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Split-liver transplantation is a well-known procedure for increasing the donor pool. The procedure is commonly used in 1 adult and 1 child, but is less commonly performed in 2 adults because of technical difficulty and poor outcome in left-lobe recipients. Preservation of caudate lobe function is important in recipients with borderline graft-recipient weight ratio to achieve better results. Herein, we report a case in which caudate lobe outflow was reconstructed in a left lobe with a caudate lobe graft in split-liver transplantation in 2 adults.

The possible involvement of endogenous opioid peptides (EOPs) in LHRH release from hypothalami of ewes during the breeding season was investigated using an in vitro perifusion system. Hypothalami were procured in December from ovariectomized (OVX; 62-65 days before the experiment; n = 6) and mid-luteal (ML; n = 7) Western White-Face ewes. Hypothalami were mid-sagitally sectioned into halves containing the preoptic area, mediobasal hypothalamus, and infundibulum (median eminence). The left half (treated) received two 30-min challenges (beginning at 130 and 250 min, respectively, after onset of perifusion) of 500 microM naloxone (NAL) followed by a 30-min 60-mM potassium (K) challenge (at 370 min after onset of perifusion). The right half served as the control, receiving only K at the same time as the treated tissue. Both NAL challenges elicited (p less than 0.05) LHRH release from tissues of both ML and OVX ewes. Release of LHRH by hypothalami from ML, but not from OVX, ewes was greater (p less than 0.01) after the second than after the first NAL challenge. These results are consistent with the view that an inhibitory opioid influence exists on LHRH release from ovine hypothalami. The release of LHRH in response to NAL was dependent on the ovarian status in vivo since the priming effect of NAL on subsequent NAL-induced LHRH release occurred only from the hypothalami of ML ewes. We suggest from these results that EOPs may modulate LHRH release from ovine hypothalami in an ovarian steroid-dependent and independent manner.

Introduction Liver transplantation is the treatment of choice for end-stage liver disease. However, the shortage of donors is still the major problem in most Asian countries. Using extended donor criteria may maximize the deceased donor pool, but some high-risk donors may show adverse recipient outcomes due to preexisting infection. Materials and Methods This study included deceased donor liver transplant patients from June 2002 through June 2007. We retrospectively reviewed the clinical manifestations of donors and recipients. The donors showed no definite infection at the time the organs were matched to the recipients. Routine sputum, urine, blood, and bile cultures were obtained from the donor during the perioperative period. According to the final reports of the cultures, the recipients divided into two groups: donor infection (DI) and no donor infection (NDI). Results This study included 59 donor and 72 recipients, including 34 who received a graft from a donor with a positive culture (47.2%) finally, defined as the DI groups, and 38 recipients (52.8%) as the NDI group. Most of them had positive sputum cultures, followed by urine cultures. Staphylococcus aureus was the most common pathogen. Using a stepwise logistical regression model to analyze the significant donor characteristics, donor admission to the intensive care unit (ICU) for 7 days or longer (P ≤ .0001), previous cardiopulmonary cerebral resuscitation (CPCR) (P = .036), and inotropic agents (P = .022) were the only three independent factors to predict donor infection. To compare the outcomes between DI and NDI groups, the days of recipient ICU or hospital admission, the 1-week or 1-month mortality rate, and the overall survival showed no significant difference between both groups. However, the hospital mortality rate was mildly higher in the DI group (P = .050). Conclusion Donors with prolonged ICU admissions, rescue by CPCR, and use of inotropic agents carried an high risk of potential infections. Our data did not show a significant increase in adverse outcomes if the recipient received a graft from a potentially infected donor. However, there may be an increased risk of hospital mortality. We should be careful in using these potentially infected donors in selective recipients.

In machining processes, geometric accuracy of a manufacturing workpiece mainly relies on the relative position of workpiece to the machining tool. Fixtures are needed to locate the workpiece relative to the machining tool in order to guarantee the manufacturing quality. Therefore, correct locating is the basic condition for designing a fixture. In addition, computer aided fixture design (CAFD) facilitates more cost effective and efficient fixture design. However, heuristic and case-based methods are still common. This paper firstly presents a general framework to verify the locating correctness so as to soundly determine locator number and positions. Secondly, within the scope of CAFD, a computing tool is developed within the Unigraph system for the correctness analysis of fixture locating schemes. Finally, a detailed discussion is made about the modeling process and its verification by means of practical examples. Analyzing results are consistent with practical ones.

Given the central role of the decapeptide LHRH in reproduction and reproductive behavior, it is important to focus on delineating the possible effects of this gene and its products in the regulation of hormone-dependent reproductive processes. In the female, ovulation is preceded by a marked increase in LHRH release; the increase in LHRH release culminates in a preovulatory LH surge, which coincides with a period of sexual receptivity. In contrast to the belief that the proteolytic metabolism of LHRH serves only as a degradative process that removes excess LHRH and attenuates signal transduction through the LHRH receptor, we hypothesized that a metabolite of the decapeptide, LHRH-(1–5), can directly regulate LHRH neuronal function. This study demonstrates the ability of LHRH-(1–5) peptide to regulate LHRH gene expression in the LHRH neuronal cell line, the GT1–7 cell. The results show that LHRH-(1–5) stimulated LHRH gene expression at the posttranscriptional level. In contrast to the LHRH suppression of its own gene expression, the coadministration of LHRH with the metalloendopeptidase, EC 3.4.24.15, an endopeptidase known to cleave LHRH to form LHRH1–5, shows a reversal of effect, a stimulation of LHRH gene expression. Finally, the effect of LHRH-(1–5) on LHRH gene expression appears to be mediated by the calcium/calmodulin-dependent protein kinase. The present study supports the hypothesis that the physiological metabolite of LHRH, LHRH-(1–5), is functionally capable of regulating the reproductive neuroendocrine system.

Graves' disease has been associated with different human leukocyte antigen (HLA) genes in different races. To evaluate the association of HLA type in Taiwanese with Graves' disease, the HLA-A, -B, and -DRB1 alleles in a total of 236 Taiwanese adults with Graves' disease and 533 racially matched normal control subjects were examined using the PCR-SSOP (sequence specific oligonucleotide probe) technique. The prevalence of HLA-A*0207, -B*2704, -B*4601, and -DRB1*0901 among patients with Graves' disease was found to be increased, with odds ratios (OR) of 2.21, 3.82, 1.76 and 1.62, respectively. However, after correction for multiple comparisons, the relative risk of HLA-A*0207 susceptibility to Graves' disease remained statistically significant and the haplotype HLA-A*3303 -B*5801 -DRB1*0301 had a significantly protective effect. None of the other 2- or 3-locus haplotypes showed any significantly increased risk. Although HLA-DRB1*1405 showed an increased relative risk in patients with GO (Graves' opthalmopathy) (OR 4.61) when compared with patients without GO, the relative risk after adjusting for the number of comparisons was not significant. Taiwanese patients with Graves' disease have HLA-associated susceptibility genes which are similar to those found in Chinese patients in Hong Kong and Singapore. However, the finding in this study of a higher frequency of HLA-A*0207 in Taiwanese with Graves' disease has not been documented in any other ethnic group.

Polychlorinated biphenyls (PCBs) cause abnormal development and physiology of the reproductive system. We hypothesized that these effects may be mediated, at least in part, by neuroendocrine cells in the hypothalamus that integrate inputs to and outputs from the central nervous system and reproductive systems. The effects of two PCB mixtures, Aroclor 1221 and Aroclor 1254, were tested on the hypothalamic GT1-7 cells, which synthesize and secrete the key hypothalamic hormone, gonadotropin-releasing hormone (GnRH). GT1-7 cells were treated for 24 h in dose-response experiments and GnRH gene expression and release were quantified. Aroclor 1221 was stimulatory to GnRH gene expression, particularly at post-transcriptional levels (GnRH cytoplasmic mRNA), and increased GnRH peptide levels, suggesting a post-translational regulation of GnRH biosynthesis. It also caused a qualitative increase in GT1-7 neurite outgrowth and cell confluency. Aroclor 1254 had very different effects from Aroclor 1221. It inhibited GnRH nuclear mRNA levels at high dosages, and stimulated GnRH mRNA at low doses, suggesting a post-transcriptional mechanism of regulation. Aroclor 1254 did not alter GnRH peptide levels. Qualitatively, Aroclor 1254 caused a retraction of GT1-7 cell processes and neurotoxicity at high dosages. In order to gauge the involvement of the oestrogen receptor in these responses, the oestrogen receptor antagonist, ICI 182,780 (ICI) was coadministered in other studies with the PCBs. While effects of Aroclor 1221 on GnRH gene expression were not blocked by ICI, its effects on GnRH peptide levels were blocked by ICI, indicating that some but not all of the effects of Aroclor 1221 are mediated by the classical oestrogen receptor alpha and/or beta. The inhibitory effects of Aroclor 1254 on GnRH gene expression were not prevented by ICI, although ICI itself had stimulatory effects on GnRH gene expression that were blocked by cotreatment with Aroclor 1254. These results demonstrate a novel mechanism for effects of the two PCBs directly on GnRH gene expression, and indicate a hypothalamic level for endocrine disruption by these environmental toxicants.

To assess the factors associated with successful discontinuation of insulin therapy after diabetic ketoacidosis (DKA) in adult patients.Patients (or= 18 years) attending the Endocrine and Metabolism Clinic at a major hospital in southern Taiwan were recruited. After recovery from the acute stage, those with no contraindications to oral antidiabetic agents, with adequate beta cell reserve, and with no antiglutamic acid decarboxylase (GAD) antibody were treated with oral agents.Sixty-six patients (38 males, 28 females, aged 18-76 years) were included, and 21 qualified for treatment with oral agents. These 21 patients were older at diagnosis of diabetes (45.5 +/- 14.0 vs. 40.0 +/- 13.8 years, P = 0.047), had shorter diabetes duration (median 0 vs. 5.5 months, P = 0.040), higher BMI (median 23.4 vs. 19.5 kg/m2, P0.001), higher serum osmolality during DKA (352.1 +/- 40.7 vs. 318.0 +/- 16.4 mmol/kg, P = 0.005), and lower insulin dose following recovery (median 0.49 vs. 0.83 unit/kg/d, P0.001) than those patients that had to continue insulin therapy. Thirteen patients (8 males, 5 females; 62%) successfully discontinued insulin for at least one year without recurrence of DKA. Multiple logistic regression analyses showed that BMIor= 25 kg/m2 (adjusted relative risk (ARR) 8.85, 95% CI 1.05, 8.39), diabetes onset ageor= 40 years (ARR 8.08, 95% CI 1.16, 6.95), and undiagnosed diabetes before DKA (ARR 8.90, 95% CI 1.19, 7.51) were significant factors associated with successful discontinuation of insulin therapy.We identified three independent clinical factors associated with successful discontinuation of insulin therapy after DKA.

Synergistic necrotizing fascitis of the scrotum, penis and perianal region was first described by Fournier in 1883. If not recognized early, this infectious process will extend along the fascia plane to the lower abdominal and back regions, causing severe morbidity and even mortality.The records of 8 patients diagnosed of Fournier's gangrene were reviewed between 1988 and 2000. The sex, age, etiology, associated diseases, bacteriological studies and treatments were analyzed.The 8 patients were all males, age ranging from 42 to 78 years old, with average 55.1 years. Six patients were due to perianal abscess, one patient was a complication of hemorroidectomy, and one patient had traumatic injury of scrotum. Six patients had poor controlled diabetes mellitus, and there were two patients with cirrhosis of the liver and hepatoma, respectively. Even with aggressive treatments, two patients died; the other 6 recovered completely. The mortality rate was 25%.Fournier's gangrene is a not common but life-threatening disease which needs radical debridement and effective antibiotics to control the infection and early reconstruction with skin graft and myocutaneous flaps. Mortality is usually due to delayed diagnosis.

A very low-birth-weight neonate developed chylus-like urine after receiving parenteral nutrition (PN) via percutaneous central venous catheters (CVC) for 7 weeks. A perirenal fluid collection could be seen under sonography. This kind of complication has not been described in literature. After withdrawing the CVC for 5 cm, the urine cleared up. For patients under prolonged PN via CVC and repeated change dressing of the CVC, close monitoring and regular evaluation of the position of the catheter tip are warranted.

The study was done to test the hypothesis that an artificial anatomical obstacle prevents the maintenance of ventricular fibrillation (VF) by stabilizing reentrant wavefronts (RWF) and increases the critical mass (CM) of myocardium required to sustain VF.Artificial obstacles can anchor RWF in simulated models of VF. Whether an artificial obstacle affects multiple-wavelet VF in real tissue is unclear.The endocardial surfaces of seven isolated, perfused swine right ventricles were mapped using a plaque of 477 bipolar electrodes with 1.6-mm resolution. An 8-mm hole was punched in the tissue. The CM was reached by tissue mass reductions, at which VF converted to periodic activity (ventricular tachycardia, VT).After the creation of the obstacle, the VF cycle length increased from 71.6+/-18.4 ms to 87.5+/-13.0 ms (p0.05). The obstacle, together with the papillary muscle, facilitated the transition from VF to VT by serving as attachment sites for the RWF. When one RWF attaches to the obstacle and another attaches to the papillary muscle, it may result in stable VT with figure-eight patterns. The CM for VF in the presence of an 8-mm hole (28.7+/-3.8 g) was higher than in the control group (swine right ventricles without holes, 24.0+/-3.4 g, p0.05).An artificial anatomical obstacle induces slowing and regularization of VF, impairs the persistence of VF as judged by an increase of the CM, and can convert VF to VT by serving as an attachment site to reentrant excitation.

Current trends in the management of type 2 diabetes mellitus, based on the 20-year United Kingdom Prospective Diabetic Study, include intensive treatment to control the blood glucose level and blood pressure in order to prevent or delay microvascular and cardiovascular complications. In the new millennium, type 2 diabetes will become epidemic in developing countries. If diabetes were to develop in 10% of the 1.2 billion population of China, the expense of intensive treatment would be immense. Laboratory tests are useful for detecting risk factors before the onset of the disease and convincing the general public to take preventive measures. Glucose tolerance testing is one of these tests. When glucose tolerance is impaired, 25% of beta-cell function is lost. Determining the plasma proinsulin level is another useful evaluation; impaired glucose tolerance accompanied by increased plasma proinsulin level is indicative of an enhanced risk that type 2 diabetes will develop within 5 years. Educating the public about eating a healthy diet and exercising may prevent the development of diabetes and thereby reduce the global prevalence of type 2 diabetes.

The glutamate analog N-methyl-D,L-aspartate (NMA) affects the regulation of GnRH and LH release in mammals. Several laboratories have reported a rapid and transient increase in GnRH mRNA levels of male rats after NMA injection. Studies employing the simultaneous measurements of nuclear GnRH primary transcript RNA, a reflection of gene transcription, and GnRH mRNA suggest that NMA's effect on GnRH gene expression in the rat is likely due to post-transcriptional regulation. Despite the increasingly widespread use of transgenic mice, surprisingly little is known about the regulation of GnRH gene expression in the mouse. In this study, we assessed in detail the effects of NMA on GnRH gene expression in adult male mice. In the first experiment, GnRH mRNA levels in mice killed 60-min post-NMA injection (20 mg/kg bw, ip; n=9/treatment group) were lower (P0.05) when compared to controls (saline vehicle). In the second experiment, mice (n=7/treatment group) were administered NMA or saline vehicle and were killed at 15-, 60- and 120-min post-injection. Consistent with the first experiment, treatment with NMA resulted in a significant decrease (P0.05) in cytoplasmic GnRH mRNA compared to control levels at 15- and 60-min but not 120-min. NMA treatment decreased the nuclear GnRH primary transcript RNA at 120-min but not at earlier time points. In summary, we have shown that regulation by NMA of GnRH gene expression in mice differs substantially from rats. This differential regulation of GnRH gene expression between rats and mice warrants further investigation.

Leptin, the ob gene product that can decrease caloric intake and increase energy expenditure, is functionally released by insulin from adipose tissue. Adenosine is thought to be an important regulator of the action of insulin in adipose tissue. The present study investigated the role of adenosine in the release of leptin by insulin in isolated rat white adipocytes. Release of leptin, measured by radioimmunoassay, from insulin-stimulated samples was seen after 30 min. Adenosine deaminase, at concentrations sufficient to metabolize endogenous adenosine, decreased insulin-stimulated leptin release. Also, the insulin-stimulated leptin release was completely blocked by the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Mediation of endogenous adenosine in this action of insulin was further supported by the assay of adenosine released into the medium from adipocytes stimulated with insulin. In addition, activation of adenosine A1 receptors by N6-cyclopentyladenosine (CPA) induced an increase in leptin release in a concentration-dependent manner that could be blocked by antagonists, either DPCPX or 8-(p-sulfophenyl)theophylline (8-SPT). In the presence of U73312, a specific inhibitor of phospholipase C (PLC), CPA-stimulated leptin secretion from adipocytes was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control for U73312. Moreover, chelerythrine and GF 109203X diminished the CPA-stimulated leptin secretion at concentrations sufficient to inhibit protein kinase C (PKC). These results suggest that, in isolated white adipocytes, the released adenosine acts as a helper and/or a positive regulator for insulin in the release of leptin via an activation of adenosine A1 receptors that involves the PLC-PKC pathway.

Endopeptidase EC 3.4.24.15 (EP24.15) is a soluble, neuropeptide-degrading metalloenzyme, widely expressed in the brain, pituitary and gonads. For the physiological metabolism of neuropeptides, the enzyme should be located extracellularly, either associated with the plasma membrane or in the extracellular milieu. Western immunoblot analyses of crude cytosolic and post-nuclear membrane fractions prepared by differential centrifugation revealed a slightly smaller molecular mass ( approximately 2 kDa) for EP24.15 in the post-nuclear membrane fraction. This smaller EP24.15 species was also present in an enriched fraction of plasma membrane prepared by Percoll gradient centrifugation. To ascertain whether EP24.15 is associated with the extracellular surface of plasma membrane, two sets of experiments were carried out. First, Western immunoblot analysis of AtT-20 cells treated with the membrane-impermeable, thiol-cleavable cross-linker, 3, 3'-dithio-bis(sulpho-succinimidyl-propionate) (DTSSP), indicated an extracellular membrane association. After cross-linking and thiol-reduction, a distinct band corresponding to EP24.15 was significantly diminished under non-reducing conditions. Second, immunocytochemical studies performed at 4 degrees C on non-permeabilized AtT-20 cells (i.e., non-fixed to prevent antibody internalization), indicated that EP24.15 was expressed on the surface of the AtT-20 cells. We furthermore determined that EP24.15 enzymatic activity is present on the extracellular surface of the cell discernable from the secreted enzyme. These results suggest that the EP24.15 is associated with the extracellular surface of the AtT-20 cell plasma membrane and is enzymatically active. Taken together, the results are consistent with a putative role in the degradation of neuropeptides acting at the external cell surface.

The melanotrophs of the neurointermediate lobe and peptidergic terminals of the neural lobe are regulated by gamma-aminobutyric acid (GABA) via GABA-A receptors and therefore, may be important sites for the modulatory actions of neurally active steroids. These steroid compounds might be produced peripherally, synthesized de novo in the pituitary, or derivatized from circulating steroids, each pathway having different physiological implications. In the present study, we show that neurointermediate lobe tissue can derivatize progesterone to the neurally active steroid 3 alpha-hydroxy-5 alpha-pregnan-20-one. The neurointermediate lobe was found to be four times as active as anterior pituitary and mediobasal hypothalamus in conversion of progesterone to 3 alpha-hydroxy-5 alpha-pregnan-20-one; mediobasal hypothalamus was relatively more active in the production of the intermediate 5 alpha-pregnan-3,20-dione. The identity of the compounds was confirmed by the method of serial isotopic dilution. We observed rates of synthesis in the neurointermediate lobe consistent with the production of physiologically relevant quantities of 3 alpha-hydroxy-5 alpha-pregnan-20-one from concentrations of progesterone which can occur naturally. In support of these findings, we demonstrate the presence of 3 alpha-hydroxysteroid oxidoreductase in neurointermediate lobe by immunocytochemistry.

Continuous spinal anesthesia (CSA) has been considered to be better in temporal and dose flexibility, as well as hemodynamic stability than single dose spinal anesthesia. However, the failure of spinal anesthesia is not a rare experience for anesthesiologists. Here we present our experience in solving the problem and discuss the possible causes for the failure.236 cases were studied retrospectively from January to December in 1996. All were over 65 years old, ASA III, scheduled for transurethral procedures or orthopedic operation. CSA was performed with 0.2% bupivacaine. Failed CSA was confirmed by positive pin-prick test at T10 dermatome(umbilicus) 30 minutes after 20 mg bupivacaine was injected. For failed cases, 5 mL 1% lidocaine was injected intrathecally for rescue. The failure rate, sensory and motor blockade, success rate by changing to lidocaine and its dosage were recorded.Eleven of 236 cases (4.7%) were considered spinal failure since the initial 20 mg bupivacaine could not provide adequate T10 anesthesia in 30 minutes. Addition of 5 mL 1% lidocaine produced a profound sensory and motor blockade in 9 cases, while further lidocaine injection was required in two cases. The success rate by rescuing lidocaine was 100% with an average lidocaine consumption by 52.5 +/- 4.5 mg.Factors contributed to failure spinal anesthesia including failure of technique, errors of judgment, maldistribution and failure of local anesthetic itself. However, we thought that change of pH value of local anesthetic in CSF may play a great part in these failed CSAs. Despite the reasons for failure, we demonstrate that failure of continuous spinal anesthesia by 0.2% bupivacaine can be readily resolved by 1% lidocaine.

A comparison was made of the outcome of 73 neonates born with their birth weight of 500-999 gm in National Taiwan University Hospital during the period between January 1, 1993 and December 31, 1996 (Period II), with the outcome of 21 such neonates born between April 1, 1988 and October 31, 1992 (Period I). Exclusion criteria included parental refusal for resuscitation, and major anomalies. Data were collected via a predetermined record sheet. The incidences of the extremely-low-birth-weight infants were 23/10,173 (0.23%) and 81/13,835 (0.59%) in Periods I and II, respectively. Early neonatal mortality rate was significant decreased in Period II (43% versus 14%). The limit of viability was improved from gestational age of 26 weeks or 700 gm to gestational age of 24 weeks or 600 gm. The incidence of neonatal morbidity (80% versus 50%) and total survival rate (48% versus 60%) have not changed significantly as seen in this limited number of cases. This study concluded that, with the introduction of exogenous surfactant and modern neonatal care, early neonatal survival rate and the limit of viability were improved.

We retrospectively evaluated the outcome and the risk factors for mortality among extremely low birth weight (ELBW) infants born at National Taiwan University Hospital. The records of all live-born infants with body birth weight of less than 1,000 g from January 1, 1993, to December 31, 1996, were evaluated. Infants with major anomalies or whose parents refused resuscitation were excluded from the analysis. There were 81 ELBW infants (0.59%) among a total of 13,835 live births during the study period, and 73 cases were enrolled for study. The mean gestational age (GA) was 27.2 (range, 24-34) weeks. Sixty-six percent of the ELBW infants were born by cesarean delivery. Respiratory distress syndrome occurred in 64% of infants and exogenous surfactant therapy was given to 47%, while intermittent mandatory ventilation was given to 85%. Symptomatic patent ductus arteriosus occurred in 34% of infants, septicemia in 30%, chronic lung disease in 48%, grade III to IV intraventricular hemorrhage in 27%, stage III to V retinopathy of prematurity in 33%, and necrotizing enterocolitis in 8%. Neonatal survival was 74%, survival to discharge was 60%, and intact survival was 50%. The survival rate was 40% for infants with a birth body of weight less than or equal to 750 g, and 68% for those with a birth body weight of greater than 750 g. While survival was 27% for infants with a GA of less than 26 weeks, it was 75% for those with a GA of greater than or equal to 26 weeks. The survival rate improved year by year for those with a GA less than 28 weeks. Cox regression analysis of survival showed that Apgar score at 1 minute (p = 0.0063), pulmonary hypertension (p = 0.012), and severe intraventricular hemorrhage (p = 0.0031) were the most important factors associated with mortality. Though the outcome of ELBW infants in our institute seems poorer than in some more developed countries, it is improving. The prognosis for ELBW infants of 24 to 25 weeks' GA remains guarded under our present care.A review of the records of all live-born neonates with a birth weight below 1000 g born in 1993-96 at National Taiwan University Hospital was conducted, with emphasis on outcomes and risk factors for mortality. There were 81 extremely-low-birth-weight infants (0.59%) among the 13,835 live births recorded during the 3-year study period and, after exclusion of infants with major anomalies, 73 cases were enrolled for study. The mean gestational age was 27.2 weeks (range, 24-34 weeks). The most common complications of pregnancy leading to premature delivery were antepartum hemorrhage (44%) and pregnancy-induced hypertension. Respiratory distress syndrome occurred in 64%; exogenous surfactant therapy was provided to 47% and 85% received intermittent mandatory ventilation. Symptomatic patent ductus arteriosus occurred in 34% of infants, septicemia in 30%, chronic lung disease in 48%, grade III-IV intraventricular hemorrhage in 27%, stage III-V retinopathy of prematurity in 33%, and necrotizing enterocolitis in 8%. 54 infants (74%) survived the neonatal period and 44 (60.3%) survived until discharge. The survival rate was 40% for infants with a birth weight of 501-750 g and 68% for those weighing 751-999 g. Survival was 27% for infants with a gestational age under 26 weeks compared with 75% for those with a gestational age of 26 weeks and above. Cox regression analysis of survival indicated that Apgar scores at 1 minute, pulmonary hypertension, and severe intraventricular hemorrhage were the most significant contributing factors to mortality.

Abnormalities of carbohydrate metabolism in hyperthyroid patients have been long noted. Elevated proinsulin level is considered as an early marker of B-cell impairment. Proinsulin levels in hyperthyroid patients decreased after antithyroid drug therapy. However, proinsulin in hypothyroid patients was only rarely reported, and the difference was only demonstrated after glucose stimulation-there was a greater response of proinsulin secretion after thyroxine therapy-and the basal fasting proinsulin level was not different after therapy. One of the reasons might be that the assay was not sensitive enough to detect the change of basal proinsulin levels in patients with hypothyroidism after therapy. A newly developed immunochemiluminometric assay of proinsulin was used to demonstrate that the suppressed proinsulin level increased after thyroxine therapy in hypothyroid patients (4.2 +/- 2.4 vs. 10.0 +/- 5.6 pmol/L, p0.05; n = 7). On the other hand, our study also confirmed that the proinsulin levels decreased in hyperthyroid patients after antithyroid therapy by methimazole (27.8 +/- 26.0 vs. 15.8 +/- 15.7 pmol/L, p0.05; n = 12). In conclusion, proinsulin increased in hypothyroid patients after thyroxine therapy and decreased in hyperthyroid patients after methimazole therapy. The results demonstrated there is a high correlation between thyroid function and B-cell function in hypothyroid as well as hyperthyroid patients.

Diabetic ketoacidosis (DKA) is not rare among adults. We retrospectively analyzed the precipitating factors, diabetic history, clinical features, and outcomes of adult DKA patients treated at a tertiary referral medical center in southern Taiwan between January 1994 and May 1996. Seventy-eight patients, aged from 18 to 80 years (median 47), had 87 episodes of DKA (44 males had 49 episodes; 34 females had 38 episodes). Twenty-two episodes occurred in patients with no history of diabetes mellitus (age 18-77 yr, median 40.5). The most common precipitating factor was infection (53 episodes), especially in patients aged more than 40 years. Fifteen patients died during the 87 episodes, giving a case fatality rate of 17%; DKA was precipitated by cerebrovascular accidents in two of the 15 patients and by infection in 13. Among the 53 episodes precipitated by infection, multiple logistic regression analysis showed that old age, requirement for endotracheal intubation, and low body temperature on arrival were associated with fatality. Of the 63 patients who were discharged, 39 required insulin therapy; plasma glucose was well-controlled by oral hypoglycemic agents or diet in only eight (age 29-75 yr, median 57; hemoglobin A1c 5.1-7.8%, median 6.6). The high rate of previously undiagnosed diabetes in adult DKA patients indicates a deficiency in early recognition of, and timely therapy for, diabetes in southern Taiwan.

A number of algorithms exist for searching genetic databases for biologically significant similarities in DNA sequences. Past research has shown that word-based search tools are computationally efficient and can find similarities or dissimilarities invisible to other algorithms like FASTA. We characterize a family of word-based dissimilarity measures that define distance between two sequences by simultaneously comparing the frequencies of all subsequences of n adjacent letters (i.e., n-words) in the two sequences. Applications to real data demonstrate that currently used word-based methods that rely on Euclidean distance can be significantly improved by using Mahalanobis distance, which accounts for both variances and covariances between frequencies of n-words. Furthermore, in those cases where Mahalanobis distance may be too difficult to compute, using standardized Euclidean distance, which only corrects for the variances of frequencies of n-words, still gives better performance than the Euclidean distance. Also, a simple way of combining distances obtained at different n-words is considered. The goal is to obtain a single measure of dissimilarity between two DNA sequences. The performance ranking of the preceding three distances still holds for their combined counterparts. All results obtained in this paper are applicable to amino acid sequences with minor modifications.

The endopeptidase EC 3.4.24.15 (EP24.15) is a zinc metalloendopeptidase that is widely distributed in a variety of tissues, including the testes, pituitary and the central nervous system. Among its numerous roles in metabolizing and processing biologically-active peptides, the enzyme degrades gonadotropin-releasing hormone (GnRH) by cleaving the central Tyr5-Gly6 bond. The aim of the present studies was to determine whether EP24.15 can modulate the concentrations of GnRH within the hypothalamo-hypophysial portal blood and thereby play a physiological role in reproduction. Our data suggest the presence of immunoreactive EP24.15 in the perivascular space of the median eminence and that this enzyme is secreted into portal blood. We have also shown a physiological role for this enzyme in that an inhibition of its activity with a specific inhibitor augmented the steroid-induced LH increase in ovariectomized rats. The present results suggest that secretory and post-secretory mechanisms are important in shaping the GnRH signal from the central nervous system; GnRH metabolism by EP24.15 may be one such mechanism.

In ongoing efforts to study the ontogeny of gonadotropin-releasing hormone (GnRH) neurons, we serendipitously observed that increasing times of incubation in antibodies enhanced signal detection. Here, we describe significant differences in the early migration pattern, population dynamics, and growth cone morphology from published reports. The first immunoreactive GnRH cells were detected in the mouse at E10.75 (7.6 +/- 2.8 cells; morning after mating = E0.5), prior to the closure of the olfactory placode. Although half of these cells were in the medial wall of the olfactory pit, the other half had already initiated their migration, and approximately one quarter had reached the telencephalic vesicle. Although the migratory pattern of the GnRH cells after E11.00 was identical to that described previously, these earliest migrating cells traveled singly rather than in cords, with some reaching the presumptive preoptic area (posterior to the ganglionic eminence) by E11.75. The number of GnRH cells increased significantly (p0.05) to 777 +/- 183 at E11.75 and peaked at 1949.6 +/- 161.6 (p0.05) at E12.75. The adult population was approximately 800 cells distributed between the central nervous system (CNS) and the nasal region. Hence, the population of GnRH neurons during early development is much larger than previously appreciated; mechanisms for its decline are discussed. Neuritic extensions on the earliest GnRH neurons are short (30-50 microm) and blunt and may represent the leading edge of the moving cell. By E12.75, GnRH axons in the CNS had a ribboned or beaded morphology and increasingly more complex growth cones were noted from this time until the day of birth. The most complex growth cones were associated with apparent choice points along the axons' trajectory. By E13.75, GnRH axons were seen at the presumptive median eminence in all animals, and it was at this stage that the axons began to branch profusely. Branching, as well as the presence of growth cones, continued post-natally. These results provide further insights into the pathfinding mechanisms of GnRH cells and axons.

A retrospective study of 143 very-low-birthweight infants cared in a level III neonatal intensive care unit who had survived for at least 28 days. Initial eye ground evaluation was done at the postnatal age between 4 and 6 weeks. Follow-up evaluation was done every one to two weeks at the discretion of the ophthalmologists. Thirty-four variables were reviewed for each case. Statistical analysis was done for each variable, with the development of retinopathy of prematurity (ROP), severity of ROP and development of threshold ROP as the dependent variables, by Mann-Whitney U test or X2 test when adequate. Variables with P-valu0.05 were included in multiple regression. One hundred and thirty-eight cases were survived for more than 28 days with their eyes been checked. Twenty-six (18.8%) of them developed ROP. The prevalence of stage I was 2.2% (3/138), stage II was 3.6% (5/138), stage III was 12.3% (17/138), and stage V was 0.7% (1/138). Threshold disease, stage 3 (+) and above, was found in 5 cases (3.6%). Seventeen variables were found to be correlated with the development of ROP. Only the duration of continuous positive airway pressure (CPAP) was significantly correlated to the development of ROP in multivariate logistic regression. Fifteen variables were correlated with the severity of ROP, but only peak direct bilirublin level, peak total bilirubin level and duration of CPAP could entered multiple stepwise linear regression. Thirteen variables were correlated with the development of threshold ROP, but only episodes of septicemia enter the multivariate logistic regression. We postulate that the longer duration of CPAP in ROP cases may reflect the severity of apnea and episodes of hypoxic attacks. Reducing episodes of apnea may prevent the development of ROP. The number of episodes of septicemia was the only significant variable for threshold ROP so that infection control is important for the prevention of threshold disease.

An immunochemiluminometric assay of parathyroid-hormone-related peptide (PTHrP) was developed with purified antisera produced from a single goat immunized with (1-86) PTHrP. One batch of purified antibodies was labeled with acridinium ester used as tracer antibodies; a second batch of the purified antibodies was immobilized onto plastic bead. Sensitivity of the assay was 0.1 pmol/L. The assay had no cross-reactivity with PTH. Seventy-five percent of healthy individuals had undetectable PTHrP (mean +/- S.D. were 0.73 pmol/L +/- 0.6; n = 110). The 95 percent upper reference limit was 2.0 pmol/L. Five of the seven patients with humoral hypercalcemia associated with malignancy (HHM) of solid-tumor had PTHrP greater than 2.0 pmol/L. The test efficacy in detecting HHM was 71 percent, which is similar to previous extraction radioimmunoassay (RIA) or immunoradiometric assay (IRMA). The new assay lowered the detection limit to 0.1 pmol/L, which is a great improvement from that of RIA at 2.0 pmol/L and IRMA at 1.0 pmol/L; however; it did-not improve the test efficacy in detecting patients with HHM. It may indicate the patients with HHM only have elevated plasma PTHrP in 70 percent of them. Technically, the method can be used as a model to develop chemiluminescent esoteric test for research or reference laboratories.

Information about accessory pathways conducting only in the antegrade direction is limited. The purposes of the present study were to prospectively investigate the clinical features, electrophysiological characteristics, effects of radiofrequency catheter ablation and recurrent atrial fibrillation after successful ablation in patients with accessory pathways conducting only in the antegrade direction, and to compare them with those who had pathways capable of bidirectional conduction in a consecutive series of 759 patients. Electrophysiological studies and radiofrequency catheter ablation were performed in 33 study patients with antegrade-only accessory pathways and in 377 patients with bidirectional accessory pathways for comparison. The patients with accessory pathways conducting only in the antegrade direction were older (47 +/- 16 vs 40 +/- 16 years, P = 0.037) and had a higher incidence of atrial fibrillation (100% vs 27.1%, P < 0.001) as well as related syncope (33.3% vs 10.1%, P = 0.001). The study patients also had more accessory pathways located in the posterior septum and a higher incidence of retrograde atrioventricular nodal conduction. The biophysical variables, success and complication rates of radiofrequency ablation were similar in both groups. During the follow-up period of 32 +/- 12 months, symptomatic atrial fibrillation after successful ablation did not recur in 79% and 81% of patients with unidirectional and bidirectional accessory pathways, respectively. Furthermore, old age and cardiovascular diseases were independent predictors of recurrent atrial fibrillation after radiofrequency ablation. In conclusion, this study showed that atrial fibrillation with preexcitation was the usual presentation in patients who had symptomatic Wolff-Parkinson White syndrome with an antegrade-only accessory pathway, and might be related to antegrade conduction of the accessory pathway. Therefore elimination of antegrade-only and bidirectional pathways by radiofrequency ablation could prevent the recurrence of symptomatic atrial fibrillation in younger patients without cardiac disease.

Two infants, one male and one female, with elevated serum ammonia levels, were shown, based on urine organic acid analysis and DNA studies, to have ornithine transcarbamylase (OTC) deficiency. OTC deficiency is one of the most common urea cycle disorders. Hyperammonemia occurred at 3 days of age in the male infant, and at approximately 7 days of age in the female infant. Administration of sodium benzoate and sodium phenylacetate lowered the serum ammonia level effectively in both cases. Other modalities, including peritoneal dialysis and protein restriction, were also important in the control of the serum ammonia level. The mother of the male infant was shown to be a carrier of the OTC gene mutation by allopurinol loading test. The mutation site of the OTC gene for the female infant was identified, but her mother did not have the mutation. OTC deficiency, an incompletely dominant X-linked disorder, is a severe disease even for females and prompt treatment and precise genetic counseling are mandatory.

To determine the efficacy of cortisol and its metabolite, cortisone, measured simultaneously by high performance liquid chromatography (HPLC) in the diagnosis of Cushing's syndrome, we retrospectively reviewed the histories of 29 surgically proven Cushing's syndrome patients (20 Cushing's disease, 5 ectopic ACTH syndrome, and 4 adrenal Cushing's syndrome) and 6 patients with exogenous Cushing's syndrome. These 35 patients had urinary free cortisol determined by both HPLC and competitive binding methods. The efficacy of the HPLC assay using cortisol alone was equivalent to that of the competitive binding assay; 22 of 29 (76%) patients had increased cortisol. Cortisone also aided in the diagnosis; 25 of 29 (86%) had increased cortisone. Twenty-seven of the 29 (93%) patients had either both cortisone and cortisol (n = 19) or at least 1 of the 2 (n = 8) increased. All 6 patients with exogenous Cushing's syndrome had suppressed urinary free cortisol, cortisone, and the presence of prednisone and prednisolone. In the competitive binding assay, all exogenous Cushing's patients had falsely increased cortisol results. In conclusion, urinary free cortisol plus cortisone determined simultaneously by HPLC added a new dimension to the diagnosis of Cushing's syndrome. It should be considered when exogenous Cushing's syndrome is suspected or when only one urinary cortisol test is allowed to be ordered.

The report describes a premature infant with necrotizing enterocolitis who developed symptoms of zinc (Zn) deficiency after three to four weeks of total parenteral nutrition (TPN). Clinical presentations included characteristic skin rash, alopecia, retarded growth, generalized edema and decreased serum alkaline phosphatase (ALP). Immune function studies revealed impaired neutrophil adhesion and mitogen-induced lymphoproliferation, whereas phagocytosis, chemotaxis and lymphocyte subsets remained normal. A high dose of elemental Zn (2.5 mg/kg/day), administered orally, improved the clinical symptoms and restored the immune function. In patients with Zn deficiency, impaired neutrophil adhesion and lymphocyte function may contribute to immunodeficiency which can be reversed with adequate Zn supplementation.

We used FOS expression, widely accepted as a marker for neuronal activation, to evaluate physiologically induced activation of gonadotropin-releasing hormone (GnRH) neurons within intraventricular preoptic area grafts in hypogonadal (hpg) female mice. Hpg mice lack endogenous GnRH due to a mutated gene, but can respond to grafted GnRH neurons with reproductive development. The purpose of this study was to determine the degree to which the host brain regulates grafted GnRH neurons. FOS expression in grafted GnRH neurons was induced in progesterone-primed female mice paired with sexually active males. The degree of sexual activity did not affect the outcome, with 40.9 +/- 12.2% of the grafted GnRH cells expressing FOS when male partners performed intromissions, and 47.5 +/- 10.2% when they also ejaculated. There was little or no FOS expression in the grafts of unprimed hpg mice paired with sexually active males, in unpaired mice primed with progesterone or sequential estradiol benzoate and progesterone, or in controls. The pattern of FOS expression in the brains of the female hpg mice engaged in mating behavior was similar to that reported in other species, with moderate to high expression in the medial preoptic area, ventromedial nucleus, and medial amygdala in females paired with males that ejaculated. The present results support the hypothesis that host-derived activation of grafted GnRH neurons underlies aspects of reproductive responses seen in hpg mice with grafts, and further, that at least a portion of the host-graft connectivity is steroid sensitive.

To evaluate the incidence, clinical course, and possible risk factors of cholestasis in very low-birth-weight infants. A retrospective study of 143 very low-birth-weight infants was performed. Cholestasis was defined as direct-reacting bilirubin2 mg/dL for more than 14 days. The clinical course of cholestasis was described, and perinatal risk factors were evaluated for associations with the development and severity of cholestasis. Cholestasis was present in 31 infants (21.7%). The mean (SD) age of onset was 30.3(15.3) days after birth or 26.0 (15.6) days after receiving parenteral nutrition, and the mean (SD) duration was 77.1 (33.8) days. In half of the cholestatic infants, bilirubin continued to rise after discontinuing parenteral nutrition. One infant developed signs of liver cirrhosis and died, two infants died with progressive cholestasis, while the other 28 patients recovered. Analysis of risk factors revealed that birthweight and duration of fasting significantly correlated with the development of cholestasis, and that sepsis significantly influenced the severity of cholestasis. Cholestasis is a common complication of extreme prematurity. The clinical course seems benign but long-term sequelae are unknown. Immature liver function and absence of stimuli for intestinal motility and hormonal secretion predispose to decreased bile flow, while sepsis further impairs hepatic ductular secretion and aggravates cholestasis.

Systemic air embolism is a rare but fatal complication of the ventilatory support. We reported a case with this complication after surfactant therapy. This 1175 gm neonate was born at the gestational age of 28 weeks. Endotracheal intubation was performed after birth for positive pressure ventilation. Surfactant therapies (Exosurf Neonatal) were given at two and fourteen hours of age. The ventilator settings were gradually weaned. Unfortunately, tachycardia, hypotension, pallor and O2 desaturation developed at thirty-nine hours of age. Many air bubbles were withdrawn from the arterial line. The chest radiography showed lucency in the heart and major vessels. The neonate died twenty-one hours later, despite aggressive resuscitation.

Accessory atrioventricular (AV) pathway located at or near the region of aorta-mitral continuity has rarely been mentioned. This report describes one such case with a concealed accessory AV pathway at the anteromedial mitral annulus adjacent to aorta-mitral continuity. The location of the accessory pathway was confirmed by successful radiofrequency catheter ablation. This patient was a 26-year-old male. His 12-lead surface ECG showed no evidence of ventricular preexcitation during sinus rhythm. The earliest retrograde atrial depolarization recorded from the routine catheters was at the His bundle area during ventricular pacing and orthrodromic AV reentrant tachycardia; paradoxically, the earliest left-sided atrial activation recorded from the coronary sinus catheters was at the distal coronary sinus area. The unique retrograde atrial activation sequence over the left atrium and His bundle area was not true for patients with left lateral or anterolateral accessory pathway. During tachycardia, the local electrogram from the successful ablation site showed local VA fusion in the anteromedial mitral annulus. After delivering one pulse of radiofrequency energy (30W), the accessory AV pathway was successfully eliminated without complication. This report presents a concealed left-sided accessory AV pathway at an unusual location. It is very important to describe special electrophysiologic characteristics and ablation technique in this unusual accessory pathway to improve knowledge in the era of interventional electrophysiology.

A female infant, born at the gestational age of 29 weeks with a birthweight of 1,350 gm, developed progressive hepatomegaly at 10 days of age. Congestive heart failure gradually developed, and hepatic hemangioendothelioma was diagnosed at 1 month of age by open biopsy. Due to rapid enlargement of the tumor and progressive heart failure, steroid therapy was given from 36 days of age, including methylprednisolone 15 mg/kg/day for 3 days and 10 mg/kg/day for 4 days, then prednisolone 4 mg/kg/day for 20 days followed by tapering till 74 days of age. The tumor regressed gradually and was not detectable by sonography at 33 months of age. We suggest that, even in very-low-birthweight infants, the prognosis of hepatic hemangioendothelioma may be improved with aggressive therapy when symptoms develop during tumor progression, and that steroid should be the initial treatment.

A female, term neonate presented with generalized edema, heavy proteinuria, hypoalbuminemia and hyperlipidemia in the second week of life. The clinical and laboratory features were compatible with the diagnosis of congenital nephrotic syndrome. Treatment included albumin infusion, empirical penicillin, steroid and continuous arterio-venous hemofiltration. Intestinal perforation developed at the 19th day of age and led to a fatal outcome. At autopsy, thrombosis of the superior mesenteric artery and its branches was noted, and histology of the kidney was compatible with congenital nephrotic syndrome of the Finnish type. The risk of thromboembolism, arterial or venous, should be considered in patients with nephrotic syndrome, even in the neonatal period. Preventive measures, including avoiding volume depletion and femoral arterial/venous puncture, are essential in managing these patients. Prophylactic anticoagulation and infusion of fresh frozen plasma may be warranted to avoid such potentially lethal complications of thromboembolism.

Proinsulin, the precursor of insulin and C-peptide, is detectable in the circulation and is a potential marker of beta-cell dysfunction. Currently, circulating proinsulin can be measured accurately without the interference of insulin or C-peptide by immunometric assays and a few specific radioimmunoassays. An immunochemiluminometric assay was developed in our laboratory by using two immunopurified polyclonal antibodies of C-peptide and insulin from two goats. The C-peptide antiserum was labeled with acridinium ester. The insulin antiserum was immobilized onto a plastic bead. With this assay, proinsulin levels found in noninsulin-treated patients with noninsulin-dependent diabetes mellitus (63 +/- 58 pmol/L; n = 19) were significantly higher (p0.05) than levels in insulin-treated patients with noninsulin-dependent diabetes mellitus (30 +/- 24 pmol/L; n = 43), and both were significantly higher (p0.001) than proinsulin levels in patients with insulin-dependent diabetes mellitus. In addition, there was a negative correlation between proinsulin levels and duration of years on insulin therapy in patients with noninsulin-dependent diabetes mellitus (r = -0.4795; p0.01).

To evaluate the clinical effects of magnesium sulfate (MgSO4) in the treatment of persistent pulmonary hypertension of the newborn (PPHN) in premature infants.This was a prospective, nonrandomized, clinical study. Seven premature neonates with PPHN were treated with MgSO4 as soon as documentation of an interatrial right-to-left shunt was made. A loading dose of 200 mg/kg was infused over 30 minutes, followed by a maintenance dose of 20 to 50 mg/kg/h. Alveolar-arterial oxygen tension difference (AaDO2) and oxygenation index were followed up sequentially as the primary outcome measures. Blood pressures and serum electrolytes were also monitored.Six cases responded clinically. The decrease of AaDO2 reached significance at 36 hours, but the decrease of oxygenation index was not significant over 72 hours. Four infants survived. No significant side effects were encountered.Our results suggest that MgSO4 may be considered as an alternative treatment of PPHN in premature infants.

Recurrence rate of atrioventricular (AV) nodal reentrant tachycardia after successful radiofrequency ablation varies widely, and the determinants of recurrent AV nodal reentrant tachycardia remain controversial. Furthermore, true or pseudorecurrence of tachycardia after successful ablation in patients with different forms of AV nodal reentrant tachycardia has not been evaluated systematically. Three hundred sixty-two patients (161 men and 201 women [mean age 52 +/- 16 years]), including 314 patients with typical-form, 10 patients with atypical-form, 4 patients with variant-form, and 34 patients with multiple-form AV nodal reentrant tachycardias, received selective radiofrequency ablation of the anterograde and/or retrograde slow AV nodal pathway. During a mean follow-up of 27 +/- 11 months, 9 patients (2.5%) experienced recurrent AV nodal reentrant tachycardia (true recurrence, group A), and 8 (2.2%) had inappropriate sinus tachycardia or paroxysmal atrial tachyarrhythmias (pseudorecurrence, group B). Neither the true nor pseudorecurrence rate was different among the 4 different forms of tachycardia. Factors including presence of residual slow pathway conduction, a single AV nodal reentrant echo beat, absence of an accelerated junctional rhythm during successful ablation, facilitating induction of tachycardia by isoproterenol, radiofrequency pulse number, and successful ablation site were not associated with an increased risk of recurrent AV nodal reentrant tachycardia. The onset time of recurrent tachycardia was significantly late in group B patients (30 +/- 21 vs 292 +/- 240 days, p = 0.04). Thus, this study demonstrated that both true and pseudorecurrence could occur after successful ablation.

Accessory pathway-mediated tachyarrhythmias and AV nodal reentrant tachycardia represent a large portion of supraventricular tachycardia in younger patients. Reports comparing electrophysiologic characteristics and results of radiofrequency ablation between teenagers and adults from the same electrophysiology laboratory are rare, and these deserve further study. This study included 49 teenage patients (mean age 17 +/- 3 years, range from 10 to 20) and 1008 adult patients (mean age 50 +/- 13 years, range from 21 to 92) referred for electrophysiologic study and radiofrequency ablation for treatment of accessory pathway-mediated and AV nodal reentrant tachycardia. The results showed that: (1) mean duration of tachyarrhythmia was shorter in teenagers, but incidences of syncope, cardioversion for hemodynamic compromise and associated cardiovascular diseases were similar in both groups; (2) teenagers had a higher incidence of right-sided free wall accessory pathways (34.1% vs 14.9%, p = 0.048) and better conduction properties of accessory pathways and AV nodal pathways; (3) fast-slow and multiple forms of AV nodal reentrant tachycardia were significantly less frequent (p = 0.026) in teenagers, whereas atrial fibrillation with ventricular preexcitation was common in adults; (4) success rate, incidence of recurrent tachycardia, total procedure time, radiation exposure time and number of radiofrequency pulses for successful ablation did not differ significantly between teenagers and adults.(1) different electrophysiologic characteristics were found between teenagers and adults; and (2) radiofrequency ablation was effective and safe in teenagers with paroxysmal supraventricular tachycardia.

Body composition measurements using bioelectrical impedance analysis (BIA) were performed on 50 uremic patients immediately before and after hemodialysis (HD) therapy, on 10 uremic patients under continuous ambulatory peritoneal dialysis (CAPD) therapy before and after the fluid was drained out of the peritoneal cavity and on 3 cirrhotic patients before and after abdominal paracentesis. Thirty-two pairs of measurements were performed on the CAPD patients and 3 pairs on the cirrhotic patients. Significant increases in both resistance and reactance were noted after HD. However, resistance and reactance before and after peritoneal fluid had been drained were not significantly different. In HD, body fluid loss as estimated by BIA (LBIA) was higher than that from the body weight method (LBW). The relationship between the two is described by the equation LBW = 0.841LBIA + 0.588. The total body fat estimated before HD was significantly lower than after HD, and it was significantly higher when measured with peritoneal fluid retention than with fluid drained. Generalized edema caused an increase in resistance and reactance, while local peritoneal fluid retention did not cause any significant changes. When total body fluid is measured by the BIA method, it is often overestimated in the case of generalized edema and underestimated in case of peritoneal fluid retention. Therefore, total body fat is underestimated by BIA in generalized edema before HD and overestimated in peritoneal fluid retention.

Reverse alternating Wenckebach periods (RAWP) have rarely been described, and the significance of dual AV nodal pathways in atrial pacing-induced RAWP is unknown. Forty-five of 50 consecutive patients (M/F = 23/27, mean age 40 +/- 5 years) with common type AV nodal reentrant tachycardia had discontinuous antegrade conduction curves. Atrial pacing revealed that pattern A RAWP (23 patients) had the fourth paced beat conducted over the fast pathway, and pattern B (18 patients) over the slow pathway. Four patients had both pattern A and B RAWP during different pacing cycle lengths. All episodes of atrial pacing-induced RAWP emerged from (or started as) 3:2 AH block, which thereafter were followed by runs of 2:1 AH block. Comparisons between patterns A and B showed (1) maximal atrial pacing cycle length with RAWP was longer in pattern A; (2) A2H2-A1H1 and A4H4-A1H1 were significantly greater in pattern B; (3) A2H2-A4H4 and H2A4/A2H2 were significantly greater in pattern A. It is concluded that atrial pacing-induced RAWP is a common electrophysiologic phenomenon in patients with dual AV nodal pathways. Furthermore, intermittent slow pathway conduction associated with different AnHn and HnAn+2 parameters helped the interpretation of different conduction patterns.

Experiments were conducted to identify neurons in the bovine brain that express the LHRH gene and to determine whether LHRH mRNA levels are influenced by the ovaries. Two groups of postpubertal heifers were utilized: heifers killed during the mid-luteal phase of the estrous cycle (LUTEAL, n = 5) and heifers killed 14-16 wk following ovariectomy (OVX, n = 5). In situ hybridization was performed through use of a 32P-end-labeled deoxyoligonucleotide (59 mer) complementary to the human LHRH mRNA sequence. LHRH-expressing neurons were identified in the diagonal band of Broca, the preoptic area, and the anterior hypothalamus in a manner consistent with immunocytochemical localization. Reduced silver grains, proportional to LHRH mRNA content, were quantified (in pixels, 45x objective) with an image analysis system. Expected serum hormone concentration differences between endocrine states were confirmed by radioimmunoassay for progesterone (LUTEALOVX, p0.01) and for LH (OVXLUTEAL, p0.01). Compared to the OVX group, LUTEAL heifers had 34% fewer LHRH-expressing neurons (p0.05); on the average, these neurons possessed 28% fewer pixels/cell (p0.01), indicating fewer copies of LHRH mRNA per cell. When the numbers of pixels in all labeled cells were totalled, LUTEAL animals had 57% fewer pixels (p0.05) than did the OVX females--probably reflecting a decrease in LHRH synthetic capacity in the LUTEAL animals. Therefore, during the mid-luteal phase of the bovine estrous cycle, ovarian steroid (i.e., luteal progesterone) suppression of LHRH release (as reflected by serum LH) is coincident with decreased LHRH mRNA in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)