Effects of combined resistance and aerobic training program on myoelectric activity of Vastus Lateralis in patients with breast cancer during adjuvant chemotherapy period.

OBJECTIVE: Chemotherapy and/or radiation are normally the predominant therapies administered to cancer patients. Commonly, patients express complaints of fatigue during adjuvant treatment. Furthermore, regular practice of physical exercise during adjuvant treatment seems to have positive effects. The aim of this study was to investigate the effects of combined muscle strength, and a supervised aerobic training program on myoelectric activity of Vastus Lateralis during isometric test in patients with breast cancer undergoing adjuvant chemotherapy. PATIENTS AND METHODS: Thirty-two women with breast cancer (20 patients in the training group and 12 patients as controls) undergoing adjuvant chemotherapy participated in the study. They took part in a 6-week training period. A muscle-strength program included isometric contraction and electrical muscle stimulation (EMS). Aerobic training program consisted of supervised intermittent cycling exercise and home-based walking exercise. The outcome measures were Root Mean Square (RMS), Mean Power Frequency (MPF), Maximal Voluntary isometric Contraction (MViC), and Endurance Time (ET) of Vastus Lateralis, before and after the training period in the two groups. RESULTS: Compared to controls, a significant increase in MViC (p=0.001) and ET (p=0.005) in quadriceps accompanied by a significant decrease in RMS (p=0.007) and a significant increase in MPF (p=0.002) has been obtained in the training group. CONCLUSIONS: Supervised muscle strength and supervised aerobic training programs enhanced muscle activity and muscular performance in women with breast cancer during adjuvant chemotherapy treatment and optimized the decrease of muscular fatigue.

Pial arterial pressure contribution to early ischemic brain edema.

The effect of pial arterial pressure (PAP) on brain edema was examined in cats with middle cerebral artery (MCA) occlusion. Measurements of PAP and regional CBF (rCBF) were collected in the central core and the peripheral margin of the MCA territory over 180 min post MCA occlusion. Brain water content in each region was determined at the end of the experiment. MCA occlusion resulted in decreased PAP and rCBF in both the core (PAP = 13 mm Hg, rCBF = 9 ml/100 g/min) and the peripheral region (PAP = 15 mm Hg, rCBF = 18 ml/100 g/min). Brain edema developed in both the core and the peripheral region. Brain water content was correlated inversely with PAP in the core region and positively in the peripheral region. The results indicate that decreased blood flow contributes to cytotoxic edema in the core, and a hydrostatic pressure gradient preferentially enhances edema formation in the peripheral region. Maintenance of high perfusion pressure early after ischemia onset may suppress brain edema in the core region.

Flow thresholds for cerebral energy disturbance and Na+ pump failure as studied by in vivo 31P and 23Na nuclear magnetic resonance spectroscopy.

The relationships among CBF, cerebral energy metabolism, Na+ pump activity, and electrocorticograms (ECoG) following graded hypotension were studied in 48 gerbils. Energy metabolism and Na+ pump activity were estimated by in vivo 31P and 23Na nuclear magnetic resonance (NMR) spectroscopy, and CBF was determined by [14C]iodoantipyrine methods at the end of the experiments. The CBF measured in normotensive animals was 0.51 +/- 0.07 ml/g brain/min. Following graded hypotension, no 31P spectral change was observed until CBF fell to 0.21-0.27 ml/g brain/min, at which level the intracellular pH began to decrease in association with ECoG voltage reduction. At a CBF level of 0.18-0.23 ml/g brain/min, phosphocreatine (PCr) began to decrease in association with inorganic phosphate (Pi) elevation. At this level, ECoG became isoelectric, although no adenosine triphosphate (ATP) change yet resulted. At a flow level of 0.12-0.14 ml/g brain/min, ATP began to decrease gradually. At 0.04-0.05 ml/g brain/min, PCr and ATP virtually disappeared, and the 23Na signal intensity suddenly changed. The present study demonstrated flow thresholds for the development of tissue acidosis, PCr-Pi changes, and ATP reduction. It appears that functional suppression occurs prior to ATP changes, whereas Na+ pump failure results after ATP depletion.

Dysautoregulation of the cerebral circulation in primary systemic amyloidosis.

A case of primary systemic amyloidosis associated with marked dysautoregulation of the cerebral circulation in response to hypotension is reported. The major amyloid protein was immunoglobulin A lambda type. An autonomic nerve function test showed severe and extensive disturbances of the autonomic nervous system. The cerebrovascular reactivity to 5% CO2 inhalation was spared. To our knowledge, this is the first case to demonstrate that amyloid peripheral autonomic neuropathy can be accompanied by dysautoregulation of the cerebral circulation.

Pharmacokinetics and pharmacodynamics of intravenous OPC-18790 in humans: a novel nonglycosidic inotropic agent.

OPC-18790, a nonglycosidic intropic agent, is now under clinical development for treatment of congestive heart failure. Two separate studies (one placebo-controlled) were conducted to evaluate its pharmacokinetics and pharmacodynamics after intravenous administration to a total of 36 healthy male subjects. The drug was administered both rapidly as a .05-, .1-, .2-, or .4-mg/kg intravenous dose, and as a 1-hour infusion of .5, 1.0, 2.5, 5.0, 10.0, or 15.0 micrograms/kg/minute. Echocardiograms (ECHO) were evaluated before and immediately and 4 hours after the rapid administrations. Blood pressure (BP), heart rate (HR), and QTc in the electrocardiogram also were monitored in the rapid administration study. OPC-18790 was generally well tolerated by all subjects. Maximum peak plasma concentration and area under the curve increased linearly with dose in both studies. The t1/2, total body clearance of drug from plasma (CL), and the dose fraction excreted unchanged in the urine (fe) were comparable and dose-independent at the doses tested in both studies. The overall mean values of t1/2 alpha, t1/2 beta, CL, and fe were .08 +/- .01 hours, 3.64 +/- .22 hours, .46 +/- .01 L/kg, and 43.5 +/- 1.0%, respectively. Echocardiograms showed that, immediately after rapid administration of up to .4 mg/kg, OPC-18790 increased left cardiac function dose-proportionally (P < .05 to .01): the ejection fraction by 21.1% and fractional shortening by 26.5% compared with the predose values, blood pressure, heart rate, and QTc did not differ between subjects given OPC-18790 and these receiving placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of an antithrombotic agent (MD-805) on progressing cerebral thrombosis.

The effects of the newly developed synthetic selective antithrombin agent MD-805 were examined in 11 patients with progressing cerebral thrombosis, as an open trial. Nine (82%) of 11 patients improved after 1 week of intravenous drip infusion. No hemorrhagic complications were observed during the therapy. These results suggest that MD-805 is a safe and effective agent for treatment of progressing cerebral thrombosis.

Adrenomedullin in the gastrointestinal tract. Distribution and gene expression in rat and augmented gastric adrenomedullin after fasting.

The aim of this study was to investigate the regional distribution, molecular forms, and gene expression of adrenomedullin in the rat gastrointestinal tract and to examine physiological changes in gastric adrenomedullin after 24-h fasting. The tissue concentration was measured by radioimmunoassay. The molecular forms were analyzed by high performance liquid chromatography. mRNA levels were quantified by Northern blotting and cells positive for adrenomedullin immunoreactivity were localized by immunohistochemistry. A high concentration of adrenomedullin was found in stomach, cecum, and colon (450-520 fmol/g wet tissue). Adrenomedullin immunoreactivity was also detected in duodenum, jejunum, and ileum (200-250 fmol/g wet tissue). Transcripts of the adrenomedullin gene were widely expressed throughout the gastrointestinal tract. The major form of adrenomedullin immunoreactivity in stomach and colon corresponded precisely with authentic adrenomedullin peptide. Adrenomedullin immunoreactive cells were present in the gastrointestinal endocrine system. The concentration and mRNA level of gastric adrenomedullin after fasting were significantly increased compared with findings in controls. Adrenomedullin is ubiquitous in the gastrointestinal tract, and may be produced by endocrine cells. The results suggest that adrenomedullin, through its potent vasodilating activity, may play some role, in the stomach including the regulation of the mucosal blood flow.

Distribution and expression of adrenomedullin in human gastrointestinal tissue.

Adrenomedullin (AM) is a biologically active peptide recently isolated from phaeochromocytoma. We report here the distribution and characterization of immunoreactive AM and gene expression of AM in human gastrointestinal tissue. Using a sensitive radioimmunoassay system for the peptide, immunoreactive human AM was detected in the stomach, duodenum, jejunum, ileum and colon. The AM concentration of these tissues was about 0.4-0.8 pmol/g wet tissue. Reverse phase and gel filtration high-performance liquid chromatographies showed that most of the immunoreactive AM in stomach and jejunum was identical to authentic human AM. By northern blot analysis, human AM mRNA was found to be expressed ubiquitously in the human gastrointestinal tissues. Furthermore, an immunohistochemical study revealed that immunoreactive AM cells were present in the gastrointestinal glands. These results suggest that AM may play some role as a gastrointestinal hormone.

Effect of long-term administration of buflomedil on regional cerebral blood flow in chronic cerebral infarction.

The influence of long-term oral administration of buflomedil on regional cerebral blood flow was investigated in 10 patients with chronic cerebral infarction and mild to moderate mental deterioration. Patients were given 150 mg buflomedil three times daily for a period of eight weeks. Regional cerebral blood flow (rCBF) was measured in patients before they began buflomedil treatment and during the last week of treatment. The interval of the rCBF measurements in the control subjects (n = 12) ranged from seven to forty-eight days. Mental function in the patients studied was evaluated by use of Hasegawa's simple intelligence scale for the aged and Zung's self-rating depression scale, before and during the last week of buflomedil treatment. The results showed a mean increase in rCBF of 10.5% +/- 12.1% in the patient group. The control group demonstrated virtually no change in rCBF measurements. Improvements in the mental function scores of the buflomedil-treated group were noted, and 5 of the 10 patients reported improvement in subjective symptoms.

[Unilateral posterior spinal artery syndrome of the upper cervical cord associated with vertebral artery occlusion].

Upper cervical cord infarction in the territory of the posterior spinal artery is very rare. We present here an elderly man who developed right upper cervical (C1-2) posterior spinal artery syndrome associated with vertebral artery occlusion. A 62-year-old man suffered a right upper cervical (C1-2) posterior spinal artery syndrome. The onset was associated with neck flexion. Magnetic resonance imaging clearly showed an ischemic lesion. Cerebral angiography revealed occlusion of the distal end of an ipsilateral vertebral artery. The occlusion of the vertebral artery probably caused the cervical cord infarction. The neck flexion possibly induced thrombogenesis in the vertebral artery. Unilateral upper cervical posterior spinal artery syndrome associated with vertebral occlusion following neck flexion was suggested.

[Acute respiratory arrest associated with medullary lesion in a case of multiple sclerosis].

We present a case history of a patient with multiple sclerosis who developed an abrupt onset of respiratory arrest associated with medullary lesion. A 27-year-old man developed shallow, totally irregular, ataxic respirations with aggravation of bulbar palsy and quadriplegia in the course of multiple sclerosis. As respiration was almost arrested, artificial respiration was started and continued for five days. Respiration was almost normal after 16 days from the onset of respiratory arrest. MRI showed bilateral, medullary lesions without upper cervical lesions. Pyramidal tracts, medial lemnisci, and paramedian reticular formations in medulla were damaged bilaterally. We supposed that the medullary lesions involved dual respiratory systems: a voluntary system and an automatic system, and caused acute respiratory arrest.

[A case of diffuse fasciitis and its MRI findings].

A 36-year-old woman with diffuse fasciitis and her MRI findings are reported. The patient developed pain and swelling in the calves, right forearm, and left arm, predominantly in the right calf muscle. Her body temperature was 38.4 degrees C, the ESR 104 mm/2 hours and white blood cell count 8,000/microliter without eosinophilia. The fascia and muscle were biopsied from her right calf. The light microscopy showed that the fascia was thickened and infiltrated with mononuclear cells with no eosinophils, mostly in perivascular areas. The muscle fibers were spared. MRI of legs revealed marked hyperintensities on T2 and mild hyperintensities on T1-weighted images in the fascia, superficial flexor muscles, especially soleus muscle, and Achilles tendons. Moderate dose of prednisolone was very effective and the abnormal signals on MRI almost disappeared within a month. T2 weighted MRI was very useful to detect the lesions and to evaluate the course of diffuse fasciitis.

[A case of hereditary motor and sensory neuropathy with vocal cords palsy and diaphragmatic weakness].

A case of hereditary motor and sensory neuropathy (HMSN) type 1 (Charcot-Marie-Tooth disease (CMT)) is reported with vocal cords palsy, deafness, diaphragmatic weakness, and cerebellopontine atrophy. A 42-year-old man was admitted to our hospital in April, 1991 with marked respiratory distress. He had been diagnosed as having CMT 14 years previously. On admission to our hospital, he revealed dyspnea with marked stridor during inspiration. Physical examination showed marked use of respiratory accessory muscles with thoracoabdominal paradox in the supine position. Neurologic examination revealed tonic pupils, mild bilateral weakness of facial muscles, deafness, mild bulbar palsy, severe wasting and weakness in both proximal and distal muscles of the arms and legs, areflexia, distal loss of all sensory modalities. Pes cavus and hammer toe were present. Movement of upper extremities was ataxic. No hypertrophic changes were noted in his peripheral nerves. Peripheral nerve conduction study showed undetectable both sensory and motor action potentials. Electromyography showed evidence of denervation, more marked in distal muscles. Auditory brain stem response was undetectable. Chest radiographic film showed a normal-sized heart with marked elevation of both hemidiaphragm. Laryngofiberscopy confirmed the presence of bilateral vocal cord paralysis without tumor formation, inflammation or anomaly. The vocal cords lay near the midline and did not show any movement during respiration. Moderate cerebellopontine atrophy was confirmed on MRI scan. A sural nerve section showed severe decrease of myelinated fibers, and onion bulbs. Diagnosis of HMSN type 1 was made by clinical, electrodiagnostic, and sural nerve sections study.(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of Avellis' syndrome with ipsilateral central facial palsy due to a small medullary infarction].

We report a 51-year-old man with mild left central facial palsy and left Avellis' syndrome due to a small medullary infarction. On admission, neurological examination revealed hoarseness, dysphasia, absent left gag reflex, palsies of the left vocal cord and left soft palate, and hypalgesia and thermohypesthesia on the right side of the trunk and extremities. In addition, he had a mild left central facial palsy. He had no nausea, vomiting, vertigo, hiccups, nystagmus, Horner's sign, facial numbness, or paresis or ataxia of the limbs. A T2 weighted MRI showed a small, high signal intensity area in the left dorsal region of the medulla and this lesion was presumed to involve the nucleus ambiguus and a part of the spinothalamic tract. These findings suggest that an aberrant supranuclear pathway, looping around the nucleus ambiguus to the facial nucleus exists in our patient.

[Cognitive function, cerebral blood flow and brain atrophy in olivo-ponto-cerebellar atrophy].

UNLABELLED: Eighteen cases of OPCA (9 males and 9 females, age 39-70, mean 57.8 +/- 8.1 years). Mean duration of illness was 65.7 +/- 36 months. Age-matched controls for Brain-CT were 34 cases (13 males and 21 females) (age 39-70, mean 56.8 +/- 9.4 years), in which CT was examined because of functional disorders, and 50 healthy volunteers (25 males and 25 females) (age 36-72, mean 56.6 +/- 7.9 years) for regional cerebral blood flow (rCBF) and mental function. Brain Atrophy Index (BAI) and Ventricular Atrophy Index (VAI) were calculated by digitizer (PCPAD) on CT films in the slice of lateral ventricle level, basal ganglia level and cerebello-pontine level. There were 10 patients of OPCA who examined CT prior to this study. Interval of the two examinations was 21-76 months, mean 53 months. Regional cerebral blood flow (rCBF) were measured by 133 Xe inhalation methods. Intelligence were evaluated with Okabe's Intelligence Scale (Shortened and modified Wechsler's Memory Scale for Japanese Aged) and Kohs' Block Design Test. Depressive state was evaluated with Zung's Self-rating Depression Scale (SDS). RESULTS: 1) Cerebello-pontine atrophy was significantly prominent but no cerebral atrophy was observed in OPCA. 2) The rCBF was mildly but significantly reduced in OPCA. 3) Performance and verbal intelligence were significantly low in OPCA. 4) OPCA patients showed significant depressive state. 5) Grade of ADL did not show significant participation in the rCBF, intelligence and depressive state. 6) There was no significant correlation between duration of illness and rCBF or mental functions. 7) Cerebello-pontine atrophy significantly progressed in OPCA patients followed-up.(ABSTRACT TRUNCATED AT 250 WORDS)

[Responses of cerebral arteries to the changes in cerebral perfusion pressure].

The responsiveness of cerebral pial arteries and arterioles to changes in systemic arterial blood pressure (SAP) was investigated. Using 9 cats anesthetized with chloralose and urethane, direct, simultaneous measurements of pial arterial pressure (PAP) and cerebral blood flow (CBF) were made during changes in SAP. SAP was varied between 25 and 140 mmHg by the hemorrhage and blood infusion methods. After a partial craniotomy. PAP was measured with a micropipette connected to a servo-controlled micropressure recording system. Punctured pial arteries were grouped into three types according to their diameters, 1A (291 +/- 33 microns), 2A (16 +/- 26 microns), and 3A (70 +/- 10 microns). CBF on the exposed cortex was measured with hydrogen clearance method. The PAPs measured were a linear function of SAP; PAP (1A) = 0.73/SAP-6.6 (r = 0.96), PAP (2A) = 0.62 X SAP-6.6 (r = 0.90), PAP (3A) = 0.61 X SAP-6.4 (r = 0.93). The result indicates that PAPs are entirely dependent on SAP and that SAP induced changes in PAPs are less in the smaller pial arteries. Regional CBF remained constant (55 +/- 4 ml/100 g/min) between 60 and 140 mmHg of SAP. A significant decrease in CBF was observed below 60 mmHg of SAP. Cerebrovascular resistances were calculated segmentally using the following formulas; large vessel resistances (LVR) = (SAP-PAP(1A]/CBF, middle vessel resistance = (PAP (1A)-PAP (3A]/CBF, and small vessel resistance = PAP (3A)/CBF. The changes in LVR, MVR, and SVR were almost identical between 70 and 140 mmHg of SAP. Below 70 mmHg of SAP, SVR showed the greatest decrease in resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

[A case of leiomyosarcoma of the jejunum with postoperative hepatic encephalopathy].

We report a case of leiomyosarcoma of the jejunum with postoperative hepatic encephalopathy. A 60-year-old man was operated for tumor of the abdomen. He was diagnosed as leiomyosarcoma of the jejunum with disseminated peritoneal metastasis, but no liver metastasis and cirrhosis. A palliative resection of the jejunum was performed. After operation, disturbance of orientation and apraxia with electroencepharographic abnormality and hyperammonemia developed. He was diagnosed as hepatic encephalopathy without lesion of the liver, and died 11 months after surgery. We consider that the portosystemic shunt and bleeding from the digestive tract due to invasion of metastatic lesions caused hepatic encephalopathy.

[Prospective study on the influence of social activity on development of dementia in the neurologically normal elderly].

We investigated the rate of development of dementia in 84 neurologically normal elderly subjects living in an old-age home (30 subjects, mean 77.2 years) or their own home 954, 73.7) prospectively. We examined cerebral blood flow (CBF), Hasegawa's scale (HS) and Kohs' block design test 6 to 9 years before this study (1991). HS and Kohs' IQ were significantly lower in the old-age home group than that in their own home group at that time. However, there were no demented subjects. Mortality was 21%, and we confirmed 9 dementia and 6 stroke cases during the period of observation. Twenty-seven percent of the old-age home group showed dementia in 1991. This rate was significantly higher than that for the elderly living in their own home (6.7%). Occurrence of stroke was also significantly higher in the former group than in the latter group. The subjects who developed stroke during observation showed a high incidence of dementia. Mean CBF measured on the first examination was significantly lower in dementia cases with stroke than in dementia cases without it. We performed MRI in 4 demented cases in 1991 (Fig. 1). Two cases showed no significant lesions and the other cases showed cerebral infarction which could cause dementia. These results indicate that life style and social environment may have significant effect on aging of the brain and on development of dementia in the elderly.