Developmental origin of the rat adenohypophysis prior to the formation of Rathke's pouch.

In amphibians, it has already been shown that the adenohypophysis originates from the anterior neural ridge. During the migration and morphogenesis of this organ, the anterior neural ridge transiently forms a Rathke's pouch-like structure by attaching itself to the rostral tip of the foregut, and finally gives rise to the adenohypophysis by detaching from the foregut and becoming connected to the infundibulum of the hypothalamus. In order to identify the origin of the adenohypophyseal cells in mammalian embryos prior to the formation of Rathke's pouch (RP), we labeled the rostral end of the neural plate and the adjacent area focally with DiI at the open neurula stage (9.5 dpc). After a 48-hours culture of the whole embryos, strongly labeled cells were detected in the RP only when DiI was applied to a small area situated just anterior to the rostral end of the neural plate. By explanting the labeled RP for a further 7 days, we confirmed immunohistochemically that the labeled cells developed into the secretory cells of the adenohypophysis. The developmental origin of the adenohypophysis is identified for the first time in the early mammalian embryo before the formation of RP.

Cellular co-localization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies.

The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB). The microtubule-associated protein tau is an integral component of filaments of neurofibrillary tangles (NFTs). NFTs are occasionally found in brains of PD and DLB; however, the presence of NFTs or tau-epitopes within LB-containing neurons is rare. Double-immunofluorescence study and peroxidase-immunohistochemical study in serial sections, performed to examine the co-localization of tau- and NACP-epitopes in the brainstem of PD and DLB, demonstrated that four different epitopes of tau including phosphorylation-dependent and independent ones were present in a minority of LBs, but more often than previously considered. A tau (tau2)-epitope was localized to filaments in the outer layers of brainstem-type LBs by immunoelectron microscopy. Therefore, we conclude that tau is incorporated into filaments in certain LBs. Extensive investigation has enabled us to classify this co-localization into four types: type 1, LBs with ring-shaped tau-immunoreactivity; type 2, LBs surrounded by NFTs; type 3, NACP- and tau-immunoreactive filamentous and granular masses; and type 4, NACP- and tau-immunoreactive dystrophic neurites. This study raises a new question whether aggregation and hyperphosphorylation of tau in PD and DLB are triggered by the collapse of intraneuronal organization of microtubules due to NACP-filament aggregation in neuronal perikarya and axons.

[An unusual case of peroneal muscular atrophy with rigidity, polyneuropathy, mental retardation, and diabetes mellitus developed in familial Parkinson's disease].

Familial polyneuropathy mimicking Charcot-Marie-Tooth disease associated with parkinsonism and dementia has been reported in literature. We present with similar peroneal muscular atrophy, rigidity of upper extremities, severe peripheral neuropathy, mental retardation and diabetes mellitus. The patient, a 42-year-old man, developed progressive muscle weakness, mental retardation and difficulty in walking in childhood. Because of his pes cavus, he had three surgical operations. At the age of 20 years, he developed distal muscular atrophy of lower limbs. On neurological examination, all limb muscles were atrophic, especially in lower one third of the thigh. Rigidity was noted in the upper extremities. Deep tendon reflexes were hyperactive in the upper and diminished in the lower extremities. Muscle CT revealed low density areas in all the muscles examined, specially in the gastrocnemius and anterior tibial muscles. Needle EMG showed neurogenic change in the forearm, but not in the lower limbs, because of no voluntary contractions obtained due to severe muscle atrophy. Marked slowing of motor conduction velocity with muscle action potentials of very low amplitude was found in the ulnar nerve. Muscle action potentials were not elicited in the median and peroneal nerves. Sensory action potentials were not elicited from the median, ulnar and sural nerves. These findings were consistent with axonal polyneuropathy. In the sural nerve biopsy, the densities of myelinated fibers were markedly decreased. However, unmyelinated fiber densities were relatively preserved. Onion bulb formation was not found. This patient may be classified into hereditary motor-sensory neuropathy (HMSN) type II based on the clinical findings delayed nerve conduction velocities and axonal degeneration in the sural nerve. He has also diabetes mellitus. CT of the brain revealed nothing particular. He is one of members with familial Parkinson's disease (PD) developed in Sagamihara. Peroneal muscular atrophies are not necessarily associated with PD, though it has been occasionally complicated in various neuro-degenerative diseases including parkinsonism. We are now following the patient to detect the symptom of Parkinson's disease for early treatment.

Cardiac sports rehabilitation for patients with ischemic heart disease.

This paper summarizes data gathered from an 8 years sports cardiac rehabilitation program at Kyoto University and satellite hospital (Takeda Hospital). In total, 185 patients were rehabilitated under our original program with no serious cardiac accidents. Compliance was 58.2% after 6 months of this rehabilitation. In patients selected to evaluate the value of rehabilitation, exercise study with treadmill and 201Tl scintigraphic study showed improvement in exercise tolerance (in 58% of patients) and in perfusion on exercise (in 40%). Coronary angiographic study showed regression of arterial narrowing in 16% of the patients studied. We conclude that in addition to emotional and psychological support, our sports cardiac rehabilitation is safe and effective in improving exercise tolerance and cardiac perfusion.

Clinical evaluation of a newly developed enteric nutrient given to the neurosurgical patients with disturbances of consciousness.

An enteric nutrient 'SAN-ET-A', rich in protein and electrolytes, was given to 8 patients with disturbances of consciousness. Although the adminstered dosage had a calorie content so low that basal metabolism was barely maintained, the level of serous proteins increased following administration. Electrolyte imbalance was not found, and the patients did not suffer from severe renal or liver dysfunctions. No notable gastrointestinal troubles occurred except in one case. It is concluded that a low dosage of SAN-ET-A was sufficient to maintain the patients in good nutritional condition. Furthermore, it is suggested that this nutrient can be safely given for a long period.

[Hypertensive recurrent intracerebral hemorrhage accompanied with orthostatic hypotension and labile hypertension].

Authors reported a case of recurrent intracerebral hemorrhage accompanied by severe orthostatic hypotension. A 51-year-old women had recurrent intracerebral hemorrhage 3 times during a period of 2 years. The first and third hemorrhages were located in the right putaminal region, and the second hemorrhage in the left thalamic region. Cerebral angiography revealed neither evidence of vascular malformation nor that of tumor vessels. At the third admission, she became unconscious for three hours after admission, and emergent fronto-temporal craniotomy was performed. Light microscopic histological investigation with congo-red stain demonstrated the absence of cerebral amyloid angiopathy. Laboratory examination revealed no hemorrhagic diathesis. During hospitalization, She complained of dizziness in the standing position. When systolic blood pressure fell from 140 mmHg in the supine position to less than 80 mmHg in the standing position, she became unconscious. Her blood pressure was very labile with orthostatic changes and her systolic blood pressure was also very labile without orthostatic changes, changing from 108 mmHg to 218 mmHg. Severe orthostatic hypotension and labile hypertension made the medical control of hypertension difficult. In conclusion, both severe orthostatic hypotension and labile hypertension were risk factors of recurrence of intracerebral hemorrhage.