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Biomedical subjects

T Baba

Publications and source records attributed to T Baba.

At least 523 records · Page 29Linked to original sources
PubMed1984

[Problems in the treatment of small cell lung cancer from the standpoint of the cause of death].

Fifty patients with small cell lung cancer were treated by radiotherapy mainly with maintenance chemotherapy. Relative survival for all cases combined was 34.6% for one year, 5.9% for three years, and 6.6% for five years; in the curative irradiation group, the corresponding figures were 72.2%, 12.5% and 13.6%. The cause of death in the palliative group was local lesion in 32% and multiple metastases in 43%. But in the curative irradiation group, it was local lesion in 22% and multiple metastases in 56%. Long-term survivors more than two years were all in the curative irradiation group, of the intermediate cell type and almost all had received over 50 Gy total dose, over 80 for TDF, within a two-month treatment period.

Adult↗
PubMed1984

UV radiation and keratosis follicularis.

We carried out provocation studies on the lesions of keratosis follicularis by the use of UV radiation. Nonerythema-producing doses of UV-B elicited the lesions in uninvolved skin sites in a 34-year-old man with this disease. The elicited lesions were compatible with those of keratosis follicularis both clinically and histopathologically. Similar irradiation with UV-A produced no visible changes in the test area.

Adult↗
PubMed1984

[Effects of PS-K as adjuvant therapy for primary lung cancer--an autopsy case].

A 57-year-old woman underwent left lower lobectomy for primary lung cancer (papillary adenocarcinoma, T2NOMO). Despite postoperative adjuvant immunochemotherapy with 5-Fu, Carboquone and PS-K, bone metastases were recognized at 9 months after the surgery. She received radiation therapy and was administered PS-K alone, 3.0 g daily. As a result, long-term good condition was maintained with a positive PPD skin test. The bone metastases developed slowly, and the patient survived 5 years and 8 months after the operation. At autopsy, no obvious metastatic lesions were identified except for the bone metastases. The cause of her death was thought to be acute renal failure due to severe hemorrhage from an esophageal ulcer. Moreover, she was doomed because of advanced polycystic disease.

Adenocarcinoma, Papillary↗
PubMed1984

"Two-route chemotherapy" using high-dose ip cisplatin and iv sodium thiosulfate, its antidote, for peritoneally disseminated cancer in mice.

We studied the effects of "two-route chemotherapy (TRC)" using cisplatin given ip and its antidote, sodium thiosulfate (STS), given iv on mice bearing peritoneally disseminated cancer. Initially, a pharmacokinetic analysis of cisplatin given ip and STS given iv or sc was made. The plasma concentrations of non-protein-bound and total platinum increased rapidly to a maximum at 10 mins after ip administration of cisplatin alone. When STS alone was given sc, the peak level in the plasma was much lower than that given iv. The superiority of the iv route for STS administration was observed in the lethal toxicity tests. The iv administration of STS to mice 1 min after cisplatin given ip was the best protocol to protect against the lethal toxicity of cisplatin. The protective conditions were applied to TRC in which STS was given iv 1 min after ip cisplatin to mice bearing peritoneally disseminated cancer. Significantly superior antitumor effects were observed in mice given TRC by evaluating survival time as compared with mice given a single treatment with cisplatin at an equitoxic level. The nephrotoxic and hematotoxic effects were slight in TRC.

Animals↗
PubMed1984

Desensitization. IV: Permeability changes during active and passive desensitization.

The systemic injection of large amounts of specific antigen (active desensitization) or exogenous lymphokine-containing preparations (passive desensitization) leads to a state of anergy or hyporesponsiveness with respect to cellular immunity without effect on antibody production. In the present study, we show that desensitization is associated with the suppression of permeability alterations at the skin reaction site. This effect is not confined to delayed hypersensitivity responses; it is observed in antibody-mediated and nonimmunologically induced reactions as well. Thus, although the mechanism of desensitization involves the cellular rather than the humoral limb of the immune response, it is possible for the expression of a variety of inflammatory responses to be modified during this state.

Animals↗
PubMed1984

Cell-mediated immune protection in chickens against Pasteurella multocida.

Immune protection by cellular immunity in chickens against Pasteurella multocida was investigated by in vivo and in vitro experiments using spleen cells and culture supernatants of immunised chickens. Intraperitoneal or intravenous transfer of immune splenic cells into normal chickens induced transmission of an as effective protection as that exhibited in immunised chickens. Immune protection was also obtained by intravenous treatment of chickens with culture supernatant fluid from immune splenic cells of hormonally bursectomised chickens. The in vitro experiment showed that intracellular bacterial proliferation was inhibited in peritoneal macrophages from immunised chickens, or from normal chickens sensitised with culture supernatant fluid of immune splenic cells, and the macrophages were protected from disruption by infection. Peritoneal macrophages sensitised with culture supernatant fluid from unimmunised splenic cells, or peritoneal macrophages from unimmunised chickens, allowed considerable intracellular proliferation of bacteria with almost complete breakdown of the macrophages within 24 hours after bacterial challenge. These data suggest that the protective immunity of chickens against P multocida was dependent on cell-mediated immunity by mediators such as the macrophage activating factor from T lymphocytes.

Animals↗
PubMed1983

Regulatory mechanisms of cutaneous delayed-type hypersensitivity. I. Suppression of cutaneous delayed-type hypersensitivity by migration inhibitory factor.

The macrophage migration inhibitory factor (MIF) fraction was prepared from the immunoadsorbent column by using anti-guinea pig MIF antiserum. Suppression of cutaneous delayed-type hypersensitivity was achieved by intraperitoneal injection of the MIF fraction into the animals bearing macrophage-rich peritoneal exudates. Skin reactions induced by phytohemagglutinin (PHA) were also suppressed in these animals. Reactivity to skin reactive factor (SRF) was suppressed in these animals as well. The sera obtained from these animals exhibited the inhibitory activity against production of lymphokines from sensitized lymphocytes.

Animals↗
PubMed1983

Regulatory mechanisms of cutaneous delayed-type hypersensitivity. II. Suppression of cutaneous delayed-type hypersensitivity by macrophage disappearance reaction.

Studies were performed on the behavior of cutaneous delayed-type hypersensitivity (DTH) in guinea pigs in which macrophage disappearance reaction (MDR) was induced. Guinea pigs were immunized with dinitrophenylated egg albumin (DNP-EA), followed by intraperitoneal (ip) injection of liquid paraffin in order to elicit peritoneal macrophages. Subsequently 20 micrograms of EA was injected into these animals and the animals were divided into two groups. One group of animals was sacrificed for estimation of MDR 6 hr after the subsequent ip injection. The other group received a skin test by EA at the time of the subsequent ip injection. The first group of animals sacrificed for estimation of MDR exhibited a marked reduction in the number of peritoneal macrophages. The second group of animals that received skin tests revealed suppressed skin reactions 24 hr after the subsequent ip injection. A similar experiment was performed using the guinea pigs doubly immunized with DNP-EA and dinitrophenylated bovine gamma-globulin (DNP-BGG). Induction of MDR was performed by ip injection of BGG and skin tests were done by both EA and BGG. As a result, suppression of not only BGG-induced skin reactions but also EA-induced skin reactions was observed in animals in which MDR had been induced by BGG. In addition, the guinea pigs in which MDR was induced showed hyporeactivity to phytohemagglutinin (PHA). Reactivity to skin reactive factor (SRF) was also suppressed in these animals. The culture supernatants of macrophages incubated with the MIF fraction in vitro showed the ability to suppress skin reactions of cutaneous DTH, PHA and SRF.

Animals↗
PubMed1983

Hormonal response to insulin-induced hypoglycemia in patients with Shy-Drager syndrome.

We examined the response of plasma glucose concentration and glucose counterregulatory factors (eg, glucagon, epinephrine, growth hormone, cortisol, and norepinephrine) to insulin-induced hypoglycemia in four patients with Shy-Drager syndrome and in five control subjects to determine if glucose counterregulation occurred in the patients with sympathetic and parasympathetic nervous system defects. The recovery of plasma glucose from hypoglycemia in a slower phase in the patients appeared to be almost similar to that in the control subjects, along with the absence of an initial rapid recovery phase; that is, there was no significant difference in the plasma glucose levels observed at any point between the patients and the control subjects. Although the insulin-induced hypoglycemia in the control subjects provoked a rapid release of epinephrine, followed by an increase in the plasma glucagon, growth hormone, and cortisol levels, it did not cause a significant increase in any of the glucose counterregulatory factors in the patients. Our findings that the restoration of normoglycemia after insulin-induced hypoglycemia occurred despite no significant increase in the counterregulatory hormonal factors suggest that other glucose counterregulatory mechanisms (eg, increased glucose release from the liver by the intrinsic effect of hypoglycemia on the liver) than the hormonal glucose counterregulatory factors might play an important role in the recovery of plasma glucose from insulin-induced hypoglycemia in a state of chronic deficiency of hormonal factors.

Autonomic Nervous System Diseases↗
PubMed1983

Effect of administration of anti-bursal extract or perfusate serum on the antibody production in chickens.

Antisera to bursal extracts or perfusates were prepared and the influence of such sera on antibody production in chickens was investigated by the injection of antisera during the embryonic stage. Antisera to cyclophosphamide treated bursal extracts or bursal perfusates were injected on the 15th day of embryogenesis. The level of antibodies produced by chickens treated by these antisera was equal to the controls but IgG antibodies were totally absent. These results suggested that the administration of these antisera inhibited the differentiation of IgM antibody producing cells.

Animals↗
PubMed1983

Pituitary-adrenocortical system in patients with Shy-Drager syndrome.

We examined ACTH responses to the three main mechanisms of ACTH secretion, i.e., stress, negative feedback and circadian rhythm, in six patients with Shy-Drager syndrome and in six control subjects to determine whether or not injury to the central autonomic nervous system provokes some disturbances in ACTH secretion. The patients showed a poor cortisol response to the stress of insulin induced hypoglycemia along with a normal ACTH and urinary 17-OHCS response to metyrapone and a normal cortisol circadian rhythm. The discrepancy between the above-mentioned functional tests of ACTH secretion is rare to our knowledge. These findings suggested the existence of a glucoreceptor defect in such patients, or the possibility that the stress of insulin induced hypoglycemia stimulates ACTH secretion by way of the autonomic nervous system.

Adrenocorticotropic Hormone↗
PubMed1983

The mechanism of aldosterone response to furosemide test in patients with Shy-Drager syndrome.

We examined the renin-angiotensin-aldosterone system in seven patients with Shy-Drager syndrome by studying their response to the stimulation of 1 mg/kg furosemide injection followed by sitting for 1 hour. Six of the seven patients showed a low response of plasma renin activity to the stimulation. However, in five of the low responders, the plasma aldosterone levels after stimulation were observed to be similar to those of the control subjects; in addition, an increment in the plasma cortisol level appeared although no such increment was observed in normal subjects. Next, we studied the aldosterone response to angiotensin II. The five patients who showed a low plasma renin activity response and a normal aldosterone response to furosemide administration also showed low plasma aldosterone response to angiotensin II. Furthermore, in the patients who demonstrated a low plasma renin activity response and a normal aldosterone response to furosemide administration, the pretreatment with 2 mg dexamethasone for 2 days caused a marked inhibition of aldosterone response to the stimulation. These findings suggested that in most patients with Shy-Drager syndrome, the plasma aldosterone response to the stimulation of furosemide injection followed by sitting for 1 hour might be controlled by ACTH but not by plasma renin activity.

Adult↗
PubMed1983

Renin-angiotensin system and plasma aldosterone in Cushing's syndrome.

The renin-angiotensin system was studied in eight patients with Cushing's syndrome (four with adrenal adenoma and four with adrenal hyperplasia) and in five normal controls. Basal plasma renin activity (PRA) and aldosterone concentration (PAC) were similar in supine position among Cushing's syndrome due to adrenal adenoma (PRA; 1.0 +/- 0.3 ng/ml/h, PAC; 7.4 +/- 1.0 ng/dl, mean +/- SE), those due to adrenal hyperplasia (1.0 +/- 0.2, 6.9 +/- 0.8) and the controls (0.8 +/- 0.1, 6.4 +/- 0.4). The PRA after furosemide (1 mg/kg i.v.) and 120 min. upright posture stimulation was similar among Cushing's syndrome due to adrenal adenoma (2.2 +/- 0.7 ng/ml/h), those due to adrenal hyperplasia (2.6 +/- 1.7) and the controls (2.5 +/- 1.2). However, the PAC response after the stimulation in Cushing's syndrome due to adrenal hyperplasia (7.1 +/- 1.2 ng/dl) was significantly lower than that in the controls (17.5 +/- 2.1) (p less than 0.01), although there was no significant difference between the PAC response in Cushing's syndrome due to adrenal adenoma (12.6 +/- 1.0) and the controls. These results indicate that PAC response to furosemide and upright pasture stimulation might be suppressed in Cushing's syndrome due to adrenal hyperplasia.

Adenoma↗