[The Childbearing Experiences of Taiwanese Women After a Stillbirth].

BACKGROUND: Perinatal losses are traumatic events for women and may have serious long-term consequences for the psychological health of women and subsequent pregnancies. Therefore, it is important to explore the psychological adaptation process of subsequent pregnancy after loss in order to understand the overall phenomenon of perinatal loss. PURPOSE: To explore the childbearing experiences of women who have experienced a prior stillbirth. METHODS: This qualitative descriptive study targeted a purposive sample of 15 women who had prior personal experiences with stillbirth. A total of 22 in-depth interviews were conducted in order to ensure data saturation. Women who had experienced stillbirth at one of two teaching hospitals in southern Taiwan were recruited. Data were analyzed using content analysis. RESULTS: Three themes were identified that captured the complex feelings of participants regarding their subsequent childbearing experiences: (1) looking forward to another pregnancy but afraid of being hurt again, (2) treading on thin ice, and (3) bearing another child helps heal the loss of the stillborn. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: The empirical data gathered in the present study helps build a more complete understanding of the process of recovery that women undergo following a stillbirth experience. In addition, the results suggest that healthcare professionals should be aware of and accept the worries and reactions of women during their subsequent pregnancy in order to help these women achieve a positive subsequent childbearing experience.

Transcriptional regulators of the ΔNp63: their role in limbal epithelial cell proliferation.

The surface cells of corneal epithelium are regularly shed off and replaced by new cells that are derived from limbal epithelial stem cells (LESC). LESC are believed to reside in the basal layer of the limbal epithelium and are characterized with high expression levels of ΔNp63, a transcription factor (TF) which is believed to play roles in the regulation of LESC proliferation. In this study, we examined the transcriptional regulation of ΔNp63 in limbal epithelial cell. We employed DNA pull down assay followed by LC/MS analysis and cDNA microarray analysis to identify the TFs that were capable of binding to ΔNp63 promoter or were expressed at higher levels in limbus over cornea. The TFs thus selected were further examined for their in vivo ΔNp63 promoter binding by chromatin immunoprecipitation assay. We identified six putative TFs (PAX6, EGR1, CEBPB, JUN, ATF3, and ARID5B) through the aforementioned approaches. Among them, PAX6 and EGR1 were shown to promote the transcription of ΔNp63 and led to increased cell proliferation. In contrast, CEBPB and ATF3 appeared to exert little or no effect on ΔNp63 expression, however, their silencing suppressed cell proliferation. Although JUN exhibited low promoter-binding specificity, however, it affected ΔNp63 expression and limbal epithelial cell proliferation in ways similar to that of PAX6 and EGR1. Intriguingly, ARID5B was highly expressed in the limbal epithelial cell, however, its silencing by siRNA did not obviously affect the expression of ΔNp63, nor did it reduce cell proliferation of the limbal epithelial cell.

Neurodegeneration in streptozotocin-induced diabetic rats is attenuated by treatment with resveratrol.

AIM: Diabetes mellitus-associated hyperglycemia and oxidative stress have been shown to have detrimental effects on the brain and may lead to impairment of cognitive functions. Resveratrol (Rsv), a polyphenolic antioxidant, has been shown to have moderate hypoglycemic and prominent hypolipidemic effects in diabetic rats. In the present study, we examined if Rsv improves the diabetic encephalopathy and explored its possible underlying mechanisms. METHODS: Male SD rats were treated with streptozotocin (65 mg/kg), and the diabetic rats were orally fed with Rsv (0.75 mg/kg, every 8 h) or normal saline for 4 weeks. Animals were then sacrificed and the brain tissues (hippocampus) processed for biochemical and histological studies. RESULTS: Neurodegeneration and astrocytic activation were noted in the hippocampus of the diabetic rats. Tumor necrosis factor-α, IL-6 transcripts and nuclear factor-κB expression were increased in the brain. In addition, neuropathic alterations in the hippocampus were evident in diabetic rats, including increased blood vessel permeability and VEGF expression, decreased mitochondrial number and AMP-activated protein kinase activity. In Rsv-treated diabetic rats, the aforementioned abnormalities were all attenuated. CONCLUSION: These observations suggest that Rsv significantly attenuated neurodegeneration and astrocytic activation in the hippocampus of diabetic rats. Our results suggested that Rsv could potentially be a new therapeutic agent for diabetic encephalopathy and neurodegeneration.

Resveratrol ameliorates vasculopathy in STZ-induced diabetic rats: role of AGE-RAGE signalling.

BACKGROUND: Resveratrol (RSV) has been shown to ameliorate hyperglycaemia and hyperlipidaemia in streptozotocin-induced diabetic rats. In the present study, we examined the beneficial effects of RSV on diabetes mellitus (DM)-induced vasculopathy and explored its possible mechanism. METHODS: Male Sprague-Dawley rats were injected with streptozotocin at 65 mg/kg body weight The induction of DM was confirmed by a fasting plasma glucose level > or = 300 mg/dL and symptoms of polyphagia and polydipsia. The DM rats were treated with or without RSV at 0.75 mg/kg body weight three times a day for 4-8 weeks. Animals were sacrificed and vessel wall histology was examined by microscopy. The vascular smooth muscle cell activation was assessed by the medial thickness, collagen deposition, and the expressions receptor for advanced glycation end product, NF-kappaB, proliferation cell nuclear antigen, and the levels of Erk1/2 phosphorylation. RESULTS: In RSV-treated DM rats, the vascular wall thickening, collagen deposition/cross-linking, and vascular permeability were all alleviated compared with that of the untreated DM rats. The vascular smooth muscle cell of the RSV-treated rats was characterized with less proliferation, lower NF-kappaB, and Erk1/2 activation, decreased proliferation cell nuclear antigen and receptor for advanced glycation end product expression. Moreover, the plasma fructosamine was significantly reduced in RSV-treated DM rats. CONCLUSIONS: RSV alleviated DM-induced vasculopathy through attenuation of advanced glycation end product-receptor for advanced glycation end product-NF-kappaB signalling pathway.

An occult cause of hemodialysis vascular access dysfunction.

Although hemodialysis vascular access dysfunction is often caused by venous stenosis, stenosis can occur anywhere in the circuit. Herein, we report a 75-year-old woman who received repeated percutaneous angioplasty due to insufficient flow. Finally, a culprit stenosis at the subclavian artery was found and treated. Subclavian artery stenosis is often atherosclerotic in origin and is usually delayed to be diagnosed because of caveats in the care of vascular access. This case highlights important clues that can assist in the early discovery of inflow problems and reminds the physician that inflow stenosis may be hidden at a site far from the anastomosis.

Glycated type 1 collagen induces endothelial dysfunction in culture.

Hyperglycemia-induced protein glycation is thought to be implicated in the diabetic vasculopathy. In this study, we cultured vascular endothelial cells on native or glycated collagen matrix and compared their growth and functional characteristics. At lower plating density, the cells grew equally well on both substrata; however, at higher planting density, the cells plated on glycated collagen grew slower and reached a lower confluent density compared to that of the native collagen-based cultures. Confluent cell layers formed on glycated collagen exhibited a lower diffusion barrier function and a less response to epidermal growth factor stimulated prostacyclin production, compared to their native collagen-cultured counterparts.

STAT3 regulates the proliferation and differentiation of rabbit limbal epithelial cells via a ΔNp63-dependent mechanism.

PURPOSE: To explore the roles of STAT3 in the regulation of ΔNp63-dependent proliferation and differentiation of rabbit limbal keratinocytes. METHODS: siRNAs were designed to specifically suppress the expression of STAT3 and ΔNp63, and their effects on limbal epithelial cell proliferation and differentiation were examined. Ectopically expressed ΔNp63 was used to compensate for the decreased endogenous ΔNp63. Immunoblot was used to examine the expressions of STAT3, ΔNp63, K3, integrin ß1, and involucrin. RESULTS: Limbal tissue expresses higher level of phosphorylated and nuclear translocated STAT3 compared with that of the cornea. Knockdown of STAT3 expression reduces the expression of ΔNp63, inhibits the expansion of limbal epithelial outgrowth, suppresses the expression of integrin ß1, and promotes the expression of involucrin. CONCLUSIONS: STAT3 enhances the proliferation of limbal keratinocytes through a ΔNp63-dependent mechanism. Suppression of this pathway inhibits cell proliferation with a concomitant increase of cell differentiation.