Search

Summary: 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.

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.