Gap junctional intercellular communication (GJIC) and connexin expression are frequently decreased in neoplasia and may contribute to defective growth control and loss of differentiated functions. GJIC, in E9 mouse lung carcinoma cells and WB-aB1 neoplastic rat liver epithelial cells, was elevated by forced expression of the gap junction proteins, connexin43 (Cx43) and connexin32 (Cx32), respectively. Transfection of Cx43 into E9 cells increased fluorescent dye-coupling in the transfected clones, E9-2 and E9-3, to levels comparable to the nontransformed sibling cell line, E10, from which E9 cells originated. Transduction of Cx32 into WB-aB1 cells also increased dye-coupling in the clone, WB-a/32-10, to a level that was comparable to the nontransformed sibling cell line, WB-F344. The cell cycle distribution was also affected as a result of forced connexin expression. The percentage of cells in G(1)-phase increased and the percentage in S-phase decreased in E9-2 and WB-a/32-10 cells as compared to E9 and WB-aB1 cells. Concomitantly, these cells exhibited changes in G(1)-phase cell cycle regulators. E9-2 and WB-a/32-10 cells expressed significantly less cyclin D1 and more p27(kip-1) protein than E9 and WB-aB1 cells. Other growth-related properties (expression of platelet-derived growth factor receptor-beta, epidermal growth factor receptor, protein kinase C-alpha, protein kinase A regulatory subunit-Ialpha, and production of nitric oxide in response to a cocktail of pro-inflammatory cytokines) were minimally altered or unaffected. Thus, enhancement of connexin expression and GJIC in neoplastic mouse lung and rat liver epithelial cells restored G(1) growth control. This was associated with decreased expression of cyclin D1 and increased expression of p27(kip-1), but not with changes in other growth-related functions.

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Background: Urine ketone test is commonly used to screen for diabetic ketoacidosis (DKA). Ketonuria also develops in patients with disease conditions other than DKA. However, the prevalence of DKA in patients with ketonuria is not known. We investigated the prevalence of ketonuria and characteristics of patients with ketonuria and estimated the prevalence of DKA among them to study the clinical significance of ketonuria as an indicator of DKA. Methods: We studied 1,314 adult and 1,027 pediatric patients who underwent urinalysis. The prevalence of ketonuria in the different groups of patients, classified according to the types of their visits to the institution, was investigated, and the relationships between ketonuria and albuminuria, glycosuria, and bilirubinuria were evaluated. Results: The overall prevalence of ketonuria was 9.1%. The prevalences of ketonuria in adult and pediatric patients were 4.3% and 15.2%, respectively. The prevalences of ketonuria were the highest in the adult (9.7%) and pediatric (28%) patients in the group that had visited the emergency department. Among patients with ketonuria, 7% adult and 3.8% pediatric patients showed glycosuria. Conclusions: This study showed that the prevalence of DKA in patients with ketonuria, defined as the simultaneous presence of ketone bodies and glucose in urine, was only 7%. Therefore, we concluded that ketonuria might be clinically significant as an indicator of acute or severe disease status rather than of DKA.

혈중으로 끌어오며 결과적으로 osteocalcin (OST), carboxy-terminal telopeptide of type I collagen (CTX) 등 골대사 산물의 혈중 농 도를 증가시킨다[1]. 체내 비타민 D 양의 적정성은 혈청 25(OH) Vitamin D (25(OH) VD)의 농도를 기준으로 평가한다. 일반적으로 25(OH)VD의 농도 가 10 ng/mL (25 nmol/L)미만이면 부족한 비타민 D 상태로 삼으 며 뼈의 무기질화에 영향을 미치는 것으로 알려져 있다[2]. 한편, 25(OH)VD의 농도가 30 ng/mL을 넘지 않는 경우 뼈 이외의 질환 을 잘 일으켜 장기적으로 개인의 건강에 나쁜 영향을 미칠 수 있으 므로 10-30 ng/mL 범위를 불충분한 비타민 D 상태로 정의하고 30 ng/mL 이상으로 높은 상태를 유지할 것을 권장하며 체내 비타민 D 상태를 부족(de ciency), 불충분(insuf ciency), 적정(adequacy) 의 3가지로 분류하고 있다[2].