Cavernous haemangioma and mid trimester pregnancy loss leading to severe haemorrhage and hysterectomy: a case report and review of literature.

Background: Cavernous haemangiomas are benign vascular tumours that are known to occasionally involve the female genital tract, including the uterus. They are often underdiagnosed during pregnancy, although they can also lead to severe postpartum or antepartum haemorrhage. Objectives: Describe our case of an uncommon second-trimester pregnancy loss in a woman with a diffuse cavernous haemangioma of the uterus and cervix and review the wider literature. Methods: The review was conducted using MEDLINE, Scopus and PubMed electronic databases from beginning of the database to May 2023, using the following keywords: arteriovenous malformation; cavernous haemangioma/hemangioma; uterine neoplasms; pregnancy complications; abnormal vaginal bleeding. Main outcome measures: Description of the characteristics of cavernous haemangioma during pregnancy as well as diagnostic criteria and treatment options. Results: Twenty publications were included in the review, which included English-language case reports over a period from 1959 to 2022. No pathognomonic symptoms for cavernous haemangioma of the uterus in a pregnant woman were noted. Complications including massive secondary postpartum haemorrhage, haemoperitoneum, and severe thrombocytopenia with anaemia after delivery were reported. Conclusions: Diagnosis and management during pregnancy can be challenging and requires considerable attention, with a multidisciplinary approach including gynaecologists, radiologists, and pathologists to avoid major complications. What is new?: An additional case of diffuse cavernous haemangioma of the uterus and cervix is described, that adds to the little existing literature.

Removal of viral contaminants by monoclonal antibody purification of plasma proteins.

The transmittance of pathogenic viruses by the widespread administration of protein fractions such as F VIII prepared on a large scale from pooled human plasma has been of growing concern. We have now demonstrated that significant amounts of pathogenic viruses including LAV/HTLVIII may be removed by a new large scale fractionation process for the preparation of human F VIII (Monoclate) which employs immunoaffinity chromatography. Model viruses representative of different virus families and the LAV strain of HIV were added to cryoprecipitate and then the mixture was processed as for Monoclate manufacturing. Virus titers were determined at each step of the fractionation procedures. An overall reduction of at least 6 logs was obtained for the model viruses and the HIV due to the purification process. An added heating step further increased the safety margin for the product resulting in at least an overall reduction of 7-9 logs for HIV. Clinical experience with Monoclate in virgin hemophiliacs has confirmed its viral safety. Our laboratories are exploiting a similar strategy of immunoaffinity chromatography to ensure the viral safety of FIX and protein C preparations derived from plasma.

Lung injury induced by antibody fragments to angiotensin-converting enzyme.

Rabbits given goat anti-rabbit angiotensin-converting enzyme antibodies or derived antibody fragments develop rapidly fatal pulmonary edema. Endothelial cell injury is manifested by bleb formation and the disintegration of cell membranes. Platelets are found along the injured endothelium and leukocytes block capillary lumens. The pathologic features are similar when immune IgG, F(ab')2, or Fab are given. In vitro studies of complement activation show that solubilized, purified angiotensin-converting enzyme alone activates C1, with consumption of C4 and C3. Addition of immune IgG plus converting enzyme enhances this activation. F(ab')2 plus enzyme enhances only C3 consumption, while Fab with enzyme produces no additional complement utilization. Thus, while complement activation may be involved in the pathogenesis of injury induced by IgG or F(ab')2, the mechanism of Fab-induced endothelial injury remains unclear.

Characterization of the cell cycle and synchrony in a CV-1 cell line.

Synchronous populations of CV-1 cells have been prepared by the selective detachment of mitotic cells. An approach, using a combination of standard techniques, has allowed evaluation of the degree of synchrony throughout the cell cycle. CV-1 cells have a cycle of approximately 19-hr duration, throughout which synchronous populations progress with a dispersion of 3 hr, i.e., ie, greater than or equal to 90% of the cells enter S phase and subsequently divide within a 3-hr period. A major cause of this dispersion is the differential attachment times of individual cell within the population when a synchronous culture is initiated.

Characterization of a CV-1 cell cycle. II. The role of cell-substrate attachment.

The availability of synchronous cultures of untransformed CV-I cells has allowed analysis of the role of cell-substrate attachment in cell cycle progression as well as the ability of serum and SV40 infection to override the requirement for cell-substrate attachment. Attachment to a solid substrate is required for progression through G1. Prevention of attachment results in cell cycle arrest 30 min after cytokinesis. Serum is required for attachment, but increasing the serum concentration from 2 to 20 % does not enhance cell attachment, nor obviate its need for cell cycle progression. SV40 infection does not overcome the requirement of serum for attachment nor the need of attachment for normal cycling.

T antigen banding on chromosomes of simian virus 40 infected muntjac cells.

Chromosomes were prepared from mitotic munjac cells 48 to 72 h after infection with SV40 virus. When stained for SV40 T antigen by indirect immunofluorescence, all chromosomes within an infected cell were fluorescent, indicating the presence of T antigen. Furthermore, the chromosomes were not uniformly stained but appeared to have regions of high and low fluorescence intensity. A variety of controls showed that the banding patterns are specific and highly reproducible and may indeed reflect the binding sites of T antigen. The bright, fluorescent bands T antigen were found to correspond to bands visualized by trypsin-Giesma staining (G-bands) and also by quinacrine staining (Q-bands). Current knowledge of chromosome banding indicates that Q-bands reflect the distribution of AT-rich regions along the chromosome. From the DNA sequence of SV40, it is known that one of the T antigen binding sites contains AT-rich sequences; thus, T antigen banding might be due to the base-specific binding of T antigen to chromatin. In addition, these bands have been implicated as centers for chromosome condensation and units in control of DNA replication. While the functional significance of T antigen binding has yet to be determined, the SV40-muntjac system provides an unusual opportunity to study the interaction of a known regulatory protein with mammalian chromosomes.

On the quantitation of SV40 virus by plaque assay and immunoperoxidase technique.

Procedures are described for the quantitation of SV40 virus infectivity by plaque formation within 7 days and T antigen assay by the sensitive and economical indirect immunoperoxidase technique.

Kinetics of desynchronization and distribution of generation times in synchronized cell populations.

The kinetics of the distribution of generation times in synchronized cells can be analyzed by using Fourier transform analysis. Deviations of the experimental data from the curve of completely asynchronous growth reflect the degree of synchrony at a particular time. Fourier transform analysis of these deviations yields the average generation time as well as information on the distribution of generation times characterizing a synchronized culture. A detailed analysis of synchronized cell cultures does not provide any evidence for the existence of a subcycle or a polymodal distribution in generation times. The data do indicate that cell-cell interaction occurs at cell densities as low as 2.5 X 10(3)/cm2. It is also shown that the Eyring-Stover formalism for the dynamics of survival can correctly describe the distribution of the first round of cell divisions in a synchronized culture.

Antibodies to the triplet codons AAA, AAC, and AUG: reactions with nucleic acids.

Antibodies specific for the trinucleotide codons AAA, AUG, and AAC were examined for their reactions with nucleic acids. Anti-AUG and anti-AAC precipitated denatured DNA. Anti-AAA did not, and moreover, the binding of a tritiated AAA derivative to anti-AAA was not inhibited by denatured DNA. Radioligand-binding studies showed that anti-AAA was highly specific for the triplet sequence, some cross-reactions occurring with di-A and tetra-A but little with A and poly(A). The anti-codons did not precipitate whole yeast RNA, but binding could be demonstrated with Escherichia coli 3H-rRNA. Anti-AAC and anti-AUG (but not anti-AAA) bound E. coli 14C-tRNA. Anti-AUG was found to inhibit protein synthesis in an in vitro system in which rabbit reticulocyte mRNA was being translated. Inhibition was abolished by absorption of the antibody with AUG-RSA. The results of these and previous experiments (reference 1) are interpreted to indicate that antibodies can recognize trinucleotide sequences but not with absolute specificity, and it is suggested that antibodies to longer nucleotide sequences might show specificity comparable to that shown by antibodies to polysaccharide and peptide sequences.

Effects of acridine orange on the growth of Escherichia coli.

Exposure of Escherichia coli to critical acridine orange (AO) concentrations did not result in loss of viability. However, the deoxyribonucleic acid (DNA) of cells exposed to such agents was rapidly degraded and repolymerized. On the other hand, a bacterium deficient in DNA repair (pol A(1) (-), lacking DNA polymerase) was sensitive to the action of AO. The DNA of such cells was also degraded but it was not repaired.