[Biography of Moody Meng].

Moody Meng(1897-1983) was a pioneer of pharmacy in China. He was the main editor of the first Chinese Pharmacopoeia, the first president of the National College of Pharmacy (now China Pharmaceutical University), the first director of Chongqing Union Pharmaceutical Factory during the Anti-Japanese War and the first director of the China National Institute for the Control of Pharmaceutical and Biological Products. He made important contributions in many fields of pharmacy in China.

[Clinical characteristics of adult-onset primary hypoparathyroidism: a retrospective analysis of 200 cases].

Objective: To study the clinical characteristics of primary hypoparathyroidism in adults. Methods: The clinical data of 200 cases with adult-onset primary hypoparathyroidism in Peking Union Medical College Hospital during December 1987 to December 2015 were collected and analyzed retrospectively. Among them, 128 cases were followed up for a median period of 3 years. Results: The major manifestations at their first visits were tetany and numbness in the distal extremities(81.5%, 163/200 and 62.0%, 124/200). Thirty-two percent of the cases (62 cases) had history of seizures, and 60.9%(98/161) and 74.4%(96/129) of them were with intracerebral calcifications and cataracts, respectively.Most of subjects(155/200)had more than one year delay in diagnosis. Hypercalciuria occurred in 67.2%(86/128) of the cases during the follow-up. No significant differences in the clinical characteristics and biochemical markers between the hypercalciuria subjects and the non-hypercalciuria subjects. Renal nephrocalcinosis or stones were found in 6.5%(5/77) of the cases, and kidney function decreased in 6.6%(6/91) of the patients. Kidney function was negatively associated with age and duration of disease. Conclusions: The predominant manifestations of primary hypoparathyroidism in adults included tetany and numbness in the distal extremities and seizures. It is often misdiagnosed. Calcium supplement combined with vitamin D or its metabolites effectively relieve clinical symptoms and signs. The serum and urinary calcium levels should be monitored frequently to reduce renal complications.

Ultrastructural localization of nitric oxide synthase immunoreactivity in the cat ventrobasal complex.

This study describes the ultrastructural localization of nitric oxide synthase (NOS) immunoreactivity in the cat ventrobasal complex. NOS immunoreactivity was found in the cell bodies and dendrites of local circuit neurons and in vesicle-containing profiles. The vesicle-containing profiles could be divided into two classes, those of dendritic origin (presynaptic dendrite boutons) and those of axonal origin. The NOS labelled axon terminals varied in size and packing density and were principally located in the extra-glomerular neuropil. These boutons presented a range of morphologies and it was not possible to determine the probable source based on morphological criteria. The NOS immunoreactive presynaptic dendrite boutons were found both within and outside glomeruli and established both pre- and post-synaptic relationships with other elements. Post-embedding GABA immunocytochemistry showed that some NOS immunoreactive axonal boutons and presynaptic dendrites were also immunopositive for GABA. This finding suggests that some of the NOS labelled axonal boutons are of local circuit neuron origin. These results suggest that local circuit neurons in the cat ventrobasal complex might be involved in specific, short range interactions using GABA and longer, more global interactions using nitric oxide.

Transneuronal changes of the inhibitory circuitry in the macaque somatosensory thalamus following lesions of the dorsal column nuclei.

The inhibitory circuitry of the ventroposterolateral nucleus (VPL) of the macaque somatosensory thalamus was analyzed in normal animals and in those surviving for a few days or several weeks following a unilateral lesion of the cuneate nucleus, the source of medial lemniscal (ML) axons carrying information from the contralateral upper extremity. Inhibitory synaptic terminals in the VPL were defined as those that contain flattened or pleomorphic synaptic vesicles and that can be shown to be immunoreactive for gamma-aminobutyric acid (GABA). There are two types of these profiles: F axon terminals that arise from neurons of the thalamic reticular nucleus, and perhaps from VPL local circuit neurons (LCNs); and the dendritic appendages of LCNs that form presynaptic dendrites (PSDs). ML terminals normally have extensive synaptic interactions with PSDs but not with F axon terminals. Electron microscopic analyses revealed that cuneatus lesions resulted in a rapid loss of ML terminals and a statistically significant reduction in both F and PSD synaptic profiles. Confocal scanning microscopy also demonstrated a profound loss of GABA immunoreactivity in the deafferented VPL. These changes persisted for more than 20 weeks, without any evidence of reactive synaptogenesis of surviving sensory afferents or of inhibitory synapses. The changes in GABA circuitry are transneuronal, and the possible mechanisms that may underlie them are discussed. It is suggested that the altered GABAergic circuitry of the VPL in the monkey may serve as a model for understanding changes in somatic sensation in the human following peripheral or central deafferentation.

Nitric oxide synthase immunoreactivity distinguishes a sub-population of GABA-immunoreactive neurons in the ventrobasal complex of the cat.

This study describes the presence of nitric oxide synthase (NOS-ir) immunoreactive neurons in the thalamic ventrobasal complex of the cat. NOS-ir is co-localized with gamma-aminobutyric acid (GABA-ir) in a subset of small neurons identified as local circuit neurons in previous studies. The double labeled neurons are further identified by a larger soma diameter when compared to GABA-ir only neurons. All NOS-ir somata exhibit GABA-ir but none exhibit immunoreactivity to calbindin.

[Treatment of hypoparathyroidism with 1 alpha-hydroxyvitamin D3].

2 male and 17 female patients with hypoparathyroidism including 7 idiopathic, 11 surgical and 1 pseudohypoparathyroidism received 1 alpha-OHD3 at a mean daily dose of 2.7 +/- 0.7 microgram (1.5-4.0 micrograms) combining with calcium 1 g for 14 weeks. The mean age of the patients was 37 +/- 9 old years and the mean course of disease was 15 +/- 10 years. The symptoms and signs of hypocalcium disappeared in 1-3 weeks after therapy, meanwhile the serum ionized calcium (Ca++) and total calcium (TCa) increased from 0.84 +/- 0.02 to 1.03 +/- 0.01 mmol/L and from 6.90 +/- 0.22 to 8.70 +/- 0.20 mg/dl (P less than 0.001) respectively. The serum Ca++ and TCa increased to normal volume in 58% and 63% patients respectively. The concentration of serum 1,25 (OH)2 D3 elevated significantly from 19.5 +/- 1.1 to 29.1 +/- 2.4 pg/ml (P less than 0.01 n = 17). The lever of urinary hydroxyproline was no significant change. The serum phosphate reduced markedly from 5.50 +/- 0.2 to 4.80 +/- 0.2 mg/dl (P less than 0.01). The serum Ca++ and TCa changed to the primitive level when we stopped to use 1 alpha-OHD3 alone for 1-3 weeks. No significant side effects were found. It might be suggested that 1 alpha-OHD3 is effective and safe in treating hypoparathyroidism because calcium absorption in intestine is promoted by 1 alpha-OHD3.

[Metabolism of calcium and phosphorus in Cushing syndrome with osteoporosis].

52 patients with Cushing syndrome were studied. According to the appearance of X-ray film of bones, they were divided into three groups: (I) Without osteoporosis, 12 cases (23.1%), (II) Mild osteoporosis, 17 cases (32.7%), (III) Severe osteoporosis with fractured ribs and/or wedge-shaped vertebrae, 23 cases (44.2%). It was found that the mean level of serum calcium in the patients was significantly lower than that in 94 normal subjects (mean +/- S 2.3 +/- 0.2 versus 2.4 +/- 0.1 mmol/L P less than 0.001). The mean concentrations of blood alkaline phosphatase and parathyroid hormone in the patients were much higher than those in normal subjects (65.0 +/- 27.6 versus 42.6 +/- 15.6 IU/L P less than 0.001, 44.6 +/- 22.4 versus 20.6 +/- 8.0 pg/ml P less than 0.001 respectively). The mean level of serum 25 (OH)-D in the patients was significantly lower than that in controls (10.9 +/- 5.6 versus 16.2 +/- 4.6 ng/ml P less than 0.001). Urinary calcium excretion increased in the patients as compared with that in controls (P less than 0.01). The urinary calcium excretion correlated well with the blood total cortisol and urinary free cortisol. It is suggested that hypercalciuria might cause decrease of serum calcium. Thus the parathyroid glands were stimulated and the parathyroid hormone (PTH) secretion was increased. Excess of PTH stimulates bone resorption. All of these factors are involved in the pathogenesis of osteopenia in Cushing's syndrome.