Magnesium-doped zinc oxide electrochemically grown on fluorine-doped tin oxide substrate.

Nanostructures of magnesium (Mg) doped Zinc oxide (ZnO) were successfully deposited on conducting fluorine-doped tin oxide (FTO) coated glass plates by cathodic electrochemical deposition method at different potentials and temperature conditions. The deposited samples were characterized by XRD and SEM techniques to confirm their structures, morphologies and optical properties. These measurements show that Mg doped ZnO has a wurtzite structure and that the strongest intensity of the (002) peak is found at 60 degrees C and -1.0 V. Tunable transmittance of Mg doped ZnO has a band gap energy from 3.45 eV to 3.82 eV, which is the direct evidence of doping.

Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years.

BACKGROUND: Atrophic gastritis and intestinal metaplasia are premalignant conditions for gastric cancer. Their reversibility by Helicobacter pylori eradication remains controversial. AIM: To evaluate the reversibility of atrophic gastritis and intestinal metaplasia by H. pylori eradication with long-term follow-up. METHODS: 598 subjects were prospectively enrolled and followed for up to 10 years. They were categorised as H. pylori-negative (n = 65), H. pylori non-eradicated (n = 91), and H. pylori-eradicated (n = 442). Histological assessment was performed for antrum and corpus by Sydney classification. RESULTS: Histological follow-up was performed regularly at 1, 2, 3-4 and ≥5 years, with mean follow-up of 1.07 ± 0.21, 2.29 ± 0.83, 3.93 ± 1.02, and 6.45 ± 1.28 years, respectively. Atrophic gastritis in antrum and corpus gradually and significantly (both P < .05 for all timepoints) improved only in the H. pylori-eradicated group compared to that at baseline. Significant difference in atrophic gastritis between H. pylori-eradicated and H. pylori-negative groups disappeared from 1-year follow-up. Similarly, intestinal metaplasia in antrum and corpus improved significantly (both P < .05 for all timepoints) only in the H. pylori-eradicated group in comparison with that at baseline. Significant difference in intestinal metaplasia between H. pylori-eradicated and H. pylori-negative groups disappeared from ≥5 years of follow-up in the antrum and from 3 years of follow-up in the corpus. CONCLUSION: H. pylori eradication may be a preventative strategy for intestinal-type gastric cancer by regression of atrophic gastritis and intestinal metaplasia.

Detection of response-predicting mutations in the kinase domain of the epidermal growth factor receptor gene in cholangiocarcinomas.

PURPOSE: Epidermal growth factor receptor (EGFR) signalings have recently been implicated in the genesis and progression of cholangiocarcinomas. Thus, the EGFR kinase inhibitor appears to be promising in the treatment of this cancer. The response-predicting mutations in the tyrosine kinase domain of EGFR gene have recently been detected in non-small cell lung cancers. This study was, therefore, to investigate if these mutations are also found in cholangiocarcinomas. METHODS: Twenty-two consecutive cholangiocarcinoma patients who underwent surgical resection were enrolled. Their resected paraffin-embedded cholangiocarcinoma specimens were used for mutation analysis, which was performed by DNA sequencing of exons 18, 19 and 21 in the EGFR gene. Clinical characteristics were compared between each group according to the presence or absence of mutations. RESULTS: Three patients (13.6%) harbored EGFR mutations. All the mutations found were deletions in exon 19. Mutations were more common in intra-hepatic or poorly differentiated tumors. Differences in age, sex, stage at diagnosis and survival were not observed between mutation-positive and -negative patients. CONCLUSIONS: This study, for the first time, demonstrates that a subset of cholangiocarcinoma patients has response-predicting EGFR mutations. Therefore, a highly selected application of the EGFR kinase inhibitor would be therapeutically effective in these patients.

c-Fos basal immunoreactivity decreases in rat spinal cord during normal ageing.

The pattern of distribution in rat spinal cord and changing pattern during normal ageing of c-Fos expression were investigated by immunohistochemical staining in male Sprague-Dawley rats at the age of 1 week, 5 months and 2 years. c-Fos immunoreactivity was observed diffusely in gray matters in neonatal rats, preferentially located in deep dorsal horn and around central canal. Compared with those of neonatal rats, these cells decreased prominently in adult rats. In aged rats, immunoreactive cells were not seen in any segments. c-Fos immunoreactivity in spinal cord may be related to stress response, functional differentiation, and in part, neuronal death with target dependence. In conclusion, we demonstrated for the first time that c-Fos expression patterns change during normal ageing.

Immunohistochemical study on the distribution of six members of the Kv1 channel subunits in the rat basal ganglia.

The differential expression of specialized voltage-gated potassium (Kv) channel subtypes in the nervous system probably reflects the wide range of functions. Although there have been previous reports in the cellular and subcellular localizations of various Kv mRNAs and proteins, the comprehensive study described here is the first in which the expression of six Kv1 channel subunits have been directly compared in the rat basal ganglia. In the present study, we have found that staining patterns of the six Kv1 channel subunits overlap in some areas of the basal ganglia, but each has a unique pattern of expression. It was noted that Kv 1.4 subunit had a strikingly high level of expression in the globus pallidus compared to the caudate-putamen. This distinct distribution formed the clear demarcations between caudate-putamen and globus pallidus. The dot-like staining pattern of Kv1 subunits was observed through the accumbens nucleus. Strong staining for Kv1.4 was observed in the cerebral peduncle, not in the subthalamic nucleus. In the substantia nigra, immunoreactivity for Kv1.4 subunit was prominent in the pars reticulata of the substantia nigra. The staining intensity for Kv1.2 was high in the pars compacta of the substantia nigra. Our immunohistochemical results may support the notion that the formation of heteromultimeric Kv channels possibly represents an important contribution to the generation of Kv channel diversity in the brain, especially in the basal ganglia.

Age-related changes in the distribution of Kv1.1 and Kv1.2 channel subunits in the rat cerebellum.

We have revealed age-related changes in the expression patterns of Kv1.1 and Kv1.2 in the rat cerebellum for the first time. In the aged rat, immunoreactivity for Kv1.1 was increased in the cell bodies of Purkinje cells, while the staining intensity was significantly decreased in the granule cells. The cell bodies of cerebellar output neurons showed strong Kv1.1 immunoreactivity in the nucleus medialis, interpositus and lateralis of the aged rat. Kv1.2 immunoreactivity was found in some interneurons with their processes in this region of the aged rat. Image analysis demonstrated that immunoreactivities for Kv1.1 and Kv1.2 were increased specifically in the cell bodies of cerebellar output neurons of the aged rat. This study may provide useful data for future investigations on the channels that cause brain diseases and age-related disorders.

Immunohistochemical study on the distribution of Bcl-2 and Bax in the central nervous system of the transgenic mice expressing a human Cu/Zn SOD mutation.

In the present study, we performed immunohistochemical studies to investigate the changes of Bcl-2 and Bax in the central nervous system of the transgenic mice expressing a human Cu/Zn SOD mutation. In contrast to the controls, a high density of Bcl-2-IR astrocytes were detected all around the gray matter of the spinal cord of the mutant transgenic mice. Bcl-2-IR astrocytes were also detected in the cerebellum and brainstem of transgenic mice. Specific immunoreactivity for Bax was seen in the spinal cord and brainstem of transgenic mice. Immunostaining for Bax was identified only in neurons and not in glial cells. Our present study demonstrated the distribution of Bcl-2 and Bax in detail using immunohistochemical methods through the central nervous system of the transgenic mice, for the first time.

Immunocytochemical study on the distribution of nitrotyrosine in the brain of the transgenic mice expressing a human Cu/Zn SOD mutation.

In the previous study, we reported increased NOS expression in the astrocytes in the spinal cord of the transgenic mice that are used as ALS animal model. In the present study, we performed immunocytochemical studies to investigate the changes of nitrotyrosine-immunoreactivity in the brains of the transgenic mice, and demonstrated in vivo evidence of peroxynitrite-mediated oxidative damage in the pathogenesis of ALS. In the spinal cord of the transgenic mice, immunocytochemistry showed intensely stained nitrotyrosine-IR glial cells with the appearance of astrocytes, but no nitrotyrosine-IR glial cells were observed in the spinal cord of the control mice. In the transgenic mice, nitrotyrosine-IR neurons were observed in the hypoglossal nucleus, lateral reticular nucleus, medullary reticular formation and cerebellar nuclei. Interestingly, nitrotyrosine-IR neurons were observed in the hippocampal formation and septal area of the transgenic mice. In the hippocampus, nitrotyrosine-IR neurons in the CA1 region showed intense staining, and the immunoreactivity was localized mainly in the pyramidal cell layer. Recent studies have shown that antioxidants and selective neuronal NOS inhibitor increase survival in the SOD1 transgenic mouse model of FALS. It is possible that therapy with these agents may slow the neurodegenerative process in human ALS, perhaps through reduction of nitrotyrosine formation.

Differential alterations in the distribution of voltage-gated calcium channels in aged rat cerebellum.

In the present study, we used immunohistochemistry and Western blot analysis to determine region-specific changes in the distribution of voltage-gated calcium channels (VGCCs) in aged rat cerebellum. Age-dependent changes in the staining intensity of the alpha(1C) and alpha(1D) subunits were prominent in the Purkinje cells, whereas there was no change in the expression of the alpha(1A) and alpha(1B) subunits. In the aged rat, in particular, immunoreactivity for the alpha(1C) subunits were increased in the dendrites as well as in the cell bodies of Purkinje cells. On the other hand, decreases in immunoreactivity for alpha(1A) and alpha(1D) subunits were found in the molecular or granular layers. However, only alpha(1D) subunit immunoreactivity was decreased in the aged cerebellum membrane by Western blot analysis that, while not addressing regional specificity, further confirmed an age-related decrease in alpha(1D) subunit. These age-related changes in alpha(1D) subunit expression might reflect a gradual loss of regulation for L-type Ca(2+) channels in the senescent period. The first demonstration of age-related alterations in VGCC expression may provide useful data for future investigations on aging and neurodegenerative diseases.

Spatial and temporal distribution of N-type Ca(2+) channels in gerbil global cerebral ischemia.

In the present study, we have investigated the spatial and temporal distribution of voltage-gated calcium channels in the gerbil model of global cerebral ischemia using immunohistochemistry. Distinct localizations of P-type (alpha(1A)), N-type (alpha(1B)), and L-type (alpha(1C) and alpha(1D)) Ca(2+) channels were observed in the hippocampus at days 1-5 after ischemic injury. However, increased expression of N-type Ca(2+) channels was detectable in brain regions vulnerable to ischemia only at days 2 and 3 after ischemic injury. The pyramidal cell bodies of CA1-3 areas and the granule cell bodies of the dentate gyrus were intensely stained at days 2 and 3 following ischemic injury. Transient changes in N-type Ca(2+) channel expression were also observed in the affected cerebral cortex and striatum at days 2 and 3 after ischemic injury. Although the present study has not addressed the multiple mechanisms contributing to the intracellular free Ca(2+) concentration ([Ca(2+)](i)) increase in the ischemic brain, the first demonstration of the transient increase in N-type Ca(2+) channels may prove useful for future investigations.

Immunohistochemical study on the distribution of the type I and type II voltage-gated sodium channels in the gerbil cerebellum.

In this study, we investigated the distribution of the type I and type II Na+ channels in the gerbil cerebellum by immunohistochemistry. Strong uniform staining for type I was observed in the granular layer, whereas there was little evidence of concentrated labeling in the cell bodies and processes of Purkinje cells. The most intense staining for type II was observed in the cell bodies and dendrites of Purkinje cells, with a strong signal in the molecular layer. This localization study has shown clearly that the type I and type II Na+ channel subunits have differential distribution in the gerbil cerebellum, for the first time. The present study may provide useful data for the future investigations to understand the roles of voltage-gated sodium channels in neurological pathways.

Enhanced expression of L-type Ca2+ channels in reactive astrocytes after ischemic injury in rats.

In the present study, we have examined the expression of voltage-gated calcium channels in a rat model of transient focal ischemia using immunohistochemistry. Increased expression of class C L-type Ca2+ channels was clearly detected in reactive astrocytes in each region of the hippocampus 7 days after ischemic injury. On the contrary, class D L-type Ca2+ channels were not expressed in reactive astrocytes under these conditions. These patterns were also observed in reactive astrocytes in the affected cerebral cortex and fiber tracts. Our study showed the spatial and temporal localization of class C L-type Ca2+ channels in reactive astrocytes in ischemic rat brain, for the first time. The present studies may provide useful data for future investigations to understand the role of Ca2+ channels in reactive astrocytes following ischemia or glutamate toxicity.

Spatial and temporal distribution of pituitary adenylate cyclase activating polypeptide in gerbil global cerebral ischemia.

In the present study, we used immunohistochemistry to investigate the effects of transient global ischemia on pituitary adenylate cyclase activating polypeptide (PACAP) immunoreactivity in gerbil brain regions. PACAP immunoreactivity had significantly decreased in the pyramidal cells of CA1 subfield susceptible to ischemic insult at 1-4 days after transient global ischemia. On the contrary, PACAP immunoreactivity had not changed in the pyramidal cell bodies of more resistant CA3 subfield after ischemic injury. In the Purkinje cell layer, PACAP immunoreactivity had significantly decreased 1 day following transient ischemia, and had increased 2 days after ischemia. The first demonstration of the postischemic localizations of PACAP should allow us to gain a more fundamental rationale for developing methods of treating ischemic brain damage with neuroprotective peptides such as PACAP.

Immunohistochemical study on the distribution of voltage-gated K(+) channels in rat brain following transient focal ischemia.

The present study examined the spatial localizations of voltage-gated K(+) (Kv) channels in the rat brain following transient focal ischemia, using immunohistochemistry. Increased expression of Kv1.2 was obvious in the cerebral cortex, dentate gyrus, amygdala, and hypothalamic areas at 3 days following ischemic insults. There was a significant increase in Kv1.2 immunoreactivity in several cortical regions, including cingulate cortex, infralimbic cortex, dorsal peduncular cortex and piriform cortex. On the contrary, Kv1.2 immunoreactivity had not significantly increased in the hippocampal CA1-3 regions although moderate Kv1.2 immunoreactivity was found in the cell bodies and processes of some neurons. Potentially the first demonstration of spatial changes in Kv1.2 channel expression could provide important molecular basis for altered neuronal excitability after ischemic brain injury.

Spatial and temporal distribution of Bax in rat spinal cord during normal aging.

Amytrophic lateral sclerosis is characterized by relentlessly progressive degeneration of spinal cord motor neurons. During the disease, the bcl-2 family genes have been reported to alter their expression levels. To understand the meaning of these changes, the expression pattern of Bax in rat spinal cord and its changing pattern during normal aging were investigated by immunohistochemical staining. Spatial expression of the protein showed a diffuse distribution pattern with immunoreactivity more prominent in the anterior hom. With advancement of age, the cell densities of Bax-positive cells tended to increase. The increasing expression of Bax might be positively associated with amyotrophic lateral sclerosis. This work demonstrates for the first time how Bax expression changes in rat spinal cord during normal aging.

Predictable normocapnia [correction of normocapnoea] in controlled ventilation of infants with Jackson Rees or Bain system.

We have devised a formula for ventilator settings which provide normal minute ventilation without rebreathing during controlled ventilation using a Jackson Rees or Bain system. As VT = VS + VF- VL, where VT = delivered tidal volume, VS = set tidal volume, VF = the volume of fresh gas entering during the inspiratory phase and VL = the lost volume due to the compliance of the system, VS was derived: VS = VL + VT x [1-b/(1 + a)] where a = expiratory-to-inspiratory ratio and b = the ratio of fresh gas flow to the minute ventilation. It was evaluated in 62 infants. Arterial partial pressure of carbon dioxide (mean (SD)) was 4.6 (0.5) kPa (35 (4) mmHg) with a range of 3.42-5.78 kPa (26-44 mmHg). The 90th percentile was 5.1 kPa (39 mmHg). It is concluded that predictable normocapnia [corrected] can be conveniently achieved in infants in controlled ventilation with Jackson Rees or Bain system if our formula is applied.