Specimens of gastric mucosa were obtained from 16 cases of fetal stomach, aging from 11 weeks to full term, 5 cases from gastric adenocarcinoma, one case from gastritis and one case from normal adult. The contents of their mucosubstances were compared histochemically with Mowry's alcian blue and PAS techniques. The results are as follows:The mucosubstances of gastric mucosa undergo a conspicions change during the fetal life. In general, acid mucopolysaccharide appear at first in the epithelium and rudimentary gastric pits and it is replaced subsequently by neutral mucin. This mucosaccharide replacement varies within different areas and stages. The neutral mucin always takes its appearance about the 11th week at the cardiac and pyloric regions where the mucosubstance have begun to reveal pruple colour in AB-PAS reaction. After the 4th month, the neutral mucosacchaide has completed its replacement in both areas except the lower parts of pyloric glands which still show some mixed mucins. In the corpus tomach, acid mucin is present almost during the whole fetal life but converts into mixed type only at birth. The parietal cell do not contain any mucous material during its histogenesis, but the chief cell may contain some alcianophilic granules which will change into faintly PAS-positive at birth. With alcian blue at low pH, it proves that most of the acid mucosaccarides are sulfated mucosubstance.Adjacent to the bottoms of gastric pits and the necks of gastric glands, some acid mucin often remains in 1he epithelial and neck mucous cells of normal adult just as those of newborn. The acid mucosubstance occurs in various degree within the spaces or lumen of adenocarcinoma tissue. It could be considered that the bottoms of pits and necks of glands would be a cellular bases for further development of gastric carcinnoma under certain conditions.

In order to examine whether the neuronal losses occur in cerebral and cerebellarcortices,we used two age groups of rats,the adult group aged 12 months containing8 animals and the old group aged 23～24 months,10 animals.After intraventriculardouble infusions with Koenig's acacia gum-formalin,a small piece of brain tissue,lessthan 2 mm in thickness,were removed from the cerebral and cerebellar cortices ofeach animal.All tissues were sectioned in paraffin and stained by H and E.Thecells were counted directly with an occular micrometer,in an area of 200 ?m~2 incerebral cortex and in a straight line of a length span of 5 mm in cerebellar cortexrespectively.The data from two age-groups were treated statistically.A significant neuronal loss were observed in both of cerebral and cerebellarcortices in the old rats.The pyramidal cells of V layer of parietal area fell from themean value of 22.75?1.76/200 ?m~2 in the adult group to 16.68?1.99/200 ?m~2 in theold.The decrease of percentage was 26.7%.The Purkinje cells fell from 98.87?3.72/5mm in the adult to 77.2?8.27/5 mm in the old,and the decrease of percen-tage was 21.9%.The t-test demonstrated that the difference between two age-groups both in cerebral and cerebellar cortices were significant(P

Objective: Hepatitis B surface antigen (HBsAg) loss is seldom achieved with nucleos(t)ide analog (NA) therapy in chronic hepatitis B patients but may be enhanced by switching to finite pegylated-interferon (Peg-IFN) alfa-2a. We assessed HBsAg loss with 48- and 96-week Peg-IFN alfa-2a in chronic hepatitis B patients with partial response to a previous NA. Methods: Hepatitis B e antigen (HBeAg)-positive patients who achieved HBeAg loss and hepatitis B virus DNA < 200 IU/mL with previous adefovir, lamivudine or entecavir treatment were randomized 1:1 to receive Peg-IFN alfa-2a for 48 (n = 153) or 96 weeks (n = 150). The primary endpoint of this study was HBsAg loss at end of treatment. The ClinicalTrials.gov identifier is NCT01464281. Results: At the end of 48 and 96 weeks' treatment, 14.4% (22/153) and 20.7% (31/150) of patients, respectively, who switched from NA to Peg-IFN alfa-2a cleared HBsAg. Rates were similar irrespective of prior NA or baseline HBeAg seroconversion. Among those who cleared HBsAg by the end of 48 and 96 weeks' treatment, 77.8% (14/18) and 71.4% (20/28), respectively, sustained HBsAg loss for a further 48 weeks. Baseline HBsAg < 1 500 IU/mL and week 24 HBsAg < 200 IU/mL were associated with the highest rates of HBsAg loss at the end of both 48- and 96-week treatment (51.4% and 58.7%, respectively). Importantly, extending treatment from 48 to 96 weeks enabled 48.3% (14/29) more patients to achieve HBsAg loss. Conclusion Patients on long-term NA who are unlikely to meet therapeutic goals can achieve high rates of HBsAg loss by switching to Peg-IFN alfa-2a. HBsAg loss rates may be improved for some patients by extending treatment from 48 to 96 weeks, although the differences in our study cohort were not statistically significant. Baseline and on-treatment HBsAg may predict HBsAg loss with Peg-IFN alfa-2a.