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S K Paik

Publications and source records attributed to S K Paik.

7 recordsLinked to original sources
PubMed2005

The distribution of inhibitory and excitatory synapses on single, reconstructed jaw-opening motoneurons in the cat.

In a previous study, we reported that the distribution of inhibitory input, in contrast to excitatory input, decreased somatofugally along dendrites of cat jaw-closing alpha-motoneurons [J Comp Neurol 414 (1999) 454]. The present study examined the distribution of GABA, glycine, and glutamate immunopositive boutons covering horseradish peroxidase-labeled cat jaw-opening motoneurons. The motoneurons were divided into four compartments: the soma, and primary, intermediate, and distal dendrites. Ninety-seven percent of the total number of studied boutons had immunoreactivity for at least one of the three amino acids. The proportion of boutons immunoreactive for GABA and/or glycine was lower than the proportion of boutons immunoreactive for glutamate. Boutons immunoreactive to glycine alone were more numerous than boutons double-labeled for GABA and glycine, which, in turn, occurred more frequently than boutons immunoreactive to GABA alone. The percentage synaptic covering (proportion of membrane covered by synaptic boutons) of the putatively excitatory (glutamate containing) and putatively inhibitory (GABA and/or glycine containing) boutons decreased somatofugally along the dendrites. Such systematic variations were not seen in the packing density (number of boutons per 100 microm(2)); the packing density showed a distinct drop between the soma and primary dendrites but did not differ significantly among the three dendritic compartments. Overall, the packing density was slightly higher for the putatively excitatory boutons than for the inhibitory ones. When taken together with previous analyses of jaw-closing alpha-motoneurons the present data on jaw-opening alpha-motoneurons indicate that the two types of neuron differ in regard to the nature of synaptic integration in the dendritic tree.

Amino Acid Transport System X-AG↗
PubMed1997

Estrogen-induced cyclin D1 and D3 gene expressions during mouse uterine cell proliferation in vivo: differential induction mechanism of cyclin D1 and D3.

D-type cyclins are involved in the regulation of the G1/S transition of the cell cycle in various cell types cultured in vitro. Little is, however, known about the expression pattern and functional role of D-type cyclins in physiological processes in vivo. In this report, we studied whether the expression of murine D-type cyclins correlates with the states of mouse uterine cell proliferation in vivo. Time-course changes in cyclin D1 and D3 mRNA levels in the uterine tissues of immature mice primed with 17 beta-estradiol (E2) were examined by Northern blot hybridization. c-fos and thymidine kinase (TK) mRNA levels were also examined as markers for the transition from G0 to G1 and the onset of S phase, respectively. Cyclin D1 and D3 mRNAs were induced 2.5-fold between c-fos and TK mRNA peaks. The E2-induced cyclin D1 and D3 gene expressions were blocked by antiestrogens tamoxifen and ICI 182,780. We also investigated the effects of cycloheximide (CHX), a protein synthesis inhibitor, on cyclin D1 and D3 gene expressions. When CHX was treated alone, cyclin D3, but not cyclin D1, mRNA was immediately superinduced. The E2-induced cyclin D3 gene expression was shifted by approximately 6 h when CHX was pretreated 1 hr before E2 administration. Interestingly, the 3H-thymidine incorporation experiment showed that the mouse uterine cell cycle progression also shifted by 6 hr with pretreatment of CHX. The overall results suggest that both cyclin D1 and D3 mRNAs are constitutively expressed in uterine tissues and induced by E2 at G1 phase of the mouse uterine cell cycle. However, the superinducibility and temporal shift of cyclin D3 by CHX suggest that there is a different regulatory mechanism underlying cyclin D1 and D3 gene expressions in the mouse uterine cell cycle progression.

Animals↗
PubMed1984

The natural history of diabetic nephropathy: unpredictable insulin requirements--a further clue.

Diabetic nephropathy has evolved into the single most prevalent cause of uremia among patients sustained by the United States End Stage Renal Disease program. Clarification of the natural history of kidney involvement and insufficiency in Type I and II diabetes has improved substantially over the past 5 years. However, it remains a poorly understood and relatively underreported morbid entity. This report reviews the problem, then reconstructs the natural history of diabetic nephropathy by studying the course of 50 Type I and Type II uremic diabetics treated with hemodialysis at The Long Island College Hospital. It traces the various stages from hyperglycemia to proteinuria to renal failure, and then reports morbidity, including cardiac, eye, stroke, and amputation complications. A new paradox is herein reported--the unpredictable insulin requirement, including new insulin need for the first time once hemodialysis was begun, in 8 of 50 patients studied.

Adult↗