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A Matsuki

Publications and source records attributed to A Matsuki.

At least 19 recordsLinked to original sources

Milrinone attenuates serotonin-induced pulmonary hypertension and bronchoconstriction in dogs.

UNLABELLED: We determined whether milrinone, a phosphodiesterase III inhibitor, attenuates serotonin-induced (5-hydroxytryptamine [5HT]) pulmonary hypertension (PH) and bronchoconstriction. Dogs were anesthetized with pentobarbital (30 mg/kg + 2 mg. kg(-1). h(-1)). Bronchoconstriction and PH were elicited by 5HT (10 microg/kg + 1.0 mg. kg(-1). h(-1)). Pulmonary vascular resistance was used to assess PH. Bronchoconstriction was also assessed by changes in bronchial cross-sectional area obtained from our bronchoscopic method. At 30 min after 5HT infusion started, seven dogs were given milrinone: 0 (saline), 5, 50, 500, and 5000 microg/kg at 10-min intervals. The other 12 dogs were given milrinone 5000 microg/kg 30 min after 5HT infusion, and 5 min later were given propranolol 0.2 mg/kg (n = 6) or saline (n = 6) IV. The 5HT significantly increased percentage of pulmonary vascular resistance to 208% +/- 27% and decreased percentage of bronchial cross-sectional area to 52% +/- 5% of the basal. Milrinone significantly attenuated both PH and bronchoconstriction in a dose-dependent manner. However, -log 50% effective concentration (mean ED(50) in microg/kg) of milrinone for bronchoconstriction: 4.32 +/- 0.13 (47.6) was significantly smaller than that for PH: 3.84 +/- 0.29 (144.9) (P < 0.01). In addition, the spasmolytic effects of milrinone (5000 microg/kg) were not antagonized by propranolol, although this dose significantly increased plasma catecholamines. In conclusion, milrinone attenuates 5HT-induced PH and bronchoconstriction; however, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than in pulmonary vascular smooth muscle. In addition, the relaxant effects could not be caused by beta-adrenoceptor activation because beta-blocker did not antagonize. IMPLICATIONS: We studied the effects of milrinone on serotonin-induced pulmonary hypertension and bronchoconstriction in dogs. Milrinone produces pulmonary vasodilation and bronchodilation, whose effects may not be caused by beta-adrenoceptor activation. In addition, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than that in pulmonary vascular smooth muscle.

Animals↗

Cardiopulmonary bypass produces greater pulmonary than systemic proinflammatory cytokines.

Cardiopulmonary bypass (CPB) impairs pulmonary endothelial injury in part by increasing expression of adhesion molecules that results in neutrophil influx. Although numerous proinflammatory cytokines up-regulate these responses, the extent to which systemic and pulmonary proinflammatory cytokines increase remains unknown. We therefore examined systemic and pulmonary gene expression and production of proinflammatory cytokines during CPB. Bronchoalveolar lavage and peripheral blood sampling were performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) was measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. We also measured these cytokines in cultured alveolar macrophages and plasma monocytes in standard medium alone, or in the presence of lipopolysaccharide. We found 2- to 20-fold increases in gene expression for these cytokines in both plasma and alveolar leukocytes at the end of surgery. However, the increases were 4-8 times greater in alveolar than plasma leukocytes. Alveolar macrophages obtained at the end of surgery produced 1.5-3 times more IL-6, IL-8, and TNF-alpha than those obtained at the beginning (P < 0.0001). Although plasma monocytes produced more IL-8 at the end of surgery (P < 0.001), TNF-alpha and IL-6 did not increase. The production of all cytokines was 1.5-3 times greater in alveolar macrophages obtained at the end of surgery than in plasma monocytes obtained simultaneously (P < 0.005). Our data thus suggest that CPB provokes a greater pulmonary than systemic inflammatory response.

Actins↗

Neutrophil number and interleukin-8 and elastase concentrations in bronchoalveolar lavage fluid correlate with decreased arterial oxygenation after cardiopulmonary bypass.

Atelectasis is a major cause of decreased arterial oxygenation after cardiopulmonary bypass (CPB). There is a close relationship between atelectasis and inflammatory responses. We therefore tested the hypothesis that neutrophil number and the concentrations of proinflammatory cytokines and elastase in plasma and bronchoalveolar lavage fluid correlate with changes in arterial oxygenation. Bronchoalveolar lavage was performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. Peripheral blood was sampled simultaneously. Arterial oxygenation was quantified by PaO(2)/fraction of inspired oxygen (FIO(2)) and intrapulmonary shunt (Q(s)/Q(t)). PaO(2)/FIO(2) and Q(s)/Q(t) decreased significantly at the end of surgery, whereas neutrophil number, interleukin (IL)-6, IL-8, tumor necrosis factor-alpha, and elastase concentrations in the lavage fluid increased significantly. The increase in neutrophil count from the lavage fluid correlated significantly with the increases in IL-8 and elastase concentrations. The increase in neutrophil number and IL-8 and elastase concentrations in the lavage fluid correlated significantly with PaO(2)/FIO(2) and Q(s)/Q(t) at the end of surgery. In contrast, none of the plasma values correlated with these variables. Significant correlation between immune mediators and decreased arterial oxygenation suggests that inflammatory responses in the distal airway are strongly related to a decrease in arterial oxygenation after CPB.

Bronchoalveolar Lavage Fluid↗

Sevoflurane stimulates inositol 1,4,5-trisphosphate in skeletal muscle.

UNLABELLED: Inositol 1,4,5-triphosphate (IP(3)) plays an important role in excitation-contraction coupling and malignant hyperthermia in skeletal muscle. We investigated whether sevoflurane affects IP(3) formation in L(6) skeletal muscle cells and studied the mechanisms that modulate IP(3). Sevoflurane stimulated IP(3) production from a basal level of 78.4 +/- 6.1 to 730.0 +/- 53.1 pmol. mg. protein(-1) in 2 mM of sevoflurane in a dose-dependent manner. A dose of 10 microM of U73122 (a phospholipase C antagonist) significantly decreased 0.8 mM of sevoflurane-stimulated IP(3) production from 387. 8 +/- 24.7 to 247.8 +/- 19.8 pmol. mg. protein(-1). A dose of 100 microM of (p-amylcinnamoyl) anthranilic acid (a PLA(2) antagonist) also significantly decreased sevoflurane-stimulated IP(3) production to 282.0 +/- 24.0 pmol. mg. protein(-1). Exposure to 1 microM of genistein and tyrphostin A23 (tyrosine kinase inhibitors) significantly decreased sevoflurane-stimulated IP(3) production to 241.0 +/- 35.3 and 267.4 +/- 32.9 pmol. mg. protein(-1). Sevoflurane-stimulated IP(3) production was significantly decreased by 10 microM of 8-(N,N-diethylamino) octyl-3,4-5-trimathoxybenzoate (an intracellular calcium antagonist) and 100 microM and 1 mM of guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS), a guanosine 5'triphosphate-binding protein inhibitor. Elevation of IP(3) production was significantly higher in halothane than in sevoflurane and isoflurane at the same concentration of 0.8 mM. We conclude that sevoflurane-stimulated IP(3) production involves phospholipase C, phospholipase A(2), tyrosine kinase, and guanosine 5'triphosphate-binding protein and the stimulation is associated with concentration of intracellular ionized calcium. IMPLICATIONS: Inhaled anesthetics increase intracellular ionized calcium in the skeletal muscle cell and the ionized calcium increase is partly released from the intracellular store by inositol 1,4,5-triphosphate (IP(3)) formation. IP(3) plays an important role in excitation-contraction coupling and malignant hyperthermia. We studied whether sevoflurane affects IP(3) formation and the mechanisms that modulate IP(3).

Anesthetics, Inhalation↗

Smoking decreases alveolar macrophage function during anesthesia and surgery.

BACKGROUND: Smoking changes numerous alveolar macrophage functions and is one of the most important risk factors for postoperative pulmonary complications. The current study tested the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery. METHOD: The authors studied 30 smoking and 30 nonsmoking patients during propofol-fentanyl general anesthesia. Alveolar immune cells were harvested by bronchoalveolar lavage immediately and 2, 4, and 6 h after induction of anesthesia and at the end of surgery. The types of alveolar immune cell and macrophage aggregation were determined. The authors measured opsonized and unopsonized phagocytosis. Microbicidal activity was determined as the ability of the macrophages to kill Listeriamonocytogenes directly. Finally, RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin 1beta, 6, and 8, interferon gamma, and tumor necrosis factor alpha were measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. RESULTS: The fraction of aggregated macrophages increased significantly over time in both groups, whereas phagocytosis of opsonized and nonopsonized particles and microbicidal activity of alveolar macrophages decreased significantly. The changes, though, were nearly twice as great as in patients who smoked. Gene expression of all proinflammatory cytokines in alveolar immune cells except interleukin 6 increased 2- to 20-fold over time in both groups. The expression of interleukin 1beta, interferon gamma, and tumor necrosis factor alpha, however, increased only half as much in smokers as in nonsmokers. CONCLUSION: Smoking was associated with macrophage aggregation but markedly reduced phagocytic and microbicidal activity-possibly because expression of proinflammatory cytokines was reduced in these patients. Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.

Anesthesia, General↗

Supplemental intraoperative oxygen augments antimicrobial and proinflammatory responses of alveolar macrophages.

BACKGROUND: The first goal was to test the hypothesis that 100% inspired oxygen maintained for approximately 8 h intraoperatively is not associated with impaired pulmonary oxygenation. The authors also tested the hypothesis that intraoperative inhalation of 100% oxygen augments proinflammatory and antimicrobial responses of alveolar macrophages during anesthesia and surgery. METHODS: The authors studied patients administered 100% oxygen (n = 30) and 30% oxygen (n = 30) during propofol-fentanyl general anesthesia. Alveolar macrophages were harvested by bronchoalveolar lavage immediately, 2, 4, and 6 h after induction of anesthesia, and at the end of surgery. The authors measured "opsonized" and "unopsonized" phagocytosis and microbicidal activity. RNA was extracted from harvested cells and cDNA was synthesized. The expression of interleukin(IL)-1beta, IL-6, IL-8, interferon-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) was measured by semiquantitative polymerase chain reaction. RESULTS: Gene expression of all proinflammatory cytokines except IL-6 increased fourfold to 20-fold over time in both groups. However, expression of TNF-alpha and IL-8, IFN-gamma, and IL-6 and IL-1beta was 2-20 times greater in patients administered 100% than in those administered 30% oxygen. Unopsonized and opsonized phagocytosis and microbicidal activity decreased progressively, with the decreases being nearly twice as great during inhalation of 30% oxygen versus 100% oxygen. CONCLUSION: Inhalation of 100% oxygen improved intraoperative decreases in phagocytic and microbicidal activity possibly because expression of proinflammatory cytokines was augmented. These data therefore suggest that intraoperative inhalation of 100% oxygen augments antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.

Anesthesia, Intravenous↗

Detection of capillary protein leakage by indocyanine green and glucose dilutions in septic patients.

OBJECTIVE: To determine whether indocyanine green (ICG) and glucose dilutions can detect generalized capillary protein leakage in septic patients without requiring repeated measurements. DESIGN: Prospective, clinical study. SETTING: General intensive care unit. PATIENTS: Twelve consecutive patients who met the criteria of sepsis and 16 consecutive acute myocardial infarction (AMI) patients without any underlying pathology inducing generalized protein capillary leakage. INTERVENTIONS: Both ICG 25 mg and glucose 5 g were administered simultaneously, to calculate the plasma volume determined by the ICG dilution method (PV-ICG) and the initial distribution volume of glucose (IDVG), on day 1 of sepsis or on day 1 of hospitalization for the AMI patients. The relationship between these two volumes and the PV-ICG/IDVG ratio was evaluated in two patient groups. MEASUREMENTS AND MAIN RESULTS: Although the IDVG of the two patient groups was not statistically different, the PV-ICG in the septic patients was higher than that in the AMI patients (p < .01). Consequently, the PV-ICG/IDVG ratio in the septic patients was higher than that in the AMI patients (p < .01). Eight of the 12 septic patients had a PV-ICG/IDVG ratio of >0.45, which was not observed in any of the AMI patients. The PV-ICG/IDVG ratio in the septic patients correlated inversely with the total plasma protein concentration (r2 = .46, p < .025) and mean arterial pressure (r2 = .42, p < .05). CONCLUSIONS: Our results indicate that overestimation of the PV-ICG can occur in septic patients and, further, suggest that simultaneous measurement of the two distribution volumes would help predict generalized capillary protein leakage in septic patients without repeated measurement.

Adult↗

[Tracheal mucosal bulla found on tracheal extubation in a patient with pemphigus vulgaris--a case report].

A 49-year-old female with pemphigus vulgaris underwent the removal of a meningioma under general anesthesia. Neither bulla nor erosion was observed on her skin and oral cavity mucosa. She had been on prednisolone 15 mg for six years daily to avoid the recurrence of skin lesion. Anesthesia was induced and maintained with total intravenous anesthesia with propofol and fentanyl. No adverse episodes were encountered during the operative procedure. We checked the tracheal mucosa using bronchofiberscope before extubation. A small bulla was found on the tracheal mucosa, where the cuff of the tracheal tube was located. The trachea was extubated slowly under bronchofiberscopic observation, and no other bullae were found. It would have been formed by mechanical stimulation of the tracheal tube. This case suggests that we have to pay careful attention to the formation of bullae at any part of the body by mechanical stimuli during anesthetic management of patients with pemphigus vulgaris.

Anesthesia, General↗

[Anesthesia, department of anesthesiology and anesthesiology--why has anesthesiology not been accepted socially in Japan?].

An incorrect Japanese terminology of "Masuigaku [symbol: see text]" has been used widely to express "anesthesiology" or "anaesthetics" [symbol: see text] since the first Department of Anesthesiology was established in Tokyo University in 1952. The reason why the nomenclature "Masui-gaku" is wrong is as follows: Japanese nomenclatures for clinical medical sciences should include a Chinese character "Ka [symbol: see text]" such as "nai-ka-gaku" for internal medicine, "ge-ka-gaku" for surgery and "gan-ka-gaku" for ophthalmology. Accordingly the name "Masui-gaku" is erroneous to mean "Anesthesiology" and it should be "Masui-ka-gaku" [symbol: see text]. Thus a big confusion has occurred among lay people as well as many physicians in medical field. "Ma-sui" is etymologically a Japanese word which Dr Seikei Sugita coined when he translated a Dutch edition of J. Schlesinger's monograph on ether anesthesia in 1850. "Ma [symbol: see text]" means analgesia or loss of regional sensation and "Sui [symbol: see text]" means loss of consciousness. Most people consider that "Ma [symbol: see text]" is originated from "[symbol: see text] (Hemp, Asa)" or "[symbol: see text] (Marihuana, Taima)", however, this is definitely incorrect and "Ma [symbol: see text]" of "Ma-sui" has no direct relation with the pharmacological effect of hemp. Thus the misuse of "Masui-ga-ku" might have caused serious academic and social confusions, such as misunderstanding of anesthesiologists as comedical technicians, leading to a poor social acceptance of anesthesiology and anesthesiologists for these fifty years in Japan. To correct this confused situation I would like to ask our colleagues to use correctly these nomenclatures.

Anesthesia Department, Hospital↗

[Abnormal Q wave in the right precordial leads unmasked during right bundle branch block in a patient with anteroseptal myocardial infarction: a case report].

Electrocardiography in a 77-year-old woman showed small R waves in leads V1-V3 3 hours after the onset of acute anteroseptal myocardial infarction. Abnormal Q waves appeared in leads V1-V3 only during intermittent right bundle branch block. The normal septal force disappeared after transmural septal infarction and a small force of right ventricle origin became apparent as a small R wave in V1. Right bundle branch block delayed activation of right ventricle, and thereby deleted the initial R wave and unmasked the Q wave of the septal infarction. Appearance of a Q wave in leads V1-V3 with right bundle branch block should not be assumed to reflect the extension of myocardial infarction.

Aged↗

[New studies on the history of anesthesiology (1)--A newly discovered truth on Woolley and Roe case after an interval of 50 years].

A famous medical accident that is widely known as Woolley and Roe case occurred on Oct 13th, 1947 at the Chesterfield Royal Hospital, England. The patients Albert Woolley and Cecil Roe underwent minor operations under spinal anesthesia using cinchocaine to develop spinal cord myelopathy with paralisis of bilateral legs. Both patients sued Dr James M. Graham, the anesthetist, and the Ministry of Health. Seven years later, Dr Graham and the Ministry of Health were given a verdict of not guilty, because three judges unanimously accepted the phenol theory proposed by a witness Prof Macintosh of Oxford University. He allged that phenol entered into the ampoule of cinchocaine through invisible cracks. Thus the plaintiffs were not compensated. Recentry Dr Hutter of Nottingham University found no validity of phenol theory and also no possibility of invisible cracks. Syringes and needles for spinal anesthesia were used to be sterilised by water-boiling steriliser, and mineral acid was used for descaling the deposition of line at that time. Dr Hutter concluded that the severe spinal myelopathy occurred both in Woolley and Roe would have been caused by mineral acid which was conveyed into their subarachnoidal space by acid-contaminated syringes and needles.

Anesthesia, Spinal↗

[New study on the history of anesthesiology (2)--who is the first Japanese to write a scientific paper for the journal "Anesthesiology"?].

The beginning of modern anesthesiology in Japan dates back to 1950 when Dr M. Saklad of Rhode Island Hospital came to Japan to give his lectures on endotracheal anesthesia and related procedures. Since then, many Japanese surgeons visited the United States to learn anesthesiology in depth and they began to write their papers for foreign journals. According to my survey of the journal "Anesthesiology" from Vol 1 (1940) through Vol 21 (1960), I found 12 scientific papers written by Japanese. The first paper by Japanese appeared in this journal published in 1955 entitled as "Observations on the action of thiopental (Pentothal) on the laryngeal reflex" by Akira Horita et al. He was born in the United States in 1928 as a son of Japanese immigrants. He was graduated from the University of Washington at Seattle to become professor or pharmacology. The first paper based on studies performed in Japan by Japanese authors appeared in 1956. It was entitled as "The spread of drugs used for spinal anesthesia" by Kitahara et al. This paper is the English translation of their Japanese paper which appeared in Nippon Rinsho Geka Ikai Zasshi entitled as "Basic Study on Spinal Anesthesia in 1953".

Anesthesiology↗

Physostigmine antagonizes ketamine-induced noradrenaline release from the medial prefrontal cortex in rats.

Physostigmine is known to antagonize ketamine anesthesia. In this study, effects of physostigmine (0.1 mg kg(-1) i.p.) on ketamine (100 mg kg(-1) i.p.)-induced anesthesia time and noradrenaline release from the medial prefrontal cortex in rats were examined. Ketamine produced anesthesia for 27+/-1 min and increased noradrenaline release to 405% of the basal. Physostigmine significantly reduced anesthesia time to 23+/-1 min (p<0.05), and noradrenaline to 248% (p<0.05). Therefore, noradrenaline release may play an important role in ketamine anesthesia.

Anesthesia↗

Allelic loss mapping and physical delineation of a region harboring a putative thymic lymphoma suppressor gene on mouse chromosome 12.

Our previous allelic loss analysis of gamma-ray induced thymic lymphomas in F1 hybrid and backcross mice between BALB/c and MSM strains mapped the Tlsr4 region exhibiting a high frequency of allelic loss (62%) to a 2.9 cM interval between the markers D12Mit53 and D12Mit279 on mouse chromosome 12. To narrow further the interval harboring a putative tumor suppressor gene, a high-density scan has been carried out for informative 361 thymic lymphomas. Construction of a physical map of Tlsr4 with 3 YAC and 15 BAC clones and isolation of YAC- and BAC-derived polymorphic probes lead to fine allelic loss mapping. Three successive polymorphic sites within one BAC exhibit the retention of both alleles in seven, one and four lymphomas, suggesting that a common region of allelic loss for Tlsr4 exists within the BAC region. Pulsed-field gel electrophoresis of NotI digests of this and other clones determines that the commonly lost region is a 35 kb interval with a NotI site. NotI sites are frequently associated with coding regions, and our preliminary sequencing has identified ESTs in the region. Thus, the present study facilitates the identification of genes in the Tlsr4 region that would lead to isolation of a novel tumor suppressor gene.

Alleles↗

Mutations in the p53 and scid genes do not cooperate in lymphomagenesis in doubly heterozygous mice.

Analysis of double mutant mice of the p53 and scid genes, which have a combination of cell cycle checkpoint/apoptosis and DNA repair defects, shows that the latter defect synergistically enhances lymphoma development with loss of the former function. These mice lack the ability to eliminate lymphocytes predisposed to neoplastic transformation resulting from faulty antigen receptor gene rearrangement. Here we examine the cooperativity in double heterozygotes of p53 and scid in which normal development of lymphocytes is not impaired. MSM mice carrying a p53-knockout allele were crossed with BALB/c mice heterozygous for the scid locus and 129 offspring were obtained. They were subjected to gamma-ray irradiation, 84 thymic lymphomas being generated. The tumors and host mice were genotyped of p53 and scid. Among 42 mice developing p53-deficient lymphomas, scid/+ and +/+ genotypes did not provide difference in onset and latency. Besides, allelic loss of the Scid gene occurred at a high frequency in those lymphomas but the loss exhibited no allelic bias. The results suggest that the scid/+ genotype is not a modifier of loss of p53 function in the double heterozygotes.

Alleles↗

Esophageal mucoepidermoid carcinoma containing signet-ring cells: three case reports and a literature review.

We report 3 cases of esophageal signet-ring cell carcinoma which were found in a set of 505 resected esophageal tumors. The incidence of esophageal signet-ring cell carcinoma was 0.6%. All of the signet-ring cell carcinomas were histologically mixed with squamous cell carcinoma (mucoepidermoid carcinoma). The signet-ring cells had intracellular mucin, which was positive for both periodic acid-Schiff (PAS) and alcian blue at pH 2.5. At the time of presentation, extensive extraesophageal tumor spread and local extension were found in all cases. All of the patients died within 2 years after the esophagectomy irrespective of whether they received chemotherapy or radiotherapy. Our results, and those previously reported, suggest that most esophageal carcinomas containing signet-ring cell carcinoma are aggressive neoplasms associated with a poor prognosis after esophagectomy.

Aged↗

Response to surgical stress in elderly patients and Alzheimer's disease.

PURPOSE: To determine the effect of surgical stress on plasma epinephrine, norepinephrine, ACTH and cortisol concentrations in patients aged 80-99 yr and in patients complicated with Alzheimer's disease. METHODS: A prospective controlled study was undertaken in 55 undergoing surgical reduction of femur neck fracture in Hirosaki University hospital and Hakodate Watanabe hospital; 18 patients in 80-99 yr (Group 1) and 18 patients in 40-59 yr (Group 2) and 7 patients (Group A) with and 12 patients (Group B) without Alzheimer's dementia (AD) aged 60-79 yr. RESULTS: The increase in plasma norepinephrine level (274%) of group 1 patients, 15 min after skin incision was higher than that in group 2 (191%) (P < 0.01). Mean plasma cortisol levels (40.4+/-4.7 and 44.1+/-5.2 microg x dl(-1)) of group 1, 15 min after skin incision and 60 min after the end of surgery were significantly higher than the 29.8+/-3.5 and 22.3+/-3.0 microg x dl(-1) of group 2 (P < 0.05). Plasma norepinephrine (1092.9+/-112.0 pg x ml(-1)) and cortisol concentrations (53.4+/-5.8 microg x dl(-1)) in group A were higher than in group B (772.6+/-82.4 pg x ml(-1) and 41.7+/-4.3 microg x dl(-1)) 15 min after skin incision (P < 0.05). CONCLUSIONS: Plasma norepinephrine and cortisol responses to surgical stress are activated in elderly patients and in patients with Alzheimer's disease.

Adrenocorticotropic Hormone↗