Transcranial Alternating Current Stimulation in a Patient with Ataxia-Ocular Apraxia 2: a Case Report.

Ataxia-ocular apraxia 2 (AOA2) is a rare neurodegenerative autosomal recessive disorder with no effective treatment. In this study, we present the case of a patient diagnosed with AOA2, who experienced walking instability and uncoordinated movement. The patient underwent transcranial alternating current stimulation (tACS) treatment for 4 weeks with follow-up after 1 month. The effectiveness of the treatment was evaluated using the International Cooperative Ataxia Rating Scale (ICARS), the Scale for the Assessment and Rating of Ataxia (SARA), the 9-Hole Peg Test (9HPT), and functional near-infrared spectroscopy (fNIRS). Following treatment, the patient's ataxia symptoms showed significant improvement and continued to be alleviated during the follow-up period, suggesting a lasting effect of tACS treatment. Our findings from this case study provide compelling evidence for the potential of tACS as a treatment option for AOA2.

Based on proteomics to explore the mechanism of mecobalamin promoting the repair of injured peripheral nerves.

Mecobalamin is commonly used in the adjuvant intervention of various peripheral nerve injuries. Actin cytoskeleton plays a role in the regeneration of myelin and axon. Therefore, the purpose of this study was to explore the possibility of mecobalamin regulating actin cytoskeleton in repairing nerve injury. In this study, a crush injury on the right sciatic nerve of two groups of rats (12 in each group) was established. The control group was only given normal saline (i.g.), and the intervention group was given mecobalamin 1 mg/kg (i.g.). The rats were sacrificed on 28th day and the injured nerves were collected for proteomics. The result shows that regulation of actin cytoskeleton pathway changed significantly. The expression of protein Vav1 was verified by Western blot and immunofluorescence. In the intervention group, the nerve fiber structure was complete, the axons were dense and symmetrical, and the myelin sheath was compact and uniform in thickness. The positive rate of myelin basic protein and ßⅢ-tubulin was higher than that in the control group. The findings of the study show that mecobalamin regulates the actin cytoskeleton in the repair of nerve damage and upregulates Vav1 in the regulation of actin cytoskeleton pathway.

Morphological and stage-specific transcriptome analyses reveal distinct regulatory programs underlying yam (Dioscorea alata L.) bulbil growth.

In yam (Dioscorea spp) species, bulbils at leaf axils are the most striking species-specific axillary structure and exhibit important ecological niches. Genetic regulation underlying bulbil growth remains largely unclear so far. Here, we characterize yam (Dioscorea alata L.) bulbil development using histological analysis, and perform full transcriptional profiling on key developmental stages together with phytohormone analyses. Using the stage-specific scoring algorithm, we have identified 3451 stage-specifically expressed genes that exhibit a tight link between major transcriptional changes and stages. Co-expressed gene clusters revealed an obvious over-representation of genes associated with cell division and expansion at the initiation stage of bulbils (T1). Transcriptional changes of hormone-related genes highly coincided with hormone levels, indicating that bulbil initiation and growth are coordinately controlled by multiple phytohormones. In particular, localized auxin is transiently required to trigger bulbil initiation, and be further depleted or exported from bulbils to promote growth by up-regulation of genes involved in auxinconjugation and efflux. The sharp increase in supply of sucrose and an enhanced trehalose-6-phophate pathway at T1 were observed, suggesting that sucrose probably functions as a key signal and promotes bulbil initiation. Analysis of the expression of transcription factors (TFs) predicated 149 TFs as stage-specifically expressed; several T1-specific TFs (from Aux/IAA, E2F, MYB, and bHLH families) have been shown to play key roles in triggering bulbil formation. Together, our work provides a crucial angle for in-depth understanding of the molecular programs underlying yam's unique bulbil development processes. Stage-specific gene sets can be queried to obtain key candidates regulating bulbil growth, serving as valuable resources for further functional research.

Rotenone induces nephrotoxicity in rats: oxidative damage and apoptosis.

Previous studies have examined rotenone toxicity on the human central nervous system, especially in the pathogenesis of Parkinson's disease, but few have investigated the effects of rotenone on the kidney. Here, rotenone-induced nephrotoxicity was evaluated by determining morphological, biochemical, oxidative stress-related, and apoptotic factor alterations in rat renal tissue. Morphological and biochemical analyzes showed that rotenone administration to rats damaged renal tissue. Western blot results revealed that rotenone-induced oxidative damage, causing overproduction of glutathione, malonaldehyde, and reactive oxygen species (ROS), and inhibiting superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity. Rotenone also decreased the mitochondrial membrane potential and increased voltage-dependent anion channel (VDAC), caspase-3, and caspase-9 protein levels, indicating an association of apoptosis with renal damage. Our results suggest that glutathione, malonaldehyde, and ROS may be signals of rotenone-induced oxidative damage, and that the mitochondrial pathway plays a key role in apoptosis of renal cells following rotenone administration.

IPP5 inhibits neurite growth in primary sensory neurons by maintaining TGF-ß/Smad signaling.

During nerve regeneration, neurite growth is regulated by both intrinsic molecules and extracellular factors. Here, we found that inhibitor 5 of protein phosphatase 1 (IPP5), a newly identified inhibitory subunit of protein phosphatase 1 (PP1), inhibited neurite growth in primary sensory neurons as an intrinsic regulator. IPP5 was highly expressed in the primary sensory neurons of rat dorsal root ganglion (DRG) and was downregulated after sciatic nerve axotomy. Knocking down IPP5 with specific shRNA increased the length of the longest neurite, the total neurite length and the number of neurite ends in cultured rat DRG neurons. Mutation of the PP1-docking motif K(8)IQF(11) or the PP1-inhibiting motif at Thr(34) eliminated the IPP5-induced inhibition of neurite growth. Furthermore, biochemical experiments showed that IPP5 interacted with type I transforming growth factor-ß receptor (TßRI) and PP1 and enhanced transforming growth factor-ß (TGF-ß)/Smad signaling in a PP1-dependent manner. Overexpressing IPP5 in DRG neurons aggravated TGF-ß-induced inhibition of neurite growth, which was abolished by blocking PP1 or IPP5 binding to PP1. Blockage of TGF-ß signaling with the TßRI inhibitor SB431542 or Smad2 shRNA attenuated the IPP5-induced inhibition of neurite growth. Thus, these data indicate that selectively expressed IPP5 inhibits neurite growth by maintaining TGF-ß signaling in primary sensory neurons.

Catalpol from Rehmannia glutinosa Targets Nrf2/NF-[Formula: see text]B Signaling Pathway to Improve Renal Anemia and Fibrosis.

Rehmannia glutinosa is widely recognized as a prominent medicinal herb employed by practitioners across various generations for the purpose of fortifying kidney yin. Within Rehmannia glutinosa, the compound known as catalpol (CAT) holds significant importance as a bioactive constituent. However, the protective effects of CAT on kidneys, including ameliorative effects on chronic kidney disease - most prominently renal anemia and renal fibrosis - have not been clearly defined. In this study, the kidney injury model of NRK-52E cells and C57BL/6N male mice was prepared by exposure to aristolochic acid I (AA-I), and it was discovered that CAT could ameliorate oxidative stress injury, inflammatory injury, apoptosis, renal anemia, renal fibrosis, and other renal injuries both in vivo and in vitro. Further treatment of NRK-52E cells with Nrf2 inhibitors (ML385) and activators (ML334), as well as NF-[Formula: see text]B inhibitors (PDTC), validated CAT's ability to target Nrf2 activation. Furthermore, the expression of phosphorylated NF-[Formula: see text]B p65, IL-6, and Cleaved-Caspase3 protein was inhibited. CAT also inhibited NF-[Formula: see text]B, and then inhibited the expression of IL-6, p-STAS3, TGF-[Formula: see text]1 protein. Therefore, CAT can regulate Nrf2/NF-[Formula: see text]B signaling pathway, significantly correct renal anemia and renal fibrosis, and is conducive to the preservation of renal structure and function, thus achieving a protective effect on the kidneys.

Human BDH2, an anti-apoptosis factor, is a novel poor prognostic factor for de novo cytogenetically normal acute myeloid leukemia.

BACKGROUND: The relevance of recurrent molecular abnormalities in cytogenetically normal (CN) acute myeloid leukemia (AML) was recently acknowledged by the inclusion of molecular markers such as NPM1, FLT3, and CEBPA as a complement to cytogenetic information within both the World Health Organization and the European Leukemia Net classifications. Mitochondrial metabolism is different in cancer and normal cells. A novel cytosolic type 2-hydroxybutyrate dehydrogenase, BDH2, originally named DHRS6, plays a physiological role in the cytosolic utilization of ketone bodies, which can subsequently enter mitochondria and the tricarboxylic acid cycle. Moreover, BDH2 catalyzes the production of 2, 3-DHBA during enterobactin biosynthesis and participates in 24p3 (LCN2)-mediated iron transport and apoptosis. RESULTS: We observed that BDH2 expression is an independent poor prognostic factor for CN-AML, with an anti-apoptotic role. Patients with high BDH2 expression have relatively shorter overall survival (P = 0.007) and a low complete response rate (P = 0.032). BDH2-knockdown (BDH2-KD) in THP1 and HL60 cells increased the apoptosis rate under reactive oxygen species stimulation. Decrease inducible survivin, a member of the inhibitors of apoptosis family, but not members of the Bcl-2 family, induced apoptosis via a caspase-3-independent pathway upon BDH2-KD. CONCLUSIONS: BDH2 is a novel independent poor prognostic marker for CN-AML, with the role of anti-apoptosis, through surviving.

Role of Dipeptidyl Dipeptidase 4 Inhibitors in the Management of Diabetic Foot.

Background: Patients with diabetes mellitus face difficulties in wound healing. It is important to explore therapeutic options for diabetic complications such as ulcers. This study evaluates the role of dipeptidyl dipeptidase 4 inhibitors (DPP4i) in the management of diabetic foot. Methods: Literature search was conducted in electronic databases (Google Scholar, Ovid, PubMed, Science Direct, and Springer) and studies were selected for inclusion if they reported the incidence rate of diabetic foot ulcer during DPP4i treatment or evaluated the effect of DPP4i on wound healing. Incidence rates of foot ulcer, amputation and peripheral vascular disease were pooled to achieve overall estimates. Meta-analyses of odds ratios were performed to evaluate the risk of foot ulcer, amputation, and peripheral vascular disease with DPP4i, and to examine the effect of DPP4i treatment on ulcer healing. Results: Ten studies (532354 DPP4i and 2092010 non-DPP4i treated diabetes patients) were included. Incidence rates of foot ulcer, amputation, and peripheral vascular disease were 3.80 [95% confidence interval (CI): 0.22, 7.39], 0.82 [95%CI: 0.60, 1.05], and 22.33 [95%CI: 9.14, 35.53] per 1000 person-years respectively in patients treated with DPP4i and 3.60 [95%CI: 1.77, 5.39], 0.76 [95%CI: 0.58, 0.94], and 20.9 [95%CI: 16.04, 25.81] per 1000 person-years respectively in patients treated with non-DPP4i drugs. Risk of ulcer or amputation with DPP4i was not consistent across studies. Odds of non-healing of ulcer were significantly lower with DPP4i in comparison with controls (odds ratio: 0.27 [95%CI: 0.10, 0.71]; p = 0.008). Conclusion: Incidence rates of diabetic foot and amputation are found to be similar with DPP4i and non-DPP4i drugs. DPP4i improved wound healing of diabetic foot in 3-month randomized trials.

Clinical application study of immediate implantation without bone grafting in maxillary molars: a clinical study with one-year follow up.

Our aim was to evaluate the clinical effect and feasibility of immediate implant placement combined with flap surgery with no bone grafting and non-submerged healing in the maxillary molar area. Thirty-five patients with failed single teeth in the molar area were selected. After minimally invasive extraction of the tooth, the flaps were elevated, and an implant inserted immediately; thereafter a healing abutment was connected. The mucoperiosteal flaps were sutured around the abutment without tension, and a permanent repair was performed six months later. During the study period, the implant survival rate, cone-beam computed tomography (CBCT) data, torque value, and the results of a subjective satisfaction survey conducted with a visual analogue scale (VAS), were evaluated to assess the procedure's therapeutic effect and feasibility. All 35 teeth were successfully implanted immediately after flap surgery. The mean (SD) torque value was 42.79 (5.70) N∙cm at the time of placement. During the six-month follow up and after one year of restoration, all 35 teeth showed no loosening, shedding of implants and restoration, or inflammation around the site. The mean (SD) value of the bony space around the implant immediately after the operation was 2.47 (0.56) mm. The bony spaces were filled with new bone after six months postoperatively. The mean (SD) VAS for satisfaction was 8.71 (1.05). Immediate implant placement combined with flap surgery without bone grafting and non-submerged healing is feasible for the maxillary molar area and produces a satisfactory clinical effect.

Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism.

Previous studies showed that acetyl-11-keto-beta-boswellic acid (AKBA), the active ingredient in the natural Chinese medicine Boswellia, can stimulate sciatic nerve injury repair via promoting Schwann cell proliferation. However, the underlying molecular mechanism remains poorly understood. In this study, we performed genomic sequencing in a rat model of sciatic nerve crush injury after gastric AKBA administration for 30 days. We found that the phagosome pathway was related to AKBA treatment, and brain-derived neurotrophic factor expression in the neurotrophic factor signaling pathway was also highly up-regulated. We further investigated gene and protein expression changes in the phagosome pathway and neurotrophic factor signaling pathway. Myeloperoxidase expression in the phagosome pathway was markedly decreased, and brain-derived neurotrophic factor, nerve growth factor, and nerve growth factor receptor expression levels in the neurotrophic factor signaling pathway were greatly increased. Additionally, expression levels of the inflammatory factors CD68, interleukin-1ß, pro-interleukin-1ß, and tumor necrosis factor-α were also decreased. Myelin basic protein- and ß3-tubulin-positive expression as well as the axon diameter-to-total nerve diameter ratio in the injured sciatic nerve were also increased. These findings suggest that, at the molecular level, AKBA can increase neurotrophic factor expression through inhibiting myeloperoxidase expression and reducing inflammatory reactions, which could promote myelin sheath and axon regeneration in the injured sciatic nerve.

Effects of regulatory T cells on glyceraldehyde-3-phosphate dehydrogenase vaccine efficacy against Schistosoma japonicum.

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a candidate subunit vaccine that induces protective immunity and elicits partial resistance to Schistosoma japonicum upon mouse and livestock vaccination. This study aimed to evaluate the effect of regulatory T cells (Tregs), which were defined as CD4+CD25+Foxp3+ cells, on the efficacy of a GAPDH vaccine against S. japonicum. BALB/c female mice were randomly divided into five groups as follows: normal, infected control, anti-CD25 monoclonal antibody (anti-CD25 mAb), GAPDH group, and co-treated with anti-CD25 mAb and GAPDH group. The worm reduction and liver egg reduction rates in the GAPDH group were 32.46% and 35.43%, respectively, which increased to 60.09% and 58.78%, respectively, after anti-CD25 mAb administration. Compared with those in the infected control group, the percentage of Tregs in the spleen decreased significantly when GAPDH and anti-CD25 mAb were used either alone or in combination. Furthermore, secretions associated with the Th1 response increased in splenocytes of the anti-CD25 mAb group, whereas the Th1 and Th2 responses increased in splenocytes of the GAPDH and co-treated groups. Compared to that in the infected control group, granuloma diameter in the GAPDH and co-treated groups increased slightly, but there were no significant differences among the groups. Our results indicate that the protective effect of the GAPDH vaccines can be improved by decreasing Tregs and enhancing the Th1- and Th2-type immune responses. Therefore, anti-CD25 mAb and GAPDH might exert synergistic effects to clear parasites by decreasing the frequency of Tregs and increasing the Th1- and Th2-type immune responses.

Effects of programmed cell death protein 10 on the Schistosoma japonicum female reproductive system.

This study aimed to investigate the effects of programmed cell death protein 10 (PCDP10) on the female reproductive system of Schistosoma japonicum, one of the major infectious agents of schistosomiasis. We found that PCDP10 was widely distributed in the integument, the worm parenchymal area, and the vitellarium of the female worm, but was localized to a lesser extent in the ovary and testicles. RNAi experiments successfully achieved gene knockdown, and the ultrastructural morphology of the adult reproductive organs was observed. The results demonstrated that, compared with those of the negative control group, the number of cortical granules around oocytes decreased and the number of immature oocyte cells increased. Fusion of yolk globules occurred, and the number and the diameter of yolk droplets decreased significantly. Real-time PCR showed that the expression of yolk glands reached its peak before ovulation and then decreased. The TUNEL assay results showed that apoptosis in the RNAi group was significantly higher than that in the negative control group. These results suggested that SjPCDP10 plays an important role in the female reproductive system. In conclusion, PCD10 is involved in oocyte growth and development, especially in eggshell formation, which may provide a reference for further elucidating the molecular mechanism of PCDP10 involved in egg formation and embryo development in Schistosoma japonicum.

The value of S-Detect for the differential diagnosis of breast masses on ultrasound: a systematic review and pooled meta-analysis.

AIM: To evaluate the value of S-Detect (a computer aided diagnosis system using deep learning) in breast ultrasound (US) for discriminating benign and malignant breast masses. MATERIAL AND METHODS: A literature search was performed and relevant studies using S-Detect for the differential diagnosis of breast masses were selected. The quality of included studies was assessed using a Quality Assessment of Diagnostic Accuracy Studies (QUADAS) questionnaire. Two review authors independently searched the articles and assessed the eligibility of the reports. RESULTS: A total of ten studies were included in the meta-analysis. The pooled estimates of sensitivity and specificity were 0.82 (95%CI: 0.77-0.87) and 0.86 (95%CI: 0.76-0.92), respectively. In addition, the diagnostic odds ratios, positive likelihood ratio and negative likelihood ratio were 28 (95%CI: 16- 49), 5.7 (95%CI: 3.4-9.5), and 0.21 (95%CI: 0.16-0.27), respectively. Area under the curve was 0.89 (95%CI: 0.86-0.92). No significant publication bias was observed. CONCLUSIONS: S-Detect exhibited a favourable diagnostic value in assisting physicians discriminating benign and malignant breast masses and it can be considered as a useful complement for conventional US.

Tunable single-doped single-host full-color-emitting LaAlO(3):Eu phosphor via valence state-controlled means.

A full-color-emitting phosphor of valence-varied Eu doped perovskite-type LaAlO(3) with the aid of energy transfer is demonstrated and its luminescence properties can be tuned through controllable addition of doped ions.

Guidelines and recommendations on the clinical use of shear wave elastography for evaluating thyroid nodule1.

Ultrasound elastography has been introduced into clinical practice for a decade and arisen continuous increasing attention worldwide. Shear wave elastography (SWE) is a further extension of ultrasound elastography on the basis of strain elastography, providing a two-dimensional distribution map of tissue stiffness and quantitative measurement of the tissue stiffness in Young's modulus (kPa) and/or shear wave speed (m/s). The Society of Ultrasound in Medicine, Chinese Medical Association (CMA) has recently released a series of guidelines for the use of SWE, including the technique and principle of SWE, and use of SWE in liver fibrosis, breast, thyroid, and musculoskeletal system. Herein, a part of SWE in thyroid nodules is presented. In this guideline, the background, classification and technology of SWE, examination methods, diagnostic performance, prognosis evaluation, reproducibility, and limitations are discussed and recommendations are given. The recommendations are based on the published literatures with regard to SWE with different levels of evidence, particularly a mid-term result of the prospective multi-center clinical trial of SWE in thyroid, as well as the Society of Ultrasound in Medicine, CMA expert's consensus. The document provides an overall analysis of SWE in thyroid from clinical perspective, which aimed to provide recommendations to the clinicians with regard to the management of thyroid nodules by the assistance of SWE.

Acetyl-11-keto-ß-boswellic acid extracted from Boswellia serrata promotes Schwann cell proliferation and sciatic nerve function recovery.

Frankincense can promote blood circulation. Acetyl-11-keto-ß-boswellic acid (AKBA) is a small molecule with anti-inflammatory properties that is derived from Boswellia serrata. Here, we hypothesized that it may promote regeneration of injured sciatic nerve. To address this hypothesis, we established a rat model of sciatic nerve injury using a nerve clamping method. Rats were administered AKBA once every 2 days at doses of 1.5, 3, and 6 mg/kg by intraperitoneal injection for 30 days from the 1st day after injury. Sciatic nerve function was evaluated using the sciatic functional index. Degree of muscle atrophy was measured using the triceps surae muscle Cuadros index. Neuropathological changes were observed by hematoxylin-eosin staining. Western blot analysis was used to detect expression of phospho-extracellular signal-regulated kinase 1 and 2 (p-ERK1/2) in injured nerve. S100 immunoreactivity in injured nerve was detected by immunohistochemistry. In vivo experiments showed that 3 and 6 mg/kg AKBA significantly increased sciatic nerve index, Cuadros index of triceps muscle, p-ERK1/2 expression, and S100 immunoreactivity in injured sciatic nerve of sciatic nerve injury model rats. Furthermore, for in vitro experiments, Schwann cells were treated with AKBA at 0-20 µg/mL. Proliferation of Schwann cells was detected by Cell Counting Kit-8 colorimetry assay. The results showed that 2 µg/mL AKBA is the optimal therapeutic concentration. In addition, ERK phosphorylation levels increased following 2 µg/mL AKBA treatment. In the presence of the ERK1/2 inhibitor, PD98059 (2.5 µL/mL), the AKBA-induced increase in p-ERK1/2 protein expression was partially abrogated. In conclusion, our study shows that AKBA promotes peripheral nerve regeneration with ERK protein phosphorylation playing a key role in this process.

Modulatory Potential of Curcumin and Resveratrol on p53 Post-Translational Modifications during Gastric Cancer.

The combination approach is now a well-established treatment for cancer. The present study evaluated the potential of curcumin and resveratrol on p53 post-translational modifications during gastric cancer. We segregated rats into five groups that included normal controls, dimethylhydrazine (DMH) treated, DMH + curcumin treated, DMH + resveratrol treated, and DMH + curcumin + resveratrol treated. Morphological analyses of tumor nodules confirmed carcinogenesis in rats after 25 weeks of DMH administration. The DMH treatment significantly induced carcinogenesis, as evidenced by high tumor burden in DMH-treated rats compared with controls. Moreover, DMH treatment caused a significant increase in the protein expressions of p53 as well as p53 phosphorylation in the DMH-treated rats. In addition, a significant rise was observed in 14C glucose uptake and 3H-thymidin uptakes in DMH-treated rats. Furthermore, enzyme activities of lactate dehydrogenase and alkaline phosphatase also showed a significant rise. On the contrary, significant decline was noticed in the p53 acetylation at residue 382 of DMH-treated rats. Conversely, combined treatment with curcumin and resveratrol to DMH-treated rats resulted in significant moderation in the tumor burden. In addition, a significant rise in p53 acetylation was at residue 382 of DMH-treated rats after treatment with phytochemicals. Supplementation with phytochemicals significantly modulated other biophysical and biochemical indices to near normal levels. Therefore, we conclude that curcumin and resveratrol significantly modulated p53 post-translational modifications during gastric cancer.

Dracorhodin Perchlorate Accelerates Cutaneous Wound Healing in Wistar Rats.

Dracorhodin perchlorate (DP) is extracted from Dragon's blood, which is widely used in traditional Chinese medicine, especially in wound healing. The aim of this paper is to investigate the influence of DP ointment, which contained DP dissolved in DMSO and mixed with Vaseline, on cutaneous wound healing in Wistar rats. Forty Wistar rats were divided into two groups: control and DP groups. The skin on the back of each rat was punched with two full-thickness wounds and then treated with the corresponding drug. After 3, 7, 10, 14, and 21 days, four rats were sacrificed for immunological, biochemical, and histological analyses. Compared with the control treatment, DP could significantly promote wound closure. Histological and biochemical analyses of the skin biopsies also showed that DP regulated the expression of inflammatory responses by TNF-α and IL-ß and by supporting wound tissue growth and collagen deposition. Western blot revealed that DP could also facilitate the expression of EGF and VEGF proteins. In conclusion, DP promotes wound healing.

[Correlation between hepatic immunological markers and virus genotype in patients with chronic hepatitis C].

OBJECTIVE: To investigate the hepatic expression of immunological markers relevant to a cytotoxic response in relation to viral genotype. METHODS: The frozen liver biopsies were obtained from 28 HF genotyped patients and made the sections stained. The morphometry was used to analyze the major histocompatibility complex class I (MHC-I), CD8, beta(2)-microglobulin (beta(2) -mG), HFE and CD68 in the stained sections. Biopsy data of response to therapy with interferon were available in 18 cases. RESULTS: CD8+ was usually clustered together and localized in portal tracts and sinusoids, and seen to interact with MHC I positive lining cells. MHC-I and beta(2) -mG were expressed mainly in endothelial and Kupffer cells. HFE was expressed in most round and dendritic CD68+ cells. Patients with virus genotype 3a had higher hepatic MHC-I and HFE expression, and a better sustained response to interferon (IFN) therapy than patients without. CONCLUSION: The MHC-I expression in the liver of patient with chronic hepatitis C virus infection seems to relate to viral-genotype. The hepatic MHC-I and HFE expression are higher in patients with virus genotype 3a than that in patients with non-3a genotype.

[Comparison between two methods for staining DNA of apoptotic spermatozoa].

OBJECTIVE: To compare two fluorochrome staining methods for the assessment of sperm quality. METHODS: Washed sperm cells were incubated in 0, 0.15, or 15 micromol/L camptothecin (CAM), or 0.37 or 3.7 mmol/L genistein (GEN) at 37 degrees C for 4 hours. The sperm cells were analyzed for cycle-independent apoptosis and necrosis by single-stain compared with dual-stain fluorescence microscopy to contrast the relative effectiveness of these two approaches. RESULTS: The single-stain procedure could not detect the sperm viability differences. In contrast, the dual-stain procedure identified a dosage-dependent decrease in the viability and increased necrozoospermia after topoisomerase inhibitor CAM and GEN treatments. Apoptosis was 2-fold higher with topoisomerase inhibitor treatment. CONCLUSION: The two topoisomerase inhibitors were associated with increased apoptosis and dosage-dependent necrosis. The data suggested that the dual-stain combination Hoechst 33342/PI was more sensitive than the single Hoechst 33342 stain analysis and permitted quantitative analysis of the apoptosis and necrosis in sperm.