Multifaceted complications and surgical management of bronchobiliary fistula with associated pneumonia and intrahepatic stones: A case report.

Background: Bronchobiliary fistulas (BBFs), primarily stemming from choledocholithiasis, present considerable diagnostic and treatment challenges. Their prolonged nature can lead to life-threatening situations without timely management, often complicated by lung abscesses. Case presentation: A 64-year-old man, presenting with fever, chills, and a cough initially misdiagnosed as a common cold, developed severe respiratory distress and delirium upon admission. Urgent intensive care unit (ICU) admission was prompted by a computed tomography (CT) scan revealing a right lung abscess. Enhanced CT scans and elevated bilirubin levels confirmed the biliary origin of the BBFs. Comprehensive treatment included laparoscopic partial hepatectomy, choledochojejunostomy, stone extraction, choledochoscopy, T-tube drainage, and BBFs closure. The patient was discharged with a T-tube. Follow-up CT after two months showed no recurrence. Conclusions: Managing BBFs, especially with concurrent lung abscesses in choledocholithiasis patients, remains challenging but feasible. Early diagnosis and intervention are crucial to improving survival rates and quality of life, highlighting the need for vigilance. This case underscores the importance of early detection and comprehensive treatment for successful outcomes in such complex conditions.

Aerobic granular sludge cultivated from Fe-loaded activated carbon as carrier working low-strength wastewater conditions by bioreactor.

This study proposes a new method to promote the granulation process while accelerating the degradation efficiency of nutrients. The new strategy could involve preparing Fe-loaded activated carbon (FAC) before start-up of granular cultivation and then cultivating the process of aerobic granular sludge (AGS) with such materials. In addition, this experiment could further comprehend how the preparation and characteristics of FAC affect the formation and properties of AGS. The conclusions showed that compared with the control, FAC enhanced the sedimentation performance and significant removal efficiency. Meanwhile, the values of protein (PN) and polysaccharide (PS) also increased significantly in the addition of FAC, indicating the production of substances were induced by FAC. Molecular biology methods indicated that the rapid production of granulation and removal of nutrients were considered as the abundance of various microbes and denitrifying bacteria at the addition of FAC. This research showed that the presence of FAC is a useful strategy for the initiation of sludge particle formation to promote the treatment of wastewater, containing COD and NH4+ at about 150-100 and 30 mg L-1.

Identification and characterization of nucleotide metabolism and neuroendocrine regulation-associated modification patterns in stomach adenocarcinoma with auxiliary prognostic assessment and immunotherapy response prediction.

Background: The significance of nucleotide metabolism and neuroendocrine in cellular immune response and cancer is becoming more well-established. However, the mechanisms underlying nucleotide metabolism and neuroendocrine involvement in stomach adenocarcinoma (STAD) remain unclear. Methods: First, a pan-cancer overview of nucleotide metabolism and neuroendocrine-related genes (NMNGs) was explored through the integration of expression profiles, prognostic values, mutation information, methylation levels, and pathway-regulation relationships. We next extensively assessed variations in prognosis and tumor microenvironment (TME) features across the various modification patterns, based on an extensive analysis of the NMNG modification patterns of 808 STAD samples based on 46 NMNGs. Utilizing principal component analysis methodologies, the NMNGscore was developed to measure NMNG alteration patterns of individual tumors. Results: Pan-cancer analysis shows that NMNGs mostly act as risk genes in multiple cancer types, especially in STAD. Based on the NMNGs we detected two different NMNG modification patterns in STAD. Both patterns showed distinct immune cell infiltration features and biological behavior, with NMNGcluster A exhibiting a worse prognosis and a larger amount of immune infiltration. Differentially expressed genes with prognostic relevance were used to classify the STAD samples into three genomic subgroups. Analysis of survival rates revealed that cluster B genes were associated with longer life expectancy than clusters A and C. Individual STAD patients' NMNG alteration patterns were analyzed by analyzing their NMNGscore signatures. NMNGscore and immune cells showed a statistically significant adverse correlation with each other. Increased longevity, a higher incidence of mutations, and a better response to immunotherapy were associated with patients' NMNG scores. Conclusions: Our findings provide a personalized prediction tool for prognosis and immunotherapy sensitivity in patients, as well as a promising knowledge of nucleotide metabolism and neuroendocrine in STAD.

Ecological treatment technology for agricultural non-point source pollution in remote rural areas of China.

Agricultural non-point source pollution is one of the important reasons for rural water pollution, and it is also an important source of water eutrophication. In recent years, with the rapid economic growth and social changes in rural areas, large amounts of untreated domestic sewage and agricultural wastewater entering farmland require high efficiency, low operating costs, and minimal maintenance of treatment systems in rural and remote areas to minimize their impact on water and biodiversity. Since there is little research on the ecological treatment technology of agricultural non-point source pollution in China, from the perspective of controlling agricultural non-point source pollution, some ecological treatment technologies suitable for rural areas at home and abroad are summarized. This paper introduces the practical application of ecological treatment technology, the type of process, advantages and disadvantages, and the influencing factors of ecological treatment technology in the purification of sewage engineering and summarizes the removal mechanism of pollutants in ecological treatment technology. Eco-processing technologies are cost-effective in terms of their construction, maintenance, and energy needs and can be considered a sustainable wastewater treatment method, especially in remote areas and developing countries. It provides basic ideas for the construction of rural ecological treatment technology in China and puts forward suggestions and ideas for the future development trend of ecological treatment process sewage.

Cellular glucose metabolism is essential for the reduction of cell-impermeable water-soluble tetrazolium (WST) dyes.

Water-soluble tetrazolium (WST) dyes, such as WST-1 and WST-8, are widely used in cell proliferation and anti-cell-growth drug screen assays. However, the underlying determinants for WST reduction are still largely unknown. In addition, application of tetrazolium-based assays to cellular glucose metabolism studies has not been fully explored. In the present study, we show here that WST-8 reduction is dependent on cellular glucose metabolism. In order to minimize the variance of live cell number during stimulation, we treated cells with different stimuli and performed tetrazolium-based assays within 6 hours. Withdrawal of medium glucose supply greatly attenuated WST-8 reduction but not intracellular ATP levels, while re-adding glucose reconstituted WST-8 reduction, indicating the effect was not due to cell death. The role of glucose on WST-8 reduction is specific since glutamine, fructose or galactose did not substitute for the effect of glucose on WST-8 reduction. Furthermore, inhibition of glucose transporters, intracellular glucose metabolic enzymes or EGFR-PI3K-Akt signaling also attenuated WST-8 reduction. In an attempt to screen inhibitors targeting cellular glucose metabolism from hyperglycemia-associated drugs, it turned out that HIV protease inhibitor, ritonavir, could largely block WST-8 reduction, but not cellular ATP level. Interestingly, ritonavir has been shown to acutely block glucose transport in vitro and in vivo. Taken together, our studies not only demonstrate an essential role of cellular glucose metabolism on WST-8 reduction, but also propose a novel application of tetrazolium-based assays in screening for inhibitors of cellular glucose metabolism when used in combination with ATP assay.

Chemical and genetic inhibition of STAT3 sensitizes hepatocellular carcinoma cells to sorafenib induced cell death.

Hepatocellular carcinoma (HCC) has become the second leading cause of cancer related death, with an increasing death rate in recent years. For advanced HCC, sorafenib is the first-line FDA approved drug, with no more than 3 months' overall survival advantage. Recently, a novel strategy has been proposed to improve sorafenib efficacy through enhancing the ability of sorafenib to induce cell death. STAT3 plays a key role in cancer development and recurrence by promoting cell proliferation, survival and immune evasion through its well-established function as a transcription factor in cancer. Notably, STAT3 transcription activity, indicated by its phosphorylation on Y705 is heterogeneous in different liver cancer cell lines. And sorafenib attenuates STAT3 phosphorylation on Y705. However, the role of STAT3 in sorafenib induced cell death is still largely unknown. Here, we show that liver cancer cells also exhibit heterogeneous sensitivities to sorafenib induced cell death, which co-relates with the STAT3-Y705 phosphorylation levels and JAK1/2 expression levels in Hep3B, Huh7 and HepG2 cells. Furthermore, overexpression or knockdown of STAT3 could switch HCC cells between resistant and sensitive to sorafenib induced cell death, which could be partially due to its regulation on Mcl-1, an anti-apoptotic protein. Finally, both inhibitors of STAT3 SH2 domain (S3i-201) or STAT3 upstream kinases JAKs (JAK inhibitor I) could synergistically enhance sorafenib induced cell death. Taken together, these data strongly suggest that STAT3 is not only a downstream effector of sorafenib, but also a key regulator of cellular sensitivity to sorafenib induced cell death, which provide support for the notion to develop STAT3-targeting drugs to improve clinical efficacy of sorafenib in liver cancer.

GOLPH2, a gene downstream of ras signaling, promotes the progression of pancreatic ductal adenocarcinoma.

Various studies have previously demonstrated that Golgi protein-73 (GOLPH2) is overexpressed in tumorigenesis, which has been observed in hepatocellular carcinoma and prostate cancer. However, the expression levels and specific functions of GOLPH2 in the progression of pancreatic cancer remain to be elucidated. The present study aimed to investigate the expression of GOLPH2 in pancreatic ductal adenocarcinoma (PDAC) tissues and examined the effects of GOLPH2 on the growth and migration of pancreatic cancer cells. In the present study, the mRNA levels of GOLPH2 in PDAC cancer tissues were examined using RT­qPCR. The effects of GOLPH2 on the growth and migration of cancer cells were examined using crystal violet and Boyden chamber assays. The study demonstrated that the expression of GOLPH2 mRNA and protein was elevated in PDAC clinical tissues. The growth and motility of the PDAC cells was enhanced following overexpression of GOLPH2, whereas downregulating the expression of GOLPH2 impaired the growth, motility and tumorigenesis. Furthermore, GOLPH2 was observed to interact with protein kinase B (Akt), which subsequently increased the activity of Akt. In addition, GOLPH2 was revealed as a downstream gene of Ras signaling and promoted the transformation of normal pancreatic cells. The results of the present study revealed the important functions of GOLPH2 in PDAC, and suggest that GOLPH2 may act as a promising therapeutic target for the treatment of PDAC in the future.

Ubiquitin-Specific Protease USP6 Regulates the Stability of the c-Jun Protein.

The c-Jun gene encodes a transcription factor that has been implicated in many physiological and pathological processes. c-Jun is a highly unstable protein that is degraded through a ubiquitination/proteasome-dependent mechanism. However, the deubiquitinating enzyme (DUB) that regulates the stability of the c-Jun protein requires further investigation. Here, by screening a DUB expression library, we identified ubiquitin-specific protease 6 (USP6) and showed that it regulates the stability of the c-Jun protein in a manner depending on its enzyme activity. USP6 interacts with c-Jun and antagonizes its ubiquitination. USP6 overexpression upregulates the activity of the downstream signaling pathway mediated by c-Jun/AP-1 and promotes cell invasion. Moreover, many aberrant genes that are upregulated in USP6 translocated nodular fasciitis are great potential targets regulated by c-Jun. Based on our data, USP6 is an enzyme that deubiquitinates c-Jun and regulates its downstream cellular functions.

Construction and Identification of the RNAi Recombinant Lentiviral Vector Targeting Human DEPDC7 Gene.

Human DEP domain containing 7 (DEPDC7) gene was originally found expressing high in liver tissue and low in most other tissues, but its function was largely unknown. In this study, we construct an RNA interference (RNAi) recombinant lentiviral vector particle targeting DEPDC7 in order to knockdown its gene expression in human hepatocellular carcinoma cell line HepG2. We screened three RNAi sequences targeting DEPDC7 and a scramble sequence by the aid of short hairpin RNAs (shRNA) design tools. Then, these sequences were separately cloned into the pLV-H1-EF1α-puro vector to construct four lentiviral vectors (pshRNA-DEPDC7-NC, pshRNA-DEPDC7-RNAi1, pshRNA-DEPDC7-RNAi2 and pshRNA-DEPDC7-RNAi3). All of the recombinant plasmids were identified and confirmed by double digestion and DNA sequencing. After infecting HepG2 cells, the DEPDC7 mRNA and protein expression levels were examined by real-time PCR and western blot, respectively, and the gene expression was significantly down-regulated at both levels (P < 0.01). Cell motility and invasiveness were detected by Matrigel migration and invasion assay, and the results revealed that migration and invasion of HepG2 cells were significantly increased (P < 0.05). Our study showed successful construction of three lentiviral RNAi vectors targeting DEPDC7 gene and shRNA-mediated knockdown of DEPDC7 enable promotion of cell migration and invasion.

DEPDC7 inhibits cell proliferation, migration and invasion in hepatoma cells.

DEP Domain Containing 7 (DEPDC7) is highly and specifically expressed in normal liver tissue, belonging to the class of genes of liver-selective cell communication. Although the function of DEPDC7 remains poorly understood, its expression is decreased in liver cancer compared with normal liver tissues. It has previously been demonstrated that knockdown of DEPDC7 promotes cell growth, S phase entry and cell mobility and invasion in HepG2 cells. In the present study, it was shown that DEPDC7 expression is downregulated in four hepatoma cell lines (SMMC-7721, Huh-7, SK-Hep-1 and HepG2) and 48 hepatoma tissues, determined using western blot and immunohistochemical analysis. When DEPDC7 is overexpressed in hepatoma cell lines (SK-Hep-1 and Huh-7), it inhibits cell proliferation and cell growth; inhibits cell cycle entry; and inhibits cell motility and invasion. These results, together with the results of knockdown experiments, demonstrate that DEPDC7 may have an important role in hepatoma cells growth and metastasis and suggest it could be a therapeutic target; however, in vitro studies are required to validate this hypothesis.

Rheb phosphorylation is involved in p38-regulated/activated protein kinase-mediated tumor suppression in liver cancer.

Ras homolog enriched in brain (Rheb) is a key regulator of mammalian target of rapamycin complex 1 (mTORC1). The Rheb-mTORC1 axis is a pivotal pathway that mediates cell growth. It was previously reported that upon energy-stress stimulation, the phosphorylation of Rheb at serine 130 by p38-regulated/activated protein kinase (PRAK) results in the impaired nucleotide binding ability of Rheb and inhibits Rheb-mediated mTORC1 activation. However, the role of Rheb phosphorylation in cancer development remains to be elucidated. The aim of the present study was to determine the effect of Rheb phosphorylation on tumor growth in vitro and in vivo. In addition, tissue samples were obtained from 70 hepatocellular carcinoma (HCC) patients in order to determine any associations between Rheb phosphorylation and the clinicopathological characteristics of patients. In vitro and ex vivo kinase assays were performed to determine the phosphorylation of Rheb by PRAK. A xenograft assay was performed to assess tumorigenicity of MEF cell lines. In addition, western blot and immunohistochemical analyses were performed to detect Rheb protein expression and phosphorylation. The results of the present study revealed that Rheb phosphorylation may be induced through Ras overexpression. In addition, kinase-dead PRAK and dominant-negative PRAK mutation were demonstrated to abolish the Rheb phosphorylation induced by Ras overexpression. Xenograft assays in nude mice revealed that Rheb phosphorylation was involved in PRAK-mediated tumor suppression. Of note, the clinicopathological analysis of 70 HCC samples determined that Rheb phosphorylation was associated with poor proliferation and the progression of HCC. In conclusion, the results of the present study suggested that Rheb phosphorylation may have an important role as an intracellular barrier to cancer development.

Recognition of cytosolic DNA attenuates glucose metabolism and induces AMPK mediated energy stress response.

Both viral infection and DNA transfection expose single-stranded or double-stranded DNA to the cytoplasm of mammalian cells. Recognition of cytosolic DNA activates a series of cellular responses, including induction of pro-inflammatory genes such as type I interferon through the well-known cGAS-STING pathway. Here we show for the first time that intracellular administration of either single or double stranded interferon stimulating DNA (ISD), but not poly(dA) suppresses cell growth in many different cell types. Suppression of cell growth by cytosolic DNA is cGAS/STING independent and associated with inhibition of glucose metabolism, ATP depletion and subsequent cellular energy stress responses including activation of AMPK and inactivation of mTORC1. Our results suggest that in concert with but independent of innate immune response, recognition of cytosolic DNA induced cellular energy stress potentially functions as a metabolic barrier to viral replication.

A novel canine model of portal vein stenosis plus thioacetamide administration-induced cirrhotic portal hypertension with hypersplenism.

Current large animal models that could closely resemble the typical features of cirrhotic portal hypertension in human have not been well established. Thus, we aimed to develop and describe a reliable and reproducible canine cirrhosis model of portal hypertension. A total of 30 mongrel dogs were randomly divided into four groups: 1 (control; n = 5), 2 (portal vein stenosis [PVS]; n = 5], 3 (thioacetamide [TAA]; n = 5), and 4 (PVS plus TAA; n = 15). After 4-months modeling period, liver and spleen CT perfusion, abdominal CT scans, portal hemodynamics, gastroscopy, hepatic function, blood routine, the bone marrow, liver, and spleen histology were studied. The animals in group 2 (PVS) developed extrahepatic portosystemic collateral circulation, particularly esophageal varices, without hepatic cirrhosis and portal hypertension. Animals from group 3 (TAA) presented mild cirrhosis and portal hypertension without significant symptoms of esophageal varices and hypersplenism. In contrast, animals from group 4 (PVS + TAA) showed well-developed micronodular and macronodular cirrhosis, associated with significant portal hypertension and hypersplenism. The combination of PVS and TAA represents a novel, reliable, and reproducible canine cirrhosis model of portal hypertension, which is associated with the typical characteristics of portal hypertension, including hypersplenism.

Implementation of a fast-track clinical pathway decreases postoperative length of stay and hospital charges for liver resection.

A fast-track clinical pathway is designed to streamline patient care delivery and maximize cost effectiveness. It has decreased postoperative length of stay (LOS) and hospital charges for many surgical procedures. However, data on clinical pathways after liver surgery are sparse. This study examined whether use of a fast-track clinical pathway for patients undergoing elective liver resection affected postoperative LOS and hospital charges. A fast-track clinical pathway was developed and implemented by a multidisciplinary team for patients undergoing liver resection. Between July, 2007 and May, 2008, a total of 117 patients underwent elective liver resection: the fast-track clinical pathway (education of patients and families, earlier oral feeding, earlier discontinuation of intravenous fluid, no drains or nasogastric tubes, early ambulation, use of a urinary catheter for less than 24 h and planned discharge 6 days after surgery) was studied prospectively in 56 patients (postpathway group). These patients were compared with the remainder who had usual care (prepathway group). Outcome measures were postoperative LOS, perioperative hospital charges, intraoperative and postoperative complications, mortality, and readmission rate. Among all patients, 69 (59%) had complicating diseases and/or a history of surgery and 24 patients belonged to American Society of Anesthesiologists grade III-IV. Compared with the prepathway group, the postpathway group had a significantly shorter postoperative LOS (7 vs. 11 days, P < 0.01). The average perioperative hospital charges were RMB 26,626 for patients in the prepathway group and only RMB 21,004 for those in the postpathway group (P < 0.05), with no differences in intraoperative and postoperative complications (P = 0.814), mortality (P = 0.606), and readmission rate (P = 0.424). Implementation of the fast-track clinical pathway is an effective and safe method for reducing postoperative LOS and hospital charges for high-risk patients undergoing elective liver resection. The result supports the further development of fast-track clinical pathways for liver surgical procedures.

An aggressive approach leads to improved survival in hepatocellular carcinoma patients with portal vein tumor thrombus.

PURPOSE: Many physicians express a relatively nihilistic approach to the treatment of hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT). Consensus among surgeons regarding the indications for an aggressive approach has not been reached. Current study was aimed to determine whether an aggressive approach, with an extended resection with thrombectomy and adjuvant therapy, would lead to an improved survival for HCC patients with PVTT. METHODS: A retrospective review of 116 HCC patients with PVTT admitted from 1996 to 2006 was conducted. Patients were divided into 2 time-period (TP) cohorts, of them, 51 cases in the first 5 years (TP1) and 65 in the last 5 years (TP2). RESULTS: Surgical operations were performed on 68 patients. Twenty-one surgical resections were performed in TP1 and forty-seven in TP2. The extent of liver resections, as well as the frequency of thrombectomy, was greater in TP2 (P = 0.039). During both time-periods, an aggressive therapy was associated with improved survival (P < 0.02 TP1, P < 0.001 TP2). Overall survival of all patients in TP2 was significantly greater than in TP1 (P < 0.001), with a median survival of 15 months in TP2, whereas in TP1, the survival was only 9 months. The median 1-, 3-year survivals in TP2 (54 and 34%, respectively) were also greater than that in TP1 (31 and 7%, respectively). A multiple logistic regression analysis revealed that radical resection and adjuvant therapy were the independent predictors of overall survival. CONCLUSIONS: An aggressive approach, combining extended liver resection with thrombectomy and adjuvant therapy, leads to an improved survival in the HCC patients with PVTT.

A canine portal hypertension model induced by intra-portal administration of Sephadex microsphere.

BACKGROUND AND AIM: Big animal models of portal hypertension are important for the research into this disease. The aim of this study was to establish a canine portal hypertension model by intra-portal administration of microspheres. METHODS: Sixteen mongrel dogs were assigned to control group and experimental group randomly. The catheterization of portal vein was performed by laparotomy and the outer end of the catheter was fixed subcutaneously in the abdominal wall. The dogs of the experimental group were given intra-portal injections of microspheres at a five-day interval, six times in total. Portal hemodynamics, blood cell counting, liver and renal function test, portography, gastroscopy, liver, spleen and lung histological examination were taken to evaluate the model. RESULTS: 1, 2, 3 and 4 months after initial injection of microspheres, portal venous pressure rose from baseline 8.7 +/- 0.7 mmHg to 24.3 +/- 1.6, 20.6 +/- 2.1, 19.0 +/- 1.8 and 17.7 +/- 2.0 mmHg, respectively (P < 0.01). The diameter of portal vein increased from 7.6 +/- 0.3 to 8.6 +/- 0.3 mm, calculated portal resistance increased from 0.46 +/- 0.06 to 1.06 +/- 0.20 (mmHg/mL/min/kg body weight); velocity of portal blood flow decreased from 35.1 +/- 1.7 to 26.1 +/- 2.4 cm/s (P < 0.01, respectively). The animals of experimental group developed marked splenomegaly and profuse portosystemic collateral circulations with normal liver and renal function. CONCLUSION: Repeated intra-portal administration of microspheres can induce stable and reproducible chronic portal hypertension in dogs with normal liver and renal functions. This model can meet multiple demands of both basic and clinical research of portal hypertension.

Luteinizing hormone receptor deficiency increases the susceptibility to alkylating agent-induced lymphomagenesis in mice.

Previous studies have revealed a close link between luteinizing hormone (LH)/human chorionic gonadotropin (hCG) signaling and oncogenesis in gonadal and nongonadal tissues. To investigate whether genetic ablation of LH receptor (Lhr) affects the animal's oncogenic susceptibility, adult female wild-type (wt), heterozygous, and homozygous Lhr knockout (LhrKO) mice were intraperitoneally injected with an alkylating agent, N-methyl-N-nitrosourea (MNU, 50 mg/kg of body weight). The mice were sacrificed when they were short of breath or 10 months after the injection. The results showed that MNU induced non-Hodgkin's thymic and lymphonodus lymphomas in 70.6% and 100% of heterozygous and homozygous animals, respectively, compared with 35.7% in wt siblings. The tumor development was rapid; they were more aggressive and metastasized to the spleen, liver, and kidney in Lhr-deficient mice compared to wt siblings. All tumors were immunostained-positive for a T-cell specific marker, CD3, but not for a B-cell marker, CD22, suggesting that all the lymphomas arose from T-cells, which are known to be LH/hCG receptor-positive. There was no rearrangement of the Lhr gene locus or differences in thymic cell proliferation among the genotypes. However, apoptosis was lower in the Lhr-deficient thymuses. The thymic Bcl-2 levels were elevated and caspase-3 activation was reduced in Lhr heterozygous and homozygous animals. In conclusion, MNU induced a higher incidence and an earlier onset of aggressive lymphomas in LhrKO animals, which may be associated with a reduction in apoptosis of thymocytes.

Circulating erythroblasts in maternal blood are not elevated before onset of preterm labor.

OBJECTIVE: Preterm labor has recently been reported to be associated with an increased release of cell free fetal deoxyribonucleic acid (DNA) into the maternal circulation. We have previously observed increases in both fetal cell traffic and cell free fetal DNA in preeclamptic pregnancies. In this study, we investigated whether fetal cell traffic is also disturbed in pregnancies with preterm labor. METHODS: In a case-control study, we examined 47 pregnancies complicated by preterm contractions that occurred between 20 and 34 weeks' gestation and an equal number of matched controls. Erythroblasts were enriched for by magnetic cell sorting and enumerated. These values were then correlated with subsequent pregnancy outcome. RESULTS: In the study group 16 patients delivered prematurely (subgroup A). The other 31 (subgroup B) delivered at term, as did all those in the control group. No significant difference was noted in erythroblast numbers between either one of the subgroups and the controls. CONCLUSION: Contrary to the reported increased levels of free fetal DNA in maternal serum, erythroblasts in maternal blood are not elevated significantly in pregnancies with threatened premature labor or in those that deliver preterm.