Leg skin temperature with body-weight-supported treadmill and tilt-table standing training after spinal cord injury.

STUDY DESIGN: Randomized crossover. OBJECTIVES: Effects of body-weight-supported treadmill (BWST) and tilt-table standing (TTS) training on skin temperature and blood flow after spinal cord injury (SCI). SETTING: McMaster University, Canada. METHODS: Seven individuals with SCI participated in BWST and TTS training (3 times per week for 4 weeks, 4-week detraining between protocols). Skin temperature was measured before and after a single session of BWST or TTS, pre- and post-training. Leg blood flow was measured at rest pre- and post-training. RESULTS: Resting skin temperature decreased at four sites after 4 weeks of BWST training in comparison with the pre-training. Four weeks of TTS training resulted in resting skin temperature decreases post-training at the right thigh only. Both BWST and TTS training resulted in altered reactivity of skin temperature at all sites except the right calf in response to a single session of BWST and TTS. Post-BWST training, a single session of BWST stimulated increased temperature at all sites, whereas after TTS training a single session of TTS resulted in temperature decreases at two of the six sites. No changes were observed in resting blood flow with either BWST or TTS training. CONCLUSION: Increased resting skin temperature and decreased skin temperature reactivity have been linked to the development of pressure sores. BWST and TTS may stimulate different skin temperature responses and the impact on pressure sore development warrants further investigation.

Age-related synapse loss in hippocampal CA3 is not reversed by caloric restriction.

Caloric restriction (CR) is a reduction of total caloric intake without a decrease in micronutrients or a disproportionate reduction of any one dietary component. While CR attenuates age-related cognitive deficits in tasks of hippocampal-dependent memory, the cellular mechanisms by which CR improves this cognitive decline are poorly understood. Previously, we have reported age-related decreases in key synaptic proteins in the CA3 region of the hippocampus that are stabilized by lifelong CR. In the present study, we examined possible age-related changes in the functional microcircuitry of the synapses in the stratum lacunosum-molecular (SL-M) of the CA3 region of the hippocampus, and whether lifelong CR might prevent these age-related alterations. We used serial electron microscopy to reconstruct and classify SL-M synapses and their postsynaptic spines. We analyzed synapse number and size as well as spine surface area and volume in young (10 months) and old (29 months) ad libitum fed rats and in old rats that were calorically restricted from 4 months of age. We limited our analysis to SL-M because previous work demonstrated age-related decreases in synaptophysin confined to this specific layer and region of the hippocampus. The results revealed an age-related decrease in macular axo-spinous synapses that was not reversed by CR that occurred in the absence of changes in the size of synapses or spines. Thus, the benefits of CR for CA3 function and synaptic plasticity may involve other biological effects including the stabilization of synaptic proteins levels in the face of age-related synapse loss.

Estrogen and aging affect synaptic distribution of phosphorylated LIM kinase (pLIMK) in CA1 region of female rat hippocampus.

17beta-Estradiol (E) increases axospinous synapse density in the hippocampal CA1 region of young female rats, but not in aged rats. This may be linked to age-related alterations in signaling pathways activated by synaptic estrogen receptor alpha (ER-alpha) that potentially regulate spine formation, such as LIM-kinase (LIMK), an actin depolymerizing factor/cofilin kinase. We hypothesized that, as with ER-alpha, phospho-LIM-kinase (pLIMK) may be less abundant or responsive to E in CA1 synapses of aged female rats. To address this, cellular and subcellular distribution of pLIMK-immunoreactivity (IR) in CA1 was analyzed by light and electron microscopy in young and aged female rats that were ovariectomized and treated with either vehicle or E. pLIMK-IR was found primarily in perikarya within the pyramidal cell layer and dendritic shafts and spines in stratum radiatum (SR). While pLIMK-IR was occasionally present in terminals, post-embedding quantitative analysis of SR showed that pLIMK had a predominant post-synaptic localization and was preferentially localized within the postsynaptic density (PSD). The percentage of pLIMK-labeled synapses increased (30%) with E treatment (P<0.02) in young animals, and decreased (43%) with age (P<0.002) regardless of treatment. The pattern of distribution of pLIMK-IR within dendritic spines and synapses was unaffected by age or E treatment, with the exception of an E-induced increase in the non-synaptic core of spines in young females. These data suggest that age-related synaptic alterations similar to those seen with ER-alpha occur with signaling molecules such as pLIMK, and support the hypothesis that age-related failure of E treatment to increase synapse number in CA1 may be due to changes in the molecular profile of axospinous synapses with respect to signaling pathways linked to formation of additional spines and synapses in response to E.

Alterations in immune function and CYP450 activity in adult male deer mice (Peromyscus maniculatus) following exposure to benzo[a]pyrene, pyrene, or chrysene.

Polycyclic aromatic hydrocarbons (PAHs) are among the most common classes of chemical contaminants found at hazardous waste sites. Deer mice (Peromyscus maniculatus) exhibit a wide geographic distribution throughout North America and have been suggested as a terrestrial biomonitoring species to facilitate comparisons between superfund sites. Chemicals tested were benzo[a]pyrene (BaP; CAS number 50-32-8), pyrene (Pyr; CAS number 129-00-0), and chrysene (Chr; CAS number 218-01-9). Adult male deer mice were exposed via intraperitoneal (i.p.) injection every other day for 11 d to the PAHs (0.3, 1, 3, 10, or 30 mg/kg) or a corn oil carrier control. Both BaP and Chr suppressed the plaque-forming cell (PFC) response at all treatment levels. Pyr exposure (1-30 mg/kg) also resulted in suppression of this response. Macrophage pinocytosis was suppressed only by Chr (3, 10, and 30 mg/kg). Concanavalin A-induced proliferation was stimulated by BaP at all dose levels, by Pyr at 1-30 mg/kg, and by Chr at 30 mg/kg. Chr did not affect pokeweed mitogen (PWM)-induced proliferation; however, BaP (1-30 mg/kg) and Pyr (0.3-30 mg/kg) produced stimulation of this response as compared to respective controls. BaP and Chr stimulated cytochrome P-450 1A1 (CYP1A1) activity (3, 10, or 30 mg/kg) as measured by ethoxyresorufin O-deethylase (EROD) activity, but Pyr did not. These results indicate that immune function endpoints appear to be more sensitive to these PAHs than measured hepatic CYP450 activity.

Spasticity after spinal cord injury.

Symptoms of spasticity are often experienced by individuals with spinal cord injury (SCI) following a period of spinal shock and, in many cases, these symptoms negatively affect quality of life. Despite its prevalence, spasticity as a syndrome in the SCI population is not always managed effectively. This is likely due to the fact that the syndrome can have various presentations, each with their own specific etiology. This overview summarizes the symptoms and pathophysiology of the various presentations of spasticity in the SCI population and discusses the currently accepted management techniques. There is a need for a better understanding of the syndrome of spasticity as well as the development of a valid and reliable assessment tool.

Long-term body-weight-supported treadmill training and subsequent follow-up in persons with chronic SCI: effects on functional walking ability and measures of subjective well-being.

STUDY DESIGN: Longitudinal, prospective within-subject design. OBJECTIVES: (1) To determine the effects of long-term body-weight-supported treadmill training (BWSTT) on functional walking ability and perceived quality of life in persons with chronic incomplete spinal cord injury (SCI), and (2) to investigate whether training adaptations are maintained following cessation of the BWSTT programme. SETTING: Hamilton, Ontario, Canada. METHODS: A group of 14 individuals with chronic (mean 7.4 years postinjury) incomplete SCI (ASIA B & C) participated in thrice-weekly sessions of BWSTT for a period of approximately 12 months (144 sessions). Functional walking ability and indices of subjective well-being were evaluated during the training programme and over an 8-month follow-up. RESULTS: In total, 13 subjects successfully completed the 144 training sessions in the required study period (max. 15 months). Adherence to the thrice-weekly training frequency was 78.8%. All subjects improved in treadmill walking ability (54% reduction in required external body-weight support (BWS), 180% increase in treadmill walking speed, 335% increase in distance walked/session), and six subjects improved their capacity to walk over ground. There were accompanying increases in satisfaction with life and satisfaction with physical function, both of which were significantly correlated with improvements in treadmill walking ability. All but one subject returned for follow-up assessment 8 months post-training; while there was a slight decline in treadmill walking performance, over ground walking scores remained relatively stable. The only change in subjective well-being in the follow-up was a slight decrease in satisfaction with physical function. CONCLUSION: Thrice-weekly BWSTT for 12 months was an effective stimulus to improve treadmill walking ability and indices of subjective well-being in persons with chronic incomplete SCI, and most of these improvements were maintained for up to 8 months following the cessation of training.

Pyridostigmine bromide (PYR) alters immune function in B6C3F1 mice.

Pyridostigmine bromide (PYR) is an anticholinesterase drug indicated for the treatment of myasthenia gravis and neuromuscular blockade reversal. It acts as a reversible cholinesterase inhibitor and was used as a pretreatment for soldiers during Operation Desert Storm to protect against possible nerve gas attacks. Since that time, PYR has been implicated as a possible causative agent contributing to Gulf War Illness. PYR's mechanism of action has been well-delineated with regards to its effects on the nervous system, yet little is known regarding potential effects on immunological function. To evaluate the effects of PYR on immunological function, adult female B6C3F1 mice were gavaged daily for 14 days with PYR (0, 1, 5, 10, or 20 mg/kg/day). Immune parameters assessed were lymphoproliferation, natural killer cell activity, the SRBC-specific antibody plaque-forming cell (PFC) response, thymus and spleen weight and cellularity, and thymic and splenic CD4/CD8 lymphocyte subpopulations. Exposure to PYR did not alter splenic and thymus weight or splenic cellularity. However, 20 mg PYR/kg/day decreased thymic cellularity with decreases in both CD4+/CD8+ (20 mg/kg/day) and CD4-/CD8- (10 and 20 mg/kg/day) cell types. Functional immune assays indicated that lymphocyte proliferative responses and natural killer cell activity were normal; whereas exposure to PYR significantly decreased primary IgM antibody responses to a T-cell dependent antigen at the 1, 5, 10 and 20 mg/kg treatment levels for 14 days. This is the first study to examine the immunotoxicological effects of PYR and demonstrate that this compound selectively suppresses humoral antibody responses.

Subchronic exposure to ellagic acid impairs cytotoxic T-cell function and suppresses humoral immunity in mice.

Ellagic acid (EA) is present in a variety of foods such as grapes, strawberries, raspberries, and nuts. It is a dietary plant phenol that has been shown to inhibit oxidative stress and chemical carcinogenesis. Although several studies have examined the protective mechanisms of dietary EA including the induction of detoxifying enzymes, regulation of cell cycle, chelation of nickel, and prevention of DNA methylation, none have addressed the role of EA in immunological surveillance. This study investigates the status of immune function in B6C3F1 mice exposed continuously to EA in drinking water at 0.5, 1.0, or 2.0 mg/kg/day for 28 days. Although this range of exposure is above the estimated human daily intake (approximately 940 microg/day for 70 kg person or 13.4 microg/kg/day), these levels would not be unreasonable if EA were used as a dietary supplement or as a chemotherapeutic agent. Previous reports have demonstrated the anticarcinogenic effects of EA at levels 10- to 250-fold greater than those applied in this study. Immunological parameters assessed included natural killer (NK) cell activity, cytotoxic T lymphocyte (CTL) activity, IgM antibody plaque forming cell (PFC) response, thymus, spleen, kidney, and liver mass, and total cellularity for the thymus and spleen. Subchronic exposure to EA for 28 days in drinking water caused significant suppression of specific IgM antibody responses in the 2.0 mg/kg EA treatment group and suppressed cytotoxic T-cell function in the 0.5 and 1.0 mg/kg EA treatment groups. All other immunological parameters were within normal ranges. Kidney and liver mass were not altered after treatment with EA. The results from this study indicate that EA suppressed both IgM antibody responses and CTLs. These observations suggest important implications on human health should EA be prescribed as a chemotherapeutic agent or a preventative dietary supplement for cancer.

Attenuated lesion-induced N-methyl-D-aspartate receptor (NMDAR) plasticity in the dentate gyrus of aged rats following perforant path lesions.

Young animals demonstrate a significant upregulation of N-methyl-d-aspartate receptor 1 (NMDAR1) in the outer molecular layer (OML) of the dentate gyrus following a total unilateral ablation of the perforant path, and this response presumably facilitates a degree of functional recovery. Aged animals have attenuated responses to lesion-induced synaptic plasticity as compared with young subjects, and in fact display decreased synaptogenesis and sprouting following a unilateral perforant path lesion. To investigate the response of NMDAR1 in the dentate gyrus of aged animals to perforant path ablation, 24-month-old Sprague-Dawley male rats received a unilateral knife cut of the angular bundle. Our results demonstrated that aged animals displayed a blunted response to lesion-induced NMDA receptor-mediated plasticity, suggesting that aged animals have an impaired ability to respond to deafferentation through an increase in NMDA receptor levels in the deafferented zone.

Length of postovariectomy interval and age, but not estrogen replacement, regulate N-methyl-D-aspartate receptor mRNA levels in the hippocampus of female rats.

Estrogens and N-methyl-D-aspartate (NMDA) receptors regulate multiple aspects of morphological and functional plasticity in young animals. For example, estrogens increase spine density in the hippocampus, and NMDA antagonists block these effects. Few studies have examined the effects of age, postovariectomy interval, and duration of estrogen replacement in the hippocampus and more specifically on NMDA receptor subunits. Therefore, the present study was designed to investigate the effects of short- and long-term estrogen replacement or deprivation on mRNA levels of three NMDA receptor subunits, NR1, NR2A, and NR2B, in the hippocampus of aging female Sprague-Dawley rats. Young (3- to 4-month-old) and middle-aged (12- to 13-month-old) rats were ovariectomized for 1 month and then treated with estrogen or vehicle for either 2 days or 2 weeks. Another set of middle-aged and aged (24-to 25-month-old) animals were ovariectomized for 6 months and treated with estrogen or vehicle for 2 days or 2 weeks. RNase protection assay was used to assess changes in the NMDA receptor subunit mRNA levels. Our results demonstrated significant effects of age and length of ovariectomy on NMDA receptor mRNA levels, with little effect of the estrogen status of the animals on these parameters. The largest effect was seen for the length of the postovariectomy interval, with the results demonstrating that rats with a short-term ovariectomy have substantially higher NMDA receptor subunit mRNA levels than animals with long-term ovariectomy. The most dramatic effects of aging were seen for NR1 and NR2B mRNAs in ventral hippocampus, with large age-related increases. These data suggest that age and duration of ovariectomy impact NMDA receptor mRNA levels in the hippocampus, potentially affecting the stoichiometry and/or function of these receptors. These findings have important implications for postmenopausal or hysterectomy/oophorectomy estrogen depletion and replacement in humans.

Different modes of hippocampal plasticity in response to estrogen in young and aged female rats.

Estrogen regulates hippocampal dendritic spine density and synapse number in an N-methyl-D-aspartate (NMDA) receptor-dependent manner, and these effects may be of particular importance in the context of age-related changes in endocrine status. We investigated estrogen's effects on axospinous synapse density and the synaptic distribution of the NMDA receptor subunit, NR1, within the context of aging. Although estrogen induced an increase in axospinous synapse density in young animals, it did not alter the synaptic representation of NR1, in that the amount of NR1 per synapse was equivalent across groups. Estrogen replacement in aged female rats failed to increase axospinous synapse density; however, estrogen up-regulated synaptic NR1 compared with aged animals with no estrogen. Therefore, the young and aged hippocampi react differently to estrogen replacement, with the aged animals unable to mount a plasticity response generating additional synapses, yet responsive to estrogen with respect to additional NMDA receptor content per synapse. These findings have important implications for estrogen replacement therapy in the context of aging.

N-methyl-D-aspartate receptor mRNA levels change during reproductive senescence in the hippocampus of female rats.

Estrogen interacts with N-methyl-d-aspartate (NMDA) receptors to regulate multiple aspects of morphological and functional plasticity. In the hippocampus, estrogens increase both dendritic spine density and synapse number, and NMDA antagonists block these effects. This plasticity in the hippocampus mediated by estrogen may be of particular importance in the context of aging when estrogen levels change and cognitive function is often impaired. Therefore, the present study was designed to investigate effects of aging and reproductive status on NMDA receptor (NR) subunit mRNA levels in the hippocampus. NR1, NR2A, and NR2B mRNA levels were measured by RNase protection assay in young (3-4 month), middle-aged (12-13 month), and aged (24-25 month) Sprague-Dawley rats in different phases of the estrous cycle in cycling animals and in acyclic subjects. Our results demonstrated that NMDA receptor subunit mRNA levels were much more prominently affected by the chronological age than by the reproductive status of the animals. Age-related changes were observed in NR1, NR2A, and NR2B in the ventral hippocampus and in NR1 and NR2B in the dorsal hippocampus. However, the only relationship with reproductive status was seen for NR1 mRNA, and this was restricted to the ventral hippocampus. An interaction between chronological age and reproductive status was found, with higher levels of NR1 mRNA seen in young animals in proestrus than in those in diestrus I (high and low estrogen levels, respectively). However, this relationship was not seen in the aged subjects. These results demonstrate that the hippocampus is subjected to age-related alterations in NMDA receptor subunit mRNA levels and that animals of different ages are influenced differently by reproductive status. This shift in the NMDA receptor mRNA levels may be a possible molecular mechanism contributing to alterations in cognitive behavior during normal aging.

Hippocampal dependent learning ability correlates with N-methyl-D-aspartate (NMDA) receptor levels in CA3 neurons of young and aged rats.

Hippocampal N-methyl-D-Aspartate (NMDA) receptors mediate mechanisms of cellular plasticity critical for spatial learning in rats. The present study examined the relationship between spatial learning and NMDA receptor expression in discrete neuronal populations, as well as the degree to which putative age-related changes in NMDA receptors are coupled to the effects of normal aging on spatial learning. Young and aged Long-Evans rats were tested in a Morris water maze task that depends on the integrity of the hippocampus. Levels of NR1, the obligatory subunit for a functional NMDA receptor, were subsequently quantified both biochemically by Western blot in whole homogenized hippocampus, and immunocytochemically by using a high-resolution confocal laser scanning microscopy method. The latter approach allowed comprehensive, regional analysis of discrete elements of excitatory hippocampal circuitry. Neither method revealed global changes, nor were there region-specific differences in hippocampal NR1 levels between young and aged animals. However, across all subjects, individual differences in spatial learning ability correlated with NR1 immunofluorescence levels selectively in CA3 neurons of the hippocampus. Parallel confocal microscopic analysis of the GluR2 subunit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptor failed to reveal reliable differences as a function of age or spatial learning ability. This analysis linking age, performance, and NR1 levels demonstrates that although dendritic NR1 is generally preserved in the aged rat hippocampus, levels of this receptor subunit in selective elements of hippocampal circuitry are linked to spatial learning. These findings suggest that NMDA receptor abundance in CA3 bears a critical relationship to learning mediated by the hippocampus throughout the life span.

An aryl hydrocarbon receptor independent mechanism of JP-8 jet fuel immunotoxicity in Ah-responsive and Ah-nonresponsive mice.

JP-8 jet fuel is handled extensively by personnel in the military and commercial airlines, despite the paucity of information regarding its potential human health effects. JP-8 is a complex mixture primarily consisting of kerosene plus aliphatic and aromatic hydrocarbons. Recent reports indicate that acute JP-8 exposure via inhalation or dermal routes can overtly and persistently impair immune function in mice. Data from preliminary studies in this laboratory assessing the immunotoxicity of JP-8 indicated that oral JP-8 exposure caused an increase in liver weight, a decrease in thymus weight, and a decrease in the PFC response. As these results were similar to classic effects elicited by TCDD, a strong AhR ligand, it was hypothesized that JP-8 may exert immunosuppression via a similar mechanism. To test this hypothesis, an Ah-responsive mouse strain (B6C3F1) and a classically non-responsive mouse strain (DBA/2) bearing a lower affinity AhR were gavaged with JP-8 for 7 days. The results suggest that both mouse strains were equally sensitive to JP-8's toxicity at several endpoints including thymus weight and cellularity, liver weight, and specific IgM antibody responses. Furthermore, JP-8 did not induce CYP1A1 or promote down regulation of the AhR when evaluated by Western blot in either B6C3F1 or DBA/2 mice. In vitro studies corroborated these findings as JP-8 did not induce CYP1A1, promote down regulation of the AhR, or activate an XRE-driven reporter gene in murine Hepa-1 cells. These results suggest that JP-8 may exert its toxicity via an AhR-independent mechanism.

Circuit-specific alterations in hippocampal synaptophysin immunoreactivity predict spatial learning impairment in aged rats.

The present study examined the long-standing concept that changes in hippocampal circuitry contribute to age-related learning impairment. Individual differences in spatial learning were documented in young and aged Long-Evans rats by using a hippocampal-dependent version of the Morris water maze. Postmortem analysis used a confocal laser-scanning microscopy method to quantify changes in immunofluorescence staining for the presynaptic vesicle glycoprotein, synaptophysin (SYN), in the principal relays of hippocampal circuitry. Comparisons based on chronological age alone failed to reveal a reliable difference in the intensity of SYN staining in any region that was examined. In contrast, aged subjects with spatial learning deficits displayed significant reductions in SYN immunoreactivity in CA3 lacunosum-moleculare (LM) relative to either young controls or age-matched rats with preserved learning. SYN intensity values for the latter groups were indistinguishable. In addition, individual differences in spatial learning capacity among the aged rats correlated with levels of SYN staining selectively in three regions: outer and middle portions of the dentate gyrus molecular layer and CA3-LM. The cross-sectional area of SYN labeling, by comparison, was not reliably affected in relation cognitive status. These findings are the first to demonstrate that a circuit-specific pattern of variability in the connectional organization of the hippocampus is coupled to individual differences in the cognitive outcome of normal aging. The regional specificity of these effects suggests that a decline in the fidelity of input to the hippocampus from the entorhinal cortex may play a critical role.

A comparative analysis of huddling in infant Norway rats and Syrian golden hamsters: does endothermy modulate behavior?

In infant rats, huddling improves surface-to-volume ratios and provides metabolic savings during cold exposure. It is unclear, however, whether endothermy is also a necessary component of huddling. In the present experiment, huddles composed of infant Norway rats (2- or 8-day-olds), which produce heat endogenously, or Syrian golden hamsters (8-day-olds), which do not produce heat endogenously, were exposed to decreases in air temperature. Behavioral and physiological responses were monitored throughout the test. Rats, especially at 8 days of age, were better able to thermoregulate using huddling than hamsters, due in part to endogenous heat production. Furthermore, 8-day-old rats exhibited behavioral responses that promote heat retention, suggesting that both physiological and behavioral mechanisms contribute to effective thermoregulation during huddling in the cold.

Rates of and factors associated with recurrence of preterm delivery.

CONTEXT: Information about risk of recurrent preterm delivery is useful to clinicians, researchers, and policy makers for counseling, generating etiologic leads, and measuring the related public health burden. OBJECTIVES: To identify the rate of recurrence of preterm delivery in second pregnancies, factors associated with recurrence, and the percentage of preterm deliveries in women with a history of preterm delivery. DESIGN AND SETTING: Population-based cohort study of data from birth and fetal death certificates from the state of Georgia between 1980 and 1995. SUBJECTS: A total of 122 722 white and 56174 black women with first and second singleton deliveries at 20 to 44 weeks' gestation. MAIN OUTCOME MEASURE: Length of gestation (categorized as 20-31, 32-36, or > or =37 weeks) at second delivery compared with length of gestation at first delivery, by age and race. RESULTS: Most women whose first delivery was preterm subsequently had term deliveries. Of 1023 white women whose first delivery occurred at 20 to 31 weeks, 8.2% (95% confidence interval [CI], 6.6%-10.1%) delivered their second birth at 20 to 31 weeks and 20.1% (95% CI, 17.7%-22.8%) at 32 to 36 weeks. Of 1084 comparable black women, 13.4% (95 % CI, 11.4%-15.6%) delivered at 20 to 31 weeks and 23.4% (95% CI, 20.9%-26.1%) delivered at 32 to 36 weeks. Among women whose first delivery occurred at 32 to 36 weeks, all corresponding rates were lower than those whose first birth was at 20 to 31 weeks; the rates of second birth at 20 to 31 weeks were substantially lower (for white women, 1.9% [95% CI, 1.7%-2.2%]; for black women, 3.8% [95% CI, 3.4%-4.2%]). Compared with women aged 20 to 49 years at their second delivery, women younger than 18 years had twice the risk of recurrence of delivery at 20 to 31 weeks. Of all second deliveries at 20 to 31 weeks, 29.4% for white women and 37.8% for black women were preceded by a preterm delivery. CONCLUSIONS: Our data suggest that recurrence of preterm delivery contributes a notable portion of all preterm deliveries, especially at the shortest gestations.

Visual cortical projections and chemoarchitecture of macaque monkey pulvinar.

We investigated the patterns of projections from the pulvinar to visual areas V1, V2, V4, and MT, and their relationships to pulvinar subdivisions based on patterns of calbindin (CB) immunostaining and estimates of visual field maps (P(1), P(2) and P(3)). Multiple retrograde tracers were placed into V1, V2, V4, and/or MT in 11 adult macaque monkeys. The inferior pulvinar (PI) was subdivided into medial (PI(M)), posterior (PI(P)), central medial (PI(CM)), and central lateral (PI(CL)) regions, confirming earlier CB studies. The P(1) map includes PI(CL) and the ventromedial portion of the lateral pulvinar (PL), P(2) is found in ventrolateral PL, and P(3) includes PI(P), PI(M), and PI(CM). Projections to areas V1 and V2 were found to be overlapping in P(1) and P(2), but those from P(2) to V2 were denser than those to V1. V2 also received light projections from PI(CM) and, less reliably, from PI(M). Neurons projecting to V4 and MT were more abundant than those projecting to V1 and V2. Those projecting to V4 were observed in P(1), densely in P(2), and also in PI(CM) and PI(P) of P(3). Those projecting to MT were found in P(1)- P(3), with the heaviest projection from P(3). Projections from P(3) to MT and V4 were mainly interdigitated, with the densest to MT arising from PI(M) and the densest to V4 arising from PI(P) and PI(CM). Because the calbindin-rich and -poor regions of P(3) corresponded to differential patterns of cortical connectivity, the results suggest that CB may further delineate functional subdivisions in the pulvinar.

Quality measures for unintended pregnancy prevention in health care services: opportunities and challenges.

PIP: This paper discusses the opportunities and challenges in conducting quality assessment of preventive measures for unintended pregnancy in the US. According to the 1995 National Survey of Family Growth, unintended pregnancies were either mistimed or occurred after a woman intended to have no (more) children. Further, unintended pregnancies are associated with social and economic disadvantages, late prenatal care and adverse pregnancy outcomes, and mistimed opportunities for preconception counseling. Thus it is important to conduct quality assessment of preventive measures for unintended pregnancy in the clinical setting in order to address health outcomes (such as induced abortions or adolescent pregnancies), health care processes (such as screening for risk behaviors for unintended pregnancy), or health system structures (such as availability of family planning providers). This paper further discusses how quality of health care can be measured relative to unintended pregnancy.^ieng

Does inadequate prenatal care contribute to growth retardation among second-born African-American babies?

The authors evaluated the relation between adequacy of prenatal care and risk of delivery of full term small-for-gestational-age (SGA) infants. Data were derived from maternally linked birth certificates for 6,325 African-American women whose first two pregnancies ended in singleton, full term live births in Georgia from 1989 through 1992. The authors used stratified analysis to assess the effect of prenatal care on the risk of having an SGA baby in the second pregnancy among women with and without an SGA baby in their first pregnancy. The group of women with a history of SGA birth may be more likely to include persons for whom SGA delivery is related to factors, such as genetics, that are not amenable to intervention by prenatal care. Inadequate prenatal care was not associated with the risk of SGA delivery among women who had previously delivered an SGA baby. In unadjusted analyses, inadequate prenatal care was associated with an increased risk of delivering a full term SGA baby in the second pregnancy among women whose first baby was not SGA (risk ratio = 1.28; 95% confidence interval: 1.05, 1.55). The association did not persist when data were adjusted for confounding variables (odds ratio = 1.11; 95% confidence interval: 0.89, 1.38). Regardless of outcome in the first pregnancy, adequate prenatal care did not reduce the risk of full term SGA birth among second pregnancies in this population.