Characterization of FLC, SOC1 and FT homologs in Eustoma grandiflorum: effects of vernalization and post-vernalization conditions on flowering and gene expression.

A rosette plant of Eustoma grandiflorum requires vernalization (exposure to a period of cold temperature) and long-day conditions to promote flowering, while prolonged cold or cool temperatures in post-vernalization periods delay flowering. This study aimed to investigate the effect of growth conditions on flowering regulation in Eustoma. In Arabidopsis, vernalization suppresses a floral repressor gene, FLOWERING LOCUS C (FLC) and upregulates floral promoter genes, such as SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1) and FLOWERING LOCUS T (FT).

The histopathogenesis of paralytic rabies in six-week-old C57BL/6J mice following inoculation of the CVS-11 strain into the right triceps surae muscle.

A fatal encephalomyelitis was developed after intracerebral and hind limb inoculation of in 6-week-old C57BL/6J mice by the inoculation of fixed rabies virus (CVS-11 strain), intracerebrally and into hind. After the intracerebral inoculation, virus antigens were detected in the cerebral cortex and hippocampus at 2 days postinoculation (PI), and later spread centrifugally to thalamus, brain stem, cerebellum, spinal cord and spinal ganglia. At 4 days PI, severe apoptosis and DNA fragmentation were observed in the hippocampus and cerebral cortex.

Evidence for functional nicotinic receptors on pancreatic beta cells.

Epidemiological studies associate smoking with reduced insulin secretion. We hypothesized that nicotine could negatively affect pancreatic beta-cell function. Acute or 48-hour exposures to nicotine (10(-4) to 10(-6) mol/L) moderately inhibited insulin release at basal (3.

Short-term intermittent exposure to diazoxide improves functional performance of beta-cells in a high-glucose environment.

Prolonged periods of "beta-cell rest" exert beneficial effects on insulin secretion from pancreatic islets subjected to a high-glucose environment. Here, we tested for effects of short-term intermittent rest achieved by diazoxide. Rat islets were cultured for 48 h with 27 mmol/l glucose alone, with diazoxide present for 2 h every 12 h or with continuous 48-h presence of diazoxide.

Interleukin-1beta swiftly down-regulates UCP-2 mRNA in beta-cells by mechanisms not directly coupled to toxicity.

Regulation of uncoupling protein-2 (UCP-2) in beta-cells is presently unclear but may involve oxidative stress. We tested for regulation by beta-cell toxic cytokines. Exposure to interleukin-1beta (IL-1beta, 10 ng/ml) for 6 h down-regulated UCP-2 mRNA in clonal INS-1 cells, by 37 +/- 7%, and in rat pancreatic islets, by 55 +/- 8%.

Pneumonia in horses induced by intrapulmonary inoculation of Streptococcus equi subsp. zooepidemicus.

To evaluate the possibility that Streptococcus equi subsp. zooepidemicus (S.z) the causative bacterial agent of equine shipping fever pneumonia (ESFP), as well as to investigate its pathogenesis, 10 horses (seven Thoroughbreds and three Anglo-Arab species, ranging from 2-4 years in age) were experimentally inoculated, via an endoscope, into bronchus of the lung lobe with a dose of 30 ml of 1-7 x 10(8) CFU/ml of S.

Langerhans cells within the follicular epithelium and the intradermal sweat duct in equine insect hypersensitivity "Kasen".

Histopathologic and electron microscopic observations were given on Langerhans cells (LCs) within the follicular epithelium (FE) and intradermal sweat duct (ISD) of equine "Kasen". By light microscopy, LCs were present in the greatest numbers within the FE and ISD than within the epidermal layer and the normal skin, with an occasional formation of several aggregated foci. By electron microscopy, LCs within the FE and ISD widely extended their dendritic processes between the keratinocytes and contained Birbeck granules (Bgs), mitochondria, rough endoplasmic reticula and ribosomes in the cytoplasm.

Glucosamine-induced beta-cell dysfunction: a possible involvement of glucokinase or glucose-transporter type 2.

Introduction: The mechanism for beta-cell dysfunction induced by glucosamine has not yet fully been investigated previously.

Aim: To investigate the effects of glucosamine on insulin release or gene expression related to glucose metabolism in rat islets cultured with glucosamine for 24 hours.

Methodology: After islets were cultured with glucosamine or diazoxide, we measured glucose- or arginine-induced insulin release by using radioimmunoassay (RIA) and gene expressions by semiquantitative polymerase/chain reaction.