Relationship between the type of hormone replacement therapy and incidence of breast cancer in Korea.

OBJECTIVE: This study aimed to investigate the relationship between hormone replacement therapy (HRT) types and breast cancer (BC) incidence in postmenopausal women in Korea. METHODS: The nested case-control study used data from the National Health Insurance Service database. Among the women aged ≥50 years who menopaused between 2004 and 2007, BC incidence up to 2017 was analyzed in 36,446 women using or having used HRT for >1 year and in 36,446 women who did not use any HRT for more than 1 year. HRT types and duration were classified into three categories. RESULTS: BC risk (BCR) decreased with tibolone use for all ages. With HRT initiation in women aged ≥50 years, BCR was lower with tibolone and estrogen-progestogen therapy. HRT for <3 years showed lower BCR with tibolone, while higher BCR was observed with estrogen-only therapy. BCR was lower in women of all ages on HRT for >5 years than in the control group. CONCLUSIONS: For women in their 50s, tibolone use lowers BCR; for all ages, the use of any HRT for >5 years showed lower BCR in Korea. These divergent results from western countries could be associated with the specific characteristics of BC in Korea.

Four-Year Experience With Extracorporeal Membrane Oxygenation for Kidney Transplant Patients With Severe Refractory Cardiopulmonary Insufficiency.

BACKGROUND: Kidney transplant (KT) recipients are vulnerable to infections because of their immunosuppressive treatments, and they occasionally exhibit serious acute cardiopulmonary dysfunction. The purpose of this study was to report the clinical outcomes of using extracorporeal membrane oxygenation (ECMO) in KT recipients and to identify risk factors for ECMO weaning failure. METHODS: We retrospectively reviewed the electronic medical records of KT patients who experienced severe cardiopulmonary dysfunction refractory to conventional therapy and received ECMO at the Asan Medical Center Surgical Intensive Care Unit between December 2010 and December 2014. RESULTS: During the 4-year study period, 12 KT patients required ECMO management. Six of these patients were successfully weaned from ECMO; the mean duration of ECMO support was 9.1 days (range, 3.5-15.1 days). Indications for ECMO included pneumonia (8 cases required venovenous ECMO and 1 case required venoarterial [VA] ECMO), stress-induced cardiomyopathy due to fungemia (1 case required VA ECMO), and septic shock due to either urinary tract infection or unknown origin (2 cases required VA ECMO). In assessing risk factors leading to a failure of ECMO weaning, the pH on arterial blood gas analysis performed just before the beginning of this intervention was significantly lower in the nonsurvivors than in the survivors (P = .046). CONCLUSIONS: ECMO can be a beneficial rescue therapy in immunosuppressed patients with cardiopulmonary dysfunction refractory to treatment. Severe acidosis before the administration of EMCO is a major determinant of ECMO weaning failure.

Up-regulation of high-affinity neurotrophin receptor, trk B-like protein on western blots of rat cortex after chronic ethanol treatment.

We previously reported that the total neurotrophic activity of hippocampal extracts was significantly (25-50%) reduced after 21-28 weeks of chronic ethanol treatment (CET) [23]. To test whether the level of a neurotrophic factor (i.e., ligand itself) is compromised, we measured nerve growth factor (NGF) protein and NGF mRNA contents using ELISA and Northern analysis. We reported that CET did not appear to reduce NGF protein, NGF mRNA or total neurotrophic activity when measured on sympathetic ganglia neurons [4]. We also observed that both NT-3 mRNA and bFGF mRNA levels were unaffected, but the BDNF mRNA levels was significantly reduced in CET rat hippocampus [18]. Neuronal degeneration and reduction of total neurotrophic activity after CET appear to be induced, at least partially, by compromised transcription of BDNF gene. CET may also induce functional changes in receptors for the neurotrophic factors. To investigate possible changes in neurotrophic factor-receptors, we examined Western blots (immunoblots) of rat cortex after 28 weeks of CET. After sonication and ultra-centrifugation, the supernatant of crude lysates of the cortex from individual animals was subjected to SDS-PAGE, electrotransfered to nitrocellulose membrane, incubated with anti-trk B antibody and secondary antibody conjugated to alkaline phosphatase, and reacted with chemiluminescent substrate. The membranes were then exposed to Kodak XAR film. Compared to controls (n = 6), CET rats (n = 6) appeared to have significantly higher band intensity (P < 0.01) of trk B-like protein at about 145 kDa, which suggests an up-regulation of trk B-like proteins to compensate the compromised level of certain subset (i.e., BDNF or NT-4/5, but not NGF) of neurotrophins in cortex.

Principal neurons of the lumbar sympathetic ganglia increase in number with body size.

Neuron number appears to be matched to body size during early development by the modulation of the processes of proliferation and naturally occurring cell death. However, body size increases rapidly as the juvenile becomes an adult, long after these processes cease to operate. The present study shows that principal neurons of lumbar sympathetic ganglia increase in number four- to fivefold during postmetamorphic life of the bullfrog. Rana catesbeiana. This increase in neuron number cannot be attributed to either counting error or selection bias and was associated with greater innervation of particular hindlimb targets, as demonstrated by retrograde labeling with horseradish peroxidase. Injection of [3H]thymidine (a marker of DNA synthesis) every third day for 20-22 weeks failed to provide evidence of neuron proliferation, although, on the basis of changes in body length during this period, substantial numbers of neurons likely were added. These results combined with previous studies of hindlimb motor and sensory neuron addition are consistent with the hypothesis that the population of sympathetic neurons is augmented by late differentiation of existing precursor cells.

Chronic alcohol ingestion: nerve growth factor gene expression and neurotrophic activity in rat hippocampus.

Chronic ethanol treatment induces memory deficits accompanied by anatomical and biochemical changes in basal forebrain and hippocampus. Cholinergic neurons in the septohippocampal pathway are especially vulnerable to alcohol neurotoxicity. Several studies showed that an adequate supply of neurotrophins, such as Nerve Growth Factor and Brain-Derived Neurotrophic Factor, is required for the normal function and survival of cholinergic neurons in basal forebrain and medial septal nuclei. We tested the hypothesis that chronic alcohol ingestion may alter the gene expression level of Nerve Growth Factor in hippocampus, the major source of neurotrophins to the cholinergic neurons in the septohippocampal pathway. We measured Nerve Growth Factor protein and Nerve Growth Factor mRNA contents using sensitive two-site ELISA and Northern analysis. We also tested the endogenous neurotrophic activity, including and excluding Nerve Growth Factor, contained in 5%, 2%, 1%, 0.5% and 0.1% (w/v) hippocampal tissue extracts on sympathetic ganglia neurons. Twenty-eight weeks of chronic ethanol treatment did not reduce Nerve Growth Factor protein, Nerve Growth Factor mRNA, or total neurotrophic activity contained in the rat hippocampus when measured on sympathetic ganglia neurons.