After Birth Ebook
Getting Back Into Shape After The Pregnancy
Once your pregnancy is over and done with, your baby is happily in your arms, and youre headed back home from the hospital, youll begin to realize that things have only just begun. Over the next few days, weeks, and months, youre going to increasingly notice that your entire life has changed in more ways than you could ever imagine.
Production, and fertile females and vasectomized males for oviduct or uterine transfer. Fertile females are either superovulated at a critical age and mated to studs, so as to obtain ample numbers of one-cell stage zygotes for pronuclear injection (see Subheadings 3.1. and 3.1.1.), or mated naturally to studs for the production and isolation of blastocysts into which genetically modified ES cells are introduced. Normal females are mated to vasectomized males to produce pseudopregnant females, which will foster transplanted, micromanipulated embryos after birth (see Subheadings 3.1. and 3.1.2.). Procedures and requirements concerning animals used for fertilized oocyte production and for oviduct transfer and guidelines for equipment and microsurgical techniques are described in excellent detail in Manipulating the Mouse Embryo by Hogan et al. (1) and in the video guide Transgenic Techniques in Mice by Pedersen and Rossant (2). In addition, these media provide comprehensive information...
Shortly after birth, a 33-week gestation infant develops tachypnea, nasal flaring, and grunting and requires intubation. Chest radiograph show a hazy, ground-glass appearance of the lungs. Presentation. Clinical manifestations occur fairly soon after birth. These include signs of respiratory distress tachypnea, nasal flaring, retractions, cyanosis, and grunting. Apnea may occur as the infant tires. The patient's condition peaks at about the third day, and improvement is signaled by a spontaneous diuresis.
Within a few months after birth, an infant makes anti-A and or anti-B, if lacking those antigens on its RBCs. Such antibodies are termed naturally occurring since they have no apparent antigenic stimulus. Experiments in chicks have shown that these antibodies probably develop as a result of exposure to bacterial antigens, closely related chemically to blood group antigens (for example, Escherichia coli has an antigen on its membrane closely resembling human B antigen). Naturally occurring antibodies to antigens other than ABO are also often encountered, particularly in the I, Lewis, P, and MN systems. These antibodies are usually lgM and react better at lower temperatures.
Another, instructive, example of a two-level data structure for which a multilevel model provides a powerful tool, is that of repeated measures data. If we measure the weight of a sample of babies after birth at successive times then the repeated occasion of measurement becomes the lowest level unit of a two-level hierarchy where the individual baby is the level-2 unit. In this case model (3) would provide a simple description with xiij being time or age. In practice linear growth will be an inadequate description and we would wish to fit at least a (spline) polynomial function, or perhaps a non-linear function where several coefficients varied randomly across individual babies, that is each baby has its own growth pattern. We shall return to this example in more detail later, but for now note that an important feature of such a characterization is that it makes no particular requirements for every baby to be measured at the same time points or for the time points to be equally spaced.
In the FSHp knockout mouse (47) or in the hypogonadal (hpg) mouse, in which a naturally occurring mutation in the gonadotropin-releasing-hormone-gene markedly reduces the synthesis of both FSH and LH from the pituitary (48), preantral follicle growth proceeds normally, confirming the gonadotropin-inde-pendence of this stage of development. However, several mouse models have clearly demonstrated that signaling from the granulosa cells to the oocyte, as well as from the oocyte to the granulosa cells, is necessary for preantral follicle growth and does not require extragonadal input (Table 4B). For example, intrafollicular signaling of kit ligand from granulosa cells to c-kit on the oocyte is critical for preantral follicle development. All mouse oocytes express c-kit, whereas granulosa cells of one-layered growing follicles, preantral follicles, and the outer (mural) layers of preovulatory follicles express kit ligand (49,50). Two hypomorphic kit ligand...
The RXRp gene is expressed mostly in Sertoli cells. Targeted mutation of the RXRp gene (46) reveals that approx 50 of RXRp- - mutants die in utero or shortly after birth, for unknown reasons. Homozygote females are fertile, but RXRp-deficient males are sterile. Histological analysis of the epididymis of males RXRp- - mice shows low levels of spermatozoa, most of which (95 ) remains immotile. A majority of spermatozoa from RXRp-deficient mice exhibit a coiling of the tail, and 30 have an acrosome that is indented or partially detached from the nuclear envelope. It has been suggested that the high frequency of such defects in mutant spermatozoa results from an impaired attachment of the acrosomal membrane to the nucleus. The diameter of the seminiferous tubules is normal, and the proportion and length of stages of the cycle is apparently normal. However, some of the late spermatids fail to align at the luminar side of the tubules. Moreover, remnants of spermatid heads are located inside...
Bcl2 null-mutant mice display severe kidney defects. At birth, the kidneys are considerably smaller than those of wild-type littermates, and these eventually become grossly enlarged and cystic (136,137). These defects result from problems during kidney development. Analysis of kidneys in Bcl2 homozygous mutant embryos using TUNEL staining during early stages of nephrogenesis revealed high levels of apoptosis of mesenchymal cells and a significant decrease in the number of nephrons. Prior to birth, the kidneys show irregular branching and convolution of the ureteric buds (138). At birth, the kidneys are reduced in size and usually become cystic within the first 2 wk after birth (136,139). Most Bcl2 mutants on a congenic C57BL 6 genetic background die before 3 wk of age as a result of the kidney defect.
3 wk of age, they develop a severe wasting syndrome, which is accompanied by a pronounced multifocal inflammatory response and tissue necrosis, resulting in multisystem organ failure and death (41,42). To overcome this problem, the animals were wounded at d 10 after birth.
Neonates are highly susceptible to infectious diseases (Kovarik and Siegrist, 1998). In clinical trials in newborn babies, VA supplementation on days 1 and 2 after birth reduced neonatal mortality in the first 2 months of life, especially in infants of low birth weight (Rahmathullah et al., 2003). The VA status, in terms of liver VA reserves and plasma retinol of newborns, even full-term infants of well-nourished mothers, is low as compared to that of older children and adults. Thus, neonates might well be considered physiologically VA deficient, or as of marginal VA status (Ross, 2005). Neonates are known to respond poorly to conventional vaccines due to immaturity of the immune system (Siegrist, 2001), and this has stimulated a search for better adjuvants for neonatal vaccines. As indicated in Table I, the pattern of immune deficiency reported for neonates (Marshall-Clarke et al., 2000) resembles the pattern observed in VA-deficient adult rats and mice (Ross, 1996a), with low...
Mice homozygous for the targeted deletion of the c ebpa gene died within 8 hours after birth due to hypoglycemia (Flodby et al., 1996 Wang et al., 1995). These mutant mice lack hepatic glycogen storage. C ebpa null mice also showed defects in the control of hepatic growth and lung development (Flodby et al., 1996). Specifically, the amount of c-myc, c-jun, -actin mRNA and proliferating cell nuclear antigen cyclin protein in the liver of mutant mice were increased, suggesting an active proliferative state of the liver. This demonstrates the importance of C EBPa in control of cell proliferation, which was
The risk of HIV transmission from a mother to her child is between about 15 and 40 per cent, the higher levels of risk being associated with breast-feeding. This risk can be greatly reduced by anti-retroviral drug treatment of the woman before and after birth. In many countries, including the UK, treatment of HIV-infected women has resulted in a decline in the number of HIVpositive children. Although drug treatment reduces the risk of virus transmission to children, it does not cure infected individuals.
And titers of these antibodies rise in some infants of lepro-matous mothers over 3 to 24 months after birth.61-62 Leprosy in infants under 1 year of age is well known. In one series of 49 such infants, the youngest patient was 2 months old at diagnosis,21 and the mother had clinical leprosy in only about half of these infants. This implies that during gestation the mother had a transient subclinical M. leprae bacteremia.
To more fully understand the role of activins in regulating reproduction, both the activin PA- and pB-subunits have been the target of homologous recombination in mice. Unfortunately, mice deficient in activin PA died within 24 h after birth, a likely result of craniofacial defects (169). In contrast, mice deficient in activin PB are viable, although several suffered from a lack of eyelid fusion at birth (170). The reproductive capacity of adult female mice that lack activin PB is greatly reduced, although this is apparently not caused by defects in the ovary. Indeed, although these mice have a delay in parturition, normal litter sizes are found. However, the pups soon die because the activin-pB-deficient mothers have a defect in milk let-down (170). FSH levels have been measured in male and female activin-pB-deficient animals. Both have a slight increase ( 20 ) in serum FSH levels (170). Removal of the activin-bB-subunit causes the loss of two forms of activin (B and AB) and one form...
Infants with classic phenylketonuria (PKU) are normal at birth but if untreated show slow development, severe mental retardation, autistic symptoms, and loss of motor control. Children may have pale skin and white-blonde hair. The neurotoxic effects relate to high levels of phenylalanine and not to the phenylketones from which the name of the disease derives. Infants are routinely screened a few days after birth for blood phenylalanine level. Treatment consists of a life-long semisynthetic diet restricted in phenylalanine (small quantities are necessary because it is an essential amino acid). Aspartame (N- a spa rtyl-phenylalanine methyl ester), which is widely used as an artificial sweetener, must be strictly avoided by phenylketonurics.
In comparison to postnatal mammary gland development, very few knockout or transgenic mice have been reported to have defects in embryonic development. Some of the genes implicated in embryonic mammary development are presented in Fig. 4. Presumably, disruption of genes that mediate epithelial-mesenchymal interactions would result in embryonic defects. Two such mouse models have been reported, p63 - - (45,46) and lymphoid-enhancer factor (Lef)-1 - - (47) mice. p63, a homolog of the tumor-suppressor gene p53 , is expressed in ectodermally-derived tissues of the embryo (45). Mice lacking p63 die shortly after birth, most likely a result of dehydration caused by poorly differentiated skin. Newborn mice do not have limbs (or have truncated limbs), and have no hair follicles or teeth. No mammary buds form in p63 - - mice. Interestingly, the p63 - - mice fail to induce expression of another gene that has been implicated in embryonic development, Lef-1 (45).
This may not be the case for genes of major relevance to the eye, but expressed elsewhere. Species-specific effects may also be relevant. A case in point is ornithine aminotransferase, mutations in the human gene for which cause gyrate atrophy of the retina (10), but no apparent systemic effects. Because of differences between human and mouse amino acid metabolism, mice with targeted disruption of the OAT gene die shortly after birth unless supplemented with L-arginine (8). Transcription factors important to eye development, but also acting elsewhere may also fall in this group. Aside from such information on function or possible function, the availability of gene and or protein specific reagents is also highly useful. For example, access to cDNA sequence and specific antibodies. The former to derive the genomic sequence of the gene and the latter to assay for disruption of expression.
Unlike the pB-null mutants, pA-deficient mice are not viable and die within the first 24 h after birth (42). These animals fail to develop whiskers and show craniofacial defects, including a lack of upper incisors and lower molars. Many animals also show cleft or incomplete palate formation, and therefore fail to suckle after birth. Mice completely devoid of activins and inhibins have also been generated by interbreeding PA- and PB-null heterozygotes and then interbreeding the compound heterozygous offspring to produce compound homozygotes lacking both PA and PB (42). Not surprisingly, the double mutant mice are not viable and die shortly after birth probably because of cran-iofacial defects similar to those observed in PA mutants. The defects appear to represent an additivity of the individual subunit mutants, including an eyelid-fusion defect, lack of whiskers, palate defects, and tooth defects. These data suggest that within the individual PA or PB mutant mice, there is little or...
The Apgar scoring system was devised by an American anesthesiologist to assess the physical condition of a newborn baby. This method assesses various aspects of the newborn's health at one minute after birth and at five minutes after birth. Evaluated are the infant's color (appearance), respiratory effort, muscle tone, reflex irritability (grimace in response to slap), and heart rate (pulse). Each feature is given a score of from 0 to 2. The numbers are added to give a total possible score of 10 (2 points in each of the 5 categories).
It is not surprising that major alterations in the metabolic milieu in which a fetus grows can markedly affect its development. Cross-fostering studies in which pups are placed with surrogate dams shortly after birth suggest that prenatal factors account for 61 to 96 of the variance in body weight gain in male and 35 to 92 in female offspring (68). Offspring of dams fed a high-fat diet during gestation became more obese than those whose dams were fed a low-fat diet, even if the high-fat offspring were fostered with dams on a low-fat diet throughout lactation (49,69). As suggested by human epidemio-logical studies, malnutrition during gestation can also result in obese offspring. To model these studies, Jones and colleagues (70,71) restricted the caloric intake of dams by up to 50 during the first two trimesters of pregnancy. Male (but not female) offspring of these calorically restricted dams became hyperphagic, gained more weight beginning at weaning (71), and became obese as adults...
In female embryos, once PGCs have entered the fetal ovary, they complete mitotic divisions and enter meiosis. They eventually arrest meiosis at Prophase I, and each germ cell will become invested by a layer of flattened somatic cells that are the precursors of the follicle or granulosa cells. Therefore, in the ovary, just as in the testis, germ-cell survival, growth, and differentiation is controlled by the complex interaction between the germ cells and the surrounding somatic cells (62,63) (see Chapter 4). The structure described here, which contains a germ cell surrounded by follicle cells, is called a primordial follicle. Within a few days of birth, the ovary is filled with oocytes within these primordial follicles. But as the oocyte grows in size, the follicle cells differentiate into cuboidal cells. The appearance of these changes represents the hallmark of the next stage of follicle development, the primary follicle. About 2 wk after birth, secondary follicles containing at...
To control bleeding after childbirth. This is the most important use of these medicines. In a case of heavy bleeding after the placenta has come out, inject one 0.2 mg. ampule (or give two 0.2 mg. tablets) of ergonovine or ergometrine maleate (Ergotrate, etc., p. 391) once every hour for 3 hours or until the bleeding is under control. After the bleeding is controlled, continue giving 1 ampule (or 1 pill) every 4 hours for 24 hours. If there is no ergonovine or if heavy bleeding starts before the placenta comes out, inject oxytocin 2. To help prevent heavy bleeding after birth. A woman who has suffered from heavy bleeding after previous births can be given 1 ampule (or 2 pills) of ergonovine immediately after the placenta comes out, and every 4 hours for the next 24 hours.
Many viruses can be spread vertically. Congenital infection of the fetus in utero or during passage of the infant through the birth canal occurs with viruses such as HIV, cytomegalovirus (family Herpesviridae), and rubella virus (genus Rubivirus, family Togaviridae). Vertical transmission can also occur shortly after birth, by breast feeding for example. HTLV I (family Retroviridae), which causes leukemia in humans, is such a virus.
As summarized in Table 1, all of the female homozygous mutants possessed a uterus with oviducts and ovaries that were morphologically normal. In addition, all of the females were fertile. Therefore, although MIS is expressed in a regulated manner in the ovary of wild-type mice after birth, there is apparently no requirement for MIS expression for normal ovarian function. One possible explanation is that related molecules proteins expressed in granulosa cells may provide redundant or compensatory functions in the absence of MIS. Candidates for such related molecules include activins and inhibins.
Ocular toxoplasmosis may be acquired by infection after birth, but in a substantial percentage of cases the etiology of human ocular toxoplasmosis seems to be connected with in utero infection of the fetus via a mother whose primary infection was acquired during gestation (for review, see Holland, 2003). Consequently, ocular toxoplasmo-sis may be considered to be on the one hand a postnatally acquired disease, and on the other a late manifestation of congenital toxoplasmosis. However, it seems to be practical for a description of animal models to produce an ocular disease mainly by a primary infection of adults, although there have been efforts which have successfully established an ocular disease as a consequence of a transplacental Toxoplasma transmission (Hutchison et al., 1982 Lee et al., 1983 Hay et al., 1984 Dutton et al., 1986). In patients with underlying immunosuppres-sion or immune defects, such as with bone-marrow transplantation or HIV, toxoplasmic chorioretinitis is often...
These may result from something that went wrong with the development of the baby in the womb or from damage to the baby while he was being born. Examine the baby carefully immediately after birth. If he shows any of the following signs, something is probably seriously wrong with him
In the first 2 days of life, if a newborn baby's eyes get red, swell, and have a lot of pus in them, this is probably gonorrhea (p. 236). It must be treated at once to prevent the baby from going blind. If the eye infection begins between 1 and 3 weeks after birth, she may have chlamydia. The baby has picked up one or both of these diseases from the mother at birth.
Antibody production does not normally begin until after birth. Newborns have their mother's IgG antibodies, but these are passively received through placental transfer, not actively produced. Anti-A and anti-B production begins in the first few months of life, with titers rising for the first 5 or 6 years, and then remaining functionally the same until late in adult life. In very old people, levels of anti-A and anti-B are significantly lower than in young adults.
Timing of presentation depends on the drug, its half-life, and the last maternal dose. Signs include hyperactivity, irritability, fever, diarrhea, tremors jitters, high-pitched crying, sneezing, restlessness, vomiting, nasal stuffiness, poor feeding, seizures, and tachypnea. Heroin withdrawal usually presents within 48 hours after birth. Onset of symptoms for methadone withdrawal usually is several weeks (2-6), and there is higher risk for seizures. Phenobarbital withdrawal occurs at 1-2 weeks.
Cardiac hypertrophy occurs as an adaptive response to many forms of cardiac disease, including high blood pressure (hypertension), myocardial infarction, cardiac arrhythmias, genetic defects in cardiac contractile proteins, and endocrine disorders. Cardiac hypertrophy is characterized by an increase in myocyte cell size (in the absence of cell division) and by a number of qualitative and quantitative changes in gene expression. Many pathological stimuli induce the heart to undergo adaptive hypertrophic growth. Although the initial hypertrophic response may be beneficial, sustained hypertrophy often results in a transition to heart failure, which is a leading cause of mortality and morbidity worldwide, and is characterized by a progressive deterioration in cardiac function. Cardiac hypertrophy is generally associated with the expression of atrial natriuretic peptide (ANP) that is restricted to the atria shortly after birth, and is reexpressed in the ventricles following hemodynamic...
Developmental anomalies of teeth are marked deviations from the normal standards in color, contour, size, number, and degree of development of the teeth. Systemic as well as local factors may operate to produce these developmental disturbances. Such influences may begin before or after birth so that either deciduous or permanent teeth may be involved. Usually, it is the permanent teeth that are influenced and, in all instances, only those not completely formed at the time of the disturbance.
Owing to the high prevalence of the infection in the pre-vaccine era, its high transmissibility, and the fact that infected persons are contagious 24 to 48 hours before clinical signs occur, it is difficult to prevent infection by isolation. However, reverse isolation is recommended for hospitalized patients with varicella and for children or immunocompromised adults with herpes zoster. Patients with varicella should be bathed often to prevent staphylococcal and streptococcal superinfection. Immunocompromised children, neonates born to mothers who present with varicella during the week prior to and a few days after birth, and seronegative pregnant females should be treated with varicella-zoster immune globulin (VZIG) within 96 hours of exposure.145 VZIG, however, has no effect on the course of herpes zoster or on risk of reactivation.
Steroidogenic factor-1 (SF-1) is a transcription factor implicated in the expression of steroid hydroxylases (76,77). Homozygous SF-1 null mutants exhibit gonadal and adrenal agenesis, are phenotypically female (by appearance of external genitalia), and die shortly after birth because of adrenocortical insufficiency (78). However, animals treated with steroids are viable. These animals also exhibit pituitary and hypothalamic defects. In the pituitary, FSHp mRNA and FSH protein are barely detectable (as is the case for LHp and LH protein). The a-subunit of the gonadotropins is expressed, but at lower levels relative to controls, while expression of TSH, growth hormone, prolactin, and ACTH are normal (79). The downregulation of FSH (and LH) is interesting in light of the fact that SF-1 is expressed specifically within the gonadotrope cells of the pituitary.
Mycetoma is characterized by tumefaction and abundant draining sinus tracts (Fig. 11.3). Sometimes granulation tissue appears nodular (Fig. 11.4). Also there can be ulceration with meliceric crusting and scarring. The course is slow and inexorable without spontaneous regression, except in women after pregnancy. Symptoms are not important. Subcutaneous tissue, muscle, and bone may also be involved. Small bones of the foot and vertebrae may be destroyed. Large bones such as the tibia and femur seem resistant to severe involvement (Fig. 11.5). Mycetomas affecting the vertebrae can involve the spinal cord causing paraplegia. Mycetomas of the thorax can invade pleura and lung. There can be functional incapacity.
Gestational diabetes most often develops between the 24th and 28th week of pregnancy, occurs in 2-5 of pregnancies, and usually disappears after birth. Gestational diabetes is more common in older, obese, or diabetes-prone ethnic groups, and in those with a positive family history. Most (80-94 ) women with gestational diabetes will return to normal after delivery. Hispanic females and Native Americans are especially prone to developing diabetes after an episode of gestational hyperglycemia, with the occurrence rate being as high as 50 within 5 years of pregnancy termination. The other gestational diabetics will have a 30-40 chance of developing diabetes in 10-20 years.
Fetal circulation involves three shunts ductus venous, ductus arteriosus, and foramen ovale (Figure III-2-10). After birth, a number of changes occur in the circulatory system because of the cessation of placental blood flow and start of lung respiration (Table III-2-3). Changes After Birth
(B) After birth, higher blood oxygen concentration stimulates prostaglandin production, causing gradual closure of the ductus arteriosus. (C) After birth, clamping of the cord and increased pulmonary venous return cause increased left-sided heart pressures, which results in functional closure of the foramen ovale. A mother brings her 4-year-old girl with Down syndrome to the office because the child has a fever and a skin rash. The child takes no medications and has no significant medical history otlier than repair of a ventricular septal defect shortly after birth. The child is pale and somewhat lethargic compared with normal. The child's temperature is 102 F, pulse is 126 beats min, and respiratory rate is 22 min. Blood pressure is normal. The child has severe, exudative pharyngitis and widespread peteehiae. A complete blood count reveals the following
Vegetarians may be similar in weight to the general populace or weigh somewhat less.16 This is particularly true of vegans, who may weigh as much as 10-20 less than omnivores or LOVs.2,17 This may, in part, be due to dietary factors such as the higher intake of plant foods, which contain much more fiber and are usually less energy dense than animal food products, as well as the somewhat lower fat intake. Thus, some vegetarians may enter pregnancy at a lower weight for height and may need more careful monitoring of weight status. Birth weight among macrobiotic infants was positively associated with maternal weight gain in pregnancy, as it was in the recent study of LOVs.5,18
(3) Premature birth or neonatal separation. Premature babies, being smaller at birth, needing to be fed more often, and sleeping shorter periods of time, also place stress on a family unit. Some parents cannot cope with that stress. Also, if a newborn baby, premature or not, must stay in the hospital for a period of time after birth to overcome physical problems, proper bonding between the baby and the parents may not take place.
Matrix-Gla-protein (MGP) produced by chondrocytes and by smooth-muscle cells prevents mineralization of cartilage and blood vessels. MGP-deficient mice died a few weeks after birth from calcification of blood vessels (109). Histological examination of mutant mice demonstrated that mineralization also occurred throughout the growth plate, which preceded growth-plate closure. These results suggest that calcification of the cartilage extracellular matrix may explain the closure of the growth plate at the end of puberty. The function of the osteoblast is to form bone by producing matrix constituents, predominantly type I collagen. Mutations in the genes encoding type I collagen cause the congenital disease osteogenesis imperfecta (110), characterized by a low bone mass and fragile bones. In addition to collagen type I, osteoblasts also secrete a variety of noncollagenous proteins, such as osteopontin, bone sialoprotein, decorin, osteonectin, biglycan, and osteocalcin (bone gla-protein)....
A 25-year-old woman presents to the delivery room in labor. She has had no prenatal care. The female newborn weighs 4.5 pounds and has episodes of seizures shortly after birth. Irritability and hyper-tonicity are also noted. The most likely cause for these findings in the newborn is
The answer is a. (Behrman, 16 e, pp 519-521. McMillan, 3 e, pp 359-362. Rudolph, 20 e, pp 1168-1170, 1176-1180, 1203-1207.) The absence of a major blood group incompatibility and the finding of a normal reticulocyte count argue strongly in favor of a recent fetomaternal transfusion, probably at the time of delivery. A Betke-Kleihauer stain for fetal hemoglobin-containing red cells in the mother's blood would confirm the diagnosis. After birth, erythropoiesis ceases, and the progressive decline in hemoglobin values, reaching a nadir at 6 to 8 wk of age, has been termed physiologic anemia of infancy. Iron-deficiency anemia is common in the term infant between 9 and 24 mo of age, when the iron stores derived from circulating hemoglobin have been exhausted and an exogenous dietary source of iron has not been provided. The manifestations of sickle cell disease do not appear until 4 to 6 mo of life, coincident with the replacement of fetal hemoglobin with sickle hemoglobin.
You see a healthy 40-year-old multiparous patient for preconception counseling. She is extremely worried about her risk of having a baby with spina bifida. Five years ago, this patient delivered a baby with anencephaly who died shortly after birth. How would you counsel this woman regarding future pregnancies
To explore the roles of StAR in a system amenable to experimental manipulation, we used targeted gene disruption to create StAR knockout mice (6). At birth, StAR knockout mice were indistinguishable from wild-type littermates, with an equal ratio of genetic males and females, but all pups had female external genitalia. A subset ( 30-40 ) exhibited signs of respiratory distress and died within 24 h after birth the rest failed to grow normally and died within 2 wk after birth from adrenocortical insufficiency. Hormone assays revealed severe defects in adrenal steroids, and elevated ACTH levels consistent with a loss of negative feedback regulation at hypothalamic-pituitary levels. In contrast, gonadal hormones did not differ significantly from levels in wild-type litter-mates in the prepubertal state. Fig. 2. Histology of the adrenal gland and gonads from newborn wild-type (WT) and StAR knockout (KO) mice. Steroidogenic organs were isolated from WT and StAR KO mice 1-6 d after birth,...
In hypoplasia (figure 2-14), there is a lack of development or a defective development of the enamel of the tooth before its eruption. In deciduous teeth, enamel hypoplasia can be caused by a disturbance in the enamel formation before birth and, for some deciduous teeth, after birth. In permanent teeth, enamel hypoplasia can only be caused by some disturbance after birth since enamel formation of the permanent dentition begins at birth. Enamel prisms are deposited by the enamel organ in a definite pattern to form the crown of the tooth. A local disturbance may interfere with this process and result in defective development. The degree of the defect (hypoplasia) varies from mild, shallow depressions or grooves to extensive grooves or pits arranged in horizontal rows around the crown. These grooves or pits extend into the enamel as far as the dentinoenamel junction. The defect may be a lack of development of all or part of the enamel, leaving exposed dentin. Hypoplastic enamel and...
Hemangiomas may be present at birth, but most develop in the first few weeks after birth. These dynamic lesions can enlarge over a period of a few weeks. Hemangiomas are composed of proliferative vascular elements including capillaries and supportive dermal tissue they are soft, raised, and intensely red. If treated early by laser therapy, a small hemangioma may be prevented from growing into a much larger lesion. The common mole or melanocytic nevus is by far the most prevalent pigmented lesion. A mole is usually brown due to the production of melanin by the nevus cells. Depending on the location of the nevus cells and their number, the mole may be flat, slightly raised, or dome shaped. The great majority of nevi are acquired (appear after birth), but some are congenital (present at birth). Whereas acquired nevi are usually small (less than a quarter inch in diameter), congenital nevi are generally larger and can even cover a significant percentage of the body surface.
Protein C and S deficiencies have relatively the same incidence. They both result from numerous different mutations. A heterozygote pattern is much more frequent as homozygotes present soon after birth with purpura fulminans or massive venous thrombosis. Protein C has type I and type II deficiencies. Type I deficiencies are those mutations causing a decrease in levels and in activity most of these are missense mutations. Type II deficiencies are those in which levels are normal but activity is affected most of these are point mutations. Patients with protein C deficiency tend to present with VTE and fetal loss and rarely with arterial thrombosis. Protein S deficiency is harder to define. Many studies have shown the coexistence of protein S deficiency with APCR in as high as 40 of the patient population studied. This makes it hard to determine which is more important. However, there are more numerous reports of arterial thrombosis with protein S deficiency, including stokes, compared...
Seizures usually present within 12-24 h after birth. Intraventricular hemorrhage is more common in preterm infants. It is rarely present at birth but occurs at 1-3 days of age. A bulging fontanel or bloody cerebrospinal fluid on lumbar puncture is seen. Metabolic causes of seizures include hypoglycemia and hypocalcemia. Infections are also responsible for seizures.
The Apgar score is a useful tool for immediate assessment of the newborn. It helps identify those infants who require resuscitation. The score is also helpful in evaluating your resuscitation efforts. Scores are given at 1 and 5 min after birth and may be given every 5 min afterwards. Poor scores (0-3) at 1 min require resuscitation. Poor scores at 5 min do not predict subsequent cerebral palsy, although poor scores at 20 min are predictive of higher morbidity and mortality. A score of 8-10 is considered good. The table below demonstrates the scoring system.
The second peak in apoptotic death of male germ cells occurs postnatal. Shortly after birth, mitosis resumes and the first wave of spermatogenesis begins. During the first week, prospermatogonia differentiate into type A spermatogonia, the stem-cell population of the testis. This is followed by a period of spermatogonial proliferation until postnatal d 10, at which time germ cells initiate meiosis (161). Many apoptotic spermatogonia and spermatocytes are seen in the testis in the second and third weeks after birth (157,162). The incidence of cell death declines following the third week, when haploid cells are first found in the testis. While apoptosis is observed in male germ cells throughout adult life, the incidence of this never approaches that seen in prepubertal animals. Bax is expressed in spermatogonia of prepubertal and adult testes (161). Analysis of prepubertal animals suggests that Bax expression in testis is maximal during the second and third weeks after birth with...