Role of uterine artery doppler in prediction of pre-eclampsia

Background: Approximately 5-10 % of pregnancies are complicated by pre- eclampsia and it is a prime cause for maternal and perinatal mortality and morbidity worldwide, particularly in developing countries. In pre-eclampsia insufficient invasion of maternal spiral arteries by the trophoblast early in gestation due to abnormal implantation or maternal vascular disease results in impaired placental perfusion. Aspirin is a potent anti-inflammatory drug, has been shown to inhibit the biosynthesis and release of prostaglandins, even in low dosage. Ingestion of low dose aspirin may result in a decrease in the incidence of pre-eclampsia and fetal growth restriction and the precise mechanism by which it prevents preeclampsia in some women is also uncertain. Methods: The present prospective observational study was carried out in females between 18-20 weeks of gestation with raised uterine artery PI attending antenatal clinic in obstetrics and gynaecology department in SVP Hospital Ahmedabad from May 2023 to December 2023 using Microsoft excel and SPSS version 23. Results: In this study all the females were with raised uterine artery PI in 18-20 weeks ultrasound among them 51.85% were normotensive in later pregnancy. 48.14% developed pre-eclampsia in later pregnancy. In our study the middle cerebral artery indices in doppler ultrasound showed increased diastolic flow (including brain sparing effect) among 37% of the patients. The umbilical artery doppler showed that 62.9% of subjects were having normal umbilical artery indices, 18.5% of the patients were having decreased diastolic flow, 11.1% of the patients were having reversal of diastolic flow and 7.4% of the patients were having absent end diastolic flow Conclusions: Doppler study for fetal surveillance in pre-eclampsia is a very useful and non-invasive method and abnormal uterine artery velocimetry lead to the worse pregnancy outcomes in the present study. The knowledge of uterine and umbilical artery doppler is very helpful to improve pregnancy management and to identify and assess hypertensive disorder of the pregnancy at early gestational age compared to other antepartum test modalities

A vision of the future for BMC Medicine: serving science, medicine and authors

In June 2009, BMC Medicine received its first official impact factor of 3.28 from Thomson Reuters. In recognition of this landmark event, the BMC Medicine editorial team present and discuss the vision and aims of the journal

Targeting CXCR7/ACKR3 as a therapeutic strategy to promote remyelination in the adult central nervous system

Current treatment modalities for the neurodegenerative disease multiple sclerosis (MS) use disease-modifying immunosuppressive compounds but do not promote repair. Although several potential targets that may induce myelin production have been identified, there has yet to be an approved therapy that promotes remyelination in the damaged central nervous system (CNS). Remyelination of damaged axons requires the generation of new oligodendrocytes from oligodendrocyte progenitor cells (OPCs). Although OPCs are detected in MS lesions, repair of myelin is limited, contributing to progressive clinical deterioration. In the CNS, the chemokine CXCL12 promotes remyelination via CXCR4 activation on OPCs, resulting in their differentiation into myelinating oligodendrocytes. Although the CXCL12 scavenging receptor CXCR7/ACKR3 (CXCR7) is also expressed by OPCs, its role in myelin repair in the adult CNS is unknown. We show that during cuprizone-induced demyelination, in vivo CXCR7 antagonism augmented OPC proliferation, leading to increased numbers of mature oligodendrocytes within demyelinated lesions. CXCR7-mediated effects on remyelination required CXCR4 activation, as assessed via both phospho-S339-CXCR4–specific antibodies and administration of CXCR4 antagonists. These findings identify a role for CXCR7 in OPC maturation during remyelination and are the first to use a small molecule to therapeutically enhance myelin repair in the demyelinated adult CNS

CXCR7 influences leukocyte entry into the CNS parenchyma by controlling abluminal CXCL12 abundance during autoimmunity

During CNS autoimmunity, brain endothelial cell CXCR7 internalizes CXCL12 from the perivascular space, thereby permitting leukocyte migration into the CNS parenchyma

Conventional and microwave induced synthesis of various azetidinone and thiazolidinone derivatives from 3-[(1E)-1-aza-2-(2-chloro-7-methoxy-3-quinolyl)-vinyl]-4-(aryldiazenyl) phenol and their antimicrobial screening

1695-17003-Chloro-4-(2-chloro-7-methoxy-3-quinolyl)-1-[3-hydroxy-6-(aryldiazenyl) phenyl] azetidin-2-one 2 and 2-(2-chloro-7-methoxy-3-quinolyl)-3-[3-hydroxy-6-(aryldiazenyl) phenyl]-1, 3-thiazolidin-4-one 3 have been synthesized by the reaction of 3-[(1E)-1-aza-2-(2-chloro-7-methoxy-3-quinolyl)-vinyl]-4-(aryldiazenyl) phenol 1 with chloroacetylchloride and mercapto acetic acid, respectively. Both the reactions have been carried out by conventional and microwave methods. These compounds have been screened for their antibacterial, antifungal and antitubercular activity against different microorganisms

UTILITY OF ANKLE BRACHIAL PRESSURE INDEX AS A SCREENING TEST TO DETECT PERIPHERAL ARTERIAL DISEASE IN DIABETES MELLITUS

Introduction: Chronic hyperglycemia in diabetic patients cause many microvascular and macrovascular changes in the body. PAD is considered to be an important macrovascular complication of diabetes mellitus, especially among those with prolonged duration of diabetes. As PAD can be asymptomatic initially, it can lead to important morbidities including amputation of limbs if not detected early. ABPI is a cheap, easy and useful tool to assess PAD even in asymptomatic diabetic patients. Methods: This is a randomized cross-sectional study of 120 diabetic patients, asymptomatic for peripheral arterial disease, attending Medicine OPD or admitted in our tertiary care hospital of South Gujarat. Pretested proforma was used to collect data after taking informed consent. Investigations including ABPI with sphygmomanometer and colour doppler as mentioned in the proforma was carried out. Final analysis has been done with the help of Open EPI and SPSS software. Results: 30.83 % of patients of our study population were found with abnormal ABPI. Our data shows PAD is directly associated with high HbA1c, duration of DM, and BMI. No correlation was found between age and gender. Out of 37 significant ABPI patients, 28 patients were found to have PAD by colour doppler also. Conclusion: Among diabetic patients, high HbA1c, prolong duration of DM and high BMI were associated with abnormal ABPI, which was suggestive of PAD

Central nervous system pathology progresses independently of KC and CXCR2 in globoid-cell leukodystrophy.

Globoid-cell Leukodystrophy (GLD; Krabbe's disease) is a rapidly progressing inherited demyelinating disease caused by a deficiency of the lysosomal enzyme Galactosylceramidase (GALC). Deficiency of GALC leads to altered catabolism of galactosylceramide and the cytotoxic lipid, galactosylsphingosine (psychosine). This leads to a rapidly progressive fatal disease with spasticity, cognitive disability and seizures. The murine model of GLD (Twitcher; GALC-/-) lacks the same enzyme and has similar clinical features. The deficiency of GALC leads to oligodendrocyte death, profound neuroinflammation, and the influx of activated macrophages into the CNS. We showed previously that keratinocyte chemoattractant factor (KC) is highly elevated in the CNS of untreated Twitcher mice and significantly decreases after receiving a relatively effective therapy (bone marrow transplantation combined with gene therapy). The action of KC is mediated through the CXCR2 receptor and is a potent chemoattractant for macrophages and microglia. KC is also involved in oligodendrocyte migration and proliferation. Based on the commonalities between the disease presentation and the functions of KC, we hypothesized that KC and/or CXCR2 contribute to the pathogenesis of GLD. Interestingly, the course of the disease is not significantly altered in KC- or CXCR2-deficient Twitcher mice. There is also no alteration in inflammation or demyelination patterns in these mice. Furthermore, transplantation of CXCR2-deficient bone marrow does not alter the progression of the disease as it does in other models of demyelination. This study highlights the role of multiple redundant cytokines and growth factors in the pathogenesis of GLD

Cytokine and chemokine levels in the CNS of Twitcher mice.

<p>The fold-elevation of various cytokines/chemokines in the brain is shown. Among all the assayed molecules, the chemokine KC showed the greatest fold change in the brains (>15-fold increase) of the Twitcher mice (A). The levels of KC in the brains (B) and the spinal cords (C) of the Twitcher mice showed a progressive increase with time. The vertical bars represent the means and the error bars represent one SEM; **p<0.01, ***p<0.001.</p