PubMed Health⌕ Search

Biomedical subjects

S Baba

Publications and source records attributed to S Baba.

At least 703 records · Page 39Linked to original sources
PubMed1988

Glycation of cataractous lens in non-diabetic senile subjects and in diabetic patients.

Early- and advanced-stage products in the Maillard reaction, glycation, were measured in patients with diabetic or senile cataracts. Early-stage products were measured by means of furosine, which is an acid-hydrolysis product derived from fructose-lysine. Advanced-stage products were measured by fluorometry using high-performance liquid chromatography. Furosine levels were high (listed in descending order) in capsule, cortex and nucleus in both diabetic and senile cataracts. The advanced-stage products were also high (listed in descending order) in nucleus, cortex and capsule in both diabetic and senile cataracts. These results suggest that advanced-stage products might accumulate in larger amounts in the nucleus and cortex than in the capsule, resulting in the formation of cataracts. The study also revealed that the Maillard reaction plays an important role in causing not only diabetic cataracts but also senile cataracts.

Aged↗
PubMed1988

The antibiotic susceptibilities and beta-lactamase production of clinical isolated Branhamella catarrhalis from acute otitis media in children.

Branhamella catarrhalis has been misconsidered as a normal resident in human respiratory tract for a long time. However, many authors recently have reported its pathogenecity and isolated it from the otolaryngological region. In our study, this organism can be isolated from the ear and nasal discharge in the child with acute otitis media by the rate of 7.5% and 21.4% respectively. Out of this 107 isolated strains, 97 strains (90.7%) were found to be beta-lactamase producing organisms. The MIC measurement of penicillins and cephems (except CEX) for inhibition of all these strains in our study is 6.25 micrograms/ml or less and because of the unreliability of the ABPC's susceptibility test by disk method, it is necessary to check the beta-lactamase production in each strain. Becoming of the high emergence rate of beta-lactamase producing strains, B. catarrhalis should be considered to be as important pathogen as Streptococcus pneumoniae and Haemophilus influenzae in upper respiratory tract infections in children.

Acute Disease↗
PubMed1988

An improved method for the isolation of islets from the rat pancreas.

The conventional method for rat islet isolation was improved by injection of collagenase solution (1.3 mg/ml) into the bile duct and the concomitant dissection of the inferior vena cava, static incubation of the removed distended pancreas for 15 min at 37 degrees C and filtration of the digested tissue through two different meshes of 1190 and 590 micron in pore size. This new technique led to about 2.5 times higher yield of viable islets than the conventional method.

Animals↗
PubMed1988

Pancreatic secretagogues regulate somatostatin binding to acinar cell membranes via two-functionally distinct pathways.

Pretreatment of pancreatic acini with vasoactive intestinal peptide (VIP) or secretin for 120 min reduced subsequent [125I-Tyr1]somatostatin binding to membranes prepared from these acini, with a maximally reduced binding being 79.2% or 77.4% of control, respectively. In addition, exogenously added cyclic AMP derivatives or a phosphodiesterase inhibitor mimicked the effect of VIP or secretin. Scatchard analysis of [125I-Tyr1]somatostatin binding demonstrated that the decrease in the labeled somatostatin binding induced by VIP or dibutyryl cyclic AMP (dbcAMP) pretreatment was due to the decrease in the maximum binding capacity without a significant change in the binding affinity. The effect of simultaneous pretreatment of acini with VIP and carbamylcholine (carbachol) on subsequent labeled somatostatin binding appeared to be almost equal to the calculated additive value for each peptide. Results obtained, therefore, indicate that the binding of somatostatin to its receptors in the pancreas may be regulated via two functionally distinct pathways.

Animals↗
PubMed1988

A study of the age-related acceleration of glycation of tissue proteins in rats.

The relationship between age-related glycation and a fluorescent product attributable to the advanced Maillard reaction was investigated in the aortas of rats between 4 and 120 weeks of age. The early-stage product of the Maillard reaction was measured using furosine (epsilon-N-(2-furoylmethyl)-L-lysine) as a marker. The advanced product was measured by fluorescence high-performance liquid chromatography. The level of furosine in the aorta increased with aging to reach a maximum value in rats of 50 to 70 weeks of age, and decreased in rats from 90 to 120 weeks of age. By contrast, the level of the putative advanced product reached a maximum in 90-week-old rats and remained at the maximum level in 120-week-old rats. The level of glycated hemoglobin showed no significant change in rats of more than 14 weeks of age. The advanced Maillard products may play an important role in the pathophysiology of aging arteries.

Aging↗
PubMed1988

Penetration of fleroxacin into maxillary sinus mucosa and palatine tonsil.

Ten patients undergoing tonsillectomy or operation on the maxillary-antrum were given 200 mg fleroxacin orally 1-2 h before surgery. The concentration of fleroxacin in maxillary sinus mucosa (mean 2.61 mg/kg) was similar to that in serum samples collected simultaneously (mean 2.46 mg/l); and similar results were obtained with tonsillar tissue (mean 3.27 mg/kg; simultaneous serum samples, mean 2.84 mg/l).

Anti-Infective Agents↗
PubMed1988

Pancreatic secretagogues regulate somatostatin binding to its receptors on rat pancreatic acinar membranes.

Labeled somatostatin binding to pancreatic acinar membranes was examined to investigate how pancreatic secretagogues regulate somatostatin receptors in the pancreas. Pretreatment of pancreatic acini at 37 degrees C for 120 min with not only pancreatic secretagogues, such as carbachol and bombesin, but also vasoactive intestinal peptide (VIP) and secretin reduced subsequent labeled somatostatin binding to the acinar membranes in a dose-dependent manner. The inhibitory effects of these secretagogues on labeled somatostatin binding were also time dependent. Both types of secretagogues maximally reduced subsequent somatostatin binding when acini were incubated with them for more than 120 min. However, the degree of the inhibition was greater with carbachol or bombesin than VIP or secretin; the former secretagogues reduced the binding to 40-45%, and the latter to 75-80% of a control, respectively. These pancreatic secretagogues had no inhibitory effect on somatostatin binding when added directly to the binding media. Furthermore, the inhibitory effect of carbachol was attenuated by the presence of 1 mM EDTA in media for pretreatment, suggesting that intracellular pathways activated by pancreatic secretagogues may be responsible for somatostatin receptor modulation. Interestingly, when combined with VIP, pretreatment of acini with carbachol produced an additive inhibition of labeled somatostatin binding to the membranes. Results, therefore, suggest that somatostatin binding to its receptors in the pancreas may be regulated via two functionally distinct intracellular pathways.

Animals↗
PubMed1988

Effects of hydrocortisone on glucose- and cholecystokinin-induced insulin release from the isolated perfused rat pancreas.

The acute and chronic effects of hydrocortisone on insulin secretion were examined in the isolated perfused rat pancreas. In the first part of this study, the chronic effects of hydrocortisone on insulin release were examined using isolated perfused pancreas prepared from rats that had been given subcutaneous injections of hydrocortisone at doses of 1.25, 2.5, 5.0, and 10.0 mg/kg body weight once daily for 7 days. Hydrocortisone treatment led to a dose-dependent increase in insulin secretion in response to 8.3 mM glucose. The insulin response to 100 pM cholecystokinin (CCK-8) was also significantly higher in the hydrocortisone-treated rats than in the control group. However, the increment of insulin level over the value before CCK-8 addition in rats treated with hydrocortisone was not significantly different from that in the control rats. In the second part, the acute effects of hydrocortisone on insulin release were studied. Hydrocortisone (17-hydroxycorticosterone) at a concentration of 100 microM caused significant inhibition of the stimulatory effect of CCK-8 on insulin secretion. The inhibition started within 1 min of the beginning of hydrocortisone administration and ceased immediately after the termination of its infusion. We have demonstrated in this study a dual effect of hydrocortisone on insulin release: first, the potentiation of the insulin secretion stimulated by glucose but not by CCK-8 and, second, the inhibition of CCK-8-stimulated insulin secretion.

Animals↗
PubMed1988

The protective effect of the trypsin inhibitor urinastatin on cerulein-induced acute pancreatitis in rats.

We examined the protective effects of the trypsin inhibitor, urinastatin, extracted from human urine in experimental acute pancreatitis in conscious rats. Acute pancreatitis was induced by four subcutaneous injections of 20 micrograms/kg body weight of cerulein at hourly intervals. Urinastatin at a dose of 50,000 U/kg body weight/6.5 h was given by continuous i.v. infusion beginning 0.5 h before the first cerulein injection and continuing until 3 h after the last one, for a total of 6.5 h. Urinastatin significantly reduced serum levels of amylase, lipase, and anionic trypsin(ogen) but did not affect pancreatic wet weight or protein or enzyme content. Urinastatin also significantly reduced the degree of acinar cell vacuolization, interstitial edema, and cellular infiltration. These results suggest that urinastatin does not block the induction of acute pancreatitis by cerulein but does substantially reduce its severity.

Acute Disease↗
PubMed1988

Cell kinetics analysis of background colonic mucosa of patients with intestinal neoplasms by ex vivo autoradiography.

Studies of the cell kinetics of the colonic crypts could explain the morphogenesis of colonic adenomas and results suggest that a derangement of the proliferative zone of the colonic crypts takes place before adenoma development. This study was conducted to determine whether this is the case or not. The labelling distribution and labelling index (LI) of the colonic crypts was examined with ex vivo autoradiography. Eight patients with intestinal neoplasms, three with familial polyposis coli, four with ordinary colon cancer, and one with two colonic adenomas. Similar labelling distributions and absent upward shift of the active proliferative zone in crypts were observed in patients with familial polyposis and in those with non-polyposis cancer, or adenomas. The non-proliferative zone of the crypts was well preserved in all eight patients. The mean of the labelling index of the three patients with familial polyposis coli was 8.35% (3.17), values expressed as means (SD) and that of the five patients with non-polyposis cancer, or adenomas was 8.55% (3.20). None of the eight patients showed derangement of the proliferative zone of colonic crypts. This result is compatible with the hypothesis that adenomas are detected first as 'buds of adenomas', which sprout into the lamina propria mucosae in the middle part of normal crypts.

Adenocarcinoma↗
PubMed1988

G protein in stimulation of PI hydrolysis by CCK in isolated rat pancreatic acinar cells.

To clarify the possible role of a guanine nucleotide-binding protein (G protein) in the signal transducing system activated by cholecystokinin (CCK), actions of CCK on rat pancreatic acini were compared with those of fluoride, a well-known activator of stimulatory (Gs) or inhibitory (Gi) G protein. When acini were incubated with increasing concentrations of either CCK-octapeptide (CCK8) or NaF, a maximal stimulation of amylase release from acini occurred at 100 pM CCK8 or 10 mM NaF, respectively; this secretory rate decreased as CCK8 or NaF concentration was increased. NaF caused an increased in cytoplasmic Ca2+ concentration from the internal Ca2+ store and stimulated accumulation of inositol phosphates in acini, as observed with CCK. However, NaF-stimulated Ca2+ mobilization had a lag period before detectable stimulation and was potentiated by AlCl3. These stimulatory effects of NaF appeared to be independent of cellular adenosine 3',5'-cyclic monophosphate (cAMP). Pretreatment with cholera toxin or pertussis toxin did not affect CCK8- or NaF-induced inositol phosphate accumulation or Ca2+ mobilization. 5'-Guanylimidodiphosphate activated the generation of inositol phosphates in the [3H]inositol-labeled pancreatic acinar cell membrane preparation, with half-maximal and maximal stimulation at 1 and 10 microM, respectively. Furthermore, the effects of submaximal CCK concentrations on inositol phosphate accumulation in membranes were markedly potentiated in the presence of 100 microM GTP, which alone was ineffective. Combined findings of the present study strongly suggest that pancreatic CCK receptors are probably coupled to the activation of polyphosphoinositide (PI) breakdown by a G protein, which appears to be fluoride sensitive but is other than Gs- or Gi-like protein.

Amylases↗
PubMed1988

Quantitative therapeutic plan for the treatment of obesity and a simple method for estimating appropriate caloric intake by using previous rate of weight loss.

We have formulated an equation for the calculation of the caloric intake in a reducing diet that is suited to individual obese patients. We have designed a system in which the weight loss achieved after the intake of a fixed number of calories over a given period is used as a basis for the next weight-reducing plan for a given patient. We devised the formula Y = X - 1000 (b2/a2-b1/a1) for calculating the daily caloric intake (Y). X is the previous caloric intake; b1 is achieved weight loss (kg) in the previous period (a1 weeks); and b2 is the planned reduction in weight in the subsequent target period (a2 weeks).

Energy Intake↗
PubMed1988

Glycation of hair protein in the assessment of long-term control of blood glucose.

Glycation of hair protein was assessed in diabetic patients by the measurement of furosine, which is derived from fructose-lysine, a glycated lysine residue in protein. The level of furosine in 12-cm-long hair which grew over the course of one year was significantly better correlated with the mean values of four determinations of fasting plasma glucose (FPG) and four determinations of hemoglobin A1c (HbA1c) performed at three-month intervals than with FPG and the level of HbA1c, respectively, at the time of hair sampling. The level of glycation in hair, which corresponds to the time taken for hair growth, may represent the mean level of blood glucose during the time corresponding to the growth period. These results suggest that the determination of glycation in hair may be useful as an indicator of long-term control of blood glucose levels if appropriate lengths of hair are taken from the scalp.

Adult↗
PubMed1988

Secretin-induced exocrine secretion in perfused pancreas isolated from diabetic rats.

Exocrine secretory function in response to 10 pM to 10 nM synthetic secretin was evaluated in perfused pancreas isolated from control, streptozocin-induced diabetic (STZ-D), alloxan-induced diabetic (ALX-D), and insulin-treated STZ-D rats. In STZ-D rats, the basal rate of pancreatic juice flow was significantly increased (10.3 +/- 1.0 microliters/20 min) compared with control rats (4.4 +/- 0.2 microliters/20 min). The basal rate of amylase output as well as pancreatic amylase content were significantly decreased to less than 5% of control values. The basal rates of protein and trypsinogen outputs were similar in both groups. In both control and diabetic rats, secretin caused a dose-dependent increase in exocrine secretion. Secretin (10 pM to 10 nM) induced 1.1- to 11.7-fold increases in exocrine secretion in STZ-D rats. These increases were significantly lower than the 2.1- to 20.8-fold increases in control rats. Furthermore, there was no significant increase in exocrine secretion from STZ-D rats in response to 10 pM secretin, although this concentration of secretin caused a significant increase in control rats. Secretin-induced exocrine secretion in ALX-D rats was similar to that in STZ-D rats. In insulin-treated STZ-D rats, the basal rates of pancreatic secretion were not significantly different from those of control rats. These results suggest that insulin resistance in this patient was due to a circulating factor of low molecular weight that uncoupled insulin stimulation of glucose transport from receptor binding and phosphorylation. The factor appears to increase the binding activity of the alpha-subunit of the insulin receptor without affecting the kinase activity of the beta-subunit.

Amylases↗