Papillary renal-cell carcinoma demonstrating prominent foamy macrophages by cytobrush scrapings: a case report.
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Adult↗
Biomedical subjects
H Araki
Publications and source records attributed to H Araki.
Protease inhibitor reduces loss of tensile strength in rat anastomosis with peritonitis.
BACKGROUND: The tensile strength in intestinal anastomoses decreases postoperatively in association with degradation of the extracellular matrix, and these changes would be expected to be more intense in the presence of peritonitis. MATERIALS AND METHODS: In this study, we investigated extracellular matrix degradation and tensile strength in a rat model of intestinal anastomosis with peritonitis. In the chemical peritonitis model, peritonitis was induced 24 h earlier with intraperitoneal HCl. A serine protease inhibitor, nafamostat mesilate (NM), was given intraperitoneally to some animals every 12 h from immediately after the operation for 3 days. Immunostaining was performed by the standard streptavidin-biotin-peroxidase method after fibronectin (Fn) and factor XIII antigen retrieval on paraformaldehyde-fixed, paraffin-embedded tissue sections. RESULTS: In comparison with controls, administration of NM reduced the loss of tensile strength on Day 3 in a dose-dependent manner, and high-dose NM (20/mg/kg) significantly prevented the loss of tensile strength on Day 3 (P < 0. 05). In the control group, degradation of the collagen layer in the anastomosis was associated with disappearance of Fn and factor XIII staining on Day 3. The administration of NM attenuated these changes with intense immunostaining for Fn and factor XIII seen particularly between collagen fibers on both sides of the anastomosis on Day 3. In the chemical peritonitis model, administration of NM also significantly prevented the loss of tensile strength on Day 3 without disappearance of collagen fibers. CONCLUSION: These findings suggest that NM may be clinically useful for preventing intestinal leakage, particularly when anastomoses are performed under protease-activating conditions, such as intestinal edema and inflammation.
Anastomosis, Surgical↗
Determination of intracellular and extracellular beta-lactamase activities of Pseudomonas aeruginosa after exposure to beta-lactams in vitro and in vivo.
Beta-lactamase production in Pseudomonas aeruginosa was determined in in-vitro models and in rat pouch infection models after exposure to ceftazidime, imipenem, and piperacillin. Exposure of 28 P. aeruginosa strains to 1/4 minimum inhibitory concentration (MIC) of ceftazidime, imipenem, and piperacillin for 24 h enhanced intracellular beta-lactamase activities in 14, 22, and 6 strains, respectively, of the 28 clinical strains tested, and enhanced extracellular beta-lactamase activities which were not detected without exposure to antibiotics, in 7, 23, and 1 of the 28 strains, respectively. Extracellular beta-lactamase activity from P. aeruginosa S-1278, producing an inducible beta-lactamase, scarcely increased after exposure to ceftazidime and piperacillin 24 h after incubation, while the activity increased after exposure to imipenem over the range of 1/8 to 8 MIC. In the rat granuloma pouch models infected with P. aeruginosa S-1278, ceftazidime and piperacillin, after single administration (20 mg/kg) and serial administration (20 mg/kg per day x 3 days), did not enhance extracellular beta-lactamase activities. However, the activities were enhanced with single and serial administrations of imipenem, and levels over 10 mU/ml were detected until the third day. The beta-lactamase activity, similar to the activity found in rat pouches after serial administration of imipenem, inactivated various cephalosporins. In conclusion, extracellular beta-lactamase activity was detected both in vitro and in vivo after exposure to a good inducer, and extracellular beta-lactamase remained at infection site at levels that could inactivate cephalosporins.
Animals↗
A new model of pulmonary superinfection with Aspergillus fumigatus and Pseudomonas aeruginosa in mice.
We have produced a new model of pulmonary super-infection with Aspergillus fumigatus and Pseudomonas aeruginosa in immunosuppressed mice. Male ICR mice were given an intratracheal inoculation of 4 x 10(5) conidia of A. fumigatus in agar beads, and were immunosuppressed with 100 mg/kg subcutaneous injections of cortisone acetate on days 7, 9, 12, 14, and 16 after inoculation. Twelve days after inoculation, with the agar beads, the mice were challenged with the intranasal instillation of 2 x 10(6) CFU of P. aeruginosa. The survival rates of superinfected, A. fumigatus-alone, P. aeruginosa-alone, and non-infected mice were 50%, 30%, 90%, and 100% 14 days after pseudomonal infection (26 days after inoculation of A. fumigatus), respectively. In the superinfected mice, both A. fumigatus and P. aeruginosa were detected more than 10 days after pseudomonal infection (22 days after inoculation of A. fumigatus). Histopathological examination revealed peribronchial necrosis around A. fumigatus hyphae and inflammation by P. aeruginosa. This infection model in mice would be useful for studying the pathogenesis of superinfection.
Animals↗
Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100: a novel mechanism for regulating B cell signaling.
We have identified the lymphocyte semaphorin CD100/Sema4D as a CD40-inducible molecule by subtractive cDNA cloning. CD100 stimulation significantly enhanced the effects of CD40 on B cell responses. Administration of soluble CD100 markedly accelerated in vivo antigen-specific antibody responses. CD100 receptors with different binding affinities were detected on renal tubular cells (K(d) = approximately 1 x 10(-9)M) and lymphocytes (K(d) = approximately 3 x 10(-7)M). Expression cloning revealed that the CD100 receptor on lymphocytes is CD72, a negative regulator of B cell responsiveness. CD72 thus represents a novel class of semaphorin receptors. CD100 stimulation induced tyrosine dephosphorylation of CD72 and dissociation of SHP-1 from CD72. Our findings indicate that CD100 plays a critical role in immune responses by the novel mechanism of turning off negative signaling by CD72.
Animals↗
The roles of prostaglandin E receptor subtypes in the cytoprotective action of prostaglandin E2 in rat stomach.
AIM: To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors. METHODS: Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 mM HCl in 60% ethanol). Rats were given various EP agonists i.v. 10 min before HCl/ethanol: PGE2, sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist), 17-phenyl-omega-trinorPGE2 (17-phenylPGE2: EP1 agonist), ONO-NT012 (EP3 agonist) and 11-deoxyPGE1 (EP3/EP4 agonist). In a separate study, the effect of PGE2 on HCl/ethanol lesions was examined in EP1- and EP3-receptor knockout mice. RESULTS: Gastric lesions induced by HCl/ethanol were dose dependently prevented by PGE2: this effect was mimicked by sulprostone and 17-phenylPGE2 and was significantly antagonized by ONO-AE-829, an EP1 antagonist. Neither butaprost, ONO-NT012 nor 11-deoxyPGE1 exhibited any protective activity against HCl/ethanol-induced gastric lesions. PGE2 caused an inhibition of gastric motility as well as an increase of mucosal blood flow and mucus secretion, the effects being mimicked by prostanoids activating EP1 receptors, EP2/EP3/EP4 receptors and EP4 receptors, respectively. On the other hand, although HCl/ethanol caused similar damage in both wild-type mice and knockout mice lacking EP1 or EP3 receptors, the cytoprotective action of PGE2 observed in wild-type and EP3-receptor knockout mice totally disappeared in mice lacking EP1 receptors. CONCLUSION: The gastric cytoprotective action of PGE2 is mediated by activation of EP1 receptors. This effect may be functionally associated with inhibition of gastric motility but not with increased mucosal blood flow or mucus secretion.
Animals↗
Activity of interleukin 6 in the differentiation of monocytes to macrophages and dendritic cells.
Peripheral blood monocytes are common precursor cells of dendritic cells (DCs) and macrophages. We have searched for factors with the potential to regulate the differentiation of monocytes to DCs and macrophages. When CD14+ monocytes are cultured with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL) 4, the CD14+CD1a- population, which consists of macrophages, was found in the serum-containing cultures but not in the serum-free cultures. Addition of IL-6 receptor-neutralizing monoclonal antibody (mAb) or gp130-neutralizing mAb to the serum-containing cultures resulted in a decreased population of CD14+CD1a- cells. An increase in the CD14+CD1a- population with reduction in CD14-CD1a+ DCs was observed with the addition of IL-6 to cultures, whereas IL-11, leukaemia inhibitory factor, oncostatin M or macrophage colony-stimulating factor did not affect the differentiation of monocytes in the presence of GM-CSF plus IL-4. This effect of IL-6 was blocked by tumour necrosis factor alpha (TNF-alpha), lipopolysaccharide (LPS), IL-1beta, CD40 ligand (CD40L) and transforming growth factor beta1 (TGF-beta1). Among these factors, TNF-alpha was most potent in interfering with the action of IL-6. These results suggest that IL-6 inhibits the differentiation of monocytes to DCs by promoting their differentiation toward macrophages, which is modulated by factors such as TNF-alpha, LPS, IL-1beta, CD40L and TGF-beta1.
Adult↗
Regulatory mechanism of acid secretion in the damaged stomach: role of endogenous nitric oxide.
The present article overviews the regulatory mechanism of acid secretion in the stomach after damage with taurocholate (TC), one of the bile acids. Mucosal exposure of a rat stomach to 20 mmol/L TC for 30 min caused a decrease of acid secretion with a concomitant increase in nitric oxide (NO) and prostaglandin (PG) E2 (PGE2) as well as Ca2+ in the luminal contents. Prior administration of N(G)-nitro-L-arginine methyl ester (L-NAME), as well as indomethacin, significantly attenuated the reduction of acid secretion by TC and acid secretion was even increased in the presence of L-NAME. The acid stimulatory effect of L-NAME in the damaged stomach was not mimicked by aminoguanidine and was antagonized by co-administration of L-arginine but not D-arginine. Increased NO release in the damaged stomach was suppressed by pretreatment with L-NAME or co-application of EGTA and the latter also inhibited the increase in luminal Ca2+. The enhanced acid secretory response in the presence of L-NAME was also inhibited by cimetidine, FPL-52694 (a mast cell stabilizer) or sensory deafferentation. Mucosal exposure to TC caused an increase in luminal histamine output, together with a decrease in the number of mucosal mast cells in the stomach. These changes were prevented by FPL-52694 and sensory deafferentation and were also partly suppressed by indomethacin. In addition, the acid stimulatory action of L-NAME in the damaged stomach was significantly mitigated when indomethacin was administered together with L-NAME. We conclude that: (i) damage in the stomach may activate acid a stimulatory pathway in addition to a PG-, NO- and Ca2+-dependent inhibitory mechanism, but the latter effect overcomes the former, resulting in a decrease in acid secretion; (ii) acid stimulation in the damaged stomach is mediated by histamine released from the mucosal mast cell, a process interacting with capsaicin-sensitive sensory nerves; (iii) the increase in luminal Ca2+ plays a role in increasing NO production and, hence, in regulating acid secretion; and (iv) PG may have a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect, probably through enhancing the release of mucosal histamine.
Animals↗
Relationship among oxygenation, myoelectric activity, and lactic acid accumulation in vastus lateralis muscle during exercise with constant work rate.
The purpose of this study was to determine whether oxygenation in localized working muscle depended on the muscle activity and on the lactic acidosis level. Seven healthy male subjects underwent the five 6-min cycling exercises with work rates of 50 watts (25.0 +/- 5.0% VO2max), 100 watts (36.6 +/- 6.2% VO2max), 150 watts (50.6 +/- 7.7% VO2max), 200 watts (67.8 + 6.9% VO2max), and 250 watts (82.9 +/- 7.5% VO2max) while gas exchange parameters and blood lactate concentration (BL) were measured. We also measured oxygenated hemoglobin and myoglobin concentration (oxy-Hb/Mb) with continuous-wave near infrared spectroscopy (NIR) and surface myoelectric activity with surface electrodes (EMG). The NIR probe and electrodes were positioned on the vastus lateralis muscle of the right leg. The relative change in oxy-Hb/Mb was estimated by regarding oxy-Hb/Mb in the resting condition as 100% and that obtained during thigh occlusion as 0%. The mean values of oxy-Hb/Mb and integrated EMG (iEMG) were determined from 5'30" to 6'00" at each work rate. The percentage of oxy-Hb/Mb was sustained at the first two work rates corresponding to 25.0 +/- 5.0 and 36.6 +/- 6.2% VO2max and decreased slightly at 150 watts corresponding to 50.6 +/- 7.7% VO2max, which was followed by a linear decrease at 200 and 250 watts corresponding to 67.8 +/- 6.9 and 82.9 +/- 7.5% VO2max. The iEMG, however, was increased slowly at 25.0 +/- 5.0 to 50.6 +/- 7.7% VO2max, and a rapid increment of the iEMG occurred at 67.8 +/- 6.9 and 82.9 +/- 7.5% VO2max. BL was sustained at 25.0 +/- 5.0 to 50.6 +/- 7.7% VO2max and increased linearly at 67.8 +/- 6.9 and 82.9 +/- 7.5% VO2max. There was a significant negative correlation for each subject between the percentage of oxy-Hb/Mb and iEMG (r = -0.947 to -0.993), between the percentage of oxy-Hb/Mb and BL (r = -0.890 to -0.982), and between the percentage of oxy-Hb/Mb and VO2 (r = -0.929 to -0.994) These results indicated that oxygenated hemoglobin/myoglobin concentration measured with NIR reflected the muscle activity and the lactic acidosis.
Acidosis, Lactic↗
Therapeutic effects of parenteral beta-lactam antibiotics on experimental otitis media caused by penicillin-resistant Streptococcus pneumoniae in guinea-pigs.
The therapeutic effects of parenteral beta-lactam antibiotics were evaluated in experimental acute otitis media caused by penicillin-resistant Streptococcus pneumoniae (PRSP) in guinea-pigs. Cefotaxime, ceftriaxone and piperacillin significantly reduced viable cell counts of PRSP in the middle ear at a dose of 50 mg/kg bd for 3 days (P < 0.01 compared with control). The therapeutic effects of cefotaxime, ceftriaxone and piperacillin were superior to those of cefotiam and ceftazidime. These therapeutic effects reflected both in vitro activity and pharmacokinetic properties of the drugs.
Animals↗
Dpb11 controls the association between DNA polymerases alpha and epsilon and the autonomously replicating sequence region of budding yeast.
Dpb11 is required for chromosomal DNA replication and the S-phase checkpoint in Saccharomyces cerevisiae. Here, we report detection of a physical complex containing Dpb11 and DNA polymerase epsilon (Dpb11-Polepsilon complex). During the S phase of the cell cycle, Dpb11 associated preferentially with DNA fragments containing autonomously replicating sequences (ARSs), at the same time as Polepsilon associated with these fragments. Association of Dpb11 and Polepsilon with these fragments was mutually dependent, suggesting that the Dpb11-Polepsilon complex associates with the ARS. Moreover, Dpb11 was required for the association of Polalpha-primase with the fragments. Thus, it seems likely that association of the Dpb11-Polepsilon complex with the ARS fragments is required for the association of the Polalpha-primase complex. Hydroxyurea inhibits late-origin firing in S. cerevisiae, and the checkpoint genes, RAD53 and MEC1, are involved in this inhibition. In the presence of hydroxyurea at temperatures permissive for cell growth, Polepsilon in dpb11-1 cells associated with early- and late-origin fragments. In wild-type cells, however, it associated only with early-origin fragments. This indicates that Dpb11 may also be involved in the regulation of late-origin firing. Overall, these results suggest that Dpb11 controls the association between DNA polymerases alpha and epsilon and the ARS.
Cell Cycle Proteins↗
Effects of long-term treatment with calcium antagonists on periarterial nerve function in the mesenteric artery of spontaneously hypertensive rats.
The effect of long-term treatment with dihydropyridine calcium antagonists (amlodipine, pranidipine, nicardipine) on the periarterial nerve function was investigated in the perfused mesenteric vascular bed isolated from spontaneously hypertensive rat (SHR). Male 8-week-old SHR received amlodipine (0.01% and 0.02%) and nicardipine (0.1%) in drinking water and pranidipine (0.0035% and 0.035%) in rat chow for 7 weeks. Mean blood pressure in SHR was significantly lowered by long-term treatment with each calcium antagonist. In mesenteric vascular preparations treated with each calcium antagonist, vasoconstriction induced by periarterial nerve stimulation (PNS; 4, 8 and 12 Hz) was significantly smaller than that in non-treated SHR. The PNS (8 Hz)-evoked norepinephrine (NE) overflow in the perfusate was significantly decreased by amlodipine and pranidipine treatment, whereas nicardipine-treatment significantly enhanced the overflow of NE. In preparations with active tone produced by methoxamine and guanethidine, the PNS-induced vasodilation mediated by calcitonin gene-related peptide (CGRP)-containing (CGRPergic) vasodilator nerves was not affected by these drugs. These results suggest that long-term treatment of SHR with long-acting drugs, amlodipine and pranidipine, reduces sympathetic adrenergic nerve function but calcium antagonists have no effect on CGRPergic nerve function.
Amlodipine↗
Type II citrullinemia in an elderly patient treated with living related partial liver transplantation.
A 60-year-old woman was admitted to our hospital for repeated consciousness disturbance. Blood examination showed hyperammonemia, and plasma amino acid analysis revealed a marked increase in the citrulline level. To establish a diagnosis, a percutaneous needle biopsy of the liver was performed. The determination of the urea cycle enzyme activities revealed a selective marked decrease in argininosuccinate synthetase activity, indicating the final diagnosis of type II citrullinemia. The mean survival period of this disease after the appearance of symptoms has been reported as 26.4 months, and most conservative treatments are not effective. We performed a living related partial liver transplantation. Over the subsequent 13-month follow-up, the patient's condition has remained fairly good.
Biopsy, Needle↗
Bcl-2 in cell-cycle regulation of hematopoietic cells by transforming growth factor-beta1.
We reported that several growth factors regulate the doubling time of hematopoietic progenitor cells by modulating the time required to pass through the G1 phase. As recent studies revealed the link between cell death and cell-cycle progression, we asked if cell death regulators such as Bcl-2 play a role in regulating the cell-cycle of hematopoietic cells by growth factors. Among growth factors, transforming growth factor-beta1 (TGF-beta1), a negative regulator of hematopoiesis, was chosen. When a large number of cells was required for analysis, we used IL-3-dependent Ba/F3 cells instead of primary hematopoietic progenitor cells because the response of Ba/F3 cells to TGF-beta1 was similar to that of primary hematopoietic progenitor cells. TGF-beta1 decelerated the cell-cycling of hematopoietic cells by inducing a delay in G1 to S phase transition, an event associated with increase in the level of Bcl-2 as well as p27, a cyclin/cyclin-dependent kinase inhibitor. In experiments using Ba/F3 cells with the potential to produce Bcl-2 in an inducible manner, Bcl-2 apparently functions upstream of p27. The effects of TGF-beta1 on Bcl-2 and p27 expression as well as cell growth were abrogated by c-kit ligand. These findings suggest that Bcl-2 plays a crucial role in regulating the cell-cycle of hematopoietic progenitor cells.
Animals↗
[The relationships of mononuclear leukocyte beta-adrenergic receptors to aerobic capacity and exercise-induced asthma in asthmatic children].
beta-adrenaline receptors exist on peripheral mononuclear leukocytes as well as in lung tissue. We assessed the relationships of plasma catecholamine release by exercise to aerobic capacity and to exercise-induced asthma (EIA) in asthmatic children (Study 1). We then measured mononuclear leukocyte beta-adrenergic receptor densities at rest and assessed the relationships of the number of receptors to aerobic capacity, EIA, and bronchial responsiveness to acetylcholine (Study 2). Study 1: Eleven children (9 males, 2 females; 11-16 years old) with bronchial asthma participated in this study. The subjects underwent an incremental aerobic exercise test on a cycle ergometer to determine their aerobic capacity at the lactic threshold (LT) and VO2max. Each subject underwent an EIA test of which the intensity was 175% of LT, and plasma catecholamine concentrations were measured before and after exercise. A significant negative relationship was found between the degree of EIA and % change of plasma adrenaline concentrations to rest level (p < 0.05), and a significant positive relationship was found between VO2 max/wt and % change of plasma adrenaline concentrations (p < 0.05). Study 2: Twelve asthmatic children (10 males, 2 females; 11-16 years old) participated in this study. Aerobic capacity, and degree of EIA were also measured in each subject by the same method as that used in Study. 1. The number of mononuclear leukocyte beta-adrenergic receptors at rest was determined by (-) [125I]-iodocyanopindolol binding in each subject. A significant negative relationship was found between the number of adrenergic receptors and Max. % fall in FEV1.0 (p < 0.01), and a significant positive relationship was found between the number of adrenergic receptors and VO2max/kg (p < 0.001). These results suggested that a reduced adrenaline production and a reduced number of beta-receptors contributed to the pathogenesis of EIA.
Adolescent↗
Evaluation of the therapeutic effect of radiotherapy on cervical cancer using magnetic resonance imaging.
PURPOSE: This study was performed to evaluate magnetic resonance imaging (MRI) in determining the therapeutic effect of radiotherapy (RT) on cervical cancer. METHODS AND MATERIALS: Serial MRI studies were performed in 42 patients with predominantly advanced cervical cancer before, during, and after radiotherapy. Patients underwent external irradiation combined with high-dose-rate intracavitary (HDR) brachytherapy. T-2 weighted spin-echo pulse sequences with long repetition and echo times were used at a field strength of 1.5 T. Multiple punch biopsies of the cervix were obtained from the high-signal intensity area in all patients at the same time as the MRI. RESULT: In biopsies performed immediately after RT, no residual tumors were found in 36 patients (86%); in 6 patients, residual tumors were observed. The simultaneous MRI study demonstrated no high-signal intensity on T2-weighted images in 28 patients. A high-signal area was observed in 14 patients, and this disappeared 3 months after RT in 8 patients with a negative histological study. The sensitivity, specificity, and accuracy of MRI studies at 3 months after RT were 100%. When the relationship between reduction of tumor volume at 30 Gy and local tumor control was analyzed, every patient with a reduction under 30% gained local control. Also, patients with no residual tumors 3 months after RT gained local control. CONCLUSION: MRI studies performed at 30 Gy of external irradiation and 3 months after RT were predictive factors of local control.
Adenocarcinoma↗
A single nucleotide insertion in the 5'-untranslated region of hepatitis C virus leads to enhanced cap-independent translation.
The 5'-untranslated region (5'-UTR) of hepatitis C virus (HCV) contains an internal ribosome entry site (IRES) that directs translation of the viral open reading frame (ORF). The 5'-UTR consists of 341 nucleotides (nt) in most strains, and multiple segments within this region are important for its IRES activity. Sequencing analysis of a full-length HCV cDNA clone derived from a Japanese HCV1b-positive patient showed the 5'-UTR was 342 nt long due to a nucleotide T insertion at position 207. The influence of this T insertion on the IRES activity in directing cap-independent translation was investigated. The IRES of the 5'-UTR342 was approximately five- and two- to sevenfold more active in directing luciferase expression in monocistronic and bicistronic expression systems, respectively, when compared with the IRES of the 5'-UTR341 of a previously reported HCV1b strain. In addition to the T insertion, another point mutation involving an A to C transition at position 119 was also present in the 5'-UTR342. Simultaneous comparison of the IRES activities in engineered constructs that contained each of the two mutations indicated that the insertion at position 207 is responsible for the enhanced IRES activity of the 5'-UTR342. Further determination of the abilities of the engineered 5'-UTRs harbouring A, G, or C insertions at the same position to initiate translation indicated that both T and non-T nucleotide insertions lead to enhanced cap-independent translation.
5' Untranslated Regions↗
Determination of plasma phenobarbital concentration by high-performance liquid chromatography in rat offspring.
Plasma phenobarbital (PB) concentrations in rat offspring were determined using a 9 microl capillary by high-performance liquid chromatography (HPLC). Capillary plasma which was put into a Bond Elut cartridge column by using 1 ml of 0.01 M KH2PO4 was applied to the column with 50 microl of 2 microg/ml of acetanilide (internal standard, I.S.). After washing the column, PB and I.S. were eluted with methanol and injected into the HPLC system. There were excellent linear correlation between the amount of PB and length of the capillary at three different concentrations. Calibration for PB was linear in the range of 0-50 microg/ml. The coefficients of variation were 3.4-5.0% and 5.9-7.5% in the within-day and between-day assays, respectively. The extraction recovery rates were 87.5-105.4%. By this method, it was possible to measure plasma PB concentrations in rat offspring without killing. These results suggested that this method is very useful to determine the plasma PB concentration derived from mother's milk in newborn rats.
Animals↗