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The study subjects consisted of 14 pulmonary tuberculosis (PTB) patients with collagen disease. They are under corticosteroid treatment and the mean age is 56.4 years. The length of time from the development of collagen disease to the development of PTB averaged 4.1 years. The breakdown of collagen disease are SLE (6 patients), MCTD (3 patients), PN (2 patients), and PSS, PM, Sjogren syndrome (1 case, each). Thirteen cases were bacilli positive by the sputum examination on admission to our hospital. Chest X-ray findings on admission revealed cavitation in 3 cases and non-cavitation in 11 cases, of which 5 cases had miliary tuberculosis. Corticosteroid preparation had been administered to all of the 14 cases for more than one year. The mean dose of corticosteroid preparation administered when PTB developed was 13.9 mg (prednisolone) and it was more than 20 mg in 8 cases. The median duration from the start of the respiratory symptoms to diagnosis was 39.2 days. The delay in the discovery exceeding 1 month were seen in 9 cases. In the cases of collagen disease, when the disease course extends over a long period of time, and even when the dose of corticosteroid preparations are decreased, there is a need to be note on the risk of developing PTB. There are many non-cavitary cases with sputum smear positive. The fact suggested that an appropriate diagnosis is need so that the discovery of PTB should not be delayed.

Epidemiological trend of tuberculosis in Japan has reversed recently. The incidence of pulmonary tuberculosis (PTB) patients has increased again in Japan, and many outbreaks of PTB including nosocomial outbreaks in health-care facilities have been reported. The purpose of this study is to investigate patient's delay (interval between onset of the disease and first visit to a doctor) and doctor's delay (interval between first visit to a doctor and diagnosis as TB) in patients with PTB discovered by visiting doctors with symptoms, and especially, to investigate causes of doctor's delay in details. Of 236 PTB patients who were admitted to our hospital for treatment in 1997, 118 patients (85 males, 33 females) who were detected by their symptomatic visits were enrolled in to this study. 97 were initial treatment cases and the others were re-treatment cases. Among 34 initial treatment cases who were first seen at a general hospital and diagnosed as PTB by a close medical checkup after admission to our hospital, the 50 percentile of patient's delay was 17.0 days, and the 80 percentile was 36.4 days. The 50 percentile doctor's delay was 19.6 days, and the 80 percentile was 64.2 days. The average hospital stay was 16.2 days, the 50 percentile hospital stay was 7.8 days, and 80 percentile hospital stay was 23.5 days. On the sputum test for acid fast bacilli (AFB) performed on admission to our hospital, 26(76%) out of 34 cases were positive for tubercle bacilli, with 18 cases were positive for smear and 8 cases positive for culture. Therefore, risk of nosocomial infection was suspected. Doctor's delay had been attributed mainly to insufficient medical checkup. Among 25 initial treatment cases in whom doctor's delay as more than 4 weeks, 11 cases (44%) showed delay in chest X-ray examination and 8 cases (32%) ordered no sputum examination in spite of recognition of abnormal shadows on chest X-ray. On the sputum test for AFB on admission to our hospital, 22 (88%) out of 25 cases were positive for tubercle bacilli. Therefore, it is assumed that the delay in the adequate medical checkup was accountable for the doctor's delay. Shortening of the doctor's delay could be possible if hospitals perform the sputum examination for AFB and chest X-ray examinations properly for patients with respiratory symptoms.

We studied whether diabetics who are one of the high risk groups of developing pulmonary tuberculosis had undergone chest X-ray examination periodically. The feasibility of chemoprophylaxis in diabetics was also studied by investigating whether fibrotic lesions of tuberculosis can be found on previous chest X-ray films of these patients. Of the pulmonary tuberculosis patients admitted to our hospital for treatment, 78 patients complicated with diabetes mellitus were enrolled in this study. As to the mode of detection, the majority, 63 cases, are discovered, by undergoing medical examination because of respiratory symptoms, followed by 8 patients in whom pulmonary tuberculosis was found by health examination and only 1 patient was found by the periodic observation of diabetes mellitus. Of the 57 patients receiving the original treatment for pulmonary tuberculosis preceded by the discovery of diabetes mellitus, only 15 (26%) had undergone chest X-ray examination periodically. This fact shows that physicians treating diabetes mellitus have only a little concern on tuberculosis, thus the re-training of physicians dealing with diabetics on tuberculosis is considered to be necessary. According to chest X-ray films of 21 patients who had undergone chest X-ray examination and in whom the previous films were available, there were 6 patients without any lesion of pulmonary tuberculosis, 8 patients with fibrotic lesions and 7 patients with active lesions. The 8 patients showing fibrotic lesions have developed pulmonary tuberculosis on the average 15 years after they were diagnosed with diabetes mellitus, and the fact suggests that the prevention of the development of pulmonary tuberculosis among diabetics could be possible by chemoprophylaxis.

The complication with tuberculosis of the central nervous system (CNS) were studied in 16 patients with miliary tuberculosis who were admitted to our hospital during a period of two years from April, 1997 to March, 1999, and were examined by head MRI. Twelve cases (75%) were diagnosed as having tuberculosis of CNS. Six cases had tuberculosis of CNS which was found during the screening of miliary tuberculosis cases, and all had only cerebral tuberculoma. Meningeal irritative symptoms led to the discovery of tuberculosis of CNS in the remaining six cases, in which cerebral tuberculoma was complicated with tuberculous meningitis. Of these cases of meningitis, three cases showing disturbance of consciousness died, but no cases of death was found in cases by the screening. The length of time from the onset of symptoms to the diagnosis of tuberculosis was long in many of the cases complicated with tuberculosis of CNS compared with the cases without such a complication. In the cases of miliary tuberculosis, the rate of complication with tuberculosis of CNS is high, and the possibility of patients developing serious symptoms suddenly even when they were asymptomatic at the time of diagnosis and the paradoxical expansion that becomes intensified after initiation of treatment have been reported. Therefore, it is necessary to make a close checkup of CNS when the diagnosis of miliary tuberculosis has been made.

The frequency of complication of diabetes mellitus in patients with pulmonary tuberculosis is high, and the presence of diabetes mellitus plays an important role in the development of pulmonary tuberculosis. We studied the frequency of complication of diabetes mellitus by year, sex and age among patients with pulmonary tuberculosis who were discharged from our hospital during a period of 12 years from 1987 to 1998. The number of diabetic cases in patients with pulmonary tuberculosis was 588, namely 14.1% out of 4169 patients during the 12 years from 1987 to 1998. The frequency of complication of diabetes in every four years period showed an increasing trend; 144 cases (11.8%) out of 1225 cases from 1987 to 1990, 208 cases (14.5%) out of 1434 cases from 1991 to 1994, and 236 cases (15.6%) out of 1510 cases from 1995 to 1998. By sex, the frequency of complication with diabetes mellitus in male was about twice that of female, with 501 cases (16.0%) out of 3127 cases in male and 87 cases (8.3%) out of 1042 cases in female. By age, the frequency of complication of diabetes mellitus showed a peak in the 40s and 50s in male, being 21.3% and 23.4% respectively. In female, it showed a peak in the 60s, being 18.5%. In conclusion, in the 12 years the frequency of complication of diabetes mellitus in tuberculosis cases has been increasing, and the presence of diabetes mellitus has been playing more important role in the development of pulmonary tuberculosis.

We experienced an outbreak of tuberculosis among young adults in close contact. The index case (case 1) was 22-year-old builder and was symptomatic for 9 months before diagnosis as pulmonary tuberculosis (PTB). His sputum smear was positive for tubercle bacilli. On immediate family contacts examination carried out at our hospital, his brother and sister (case 3, case 4) were detected as having PTB. His mother (case 5) and father (case 6) were later detected as having PTB by their symptomatic visits after some months, as tuberculin test as not done at first examination. Case 7 was 19-year-old-man, and was undiagnosed for 5 months. His sputum smear was positive. Immediately, contacts examination for case 7 as carried out at our hospital, and his colleague (case 8) was detected as having PTB. By interview with the case 7, it was found that the case 1 and the case 7 were close friends and spent long time together. Case 10 was 30-year-old builder, and he was accidentally referred to our hospital and was diagnosed as PTB. By the interview with the case 10, it was found that the case 1 and case 10 were members of builders group. This fact was informed to the F health center, and contacts examination for other members of the group were carried out by the F health center, and two young men were detected as having PTB. Analysis of restriction fragment length polymorphism (RFLP) showed that the case 1, the case 5, the case 7, and the case 10 were caused by the same strain of M. tuberculosis. Based on these findings, it is highly suspected that this outbreak was origined from the case 1, and 13 developed tuberculosis and 13 were primarily infected among contacts. The characteristics of this outbreak was that the family and contacts examination were enforced and most of the cases were detected at our hospital. If the outbreak of tuberculosis highly suspected, physicians should actively cooperate with health centers for contacts examination.

It has been hypothesized that advanced Maillard reaction in vivo could explain some of the age- and diabetes-related changes. Furthermore, involvement of the Maillard reaction with Alzheimer's disease has also been suggested, as advanced glycation end products, such as pyrraline and pentosidine, were demonstrated to localize in lesions of the disease. Although aminoguanidine has been studied extensively and established as an inhibitor of the Maillard reaction, other candidates have not been investigated thoroughly. In the present study, we examined the inhibitory effect of tenilsetam [(+/-)-3-(2-thienyl)-2-piperazinone], an antidementia drug, on the Maillard reaction. Tenilsetam inhibited glucose- and fructose-induced polymerization of lysozyme in a concentration-dependent manner in vitro. Reduced enzymatic digestibility of collagen incubated with 100 mM glucose for 4 weeks was also restored to a control level by coincubation with 100 mM tenilsetam. To determine whether tenilsetam inhibits the Maillard reaction in vivo, streptozotocin-induced diabetic rats were treated with tenilsetam (50 mg/kg x day). Elevated levels of advanced glycation end-product-derived fluorescence and pyrraline in renal cortex and aorta of diabetic rats were suppressed by the administration of tenilsetam for 16 weeks. These inhibitory effects of this agent on advanced glycation in diabetic rats suggested its potential therapeutic role in controlling diabetic complications.

An analysis of 41 patients with hypopharyngeal cancer treated between April 1985 and March 1996 is presented. Our guidelines for the treatment of hypopharyngeal cancer are a combination of chemotherapy, radiotherapy and surgery. The schedule of combination therapy is as follows: chemotherapy first, preoperative radiotherapy second, and surgery last. The surgery for hypopharyngeal cancer is pharyngolaryngoesophagectomy with radical neck dissection. In many cases free jejunum transplantation was used for reconstruction. The mean age of the patients was 64.8 years, and there were 39 men and 2 women. There were 33 cases of pyriform sinus type, 4 cases of postcricoid type, 3 cases of retropharyngeal type, and 1 case of unclassified type. Histopathologically, there were 40 cases of squamous cell carcinoma and 1 case of anaplastic carcinoma. Five-year total survival rates were 23.0% and 5-year survival rates at each tumor stage were 0% (T-1), 19.9% (T-2), 32.4% (T-3), 0% (T-4). There were no statistically significant differences between tumor stages. Five-year survival rates for each nodal stage were 14.1% (N-0), 54.5% (N-1), 0% (N-2), 0% (N-3). The survival rate for stage N-1 was significantly better (p < 0.05) than that for stage N-2. Five-year survival rates for all stages were 0% (I), 0% (II), 46.3% (III), 0% (IV). The survival rate for stage III was significantly better (p < 0.05) than that for stage IV. Twenty-five patients were operated on with or without chemotherapy and radiotherapy and, 16 patients received nonsurgical treatment. The 5-year cause-specific survival rate for patients who underwent surgery was 57.7% and for patients who underwent nonsurgical treatment was 0%. The survival rate for the radical treatment group was significantly better (p < 0.05) than that for the nonradical treatment group. The 5-year cause-specific survival rate for patients who underwent radical radiotherapy was 0%. That for patients who were treated by chemotherapy was 51.4% and for patients who were not so treated was 20.1%. The results of this study suggest several significant conclusions: 1, Stage is not a good predictor of outcome in hypopharyngeal cancer. 2, Patients undergoing surgery with or without chemotherapy and radiotherapy as the primary treatment enjoyed improved survival. 3, Radical radiotherapy provided poor prognosis. We think that chemotherapy provided some survival benefit.

(1)'Antieidos' is a formlessness that results from the reverse intentionality of the life formation and is considered to be a principle of obsessive psychosis. 'Internal emptiness' is supposed to exist in the nucleus of schizophrenia. 'Antieidos' and 'internal emptiness' are in close proximity, partly overlapping each other. Obsessive psychosis and some types of simple schizophrenia are considered to have a common intentionality for the obsessive-compulsive phenomenon from the viewpoint of defensive structural dynamics. (2) The obsessive-compulsive phenomenon and the hypochondriacal phenomenon that coexist in simple schizophrenia are considered to be a 'noema' (something in which a meaning is given to the intended experience) that results from 'noesis' (action of consciousness seen in the intended experience) which has a defensive intentionality and as a result masks the basic disturbance in schizophrenia. Complementarity between the obsessive-compulsive phenomenon and the hypochondriacal phenomenon structured in this way can form one type of disease in the nonself-introspective category of simple schizophrenia.

Splitting is defined from a viewpoint of experiencing time as an 'episodic loss or sudden shift of experiencing time induced by two opposing representational groups'. According to this definition splitting phenomena are examined in four cases arranged on a spectrum from multiple personality and hysteria to borderline personality disorder (BPD). The degree of splitting was most prominent in BPD. In Contrast to the hypermnesia associated with hysteria, that of BPD had the potential to develop into paranoia. Splitting phenomena were considered to operate as a defense mechanism against the development to paranoia. In all four cases it could be seen that the overflow of 'parole', corresponding to the hypermnesia, could not be fruitfully conceptualized due to the splitting phenomena. Assuring new integration was indispensable to the therapy of the four presented cases.

Since accelerated turnover of histamine in oxyntic mucosa may be an important factor in the pathogenesis of peptic ulcers, the effect of dexamethasone and other glucocorticoids on the activity of gastric histidine decarboxylase (HDC) was studied in the rat. The activity of HDC in rat oxyntic mucosa increased significantly after dexamethasone was injected s.c. to rats at doses larger than 0.4 mg/kg body weight. The maximum response of the HDC activity to dexamethasone (4 mg/kg) was observed 8 h after the treatment. The activity of ornithine decarboxylase (ODC) increased at 4 h, while that of DOPA decarboxylase showed no significant change throughout the 16-h period following a single injection of dexamethasone. The mucosal levels of histamine, putrescine, and spermidine rose significantly after the steroid treatment, while the spermine levels remained nearly constant. There was no sex difference in these responses to dexamethasone. Betamethasone showed nearly the same effects as dexamethasone on the decarboxylase activities and the mucosal levels of diamines. Serum gastrin levels showed no significant change for the first 4 h and then rose significantly 8 and 16 h after dexamethasone treatment. Pentagastrin (0.5 mg/kg) increased the HDC activity, while it showed no significant effect on either the mucosal ODC activity or levels of polyamines and histamine. These data suggest that dexamethasone influences the metabolism of histamine and polyamines in rat oxyntic mucosa both directly and via stimulation of gastrin release.

The association of N1-acetylspermidine with human colorectal adenocarcinomas has been evaluated in this study. Free polyamines and their monoacetylated forms in adenocarcinomas, adenomas, and apparently healthy mucosae were determined using high-performance ion-exchange chromatography. The N1-acetylspermidine levels in well- and moderately differentiated adenocarcinomas were 27.30 +/- 3.13 (S.E.) (n = 99) and 22.86 +/- 3.60 (n = 22) nmol/g, wet weight, respectively. These values were significantly higher than those of benign adenomas (5.38 +/- 0.85 nmol/g, n = 31) and of control mucosae. The N1-acetylspermidine levels in control mucosae on the oral and anal side of adenocarcinomas were 5.84 +/- 1.44 (n = 57) and 7.92 +/- 2.89 (n = 50) nmol/g, respectively; no significant difference was observed between control mucosae and adenomas. The mean levels of three polyamines, putrescine, spermidine, and spermine in both adenomas and adenocarcinomas were about twice as high as those of control mucosae. The molar ratios of spermidine to spermine were significantly greater in both adenomas and adenocarcinomas than in control tissues. There was no obvious correlation between the free polyamine concentrations and the degree of malignancy of the colorectal tumors. These results suggest that the metabolism of N1-acetylspermidine in colorectal adenocarcinomas is quite different from that in adenomas and in nonneoplastic mucosae and that N1-acetylspermidine can be a promising biochemical marker of cancer in the human large intestine.