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In Japan, inguinal hernia repair is widely performed with local anesthesia. The objective of this study was to evaluate safety and efficacy of intravenous dexmedetomidine as a sedation agent with local anesthesia in inguinal hernia repair. We performed this randomized, single-blind study for 200 patients who were scheduled to undergo inguinal hernia repair with local anesthesia. Patients were randomly divided into two groups (dexmedetomidine group: Group D, midazolam group: Group M). The primary outcome was to evaluate the safety of intravenous dexmedetomidine. Secondary outcomes were to analyze results of operators’ surveys and patients’ questionnaires and evaluate implementation of conscious sedation. Incidence of respiratory depression was significantly higher in Group M than Group D (p = 0.03). Other adverse events examined did not differ significantly. All three operators’ questionnaires indicated that results were better in Group D than Group M. More than 70% of patients in both groups were satisfied with the surgery. More than 80% of Group D patients and 74% of Group M patients achieved a state of conscious sedation. This study demonstrated that intravenous dexmedetomidine during hernia repair with local anesthesia is safe and the results were satisfactory to both operators and patients.

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

✓ Cerebrospinal fluid (CSF) dynamics were correlated to the changes in ventricular size during the first 3 months posttrauma in patients with severe head injury (Glasgow Coma Scale score ≤ 8, 75 patients) to distinguish between atrophy and hydrocephalus as the two possible causes of posttraumatic ventriculomegaly. Using the bolus injection technique, the baseline intracranial pressure (ICP), pressure volume index, and resistance for CSF absorption (R0) provided a threedimensional profile of CSF dynamics that was correlated with ventricular size and Glasgow Outcome Scale (GOS) score at 3, 6, and 12 months posttrauma. Patients were separated into five different groups based on changes in ventricular size, presence of atrophy, and CSF dynamics. Group 1 (normal group, 41.3%) demonstrated normal ventricular size and normal ICP. Group 2 (benign intracranial hypertension group, 14.7%) showed normal ventricular size and elevated ICP. Group × (atrophy group, 24%) displayed ventriculomegaly, normal ICP, and normal R0. Group 4 (normal-pressure hydrocephalus group, 9.3%) had ventriculomegaly, normal ICP, and high R0. Group 5 (high-pressure hydrocephalus group, 10.7%) showed ventriculomegaly and elevated ICP with or without high R0. The GOS score in the nonhydrocephalic groups (Groups 1, 2, and 3) was better than in the hydrocephalic groups (Groups 4 and 5). It is concluded from these results that 44% of head injury survivors may develop posttraumatic ventriculomegaly. Posttraumatic hydrocephalus, as identified by abnormal CSF dynamics, was diagnosed in 20% of survivors and their outcome was significantly worse. This study demonstrates the importance of using CSF dynamics as an aid in diagnosis of posttraumatic hydrocephalus and identifying those patients who may benefit from shunt placement.

Cytotoxin-associated gene A (cagA) is the major virulence factor of Helicobacter pylori strains and affects the clinical outcome of patients. Blood group antigen binding adhesin (BabA) helps the strains adhere to the epithelial cell layer and is the most important adhesin of H. pylori.We tried to study the association between the status of babA2 and cagA in H. pylori strains and histological gastritis. methods: Thirty-six patients were included. RNA was extracted from two frozen biopsy samples of the antrum and corpus, respectively, and cagA/babA2 genotypes were analyzed with reverse transcription polymerase chain reaction and direct sequencing. Two gastric specimens of the antrum and corpus, respectively, were also stained with hematoxylin and eosin to analyze H. pylori-related gastritis.In the antrum, 56% of the specimens were babA2 positive and in the corpus 53%. The gastritis scores of activity and inflammation were associated with the presence of babA2 in antrum specimens but not in corpus specimens. cagA gene encoding in the CagA EPIYA-D region was detected in all samples, and the sequence was completely identical between those from the gastric corpus and antrum.babA2 expression is heterogeneous and correlated with the extent of gastritis in the antrum, but not in the corpus, whereas cagA shows a monotonous genotype.

To investigate whether curing Helicobacter pylori infection improves symptoms over the long-term in Japanese patients with nonulcer dyspepsia and fundic atrophic gastritis.Ninety H. pylori-positive dyspeptic patients with fundic atrophic gastritis were enrolled in this study. We performed a randomized double-blind placebo-controlled trial comparing triple therapy (n=45) with that of placebo alone (n=45). Inflammation and mucosal atrophy were scored according to the Updated Sydney System. Symptoms were scored on a scale of 0 to 3 for six items. Fasting samples of gastric juice were taken before endoscopy, and gastric pH was determined. Serum gastrin and pepsinogen levels were measured, and body mass index was determined. These patients were followed up for 3 years, and all measures were evaluated both before and after therapy.Significant improvement in dyspeptic symptoms and gastritis scores, significant decrease in gastric pH, and significant increase in body mass index were found after 3 years eradication in nonulcer dyspepsia patients treated successfully for H. pylori infection. There were no significant changes in the placebo group.Our study shows that eradicating of H. pylori results in significant long-term reduction in symptoms of nonulcer dyspepsia with fundic atrophic gastritis.

Clarithromycin has been administered to patients in Japan since 1991. Clarithromycin-resistant Helicobacter pylori strains have been on the rise in Japan. We obtained H. pylori isolates between 1989 and 2000 and examined mutations of the 23S rRNA gene, which are closely associated with clarithromycin resistance. Isolates were obtained from 356 patients with H. pylori infection treated at the Hiroshima University. Sixty-one of the patients received clarithromycin-based H. pylori eradication therapy. Mutations of the 23S rRNA gene were examined by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by sequencing analysis. Mutant strains were found in 42 of the 356 patients (11.8%). The prevalence of mutant strains increased from 0 to 20.4% during the 12-year study period. The prevalence increased to more than 10% by 1995 and then to more 20% after 1999. The H. pylori eradication rate was significantly higher in patients with wild-type strains than in patients with mutant strains (72.0 vs. 36.4%, p = 0.024). Our data indicate that clarithromycin-resistant H. pylori strains have increased rapidly since 1995 and that the effectiveness of clarithromycin-based H. pylori eradication therapies may soon be compromised. Other new therapies may be necessary as first-line treatments in Japan.

To investigate the effect of the eradication of Helicobacter pylori on histological gastritis.: Twenty-six patients with moderate to severe atrophy received successful eradication therapy of H.pylori. Four patients dropped out and 22 were followed up prospectively for 5 years. The grades of gastritis were estimated from gastric biopsy specimens. The grade of intestinal metaplasia was also evaluated by dye-endoscopy using methylene blue (methylthioninium chloride). The serum levels of pepsinogen, gastrin and anti-parietal cell antibody were also determined.: The grades of atrophy decreased in patients with successful eradication therapy in the gastric corpus (before vs. 5 years after eradication, 2.09 +/- 0.15 vs. 0.91 +/- 0.17; P0.01) and in the antrum (2.14 +/- 0.17 vs. 1.36 +/- 0.17; P0.01). The levels of intestinal metaplasia were also decreased in the corpus (0.91 +/- 0.24 vs. 0.50 +/- 0.16; P0.05) and in the antrum (1.41 +/- 0.20 vs. 1.00 +/- 0.16; P0.05), which was also demonstrated by the methylene blue (methylthioninium chloride) staining method (33.4 +/- 8.2% vs. 23.0 +/- 6.5%; P0.05). The improvement of corpus atrophy correlated well with the high serum level of pepsinogen I (P = 0.005), but showed no correlation with the levels of anti-parietal cell antibody.: These results suggest that gastric atrophy and intestinal metaplasia are reversible events in some patients.

Our previous study demonstrated that Helicobacter pylori eradication was less effective in smokers than in non-smokers. Cetraxate is an anti-ulcer drug that increases gastric mucosal blood flow.To evaluate the effect of cetraxate combined with new triple therapy for the eradication of H. pylori in smokers.This study had a single-centre, double-blind, randomized non-placebo design. A total of 106 consecutive H. pylori-positive smoking patients were randomly allocated to one of two regimens: one group received omeprazole (20 mg), amoxycillin (1500 mg), and clarithromycin (600 mg) for 7 days (OAC, n=55). The other group recieved OAC plus cetraxate (600 mg) for 7 days (OAC + CET, n=51). The success of H. pylori eradication was evaluated by histology and the 13C-urea breath test at 4 weeks after completion of treatment.By intention-to-treat analysis, the H. pylori eradication rate was 55% in the OAC group and 92% in the OAC + CET group (P0.01). By per protocol analysis, the H. pylori eradication rate was 58% in the OAC group and 94% in the OAC + CET group (P0.01).Cetraxate combined with new triple therapy increases the eradication of H. pylori in smokers.

Although several recent studies have shown that the eradication of Helicobacter pylori provokes reflux oesophagitis, the results are conflicting.To investigate the prevalence of reflux oesophagitis in patients after eradication of H. pylori and consider its association with hiatal hernia and corpus gastritis.A total of 286 patients who underwent H. pylori eradication therapy and 286 age- and disease-matched H. pylori-positive controls who did not undergo eradication therapy were followed prospectively. All patients and controls underwent endoscopy at 1-year intervals or when upper gastrointestinal symptoms recurred. The presence of hiatal hernia and histology of the gastric corpus were evaluated at the time of initial endoscopy.The estimated prevalence of reflux oesophagitis within 3 years was 18% after eradication therapy and 0.3% without therapy. Patients who developed reflux oesophagitis after therapy had a greater prevalence of hiatal hernia (P=0.0008) and more severe corpus gastritis (P=0.0005) before therapy. Cumulative prevalence of reflux oesophagitis was 26% in patients with hiatal hernia, 7.7% in those without hiatal hernia, 33% in those with corpus atrophic gastritis and 13% in those without corpus atrophic gastritis. When patients had both hiatal hernia and corpus gastritis, the prevalence of reflux oesophagitis was 37%. The newly developed reflux oesophagitis was classified as mild in 35 out of 36 (97%) patients who developed reflux oesophagitis after eradication therapy.Eradication of H. pylori increased the prevalence of reflux oesophagitis in our patient group. The presence of hiatal hernia and corpus gastritis are closely related to the development of reflux oesophagitis after H. pylori eradication therapy.

Recent studies (K. Komoto et al., Am. J. Gastroenterol., 93: 1271-1276, 1998) have shown that Helicobacter pylori infection is associated with gastric cancer. However, the mechanism of H. pylori in carcinogenesis has not been clarified. H. pylori infection leads to a sustained production of reactive nitrogen species that may contribute to cause DNA damage. In this study, we examined the expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine in gastric mucosa. The expression of iNOS and nitrotyrosine was examined by immunohistochemistry in 93 patients who initially underwent gastric biopsies between 1975 and 1992. Thirty-four individuals were later found to have gastric cancer at least 2 years after the initial biopsies (group A). The other 59 subjects have shown no evidence of gastric cancer during long-term follow-up. Fifty-one of these patients were positive for H. pylori (group B), and eight were negative for H. pylori (group C). The expression of iNOS and nitrotyrosine in the gastric mucosa was significantly higher in H. pylori-positive groups A and B than in H. pylori-negative group C. Among the H. pylori-positive patients, the expression of iNOS and nitrotyrosine was significantly higher in group A than in group B. These results suggest that high production of iNOS and nitrotyrosine in the gastric mucosa infected with H. pylori may contribute to the carcinogenesis of gastric cancer.

Recent studies have shown that the eradication of Helicobacter pylori results in a gastric acid secretion which decreases to normal levels in patients with duodenal ulcer disease. The aim of this study was to evaluate the effect of eradication of H. pylori in a 24-h study of gastric acidity in patients with atrophic gastritis of the corpus.Intragastric acidity was measured by continuous 24-h pH monitoring, and the histology of the gastric antrum and corpus were evaluated in 14 H. pylori-positive patients with histologically proven atrophic gastritis of the corpus (10 men, 4 women; mean age, 57 years) before and 1 year after anti-H. pylori therapy.H. pylori was absent in 13 of 14 patients 1 year after treatment. Both gastritis and atrophy scores were significantly lower after eradication therapy (P0.01). The 24-h median pH and the percentage of 24-h pH readings above 4.0 units were significantly decreased after eradication therapy (from 5.12 +/- 0.36 to 2.69 +/- 0.21, and from 65.5 +/- 6.6% to 28.2 +/- 6.1%, P0.01, respectively.)Eradication of H. pylori increases 24-h gastric acidity in patients with atrophic gastritis of the corpus. Improvement of the histology of the gastric antrum and corpus may lead to the normalization of gastric acidity.

We mentioned about epidemiology of gastrointestinal hemorrhage according to the clinical statistics. Most of recent reports has been investigated by emergency endoscopic examinations. Upper gastrointestinal hemorrhage was the most frequent and its clinical severity was severer than that of lower gastrointestinal hemorrhage. Hemorrhage from small intestine was rare, however they were mostly severe hemorrhage. Peptic ulcer was the most frequent disease as the upper gastrointestinal hemorrhage. Inflammation of colon was the most in the lower gastrointestinal hemorrhage. However, the varied diseases were recognized as origin of small intestinal hemorrhage, non epithelial tumor and inflammation were important.

Differential diagnosis of NPH and brain atrophy is sometimes difficult. Recently, a new method using MRI was introduced as a noninvasive, direct technique for the measurement of intracranial CSF volume. Using this new technique, we measured the intracranial and ventricle CSF volume in patients with enlarged ventricles in order to differentiate between NPH and brain atrophy. Ten healthy volunteers (control group) and 21 patients with enlarged ventricles were enrolled in this study. Eleven out of 21 patients were clinically diagnosed as having NPH (shunted group) and the remaining 10 patients were considered to have cerebral atrophy (non-shunted group). Intracranial and ventricular CSF volume in each case were measured by 3D FASE (Fast Asymmetric Spine-Echo) MR imaging sequence with region growing method. Ventricular/intracranial CSF volume ratio was also calculated. Ten out of 11 patients showed improvement in clinical symptoms and/or dementia scale after shunting. Our results clearly indicate that the ventricular volume in the shunted group was enlarged and that the ventricular/intracranial CSF ratio was significantly high. Thus we concluded that enlarged ventricle with high ventricular/intracranial CSF volume ratio strongly suggests NPH.

Chronic atrophic gastritis, which is though to be a high risk for gastric cancer, can be diagnosed by serum pepsinogen levels. We compared the usefulness of the measurement of pepsinogen levels and indirect photofluorography as indicators of gastric cancer in a mass screening involving 5,620 Japanese subjects (mean age: 60.1 years old; male : female = 2,268:3,352) in 1991 and 1992. Subjects with a serum pepsinogen I level below 30 micrograms/liter or a pepsinogen I/II ratio below 2.0 were considered to be at high risk of gastric cancer. The incidence of gastric cancer and the ratio of early cancers detected by pepsinogen levels (0.12%, 4/7) were similar to those detected by photofluorography (0.11%, 4/6). Our results showed that mass screening using pepsinogen levels was as useful as indirect photofluorography for the detection of gastric cancer in Japan. In addition, our results showed that the sensitivity of gastric mass screening was increased when the measurement of serum pepsinogen levels was combined with photofluorography.

To evaluate the association of both Helicobacter pylori (Hp) infection and advancing age with increased prevalence of atrophic gastritis.Two hundred and thirty-eight subjects who had no esophagitis, peptic ulcers, or malignancies in the upper gastrointestinal tract were divided into three groups according to age: group A,30 yr; group B, 30-49 yr; group C,or = 50 yr. Two biopsy specimens were obtained from the lesser curvature of the antrum and two from the anterior and posterior walls of the fundus to assess the degree of gastritis and histological evidence of Hp infection. Hp infection was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin (SG) and pepsinogen (PG) were determined by radioimmunoassay.In all age groups, the prevalence of atrophic gastritis was significantly more common in subjects with evidence of Hp infection. In Hp-positive subjects, the prevalence of atrophic gastritis increased with advancing age. Atrophic gastritis was extremely rare, regardless of age, in Hp-uninfected patients. SG increased, and PG I and the PG I:II ratio decreased with age in Hp-positive subjects. This trend was not apparent in Hp-negative subjects.Our results suggest that Hp infection is a stronger predictor than advancing age for atrophic gastritis.

We analyzed 66 cases (47 males and 19 females) of Crohn's disease at Hiroshima University hospital from September 1975 to October 1994 to clarify the course and prognosis of Crohn's disease. The age at onset was 21.1 +/- 7.3 years old (mean +/- SD), terms between onset and diagnosis were 21.5 +/- 33.0 months (mean +/- SD) and observation period was 65.5 +/- 44.6 months (mean +/- SD). Sites of lesion were 18 ileum, 41 ileocolon and 7 colon. Thirty-one cases, 20 cases of which had intestinal obstruction, underwent surgical operation (12 ileum types, 18 ileocolic types, 1 colon type). The cumulative probability of surgery at one, five and ten years after onset of symptoms were 12.1%, 28.8% and 56.9%, respectively. As for cumulative probability of surgical operation at one, five and ten years after diagnosis were 25.8%, 36.7% and 74.4%, respectively. Results of the cumulative probability of surgery by anatomical involvement indicated that the ileum type had a statistically significantly higher risk than other types. In each analysis compliance to nutritional therapy was also an important prognostic factor. Overall, our results indicated that the site of lesion and the compliance to nutritional therapy were important factors which have an effect on the course and prognosis of Crohn's disease patients.

Clinicopathologic characteristics of 92 colorectal laterally spreading tumors (LST) endoscopically or surgically resected were examined. Lesions were macroscopically classified into two categories according to their surface structure :(1) granular type (G type, 47 lesions), (2) flat type (F type, 45 lesions). The size (maximum diameter) of G type lesions was 24.7 +/- 11.3 mm (Mean +/- SD) and that of F type lesions was 14.2 +/- 7.4 mm. The size of G type lesions was significantly larger than that of F type lesions (p0.01). Among G type lesions, cancerous lesion was present in 2 (25.0%) of 8 lesions 10-14 mm in diameter, 2 (22.2%) of 9 lesions 15-19 mm in diameter and 19 (63.3%) of 30 lesions more than 20mm in diameter. Regarding F type lesions, cancerous lesion was present in 15 (46.9%) of 32 lesions 10-14 mm in diameter, 4 (80.0%) of 5 lesions 15-19 mm in diameter and 8 (100%) of 8 lesions more than 20mm in diameter. The incidence of carcinoma in F type lesions was higher than that in G type lesions irrespective of size. F type lesions with carcinoma showed a trend toward a higher frequency of submucosal invasion and F type lesions with adenoma revealed tendency of showing severe atypia in comparison with G type lesions. The adenomatous component of LST showed a tubulo-villous architecture in 13 (28.3%) of 46 G type lesions, however none of F type lesions had a tubulo-villous component. These results indicated that clinicopathologic characteristics of F type are obviously different from G type. Furthermore, F type had a higher malignant potential than G type and is thought to have a more important role as a precursor of colorectal carcinoma than G type.

To determine the relationship between gastric secretion and gastric carcinoma, we investigated gastric acid secretion and the fasting serum levels of pepsinogen I and gastrin in 50 Japanese patients with early gastric carcinoma. After the histological and macroscopic type of carcinoma had been determined, results were compared with findings in 50 Japanese control subjects whose gastric mucosa was endoscopically normal. The maximum gastric acid secretion and fasting levels of serum pepsinogen I were significantly lower in intestinal type gastric carcinoma than in diffuse type carcinoma and in the controls. They were also significantly lower in the non-ulcerative (elevated or flat) type than in the ulcerative (depressed) type of carcinoma. The serum gastrin levels in patients with early gastric carcinoma of either the intestinal or diffuse type were higher than those in the control subjects, though the difference was not significant. Gastric acid secretion and serum pepsinogen I levels were related with both the histological and macroscopic types of gastric carcinoma. These findings suggest that the serum pepsinogen I level might be useful as a maker for early gastric carcinoma of the intestinal type.

We examined the expression of epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), epidermal growth factor receptor (EGFR) and p185c-erbB-2 immunohistochemically and correlated the expression with growth in 66 cases of human gastric carcinoma. To evaluate growth, we used the bromodeoxyuridine (BrdU) labeling index in 51 cases and the radiographic growth rate in 15 cases. Expression of EGF was detected in 41 cases (62.1%), TGF-alpha in 42 cases (63.6%), EGFR in 34 cases (51.5%), and p185c-erbB-2 in 37 cases (56.1%). The BrdU labeling index ranged from 1.5 to 32.0%. The BrdU labeling index was higher in tumors that coexpressed EGF and EGFR or TGF-alpha and EGFR than in tumors without expression or in tumors that expressed growth factors or the receptors (p0.01). The BrdU labeling index was also significantly higher in tumors with the expression of EGFR and/or p185c-erbB-2. Tumors with simultaneous expression of EGF, TGF-alpha, EGFR and p185c-erbB-2 had an association with a high BrdU labeling index. Moreover, all of these growth factors and receptors were expressed simultaneously in gastric carcinomas with rapid growth. These results suggest that the expressions of EGF, TGF-alpha, EGFR and p185c-erbB-2 are closely related and then play an important role in the growth of human gastric carcinomas.

To evaluate the degree of gastritis and the prevalence of Helicobacter pylori in Japanese patients with pernicious anemia (PA).Histological assessment for mucosal atrophy and inflammation was performed in gastric biopsy specimens taken from 24 Japanese patients with PA and from 24 age- and sex-matched controls. The prevalence of H. pylori was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin and pepsinogens were determined by radioimmunoassay.All patients with PA had severe fundic atrophic gastritis, and 17 (71%) also had antral atrophic gastritis. Thirteen (54%) of 24 age- and sex-matched controls had fundic atrophic gastritis, and 15 (62%) also had antral atrophic gastritis. Mucosal inflammation was identified in the fundus of all 24 patients and in 15 (62%) controls and in the antrum of 22 (92%) patients and 16 (67%) controls. H. pylori was not detected by Giemsa staining or serum IgG antibodies to H. pylori in any patient with PA but was present in 16 (67%) controls. Serum gastrin levels were significantly higher, and serum pepsinogen I, II, and the I/II ratio were significantly lower in patients than in controls (p0.001).Our results confirm that H. pylori infection is infrequent in PA and is unlikely to be a factor in producing type A gastritis in PA.

✓ Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI × Δlog(ICP)/ΔPCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.

Recent advances in endoscopic diagnosis and treatments have increased the number of early gastric carcinomas being treated by endoscopic resection. However, the appropriate criteria for endoscopic resection of gastric carcinomas with submucosal invasion are not completely established. During the past 12 years from 1980 to 1992, 116 lesions in 116 patients were treated by surgical operation for differentiated type submucosal invasive gastric carcinoma. In this study, the risk factors of lymph node metastasis were investigated clinicopathologically. As the result, 1) Heterogeneity of submucosal invasive tumor margin was demonstrated in 19 (16%) of the 116 lesions of which predominant histology was differentiated adenocarcinoma. 2) Lymph node metastasis was demonstrated in 16 (16%) of the 97 lesions of which histology was differentiated type. 3) Significant risk factors of lymph node metastasis was demonstrated in submucosal massive invasion (sm3), papillary adenocarcinoma, INF gamma, lymph vessel involvement (ly(+)), and existence of ulcer (ul(+)). 4) Sm3 and papillary adenocarcinoma (pap) had a higher malignant potential than ly(+), INF gamma, and ul(+) by multivariate analysis using the logistic regression. 5) All lesions with both well differentiated adenocarcinoma (tub1) and sm minimal invasion (sm1) had no lymph node metastasis. These results suggested that the lesions with both well differentiated adenocarcinoma tub1 and sm1, which have no other risk factors such as ly(+), INF gamma, and ul(+), may be considered as the appropriate indication for endoscopic treatment of gastric submucosal carcinoma.

It is has been demonstrated that clinical outcome following head injury is correlated with the reactivity of the cerebrovasculature to carbon dioxide changes. Since CBF measurements are difficult to perform in these patients, a new technique is proposed utilizing the ICP response to capnic stimuli. In 40 head injured patients, the responses of ICP, pressure volume index (PVI) and middle cerebral artery velocities to hypocapnia and to hypercapnia were determined. Hypocapnia reduced ICP and MCA velocity while hypercapnia was followed by ICP and MCA velocity increases. Both changes were in the same magnitude supporting the concept the global ICP response reflects vascular reactivity. The fact that the velocity response to hypocapnia in lesioned hemispheres was less compared to the ICP response indicates the loss of ability to dilate in injured vessels and is consistent with earlier findings relating reduced reactivity to poor outcome.

To determine the prevalence and significance of Helicobacter pylori (H. pylori) infection, biopsies of the antral mucosa were obtained from 139 patients and 43 asymptomatic volunteers. The specimens were examined by hematoxylin-eosin staining and the ureas test. The detection rate of H. pylori by histologic examination was 91.3% in patients with duodenal ulcer, 75.0% in those with combined duodenal and gastric ulcer, 63.6% in those with gastric ulcer, 22.9% in those with gastric carcinoma, 36.4% in those with gastric adenoma, 14.3% in those with gastric hyperplastic polyp, and 51.7% in those with gastritis, and the respective percentages detected by the urease test were 91.3%, 75.0%, 54.5%, 28.6%, 27.3%, 14.3%, and 44.8%. H. pylori was also detected in 10/43 (23.3%) asymptomatic healthy volunteers by histology and the urease test. The prevalence of H. pylori was significantly higher in the patients than in the asymptomatic healthy volunteers (p0.05). H. pylori was detected in 62.9% of patients with endoscopic erosive gastritis and in 97.9% of those with histologically proven chronic active gastritis. The urease test was positive in 77/82 patients who were histologically positive for the organism (sensitivity: 93.9%), and it was negative in 98/100 patients who were negative by histology (specificity: 98.0%). Thus, there was over 90% agreement between the urease test and histology. Our investigations showed that H. pylori was closely related to peptic ulcers and antral gastritis, and that the urease test provides a simple, rapid and accurate diagnosis of H. pylori infection.

Ultrasound examinations were performed in 36 patients with Crohn's disease, 28 with ulcerative colitis, and 50 with no bowel disease. The pathological findings were classified into three types and compared with the radiographic and/or colonoscopic findings. Crohn's disease and ulcerative colitis could be detected by ultrasonography with a sensitivity of 86% and 89%, respectively. The ultrasonographic features correlated with the radiographic/colonoscopic findings and with disease activity, but did not help much in making a differential diagnosis, although the location of the pathologic changes was helpful to some extent. In conclusion, ultrasonography can serve as a useful alternative diagnostic procedure that permits us to obtain information about transmural changes in inflammatory bowel disease.

Pretreatment of mice with ammonia extract of seed shell of Pinus Koraicenis, via the intraperitoneal or intravenous route, effectively protected them from lethal infection of Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureus. The pine seed shell extract also moderately inhibited syncytium formation and cytopathogenic effect induced by human immunodeficiency virus (HIV) infection in cultured human lymphotropic virus type I (HTLV-1) positive MT-4 cells. These data suggest a medicinal potential of pine seed shell extract against opportunistic infection in HIV patients.

We report six cases of scirrhous carcinoma of the stomach in which we were able to observe the natural history of serial radiographs. All the patients developed scirrhous carcinoma of the stomach in an observation periods ranging from 2 to 15 months (mean: 5.8 months). No abnormalities or obvious findings indicative of a carcinoma were detectable, on the prior radiographs, even when they were reviewed. Endoscopy was also performed in two patients during the observation period, and no lesions were detected. At the time of diagnosis, two patients were inoperable because of metastases and died of the disease 2 and 5 months later. Three patients died of the disease 5, 8, and 26 months after gastrectomy, respectively. Only one patient is free of disease 16 months after gastrectomy. Our findings suggest that the difficulty of detection and the rapid growth of this tumor may explain why it is seldom detected at an early stage and has a very poor prognosis.

Twenty-seven patients with superficial esophageal carcinoma were investigated to determine their clinical and pathological features. All 21 male patients were habitual drinkers, and 17 were heavy smokers. Histological examination showed that three tumors were intraepithelial, five were mucosal, and 19 were submucosal. Fifteen of the 27 patients were asymptomatic, including seven of the eight with intraepithelial or mucosal carcinoma. Twelve of the 13 patients with polypoid tumors had submucosal invasion, whereas two patients with flat tumors and four of the seven with erosive tumors had either intraepithelial or mucosal carcinoma. Six of the eight patients with intraepithelial or mucosal carcinoma had normal routine radiological studies. All these eight patients had no lymph node involvement, whereas four of the 19 with submucosal carcinoma had lymph node metastases. An aggressive approach to endoscopy in asymptomatic high-risk individuals (middle-aged male drinkers and smokers) may increase the detection of early esophageal carcinoma, although the cost-effectiveness should be evaluated further. In addition, in the interest of prevention, our results show that encouraging people to stop smoking and limit their alcohol intake to an occasional drink might be an important factor in lessening the risk for esophageal carcinoma.

We prospectively studied 17 gastric cancer patients who were more than 80 yr old, in whom endoscopic therapy was performed. The patients were divided into two groups: the first group included 13 patients in whom curative treatment was attempted, and in 11 (85%) a curative response was achieved. Two patients in this group showed a positive gastric biopsy after 1 and 2 yr, respectively, of therapy: one patient is under current treatment with laser therapy, and the other patient underwent surgery with resection of the stomach. The second group included four patients in whom treatment was aimed at prolonging survival or palliation, and in all four patients, a successful response was obtained. Therefore, our results demonstrate that endoscopic therapy is effective for the treatment of gastric cancer patients over 80 yr old.

We determined serum pepsinogen I (PG I) levels by radioimmunoassay in 472 patients with duodenal ulcer and 141 normal subjects to investigate whether serum PG I levels were related to cigarette smoking, and in 225 patients to determine whether the recurrence of duodenal ulcer was related to serum PG I levels or cigarette smoking. Serum PG I levels were not influenced by cigarette smoking in either patients with duodenal ulcer or normal subjects. The recurrence rate of duodenal ulcer not under maintenance therapy was significantly higher in hyperPG I patients than in normoPG I patients, regardless of their smoking habits. Only in hyperPG I patients was the recurrence rate in smokers higher than in nonsmokers. Patients under maintenance therapy showed similar results. Multilogistic regression indicated that hyperPG I had a greater effect than cigarette smoking on ulcer recurrence. These findings indicate that serum PG I levels are not influenced by smoking, and the important characteristic in patients with recurrent duodenal ulcers is the increased serum PG I levels.

Using male Wister rats, the ornithine decarboxylase (ODC) activity in the fundic mucosa has been determined from the duodenal juice with bile of a reflux model. The activity at 24 hours postoperatively presented a value approximately 18 times higher than the preoperative level. Though this level declined subsequently, it still was approximately two times higher four weeks later. The ODC activity in the corporal mucosa of humans was compared in 25 normal persons, in 21 patients with a gastric adenoma in 29 patients with a gastric cancer, in 20 patients who had undergone a Billroth I operation and in 20 patients who had undergone a Billroth II operation. No differences in ODC activity were observed among those with a gastric adenoma, a gastric cancer, and normal cases but significantly higher values were seen in cases with a remnant stomach, particularly those who had undergone Billroth II reconstructive surgery. Further, this activity tended to be especially high from 5 to 15 years postoperatively in cases with a gastric remnant.

Rectal mucosa from normal controls (n = 25) and tumor tissue and rectal mucosa from patients with colorectal cancer (n = 38) and adenoma (n = 35) were biopsied via colonoscopy. Ornithine decarboxylase (ODC) activity was determined in order to study the role of promoters in the process of colorectal carcinogenesis. ODC activity of cancer tissue was significantly higher than that of adenoma tissue. Normal mucosal ODC activity in rectum and sigmoid colon was 2 to 4 times higher than that in the proximal colon. Moreover, rectal mucosal ODC activity was significantly higher in patients with cancer or adenoma than that in normal controls. When ODC activity is regarded as an index of promoter, the possibility is suggested that cancer and adenoma developed in similar mucosa of the large bowel. Furthermore, ODC activity in colon cancer was significantly higher than that in rectal cancer. This suggests the possibility that TPA type promoter assumes a greater role in the process of carcinogenesis of colon cancer than that of rectal cancer.

To assess the functional and morphological characteristics of the gastric mucosa of patients with fundic hyperplastic polyps (FP), the determination of gastric acid secretion, serum gastrin levels, serum pepsinogen 1 (PG1) levels and histological examination were undertaken in 24 patients with FP, 34 with foveolar hyperplastic polyps (HP) and 62 controls, who had no gastric lesions. The following were the results of our investigation. 1) There were no differences between the patients with FP and the controls as to gastric acid secretion, serum gastrin levels, and serum PG1 levels. On the other hand, hypochlorhydria, hypergastrinemia and hypopepsinogenemia were common in those with HP. 2) Histological examination using gastric biopsy specimens showed almost normal gastric mucosa in patients with FP. However, severe atrophic gastritis of the fundus was common in patients with HP. 3) It was shown that there were definite differences between the patients with FP and those with HP with regard to the gastric function and morphology, although both types of gastric polyp were histologically classified as hyperplastic.

This paper describes the morphological and histological changes of gastric cancer following OK-432 injection into and around the lesion under endoscopic observation. Of 10 cases of unresectable gastric cancer, 7 revealed morphological changes and 3 a significant reduction of tumor size. In one of these cases, all the tumor cells disappeared. In 7 cases of resected gastric cancer preceded preoperatively by OK-432 administration, no obvious morphological changes were observed. However, histologically, marked infiltration of inflammatory cells was observed at the site of injection, especially in the submucosal layer. In regional lymph nodes, a lymphocyte predominance pattern which may have resulted from augmentation of T-cell activity was observed in many cases. The results suggested that local OK-432 injection therapy does not have such a marked direct effect on tumor cells, but may be useful as a means of prevention against invasion into the submucosal layer and regional lymph nodes.

Using a population-based cancer registry, we tabulated 69 definite adult T-cell leukemia/lymphoma cases (36 males and 33 females) and 2.20 expected cases (0.95 for males and 1.25 for females) diagnosed from 1981 to 1983 in Saga, Japan. The number of human T-lymphotropic virus type I carriers was computed by applying sex- and age-specific anti-human T-lymphotropic virus type I antibody positive rates among blood donors at the blood center in 1986 to the whole population of Saga Prefecture in 1982. The age-specific incidence rates among male human T-lymphotropic virus type I carriers from 40 to 79 yr of age per 100,000 were significantly higher than those of female carriers (P less than 0.05), and the rates from 60 to 69 yr of age were the highest in both sexes. The annual crude incidence rates among carriers were 115.9 for males and 66.4 for females. The summary incidence rates with 95% confidence intervals were 115.9 (58.4 to 193.0) for males and 65.9 (30.0 to 115.9) for females. The cumulative risks were 4.5% (0.8 to 11.0) for males and 2.6% (0.3 to 7.0) for females. These morbidity figures were assumed to be underestimated partly due to the newly proposed clinical entity of adult T-cell leukemia/lymphoma.