structures radiographically appeared similar to those in MS. We conclude that in MS specific characteristics are found in the cranial base region and that radiographic analysis needs to be supplemented by histological analysis when studying this specific region.

Value of perinatal necropsy examination.

In a retrospective study of 150 stillbirths and 150 neonatal deaths carried out between 1981 and 1985 the necropsy findings were compared with the clinical diagnoses, which had been obtained from the postmortem request form, and the case notes completed before the necropsy was performed. In all cases the necropsy comprised macroscopic findings and histological examination of all organs, with microbiology, radiology, and cytogenetics where appropriate. Clinically important differences between clinical and pathological diagnoses in 54 of 150 cases (36%) were noted in the cases of stillbirth. Of the neonatal deaths, examination showed clinically important information that had not been recognised during life in 66 cases (44%). Histological examination of tissues was essential for making or confirming the pathological diagnosis in 20% of all perinatal deaths.

Gastrointestinal lymphoma in childhood.

Thirteen cases of lymphoma of the bowel in infancy and childhood are presented. There is a marked preponderance in males. The tumour most commonly presents with abdominal pain and intestinal obstruction; the prognosis is poor. Histological findings characteristic of the ;Burkitt' type of lymphosarcoma do not apparently influence survival.

Non-isotopic in situ hybridisation and immunophenotyping of infected cells in the investigation of human fetal parvovirus infection.

AIMS: To compare the use of biotinylated and digoxigenin labelled probes for diagnosis of human fetal parvovirus B19 infection in formalin fixed, paraffin wax embedded tissues; and to assess the cellular distribution of the virus in positive cases. METHODS: Sections of lung tissue from 23 cases of anatomically normal non-immune fetal hydrops presenting between 1984 and 1989, and from 13 control cases of hydrops due to chromosomal abnormality were probed for B19 DNA by in situ hybridisation using both biotinylated and digoxigenin labelled probes. The distribution of the virus was then investigated in all cases of fetal B19 infection confirmed in this laboratory to date (n = 11) by combining in situ hybridisation for viral DNA (using the digoxigenin system) with immunohistological labelling for a range of cellular antigens. RESULTS: Five unequivocal cases of B19 infection were identified among the 23 fetuses with unexplained hydrops using both probe labels. When combined with data from previous studies of the period 1974-1983, the results indicate that B19 infection was responsible for 27% of cases of anatomically normal non-immune hydrops and 8% of all cases, of non-immune hydrops presenting to this hospital over 15 years. False positive signal was seen in an additional three cases, using biotinylated probes. Digoxigenin labelled probes gave greater specificity and permitted detailed investigation of tissues high in endogenous biotin. Though most cells containing B19 DNA colabelled as erythroid precursors, viral DNA was frequently detected within mononuclear-phagocytic cells. In three cases viral signal was also found within occasional myocardial cells labelled by antibody to desmin. CONCLUSIONS: A relatively high proportion of cases of anatomically normal, non-immune hydrops are caused by B19 infection. Digoxigenin is a more reliable probe label than biotin for in situ hybridisation in archival fetal tissues. Double labelling for cellular antigens and viral nucleic acid is a powerful technique for investigating virus-host cell interactions, and provides evidence that cell types other than those of erythroid lineage may have a role in human fetal parvovirus infection.