Fertility trends in Bangladesh since 1951.
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This Bulletin examines the evidence that the world's fertility has declined in recent years, the factors that appear to have accounted for the decline, and the implications for fertility and population growth rates to the end of the century. On the basis of a compilation of estimates available for all nations of the world, the authors derive estimates which indicate that the world's total fertility rate dropped from 4.6 to 4.1 births per woman between 1968 and 1975, thanks largely to an earlier and more rapid and universal decline in the fertility of less developed countries (LDCs) than had been anticipated. Statistical analysis of available data suggests that the socioeconomic progress made by LDCs in this period was not great enough to account for more than a proportion of the fertility decline and that organized family planning programs were a major contributing factor. The authors' projections, which are compared to similar projections from the World Bank, the United Nations, and the U.S. Bureau of the Census, indicate that, by the year 2000, less than 1/5 of the world's population will be in the "red danger" circle of explosive population growth (2.1% or more annually); most LDCs will be in a phase of fertility decline; and many of them -- along with most now developed countries -- will be at or near replacement level of fertility. The authors warn that "our optimistic prediction is premised upon a big IF -- if (organized) family planning (in LDCs) continues. It remains imperative that all of the developed nations of the world continue their contribution to this program undiminished."
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We previously demonstrated the transmission of murine cytomegalovirus to syngeneic mice and preformed monolayers of mouse embryo fibroblasts with plastic-adherent peritoneal exudate cells from infected mice as a source of macrophages. In the present studies we compared this standard feeder layer method with a reverse feeder layer method in which the adhering peritoneal exudate cells remained attached to plastic and to which were added mouse embryo fibroblasts. Recovery of virus from the adherent peritoneal exudate cells of infected mice was achieved with both methods. Whereas the standard method achieved greater accuracy and usually recovered more virus, the reverse method appeared to recover virus more frequently and required fewer cells to perform the assay. Furthermore, the reverse method demonstrated the survival of murine cytomegalovirus in adhering cells after culture periods of up to 2 weeks.
UV gamma radiation-induced reversion to nar+ in a nar1-m nir1-1 strain of Ustilago maydis was found to occur under nongrowth conditions by performing the in vivo assay for functional nitrate reductase described by Resnick and Holliday (1971) who previously demonstrated that nonviable cells may still synthesize normal or near-normal levels of activity. Reversion frequencies of a signle gamma-irradiated culture were estimated in two cell populations by different methods: (A) among surviving clones after plating, and (B) among all cells (viable and nonviable) in suspension in the absence of postirradiation cell division. At gamma doses (300, 500 krad) corresponding to considerable cell killing (35%, 2% survival), reversion frequency by either method was the same. This supports the conclusion that mutation induction by gamma rays and its expression occur in nonviable cells with the same frequency as among survivors. If an error-prone repair system is assumed to be responsible for the observed gamma revertibility, then it is argued that this process is constituitive rather than inducible and that it is recombination-independent.
The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.
OBJECTIVES: To determine whether nucleophosmin/B23 mRNA expression in bladder carcinoma predicts recurrence, progression, and survival. METHODS: Real-time reverse transcriptase-polymerase chain reaction was performed on 50 fresh cancer specimens. The change in the cycle of threshold (Ct)was the difference in the Ct values derived from the nucleophosmin/B23 gene assayed and the 18S ribosomal RNA control [Ct (18S)-Ct (nucleophosmin/B23)]. RESULTS: Fifty patients diagnosed with bladder cancer were followed up postoperatively for a median of 24 months. Overexpression of nucleophosmin/B23 mRNA was observed in 37.1% of patients with Stage pT1 and 73.3% of those with pT2-T4 disease. Nucleophosmin/B23 overexpression was not associated with tumor grade (P = 0.163) but was associated with bladder cancer recurrence (68.2%) and progression (88.9%) when adjusted for the effects of clinical stage. Multivariate analysis revealed that the overall tumor stage and nucleophosmin/B23 mRNA overexpression were important prognostic indicators for bladder carcinoma (P <0.05). Patients with nucleophosmin/B23 mRNA overexpression were at a significantly greater risk of disease recurrence and progression than those with low expression of nucleophosmin/B23 mRNA. CONCLUSIONS: Overexpression of nucleophosmin/B23 mRNA was independently associated with bladder cancer recurrence and progression. In patients with muscular invasion disease, overexpression of nucleophosmin/B23 mRNA was associated with the greatest risk of recurrence and progression, suggesting a potential rationale for early definitive therapy in these patients.
Despite advances made in the care of infants with congenital diaphragmatic hernia (CDH), survival remains poor. New therapy, such as extracorporeal membrane oxygenation (ECMO), is controversial but may improve survival. Thirty-two newborns with CDH were treated. Thirteen infants were treated with jugular vein-carotid artery ECMO after CDH repair elsewhere; six (46%) survived. Three of the remaining 19 were moribund shortly after birth and first received ECMO, then underwent repair; two (67%) survived. The other 16 underwent CDH repair; 8 of 9 (89%) recovered with conventional therapy, and 4 of 7 (57%) survived when ECMO was used after conventional therapy failed. Overall survival was 63%. Parameters with which physicians may attempt to predict survival or the need for ECMO after repair--such as A-aDO2, ventilatory index versus PCO2, presence of a "honeymoon period" (PaO2 greater than 100 mm Hg after repair), or oxygenation index--were unreliable. ECMO can improve survival in infants with CDH, probably through reversal of pulmonary hypertension. Presently available methods of predicting survival after CDH repair with or without ECMO are not accurate, and thus no infant should be excluded from repair or ECMO support.
OBJECTIVE: To investigate the survival mechanisms of the reverse-flow flap. METHODS: A skin flap measuring 8.0 cm x 2.5 cm based on the left deep circumflex iliac vessel (DCIV) was designed and elevated on the rat's dorsum with 4.0 cm of it's length crossing the midline. The flap was served as the reverse-flow flap model. The survival area, the dynamic microcirculation including flow direction, microvessel number, caliber, pressure and vasculature were assessed respectively at 6 hour, 24 hour, 48 hour, 72 hour, 7 day and 14 day after operation. RESULTS: The average gradient of perfusion pressure was 0 kPa before operation and was 4.9 KPa postoperatively between the proximal and the distal site of the flap. By anastomosis of bilateral DCIV, the blood flow run in a reversed pattern in the region distal to the midline. No venous valves were observed. Distal congestion developed in 20% of the flaps within 72 h. After that, the number and caliber of venous anastomosis increased with pressure dropping in the midline region. The axial vessels extended its branches progressively along the dilated anastomotic rami. As a result, the vasculature of the flap became similar to that of the conventional axial flap by the 14th day. With these changes, flap congestion was alleviated gradually and subsided within 7 days. All the flaps survived completely. CONCLUSIONS: Anastomosis connecting the two axial vessels is the circulation route of the reverse-flow flap. By the gradient pressure between the proximal and distal region, blood is driven reversely. Within 72 h, the distal part is susceptible to congestion. In this period, increasing number and caliber and decreasing pressure of anastomosis is important mechanism to support the circulation. After that, the new vasculature similar to the conventional axial flap provides the flap with reliable and permanent blood supply.
BACKGROUND AND OBJECTIVES: The cyclin D1 gene, CCND1, is alternatively spliced to produce transcripts [a] and [b] in a manner apparently modulated by a polymorphism (A/G) at codon 241. Studies have indicated that the polymorphism can affect the prognosis of patients with different types of solid tumors. This study aimed to determine the relative levels of transcripts [a] and [b] in normal and malignant peripheral blood mononuclear cells (PBMNC), and to investigate whether these were influenced by the polymorphism. The impact of the polymorphism on the survival of a group of mantle cell lymphoma (MCL) patients was also to be studied. DESIGN AND METHODS: The polymorphism was genotyped, using restriction fragment length polymorphism analysis, in 74 patients (42 MCL, 19 chronic lymphocytic leukemia, 13 normal controls) and the relative level of transcripts [a] and [b] determined using a competitive reverse transcription polymerase chain reaction method. Kaplan-Meier survival curves and the log-rank test were used to analyze the survival data. RESULTS: Of the cases genotyped, 39 were heterozygous for the polymorphism, 24 homozygous G and 11 homozygous A. Both transcripts [a] and [b] were expressed in normal PBMNC and malignant lymphocytes, with the polymorphism affecting their relative levels. Neither the predominant transcript, nor genotype, significantly influenced survival of the MCL patients studied. INTERPRETATION AND CONCLUSIONS: Contrary to previous reports, patients who were homozygous A at the polymorphism produced more transcript [a] whilst homozygous G patients had more transcript [b]. In the small cohort studied, the polymorphism did not appear to affect the prognosis of the patients with MCL.
The issue of euthanasia is unique to veterinary clinical studies evaluating survival time. The decision to euthanize an animal is based on several factors including the health of the animal but also age and cost of treatment. The literature shows inconsistent methods used to account for observations from euthanized animals. Also, over 50% and up to 100% of animals in many studies have been euthanized. Our study illustrates the effects of different methods of accounting for observations from euthanized animals in survival analysis. Three data sets with different proportions of outcomes (alive, lost-to-follow-up, dead due to disease of interest, dead due to other disease, euthanized due to disease of interest, euthanized due to other disease) were used. Each data set was stratified according to treatment or a group characteristic (e.g. tumor type). Our methods for accounting for observations from euthanized animals were established from methods used in the literature and included right-censoring. Kaplan-Meier product-limit survival-function estimation was performed on each data set. Different methods resulted in inconsistent conclusions of significant differences between strata. At times, the ranking of the estimates of median survival time for strata was reversed. Right-censoring and use of Kaplan-Meier methods is inappropriate to evaluate observations from euthanized animals because censoring of such observations is informative. The current methods used by clinical investigators are inadequate to measure survival time reliably.
OBJECTIVE: To explore the correlation between expression of surviving gene in acute leukemic cells and its clinical effects. METHODS: By using semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) technique, surviving gene expression in 50 previously untreated acute leukemia (AL) patients was analysed. The apoptosis of primary leukemia cells cultured in vitro was assayed with terminal deoxyribonucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL). RESULTS: Surviving gene expression levels in cells of AL patients at diagnosis were significantly higher than that in normal bone marrow mononuclear cells (MNCs) (82.0% vs 33.3%, P < 0.05). The expression level was higher in ALL cells than in ANLL cells (89.5% vs 75.0%). Among 22 cases of ANLL, bone marrow remission (BMR) rate was higher in surviving gene negative expression cells from patients accepted a course of chemotherapy than in positive expression cells (83.3% vs 25.0%, P = 0.023). Among 13 ANLL patients received a course of HA regimen chemotherapy, the BMR was higher in patients surviving mRNA negative expression cells than in positive cells (100.0% vs 27.3%). Patients with surviving/beta-actin ratio>0.6 attained lower BMR. CONCLUSION: Higher expression level of surviving mRNA in AL cells may be one of the reasons that leukemic cells are insensitive to chemotherapy.
The differential display reverse transcription polymerase chain reaction method was used to detect alterations in gene expression in the superior colliculus after optic nerve crush in adult rats. One of the most prominent changes observed was the selective induction of R-esp1, a homologue of the Drosophila enhancer of split locus (Groucho). Therefore, we studied the influence of R-esp1 on nerve growth factor (NGF)-induced cell survival of PC12 cells. Overexpression of R-esp1 promotes cell survival even in the absence of NGF and, conversely, it is reduced by antisense-mediated inhibition of R-esp1 expression. In conclusion, we propose a novel model in which R-esp1 protein mediates the NGF-signaling pathway.
OBJECTIVE: To study the expression of surviving and its relationship with expression of P53, c-myc, k-ras in non-small-cell lung cancer (NSCLC). METHODS: Expression of the surviving mRNA was evaluated by reverse transcriptase polymerase chain reaction (RT-PCR) in 76 NSCLC tumor samples, 20 benign phymatoid lesion and 21 adjacent normal lung tissue samples. Immunohistochemical assay was to detect the expression of P53, c-myc, k-ras proteins. RESULTS: Expression of surviving gene was detected in a significantly greater proportion of NSCLC (61%) than phymatoid lesion (30%) and adjacent normal lung tissue (19%) (P < 0.001). There was no relationship between surviving gene expression and histologic subtype, differentiation, TNM stages, or lymph node metastases. The expression of surviving gene correlated with P53 or c-myc expression, but not k-ras expression. CONCLUSION: (1) The up-regulation expression of surviving gene in NSCLC suggested that surviving may play a role in the pathway of carcinogenesis and surviving may be identified as a potential therapeutic target in NSCLC. (2) surviving, de-activation of antioncogene P53 and up-regulation of oncogene c-myc might play synergetic roles in the process of carcinogenesis of NSCLC. But surviving and k-ras may be independently involved in the pathogenesis of lung cancer.
Coale's robust birth rate estimate, obtained by adjusting the birth rate of a stable population selected by matching the observed population of both sexes under the age of 15, C(15), and the probability of survival of births to age 5, l5, is shown to be equal to the birth rate obtainable by reverse surviving the proportion under the age of 15. Variations of matching the criterion of Coale's method to the rate of increase and C(15) or l5 are shown to lead to variants of Coale's birth rate estimate that are also nearly equal to the reverse survival birth rate based on C(15). A simplified birth rate estimate that does not require reference to models of life tables or stable populations is suggested and some of its applications are illustrated.
In the present work we analyse some properties of the pso4-1 (= xs9) mutant of the yeast Saccharomyces cerevisiae, which is blocked in both reverse mutation and recombination. We have applied the "apparent survival test" as a method to characterize putative inducible error-prone repair activities related to the PSO4 gene. As the mutagenic agent we have used bleomycin, which is an antitumour radiomimetic antibiotic. Survival, reverse mutation yield, and reverse mutation frequency were determined as a function of bleomycin concentrations (1-60 micrograms/ml) in the logarithmic phase of growth. It is shown that the PSO4 gene product is poorly involved in bleomycin sensitivity and that reverse mutation induced by this mutagen is dramatically reduced in the pso4-1 lys2 mutant strain, as compared with the isogenic SC7K (lys2) strain. M(x) functions exhibit linear-quadratic courses for both the SC7K (lys2) and the pso4-1 lys2 strains. The apparent survival functions display "humps" in both strains, corresponding to the resistant components of the survival functions. These facts suggest that the mutagenicity of bleomycin depends on at least one inducible error-prone repair pathway and that the PSO4 gene product could act as a mutation triggering factor.