A 61-year-old man, who suffered from Charcot-Marie-Tooth disease (CMT) for 44 years, was evaluated for the respiratory disorder. He had diaphragmatic dysfunction induced by phrenic nerve disturbance. In this patient, central type apnea and hypopnea related to dia phragmatic weakness occurred during REM sleep, which induced accessory inspiratory muscle inhibition. Respiratory muscle dysfunction had not been generally recognized in CMT until recently, but its significance should be emphasized. (Internal Medicine 31: 1267-1270, 1992 Key words: phrenic nerve disturbance, apnea, hypopnea, hypoxemia Case ReportA 61-year-old man was sent to our hospital for further evaluation of a respiratory disorder during sleep which was pointed during a hospital stay in November 1988. He had Charcot-Marie-Tooth disease (CMT) since age 17 and had been admitted to the previous hospital since 1973. He did not note any dyspnea or general fatigue but complained of sleeplessness for the previous 5 years. There was no history of cardiopulmonary disease. Neuro muscular disease in his family history was negative. His general status appeared to be fair, though he was not able to walk by himself, but could move using a wheelchair. His height was 168cm and weight was 49kg. No deformities of the chest wall and the vertebra were observed. Pulse was regular and the rate was 72/min. Blood pressure was 140/70mmHg. Respiration rate was 16/min. In the supine position, the abdominal wall retracted paradoxically in the inspiratory phase. No edema or clubbed finger sign were revealed. Peripheral cyanosis was recognized in the toes. Consciousness was clear and there was no problem with his intelligence. Cranial nerves were intact. Speech and swallowing were performed without any disturbance. Muscles in the bilateral hands and forearms were atrophied and claw hands were recognized. All muscles below the bilateral middle third of the thigh had atrophied showing the appearance of "stork legs." The feet were short and showed arched deformities called upes caves." The strength of the atrophied muscles was diminished and deep tendon reflexes were absent except for trace reflexes in the bilateral biceps and triceps muscles. There was no trace of pathological reflex, fasciculation or tremor. There was slight disturbance of deep sensation below the level of the tenth thoracic vertebra and touch and pain sensations were manifestly disturbed in the lower limbs, especially in the feet. The chest X-ray film showed a slight elevation of the left diaphragm, and a normal cardiac silhouette. An impairment of bilateral diaphragm movement was recognized fluoroscopically. In the laboratory data on admission, peripheral blood, biochemistry, urinalysis and the thyroid function test were normal. There was no evidence of the diabetic metabolic disorders. In the pulmonary function test, vital capacity was 3,040ml in the sitting position. On the contrary, it de creased to 2,010ml in the supine position. Especially, expiratory reserve volume which was 1,240ml in the sittig positio...
Serial changes in cardiac norepinephrine content and the beta-adrenergic system were investigated during the development of cardiomyopathy in spontaneously diabetic Chinese hamsters (CHAD strain), in comparison to age-matched control Chinese hamsters (CHA) or non-diabetic CHAD hamster littermates. Cardiac norepinephrine content and beta-adrenergic receptor density significantly increased in short-term diabetics. These changes preceded both the development of cardiac hypertrophy and the enhanced response of adenylyl cyclase to isoproterenol plus 5'-guanylylimidodiphosphate [Gpp (NH)p], sodium fluoride, or forskolin stimulation. However, as the diabetic state developed cardiac norepinephrine content, beta-adrenergic receptor density, and adenylyl cyclase activity returned to control levels. The amount of stimulatory or inhibitory guanine nucleotide binding proteins in the diabetic group was similar to those in the control groups. These data suggest that the cardiac beta-adrenergic system is enhanced by the alterations in cardiac sympathetic activity during early diabetes, which are associated with the duration of diabetes rather than with the degree of hypertrophy or strain differences.
The effects of cisplatin on the cell cycle and DNA synthesis of human lung adenocarcinoma cell line PC-9 were examined by flow cytometry. The cellular DNA content and the bromodeoxyuridine (BrdUrd) incorporation rate were measured simultaneously using a monoclonal anti-BrdUrd antibody. Following exposure to cisplatin (1.0 pg/ml) for 1 and 24 hr, the bivariate DNNBrdUrd distributions revealed a delayed S-phase transit and an accumulation of cells in the G2M phase. The BrdUrd-linked green fluorescence intensity continued to decrease with the lapse of time. However, earlyand mid-S-phase cells soon recovered DNA synthesis activity, and the former showed higher activity than the control cells. These findings suggested the vigorous DNA synthesis of cells in early S phase. However, for quantitative analysis of chemotherapeutic effects, some problems remained to be resolved regarding the condition for DNA denaturation and its alteration by the agents.Key terms: antibromodeoxyuridine, cell cycle, DNA synthesis rate, dual-parameter analysis Bromodeoxyuridine (BrdUrd) is a thymidine analogue that is incorporated specifically into DNA during the S phase of the cell cycle. In 1982, Gratzner (11) produced a monoclonal anti-BrdUrd antibody, and, in 1983, Dolbeare et al. (7) developed a procedure for simultaneous flow cytometric measurement of the cellular DNA content and the amount of incorporated BrdUrd using a n immunofluorescent antibody. They also showed that BrdUrd-linked green fluorescence was proportional to the amount of incorporated BrdUrd (7).Since then, many studies using this antibody have been reported (2,5,9,12,16,21,23). Dean et al. ( 5 ) reported that a mean BrdUrd-linked fluorescence could be taken as a n estimate of the mean DNA synthesis rate. Langer et al. (16) showed that the ratio of S-phase cells estimated by this method correlated well with the 3H-thymidine labeling index. However, there were few studies in which this technique was used to analyze the chemotherapeutic effects on cancer cell kinetics (12).We reported an analytical model of flow cytometric measurement of bivariate DNAiBrdUrd distribution for the study of the cell cycle and showed a good correlation (r = 0.85) between the "-thymidine labeling indices and the percent S-phase population obtained by this method (9). The purpose of this study was to analyze the effects of cisplatin, a n antineoplastic platinum derivative, on the cell cycle and DNA synthesis of a human lung cancer cell line. We applied the BrdUrd labeling method, simultaneous flow cytometric measurement of DNA content, and BrdUrd incorporation, for the quantitative analysis of the cancer cell kinetics. MATERIALS AND METHODS Cancer Cells and Cell Culture MethodsCultured human lung adenocarcinoma cell line PC-9 (kindly provided by Prof. Y. Hayata, Tokyo Medical College, Tokyo, Japan) was used. The cells were maintained in RPMI 1640 medium (GIBCO) supplemented with 10% heat-inactivated fetal bovine serum (FBS; GIBCO) and 40 Fgiml of gentamicin (Schering), a t 37°C in a humidified...
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