[Epidemiological and genetic characteristics of H5 subtype avian influenza virus in Guangzhou, 2014-2019].

Objective: To analyze the characteristics of spread and genetic evolution of H5 subtype avian influenza virus in Guangzhou from 2014 to 2019. Methods: H5 subtype virus was detected by fluorescence quantitative RT-PCR from the environmental samples in Guangzhou poultry markets. The genes of HA and NA of 48 isolates randomly selected were sequenced, including 46 isolates from environmental samples and 2 isolates from cases. The characteristics of molecular variation and genetic evolution were analyzed by using bioinformatics software. Results: A total of 1 094 strains of H5 subtype avian influenza virus were isolated from 52 284 samples (2.09%). All the strains belonged to Clade 2.3.4.4.C. NA gene belonged to H6N6 of Eurasian lineage. The cleavage sites of all the strains showed the characteristics of highly pathogenicity. Receptor binding sites were avian-derived receptors. However, mutations of S123P, S133A and T156A occurred, which implied that these strains could tend to bind to human receptors. There was an additional glycosylation site at 140 in strains isolated after 2017. The variation of antigen loci mainly occurred in B and E regions. Conclusions: H5 subtype avian influenza virus spread in Guangzhou from 2014 to 2019 with annual increased proportion of positive rate, and the sequencing results indicated that it belonged to Clade 2.3.4.4.C of H5N6 highly pathogenic virus, and genetic evolution and mutation continued, especially the common mutations which could enhance the binding capacity to human receptors. It is necessary to strengthen the surveillance.

Central nervous system lupus and pregnancy: 11-year experience at a single center.

OBJECTIVE: To describe the pregnancy outcomes in women with central nervous system (CNS) manifestations of lupus. METHODS: Between 1991 and 2002, the outcome of five pregnancies in four patients with CNS lupus were retrospectively reviewed. All patients had an established history of systemic lupus erythematosus (SLE), and either a history of CNS lupus or active CNS lupus. Pregnancy outcomes assessed included term and preterm birth, intrauterine growth restriction, abnormal antepartum testing, perinatal mortality, pre-eclampsia and other maternal morbidities. RESULTS: Evidence of active CNS lupus symptoms developed in three of the five pregnancies. Two pregnancies were complicated by early onset pre-eclampsia, abnormal antepartum testing and extreme prematurity, with one subsequent neonatal death. The remaining three pregnancies had good neonatal outcomes, but were complicated by severe maternal post-pregnancy exacerbations, and the eventual death of one patient. CONCLUSIONS: CNS lupus in pregnancy represents an especially severe manifestation of SLE, and may involve great maternal and fetal risks.

Diabetic Charcot's arthropathy of the wrist. Case report and literature review.

Charcot's arthropathy of the right wrist in a 55-year-old patient with diabetes is reported. Neurogenic arthropathy rarely affects non-weightbearing joints such as those of the hand and wrist; the foot, ankle, and knee most commonly are affected. When crutches are used by patients with diabetes who have Charcot's arthropathy, orthotics and platform crutches can help to relieve pressure induced by weight transfer to the wrist during ambulation.

Ultrastructural differentiation and synaptogenesis in aggregating rotation cultures of rat cerebral cells.

Cerebral cortices from fetal rats were dissociated into single cells by either trypsinization or mechanical sieving. Then the cells were allowed to form aggregates in rotation cultures. At 7, 14, 21, 28, and 35 days, aggregates were processed for electron microscopic study of morphological differentiation with special emphasis on synaptogenesis. Whether the tissue was initially dissociated by trypsin treatment or by mechanical sieving, the aggregating cultures did not exhibit any apparent differences in ultrastructural differentiation and synaptogenesis. At day 7, most neurons were immature and the extracellular space was large. Cell processes had not yet branched extensively but did contain numerous microtubules. A few immature synapses were observed. Astrocytes and oligodendrocytes displayed many of their typical cytological features. At day 14, dendritic spines had developed, some of which formed axodendritic spinous synapses. Multilayered myelin sheaths were tightly wrapped around axons. At day 21, synapses appeared mature and their number per unit area was maximal. The extracellular space had greatly decreased. At this age, asymmetrical synapses had increased approximately sixfold, whereas symmetrical synapses increased only fourfold when compared with the 7-day-old aggregates. Multifocal degeneration became apparent at 28 days and was accompanied by a significant decline in the number of synapses.

An electron microscopic study of the developing caudate nucleus in euthyroid and hypothyroid states.

Thyroid hormone exerts a powerful influence on CNS growth and maturation. Hypothyroidism early in life has long been known to cause disturbances in innate behavior, motor performance, severe and frequently irreversible mental retardation. In this deficiency, depressed caudate neurogenesis, cell migration and neuropil development during the rapid period of CNS growth may contribute to the clinical picture of perceptual handicaps often seen in cretins. Light microscopic and Golgi studies of the developing caudate nucleus in thyroid deficiency have been carried out to help attain insights into the mechanisms whereby the extrapyramidal system regulates motor function. The ultrastructural study of caudate nuclear cytogenesis and synaptogenesis in normal and hypothyroid states provides more detailed information for further analysis of the problem. Hypothyroidism was induced from birth by adding prophylthiouracil to the food and drinking water of lactating dams. Linear development of the caudate nucleus of both normal and hypothyroid rats at ages 8, 14, 20, 30 and 42 days was studied by electron microscopy. Thyroid glands were examined by light microscopy to assess the normal and deficient states. Immature cells, primitive processes and synapses were the characteristic features of the 8-day-old normal caudate nucleus. Distinctively wide cisternae of the rough endoplasmic reticulum, loosley packed Golgi apparatus and chromatin clumps throughout the nuclei of the neurons were significant early morphologic variations. The dramatic cytoarchitectural maturation in the 14- and 20-day normal caudate neuropil points to the rapidity of developmental rate. After the growth spurt of the first three weeks a maturational plateau occurs which is characterized by well-formed neuronal cytoplasmic organelles, myelinated and non-myelinated axons, axon terminals, dendrites and their spines, and synapses. Thyroid deficiency causes a marked maturational delay of approximately 7 days in caudate neuronal proliferation, the elaboration of neuronal networks and the attainment of mature synaptic contents and membranes. This delay is evidenced by comparison of the structural similarities between 8-day-old normal and 14-day-old deficient rats; and additional comparisons between the 14-day-old normal and 20-day-old hypothyroid rats. A rapid "catch up" process in fine structural morphogenesis takes place in the period between days 14 and 30 in the deficient animals. Repression of thyroid function does not entirely prevent development of the caudate nucleus but allows a fairly extensive, though critically incomplete degree of maturation. This imperfection is manifested by a decrease in the number of synaptic contacts that persists even after the rapid "catch up" phenomenon of caudate synaptogenesis.

The developing caudate nucleus in the euthyroid and hypothyroid rat.

The basal ganglia are presently implicated in learning, and thyroid deficiency induced neonatally is known to affect mentation. The effects of such a deficiency on the developing causate nucleus might be used to provide insight into structure and function of the normal subcortical brain, as well as possible influences of these extrapyramidal structures on mental retardation. Propylthiouracil was added to the diet of lactating rat dams and observations of the developing caudate nuclei of normal hypothyroid rats were made at 8, 14, 20, 30 and 42 days by using various tissue stains and Golgi-Cox preparations. Seven different types of neurons were distinguished in the caudate nucleus. Differences in the size of cell somata and the varying morphology of axons and dendrites were criteria used to make distinctions. Normally, the nucleus acquires cytoarchitectural complexity during the first three postnatal weeks. Within this period, neuron incidence increases in the caudate neuropil with age while the germinal matrix density decreases. Neuron accumulation reaches a plateau after the third week and cell migration is essentially complete at the end of the first postnatal month as shown by computer analysis of Nissl stained cell counts. Branching of cellular processes, attainment of receptor spines and complexity of the fiber network also appeared during this period. Retardation of structural development with thyroid hormone deficiency was shown by decreased numbers of neurons, inhibition of dendritic arborization, decreased numbers of dendritic spines and a reduced complexity of axonal plexuses. Thyroid deficiency delays cell migration during the first three weeks when compared to age-matched normal controls. The lack of thyroid hormone does not appear to influence the size of neuron somata, and the extent of related dendritic fields, nor does hypothyroidism affect a specific cell type population. Generalized disturbances of caudate nuclear morphological maturation are caused by the deficiency. An apparent compensatory process, including a spurt of neural growth and differentiation, takes place in the period between days 14 and 30 in the deficient animals and a seemingly "normal" caudate cytoarchitecture is seen after the third postnatal week. Quantitative data, however, show that this rapid "catch up" process is inadequate. The developmental imperfection of the caudate nucleus which persists might be a part of the underlying substrate for the mental retardation, disturbed motor performance and perceptual handicaps which are found in the human patient.