Miracle-dz/UniFAR-FTUs huggingface dataset:
Ovarian follicular and luteal physiology.

Follicular maturation and development is a complex process of interrelated intra- and extraovarian events that ultimately lead to ovulation of a mature oocyte and transformation of the ruptured follicle into a corpus luteum. The primordial follicle consists of an immature oocyte arrested in the dictyate stage of meiosis, surrounded by a single layer of relatively undifferentiated granulosa cells. The oocyte remains in the immature state because of many factors, one of which is the oocyte maturation inhibitor (OMI) secreted by granulosa cells. The oocyte subsequently increases in size, and as the antrum forms it becomes surrounded by cumulus cells. The cumulus cells may be intimately involved in the action of O,I to arrest the oocyte in the immature state within the follicle, as well as the resumption of meiosis during the LH surge. The compartments of the follicle that change most dramatically during follicular maturation are the cells lining the follicle--the granulosa and thecal cells. Under the influence of estrogen and FSH, the granulosa cells proliferate and also acquire FSH receptors. At this time, the thecal compartment differentiates and surrounds the granulosa cells, but remains separated from them by a basement membrane. Steroid secretion by the antral follicle involves the interplay of androgens, estrogens, and progestins. Both the granulosa and thecal cell compartments contribute to follicular fluid and serum levels of steroids; the interaction of both cell types may be necessary for estrogen and progesterone secretion in some species. As a consequence of the presence of an elevated number of FSH receptors, the granulosa cells of the small antral follicle are able to respond to FSH in many ways, including increased cyclic AMP accumulation, activation of the aromatase system, and induction of LH receptors, which permits the granulosa cells to later respond to LH. The mechanism by which thecal cells acquire their LH receptors is presently unknown. The granulosa cells of the follicle may indirectly control their own maturation and the number of follicles maturing through the secretion of follicular inhibin, which decreases the pituitary output of FSH. Even though the granulosa cells have acquired large numbers of LH receptors, they are prevented from luteinizing prematurely by factors in follicular fluid, including estrogen and a luteinizing inhibitor (LI). As serum LH levels increase during the preovulatory LH surge, a number of events occur: resumption of oocyte meiosis, transformation of the steroid enzyme complex from estrogen to progesterone secretion, follicular rupture, and formation of the corpus luteum. Granulosa cells form the bulk of the corpus luteum, which secretes elevated amounts of progesterone for a fixed time period depending on the species. Before ovulation the preovulatory follicle must be exposed to and respond to adequate LH and FSH levels in order for the eventual corpus luteum to secrete elevated amounts of progesterone for its normal lifespan.
Alkaline Phosphatase Activity: New Assay for the Reflotron® System. Results of the Evaluation in Eight Clinical Laboratories

Abstract A new reagent carrier, Reflotron® ALP, has been developed for the Reflotron® system, allowing easy and rapid measurement (in less than 3 minutes) of alkaline phosphatase (ALP) activity in capillary blood, venous blood, heparinized plasma or serum. The evaluation of the analytical performance of the assay was carried out at eight clinical laboratories. The study of the imprecision using the measurements in human samples resulted in coefficients of variation ranging from 1.3% to 4.6% (within-run) and from 3.2% to 4.0% (day-to-day). The analytical specificity of the Reflotron® ALP assay agrees well with ALP methods using a N-methyl-D-glucamine buffer solution. The calibration of the Reflotron® ALP assay, however, is related to the reference intervals for ALP methods using a diethanolamine buffer solution. Method comparisons were performed with the ALP method on Hitachi instruments using diethanolamine buffer. Reflotron® ALP measurements in blood and plasma in 157 randomly selected split samples showed excellent agreement (slope: 0.99; intercept: 0.7 U/l; median bias: 2.3%; median difference from the comparison method: −0.3%). Specimens from pregnant women and adolescents were excluded from this study. Differing values were obtained in a method comparison using 48 samples containing predominantly the ALP bone isoform (slope: 0.81; intercept: 31.5 U/l; median bias: 5.7%; median difference from the comparison method: −12.2%). Regression analysis of the results from 21 sera with prevailing placental ALP gave a slope of 1.51, and an intercept of −41.1 U/l (median bias: 8.6%; median difference from the comparison method: 35.6%). Reflotron® ALP was compared with three different wet chemistry procedures using different buffer compounds: N-methyl-D-glucamine or diethanolamine or 2-amino-2-methyl-1-propanol. In samples containing predominantly ALP isoforms not of liver origin, the measurements with N-methyl-D-glucamine buffer gave the best fit with respect to Reflotron®. In an interference study with 18 drugs, no effect on the test results could be detected. Total bilirubin up to 750 μmol/l and hemolysis up to 1.7 g/l free hemoglobin did not influence the test. Reflotron® ALP proved to be an easy and rapid method with excellent precision. The accuracy related to an ALP method using diethanolamine buffer was good. The systematic differences for ALP in samples from pregnant women and adolescents have to be taken into account. The assay is well suited for differential diagnosis of hepatic diseases in decentralized testing.
Gallic Acid Is an Antagonist of Semen Amyloid Fibrils That Enhance HIV-1 Infection*

Recent in vitro studies have demonstrated that amyloid fibrils found in semen from healthy and HIV-infected men, as well as semen itself, can markedly enhance HIV infection rates. Semen fibrils are made up of multiple naturally occurring peptide fragments derived from semen. The best characterized of these fibrils are SEVI (semen-derived enhancer of viral infection), made up of residues 248–286 of prostatic acidic phosphatase, and the SEM1 fibrils, made up of residues 86–107 of semenogelin 1. A small molecule screen for antagonists of semen fibrils identified four compounds that lowered semen-mediated enhancement of HIV-1 infectivity. One of the four, gallic acid, was previously reported to antagonize other amyloids and to exert anti-inflammatory effects. To better understand the mechanism by which gallic acid modifies the properties of semen amyloids, we performed biophysical measurements (atomic force microscopy, electron microscopy, confocal microscopy, thioflavin T and Congo Red fluorescence assays, zeta potential measurements) and quantitative assays on the effects of gallic acid on semen-mediated enhancement of HIV infection and inflammation. Our results demonstrate that gallic acid binds to both SEVI and SEM1 fibrils and modifies their surface electrostatics to render them less cationic. In addition, gallic acid decreased semen-mediated enhancement of HIV infection but did not decrease the inflammatory response induced by semen. Together, these observations identify gallic acid as a non-polyanionic compound that inhibits semen-mediated enhancement of HIV infection and suggest the potential utility of incorporating gallic acid into a multicomponent microbicide targeting both the HIV virus and host components that promote viral infection.
AMPA potentiator treatment of cognitive deficits in Alzheimer disease

Objective: To investigate the efficacy and safety of the positive α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid modulator LY451395 in patients with mild to moderate Alzheimer disease (AD) (Mini-Mental State Examination scores 14 to 26). Methods: One hundred eighty-one patients were randomized to treatment in an 11-week, double-blind, placebo-controlled trial. Patients received either LY451395 0.2 mg BID for 28 days and 1.0 mg BID thereafter (n = 90) or placebo (n = 91). The primary outcome measurement was the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) with several secondary outcome measurements: Clinician's Interview-Based Impression of Change, Trail Making Part A, Stylus Tapping Test, Single Digit Modality Test, and Neuropsychiatric Inventory (NPI). Results: Baseline demographics were similar between the two groups. Patients did not show any mean change from baseline in the ADAS-Cog after treatment with LY451395 for 4 weeks (p = 0.60) or 8 weeks (p = 0.83). The only secondary outcome measurement that showed changes from baseline compared with placebo was the NPI Total Score: p = 0.06 (marginal significance) after 4 weeks of treatment and p = 0.03 after 8 weeks of treatment. Ninety-two percent of LY451395-treated patients and 95% of placebo-treated patients completed the trial. Adverse events were experienced by 83% of LY451395-treated patients and 86% of placebo-treated patients, the majority of which were rated mild in severity. Conclusion: Patients treated with LY451395 did not show a statistically significant separation from patients taking placebo on the Alzheimer's Disease Assessment Scale-Cognitive Subscale, the primary outcome measure.
A compact triple-band low-jitter digital LC PLL with programmable coil in 130-nm CMOS

We present a low-jitter digital LC phase-locked loop (PLL) in a standard digital 130-nm CMOS technology, aiming at, but not limited to, clock multiplication in high-speed digital serial interface transceivers. The PLL features a fully digital core and a digitally controlled LC oscillator. The use of an integrated programmable coil enables triple-band operation in multi-GHz range (2.2, 3.4, and 4.6 GHz) on a die area as small as 0.21 mm/sup 2/. A new architecture is proposed which improves the authors' previous work and allows to achieve an outstanding long-term jitter lower than 650 fs over the whole frequency range. The PLL consumes 13 mA of current at 1.5-V supply. Its performances compete favorably with the most advanced analog PLLs and are ahead of digital PLLs. Its digital nature makes it easily realizable in the mainstream digital CMOS technologies, robust against noise, and thus ideal for application as a low-jitter clock multiplying unit in digital intensive systems on chip.
Distribution and fate of cocaine‐ and amphetamine‐regulated transcript peptide (CARTp)‐expressing cells in rat urinary bladder: A developmental study

We examined the distribution and fate of cocaine‐ and amphetamine‐regulated transcript peptide (CARTp)55–102‐immunoreactive (IR) structures in the neonatal and adult rat urinary bladder. Double‐labeling studies examining CARTp with tyrosine hydroxylase (TH), neuronal nitric oxide synthase (nNOS), or choline acetyltransferase (ChAT) were performed in wholemounts of urothelium or detrusor or cryostat sections of the bladder. In younger animals (postnatal day [P]1, P3), CARTp‐IR cell bodies in detrusor smooth muscle were observed in large clusters (∼100 cells/cluster) at the ureteral insertion and along thick bundles of nerve fibers at the bladder base. The total number of CARTp‐IR cells was significantly reduced (by five‐fold) at P14, and this reduced number persisted into adulthood. The decrease in the number of CARTp‐expressing cells was complemented with positive staining for cleaved caspase‐3, suggesting that apoptosis contributed to this decrease. At birth (P1), all CARTp‐IR cells expressed the neuronal marker Hu. After birth, CARTp was expressed by some neurons (CARTp‐IR, Hu‐IR) that represent intramural ganglion cells and by cells that lacked a neuronal phenotype (CARTp‐IR, Hu‐) but did express TH. Neither of these cell populations expressed ChAT immunoreactivity in adult bladder. These cells (CARTp‐IR, Hu‐, TH‐IR) may represent paraganglion or small intensely fluorescent (SIF) cells. The percentage of colocalization of CARTp‐IR and nNOS or TH was dependent on postnatal age and showed an inverse relationship. At P1, 67.1 % of CARTp‐IR cells expressed nNOS immunoreactivity. Decreased colocalization was observed with increasing postnatal age. In contrast, 19.5% of CARTp‐IR cells expressed TH at P1, but colocalization increased with postnatal age. The suburothelial plexus lacked CARTp‐IR nerve fibers until P14, when nerve fibers with varicosities were observed in the urethra and bladder neck region. In summary, we demonstrate 1) a decrease in the number of CARTp‐IR cells in rat detrusor in early postnatal development; 2) apoptotic events in the bladder during early postnatal development; 3) rostral migration of CARTp‐IR cells from the ureteral insertion toward the bladder body during postnatal development; 4) the presence of different populations of CARTp‐IR cells, some with and others without a neuronal phenotype; and (5) age‐dependent changes in chemical coding of CARTp‐IR cells with postnatal development. This study demonstrates that CARTp‐IR intramural ganglia and CARTp‐IR paraganglion or SIF cells exist in the postnatal and adult rat bladder, although the role of these cell types remains to be determined. J. Comp. Neurol. 489:501–517, 2005. © 2005 Wiley‐Liss, Inc.
Should the governments of ‘developed’ countries be held responsible for equalizing the indigenous health gap?

Across the globe there is significant variation between and within indigenous populations in terms of world view, culture, and socio-political forces. However, many indigenous groups do share a striking commonality: greater rates of non-communicable diseases and shorter life expectancies than non-indigenous compatriots. Notably, this health gap persists for ‘developed’ countries, including Australia, Canada, New Zealand and the United States. The question of who is responsible for equalizing the gap is complicated. Using Australia as an exemplar context, this commentary will present arguments ‘for’ and ‘against’ the governments of developed nations being held liable for closing the indigenous health gap. We will discuss the history and nature of the health gap, actions needed to ‘close the gap’, and which party has the necessary resources to do so.
5 Gbps 0.35-/spl mu/m CMOS driver for laser diode or optical modulator

This paper presents a versatile driver for laser diode or optical modulator using a 0.35-/spl mu/m CMOS process. In this driver, a quasi push-pull source follower is introduced. Combined with a dynamic amplification technique, the driver's slew rate and output voltage swing are increased; meanwhile the overshoot is efficiently reduced. The driver works well at 2.5 Gbps under 3.3 V and 5 V supply voltage, consuming typical power of 310 mW and 945 mW respectively. It can give a modulation voltage (with 50-/spl Omega/ load) ranging from 0.55 V/sub P-P/ to 4.2 V/sub P-P/ under 3.3 V supply voltage and 0.6 V/sub p-p/ to 6.2 V/sub P-P/ under 5 V supply voltage, therefore it can be used as a laser diode or optical modulator driver. When the driver was tested with a LiNbO/sub 3/ modulator, clear optical eye diagrams were measured at 2.5 Gbps and 5 Gbps, respectively. The die area is 0.57 mm/sup 2/.
Self-defining memories in post-traumatic stress disorder.

OBJECTIVE This study investigated the relationship between trauma survivors' goals and retrieval of self-defining memories in post-traumatic stress disorder (PTSD). METHODS Civilian trauma survivors with PTSD, trauma survivors with no PTSD and non-trauma-exposed control participants (N = 49) provided autobiographical memories of events that they believe shaped who they are. Participants also provided details about their major personal goals. RESULTS Participants with PTSD reported more self-defining memories that were trauma-related, negative valence and from adult years than non-PTSD and control participants. Further, retrieval of trauma-related self-defining memories was strongly associated with reporting personal goals that were related to traumatic experiences. CONCLUSIONS These findings are discussed in terms of the proposition that trauma survivors' current concerns may direct retrieval of trauma-related memories.
Phase I study of fludarabine plus cyclophosphamide in patients with previously untreated low-grade lymphoma: results and and long-term follow-up--a report from the Eastern Cooperative Oncology Group.

PURPOSE To determine the toxicity and recommended phase II doses of the combination of fludarabine plus cyclophosphamide in chemotherapy-naive patients with low-grade lymphoma. PATIENTS AND METHODS Previously untreated patients with low-grade lymphoma were entered onto dosing cohorts of four patients each. The cyclophosphamide dose, given on day 1, was increased from 600 to 1, 000 mg/m(2). Fludarabine 20 mg/m(2) was administered on days 1 through 5. The first eight patients were treated every 21 days; later patients were treated every 28 days. Prophylactic antibiotics were required. RESULTS Prolonged cytopenia and pulmonary toxicity each occurred in three of eight patients treated every 3 weeks. The 19 patients treated every 28 days, who were given granulocyte colony-stimulating factor as indicated, did not have undue nonhematologic toxicity. Dose-limiting toxicity was hematologic. At the recommended phase II/III dose (cyclophosphamide 1,000 mg/m(2)), grade 4 neutropenia was observed in 17% of all cycles and 31% of first cycles. Grade 3 or 4 thrombocytopenia was seen in only 1% of all cycles. The median number of cycles per patient was six (range, two to 11) for all patients enrolled. The response rate was 100% of 27 patients entered; 89% achieved a complete and 11% a partial response. Nineteen of 22 patients with bone marrow involvement had clearing of the marrow. Median duration of follow-up was more than 5 years; median overall and disease-free survival times have not been reached. Kaplan-Meier estimated 5-year overall survival and disease-free survival rates were 66% and 53%, respectively. CONCLUSION The recommended dosing for this combination in patients with previously untreated low-grade lymphoma is cyclophosphamide 1, 000 mg/m(2) day 1 and fludarabine 20 mg/m(2) days 1 through 5. The regimen has a high level of activity, with prolonged complete remissions providing 5-year overall and disease-free survival rates as high as those reported for other therapeutic approaches in untreated patients.
Identification and characterization of HIV‐specific RNase H by monoclonal antibody.

Human immune deficiency virus (HIV) replicates by conversion of the RNA genome into the double‐stranded DNA provirus. The reverse transcriptase is not the only enzymatic function crucial in DNA‐provirus synthesis. A viral‐coded RNase H activity which specifically degrades RNA in RNA‐DNA hybrids has been shown to be essential as well. Here we demonstrate that the HIV‐reverse transcriptase which consists of a two‐polypeptide complex, p66 and p51, copurifies with an RNase H activity which exhibits properties of a processive exonuclease. Only the p66 molecule, not p51, is active as polymerase as evidenced by activated gel analysis. p66 exhibits RNase H activity when precipitated as immune complex by a monoclonal antibody raised against a bacterially expressed carboxy‐terminal portion of p66. The monoclonal antibody which does not interfere with enzyme activity also precipitates a second population of molecules with RNase H activity which is of low mol. wt, p15. This RNase H appears therefore to be derived from the carboxy terminus of p66 during processing to the p51 polypeptide. It exhibits low template‐binding ability and is of a non‐processing mode of action which may be due to the absence of the reverse transcriptase domain. These results lend experimental support to the hypothesis that the RNase H gene maps at the carboxy terminus of the reverse transcriptase. Since both RNase H populations are virus‐coded they may be essential for retrovirus replication in general and useful targets for chemotherapeutic agents.
Endovascular implantation of covered stents in the extracranial carotid and vertebral arteries: Case series and review of the literature

BACKGROUND Covered stents are used endovascularly to seal arterial wall defects while preserving vessel patency. This report describes our experience with the use of covered stents to treat cervical pathology, and a review of the literature in regards to this topic is presented. CASE DESCRIPTION Two patients presenting with the carotid blowout syndrome and one patient with a vertebrojugular fistula were treated with covered stents. This allowed for preservation of the vessel and was a treatment alternative to cerebral bypass. CONCLUSION Covered stents provide a viable means of preserving the cervical vessels in selected patients; however, long-term follow-up is necessary to determine stent patency and permanency of hemostasis.
Endothelin B Receptor-Mediated Regulation of Endothelin-1 Content and Release in Cultured Porcine Aorta Endothelial Cell

Several cardiovascular diseases are associated with an increase in circulating levels of endothelin-1 (ET-1). Little is known about the consequences of this increase on endothelial cell responses with respect to ET-1 production and regulation. Confluent, passage 1, cultured porcine aorta endothelial cells were exposed to exogenous ET-1 (0.1 &mgr;M) for 24 h. BQ788 (1 &mgr;M, ETB receptor antagonist) but not BQ123 (1 &mgr;M, ETA receptor antagonist) significantly (p < 0.05) reduced 125I-ET-1 uptake. The effects of BQ788 were mimicked by dansylcadaverine (0.5 m M) but not nystatin (50 &mgr;g/ml). Immunoreactive ET-1 endothelial cell content doubled (p < 0.05) after 24 h of exogenous ET-1 treatment. Bosentan (10 &mgr;M, dual ETA/B receptor antagonist) reduced (p < 0.05) immunoreactive ET-1 content in control cells. Bosentan prevented exogenous ET-1-induced endothelial cell ET-1 loading, suggesting that exogenous ET-1 is partly recycled. PreproET-1 mRNA levels were reduced (p < 0.05) by exogenous ET-1 after 24 h, an effect blocked by BQ788 and bosentan. When used alone, both receptor antagonists increased mRNA levels. The results of this study suggest that part of ET-1 is recycled through ETB receptors and subsequently released to contribute to constitutive ET-1 overflow. ET-1 exerts a negative feedback on ET-1 gene transcription, which is dependent on ETB receptor activation and internalization of the complex ET-1/ETB receptor. The maintenance of this negative regulatory loop of ET-1 production may be essential for the normal endothelial physiology.
Incidence, prevalence and mortality of anorexia nervosa and other eating disorders

Purpose of review The purpose of this review is to evaluate the recent literature on the incidence and prevalence of and mortality associated with eating disorders. Recent findings General-practice studies show that the overall incidence rates of anorexia nervosa remained stable during the 1990s, compared with the 1980s. Some evidence suggests that the occurrence of bulimia nervosa is decreasing. Anorexia nervosa is a common disorder among young white females, but is extremely rare among black females. Recent studies confirm previous findings of the high mortality rate within the anorexia nervosa population. Summary The incidence of anorexia nervosa is around eight per 100 000 persons per year. An upward trend has been observed in the incidence of anorexia nervosa in the past century till the 1970s. The most substantial increase was among females aged 15–24 years, for whom a significant increase was observed from 1935 to 1999. The average prevalence rates for anorexia nervosa and bulimia nervosa among young females are 0.3 and 1%, respectively. Only a minority of people with eating disorders, especially with bulimia nervosa, are treated in mental healthcare.